CVS - Clinical/Cardiology

Drbeen Question (4001)

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A 42 years old patient presents to your clinic for a complete physical because he recently moved here from another state. He feels in good health. He has never smoked, doesn’t have diabetes, and is sure that he does not have hypertension either. He exercises regularly and eats a healthy diet.

On physical examination, you notice a slow rising pulse. His apical beat is displaced to left 6th intercostal space in the mid-axillary line. A harsh mid-systolic murmur is heard best on the right 2nd intercostal space. You notice that the murmur is radiating towards the carotids. Murmur intensity decreases with Valsalva maneuver and increases with squatting. What is the most probable diagnosis in this patient?

A. Aortic stenosis.
B. Pulmonary valve stenosis.
C. Ventricular septal defect.
D. Patent foramen ovale.
E. Hypertrophic obstructive cardiomyopathy (HOCM).


Reference ID: 4001

Check the answer here:

CVS - Clinical/Cardiology

Answer to the Drbeen’s Question 4001

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 Read the question here:


The correct answer is A.


Note the location of the auscultation point for the aorta (A) in this diagram before reading the explanation.


Patient has aortic stenosis. Aortic stenosis murmur is the best heard at the 2nd intercostal on the right side. Murmur radiates to carotids. Usually associated with ventricular hypertrophy which causes the apical beat to displace to the mid-axillary line at the 6th intercostal space on the left. There often is a systolic thrill as well.

This murmur is similar to the murmur in HOCM. However, their intensity profiles are opposite to each other. In aortic stenosis, Valsalva’s maneuver reduces the venous return which reduces the ejecting blood. The reduced outflow of blood, in turn, results in the reduced murmur intensity. Similarly, squatting increases the venous blood return, increasing the pre-load. Increased pre-load, in turn, increases the amount of blood ejecting through the aortic valve which results in higher murmur intensity. In HOCM opposite occurs. Reduced pre-load causes the obstruction to increase because of smaller chamber size which increases the murmur intensity. Increased pre-load dilates the chamber offering a wider opening for the ejecting blood, and results in the reduced intensity of the murmur.

B is incorrect. Pulmonary valve stenosis is best heard at the second intercostal space on the left side of the sternum.

C is incorrect as the ventricular septal defect is best heard at the 5th intercostal space on the left side of the sternum. It is also a holosystolic murmur.

D is incorrect because the patent foramen ovale (PFO) does not cause a murmur. Remember, on the other hand; a VSD does cause a murmur.

E is incorrect, see the answer for A for more information.


EKG – difference between MAT and PAT

MAT stands for multifocal atrial tachycardia.

PAT stands for Paroxysmal atrial tachycardia.
A student going through drbeen’s EKG interpretation lectuers asked us the difference between MAT (multifocal atrial tachycardia) and PAT (paroxysmal atrial tachycardia).

Here is a quick summary of the differences:

  1.  PAT is usually an extra focus/reentrant circuit in the atria. It is similar in pathology to PSVT but the location could be anywhere instead of near the coronary sinus (study our lecture on atrial flutter.) Due to the focus being away from the SA node, the P wave’s shape can be different but consistent. Usually, there also is a warm-up and cooling-down period.
  2. MAT is due to many reentrant circuits (but not as many as in the atrial fibrillation). Because of multiple foci present in many locations in the atria, you will find P waves of many shapes. To diagnose a MAT you must identify three different shapes of the P waves in the EKG.

One more difference of the MAT and PAT from the PSVT is that carotid massage does not affect the heart rate in these conditions. Note: study our fibrillation lecture to understand why it is difficult to cure arrhythmia due to reentrant circuits. (Hint: structural changes.)

MAT and PAT both have the common presentation of 100 to 200 bpm heart rate.

Visit for more lectures:

CVS - Clinical/Cardiology

Congestive Heart Failure (Part 3. Management)

Following 4 phases of heart failure must be in your mind when managing heart failure patients.

  • Chronic heart failure with reduced ejection fraction (HFrEF).
  • Heart failure with preserved ejection fraction (HFpEF).
  • Acute decompensated heart failure (ADHF).
  • Advanced heart failure.

General principles of treatment for heart failure

  1. Relieve symptoms.
  2. Improve functional status.
  3. Prevent (re)hospitalization.
  4. Prevent death.


General algorithm is following (each patient needs to be considered separately)

(See the typed out drug classes below the algorithm.)


  • ACE Inhibitors or ARBs (consider H-ISDN if the patient cannot tolerate either of these drug classes.)
  • MR Antagonists (anti-mineralocorticoids.)
  • Ivabradine
  • Digoxin and/or H-ISDN (Hydralazine/Isosorbide Dinitrate)
  • LVAD (Left ventricular assist device.)
Diuretics should be used to reduce the symtpoms of the congestion. They have, however, not shown to reduce rehospitalization of death.
ACEI/ARBs: titrate to evidence base dose or maximum tolerated dose below the evidence base dose.
Asymptomatic patient with LVEF =< 35% should be considred for ICD.
If MC receptor antagonist is not tolerated then an ARB can be added to ACEI.
European Medicine Agency has approved the use of Ivabradine in patients with heart rate >= 75 bpm.
CRT-P/CRT-D indication can vary depending upon the NYHA class, heart rhythm, QRS duration and morphology and LVEF.

Reference: Current Medical Diagnosis and Treatment 2016

Managing Heart Failure with Preserved Ejection Fraction (HFpEF)

Targets of the therapy are to reduce congestion, controlling the blood pressure, stabilizing the heart rate and improving exercise tolerance.


Clinical Pearls

Secondarily, managing sleep disorder and evaluation and correction of the ischemic heart disease are very important.

Excessive reduction in preload can cause underfilling of the heart leading to syncope.

Managing Heart Failure with Reduced Ejection Fraction (HFrEF)

Neurohormonal Antagonists

ACEI have shown to reduce mortality by 23% and 35% reduction in combined mortality and rehospitalization.

ACEI and ARBs have shown to safer when treating patients with renal insufficiency and tolerability in patients on beta blockers due to diabetes, asthma, and COPD.


Aldosterone antagonists are shown to reduce mortality in all stages of the HF.

Eplerenone and spironolactone are observed to reduce mortality, rehospitalization and a significant reduction in sudden cardiac death.

Hyperkalemia and renal function deterioration must be kept in mind for patient with chronic kidney disease. Monitor renal function and potassium levels.

Atriovenous vasodilation

H-ISD (Hydralazine and Isosorbide Dinitrates) are shown to improve survival. This combination is not as significant as ACEI/ARBs, however, H-ISD can be used when a patient cannot tolerate ACEI or ARBs.

Heart Rate Modification

Ivabradine (Ivf channel inhibitor) slows heart rate without reducing the strength of pumping (no negative inotropic effect.)


Digitalis Glycosides are mild inotropes, sympathoinhibitor, and blunt the carotid sinus baroreceptor activity.

Studies show that digoxin can reduce the hospitalization in heart failure patients but does not reduce mortality or improve the quality of life. This drug should be used when nuerohormonal therapies are not working.

In low doses, digoxin can help achieve treatment goals. However, higher doses can be counterproductive.

Oral Diuretics

Loop diuretics may be required to counter the neurohormonal activation in heart failure patients. Dose adjustment is important. Usual need to use diuretics is to achieve volume control and then use neurohormonal therapy.

Additional Considerations

Inflammation control is needed.

Statins to reduce cardiovascular events and to improve survival.

Anticoagulants and Antiplatelet are administered as the HFrEF is associated with hypercoagulability states. Warfarin and Aspirin both have their own pros and cons. Current guidelines support the use of Aspirin in patients with ischemic cardiomyopathy.

Fish Oil can have modest improvement of the clinical outcomes.

Micronutrients are shown to be associated with heart failure. Reversible heart failure is observed with the deficiency of thiamine and selenium.

Enhanced External Counterpulsation (EECP) it is proposed that peripheral lower extremity therapy using graded pneumatic external compression maybe beneficial.

Exercise has shown to be safe, improves patients’ sense of well being and reduced mortality.

Sleep disorder breathing should be corrected.

Anemia is common in the HF patients.

Manage depression

Atrial Arrhythmias should be managed therapeutically or with external devices.

Managing Acute Decompensated Heart Failure (ADHF)


In the hospital

Intravenous diuretics to rapidly manage the symptoms of congestion.

Start with loop diuretics. Thiazide diuretics (metolazone) combined with the loop diuretics when patient is on long-term diuretic therapy.

Weight change is a subjective metric.

Continue diuresis until euvolemia is achieved.

Cardiorenal Syndrome

This generally means the deterioration of heart when kidneys are managed or the deterioration of the kidney when heart is managed.

Possible inotropic therapy assisted circulation or cardiac transplant may be needed in the end stage disease.


Invasive fluid removal with diuretics. Proposed benefit of this is to remove neutral fluids (less ionic imbalances compared to renal excretion.)

Vascular Therapy

Vasodilators (nitroprusside) can be used to attempt to stabilize ADHF.

Inotropic Therapy

Therapeutic agents that increase the intracellular concentration of cyclic adenosine monophosphate (cAMP) are beneficial. Sympathetic amines (dobutamine) and phophodiesterawse-3 inhibitors (milrinone) can be positive inotropes used.


CVS Hemodynamics

Pulmonary Circuit

Properties of Pulmonary Circuit

The heart pumps a volume of blood into the lungs which after getting oxygenated is transported back to heart. This oxygenated blood is then pumped out of the heart and into the aorta and subsequently into the systemic circulation. As a consequence, at any given time the lungs (pulmonary vasculature) contain around 500ml of blood, thereby allowing them to function as a reservoir of the blood. This reservoir volume is increased by another 500 ml when the person is in the supine or lying down position. This is because in supine position there’s an increased venous return (due to the effect of gravity) to the right heart from the peripheries and therefore more blood accumulates in the central parts of body. Upon standing up, this extra 500ml of blood gets redistributed under the effect of gravity, to the now more dependent parts of the body which includes the peripheral tissues and the lower extremities.

The division of vasculature in the pulmonary circuit is somewhat different from that in the systemic circulation. The arteries in the pulmonary circuit divide in a binary fashion, thereby following the pattern of division of the airways. The veins too exhibit a pattern similar to the arterioles and the bronchioles, thereby finally converging into forming one large pulmonary vein. These pulmonary veins transport the oxygenated blood back to the heart.

The primary function of lungs to deliver oxygenated blood to the heart.

Apart from the primary function of lungs to deliver oxygenated blood to the heart, it has following secondary functions.


Pulmonary vascular bed acts as a filter for the blood received by the right side of the heart and before this blood leaves the left side of the heart to enter the systemic circulation. Blood arriving from the right side of the heart to the lungs may contain an embolus or a thrombus or any foreign particle that may result in obstruction of the vessels. The pulmonary artery divides into numerous small capillaries with diameters too small to allow passage of any dislodged particles into the pulmonary artery and subsequently in to the left side of the heart. Therefore, the pulmonary vascular bed acts as a filtration barrier that prevents introduction of any particles into the systemic circulation.

Metabolic Functions

The pulmonary vasculature also has some metabolic functions:

  1. The endothelium of the pulmonary vessels is lined by fibrinolytic enzymes that cause lysis of the fibrin clots which get stuck in the pulmonary vasculature.
  2. The pulmonary capillary endothelium is lined by another enzyme as well. This enzyme is called the Angiotensin Converting Enzyme (ACE). The function of ACE is to covert Angiotensin I to Angiotensin II. ACE is also present in the endothelium of other vascular beds and the plasma, however, the amount present in the pulmonary vascular bed is the highest. ACE within the pulmonary vascular bed is responsible for more than 70% of the total conversion of Angiotensin I to Angiotensin II in the body.
CVS Hemodynamics

Control of the Coronary Blood Flow

Coronary Circulation

The coronary vasculature supplies blood to the muscles of the heart (myocardium). These coronary arteries are the first branches (right & left coronary arteries) that arise from the aorta, and they run on the surface of the heart’s muscle. Branches from the arteries penetrate the muscle in order to supply blood to deeper myocardial tissues. When the heart contracts during systole, the small arteries that are embedded deeply within the heart musculature are also squeezed along with the heart. This mechanical compression of coronary arteries causes a brief period of occlusion of coronary blood flow during systole. The whole body receives oxygenated blood during systole except for the heart itself. The heart will be supplied with the oxygenated blood when the atria and ventricles are in a relaxed state which happens during diastole. At that time, the coronary vasculature is not compressed and the perfusion is at a maximum. The right heart muscles contract with lesser force compared to the left heart. Hence, a relatively small amount of perfusion is maintained in the right heart even during systole.

Even under normal resting conditions, the heart tissue extracts 80% of the total oxygen content from the blood that is supplied to it.

This high extraction of oxygen is necessary to meet the demands of highly active muscles of the heart. The demand for oxygen is increased substantially when there is an increase in the heart rate, as happens during exercise.

Compared to the cardiac muscle, the skeletal muscle extracts only 20% of oxygen from the blood at normal resting conditions.

In other tissues, when oxygen demand increases, vasodilatory metabolites such as H+ ions and carbon dioxide cause a rightward shift of the oxygen dissociation curve. This allows greater dissociation of oxygen from the hemoglobin. However, this rightward shift of the hemoglobin oxygen dissociation curve is not valid for the blood in the coronary circulation. This is because the extraction of oxygen by heart tissue is already at maximum level even under normal resting conditions. Therefore, the increased demand for oxygen during exercise can only be compensated by increasing the blood flow rate of the coronary circulation.


Auto-regulation of Coronary circulation

The flow of coronary vasculature is under the influence of both intrinsic and extrinsic mechanisms. The extrinsic mechanisms include the sympathetic and parasympathetic nervous systems.


Parasympathetic nervous system

The parasympathetic nervous system input is relayed by the right and left vagus nerves. Right vagus nerve innervates the Sinoatrial node, while the left vagus nerve innervates the AV node. The parasympathetic nervous system regulates the blood flow indirectly by controlling the heart rate (chronotropy) and the force of contraction (inotropy).


 Sympathetic nervous system

The sympathetic nervous system innervates the SA node & AV node, the myocardium and the vascular smooth muscle of coronary vessels. Hence, sympathetic nervous system regulates the heart rate, force of contraction of ventricular myocardium and the flow into the coronary vasculature. However, the extrinsic mechanisms involved in vascular diameter changes are ineffective during physiological conditions. Although there is sympathetic stimulation on the vascular smooth muscles, the effects are negated by the constant release of nitric oxide from the endothelium. If this nitric oxide release is blocked by an atherosclerotic plaque, the unchecked sympathetic stimulation causes vasoconstriction leading to the pain of angina. Atherosclerosis decreases coronary perfusion by reducing the coronary artery lumen and also by blocking the release of NO from the coronary artery endothelium.


Under physiological conditions, the metabolism induced changes in vascular caliber are more prominent. The metabolites produced by the heart tissue responsible for vasodilation are:

  • H+ ions
  • K+ ions
  • Adenosine
  • Bradykinin and Prostaglandins

Volume – Work Relationship

There is a direct relationship between the volume of blood entering the heart (preload) and the work done by the heart to pump it out. The pressure remains the same as there is no change in myocardial contractility or afterload.

This can be observed when a person is exercising during which the volume of blood returning to the heart increases.

Pressure – Work Relationship

There is a direct relationship between the pressure developed in the peripheral vasculature and the work done by the heart against it. The demand for oxygen in pressure overload situations is higher than in volume overload.

Patients with atherosclerosis show this kind of pressure – work relationship in their cardiovascular system.

CVS Hemodynamics

Blood Pressure Control By Baroreceptors

Mean Arterial Pressure

The mean arterial pressure (MAP), also considered as the perfusion pressure, is taken as the pressure difference between the arteries and the veins. The regulation of blood pressure is done in order to maintain the MAP.

The MAP dictates the amount of oxygen and nutrients that is supplied by the blood vessels and the waste that is carried away from the tissues.

Regulation Of Blood Pressure

The body has the ability to counteract long term as well as short term changes in blood pressure. The long term pressure changes cause the body to respond through the activation of renin-angiotensin system.

Rapid/short term changes in blood pressure compel the body to activate the following receptors:

  • Baroreceptors are present on the arch of aorta and carotid sinus
  • Chemoreceptors are present in the carotid sinuses, arch of aorta and medulla oblongata
  • Atrial receptors are present on the wall of right atrium


The baroreceptors are the pressure sensing bodies. They are also called stretch receptors.They are modified nerve endings attached to the cytoskeleton present within the nerve endings. The receptors  are sensitive to rapid offsets in blood pressure. The baroreceptors are densely situated on the walls of the arch of aorta and the carotid sinus. The carotid sinus is present on the base of internal carotid artery at the level of bifurcation of the common carotid artery. The sinus area is slightly dilated as the tunica media which is normally comprised of muscles, is relatively thin. The tunica adventitia, on the other hand, is thicker than usual. This is the layer of the blood vessels where the nerve receptors are situated. Same is true for the location of baroreceptors on the arch of aorta.

Rapid offsets in pressure can occur, for example, in a previously standing person who suddenly sits down. During the process, a large volume of blood is shifted from the peripheral to the central regions of the body. Consequently, a large volume of blood enters the heart and this volume overload or increased preload causes the heart to increase its cardiac output. A simultaneous increase in blood pressure will also be observed with increase in cardiac output. The increase in blood pressure is registered by the baroreceptors.

Similarly, a drop in blood pressure is registered by the baroreceptors when the person stands up suddenly from a sitting position. High blood pressure in the blood vessels causes stretch of these receptors which results in movement of sodium ions into the nerve endings, thereby, initiating an action potential.

These baroreceptors have a baseline firing pattern. That means they have an intrinsic potential to generate action potentials at a particular frequency at all times. This frequency is increased when the baroreceptors receive a stretch stimulus secondary to increase in blood pressure. The carotid sinuses increase their rate of impulse generation when the pressure in them builds up to values greater than 50 mm Hg. Below this threshold pressure, the carotid baroreceptors fail to initiate an action potential. On the other hand, the arch of aorta can record drops in blood pressure up to 30 mm Hg. The upper limit for blood pressure, after which the frequency of action potential stops increasing, is 175 mm Hg. The normal MAP is calculated to be 93 mm Hg. At this pressure, the baroreceptors are believed to be the most sensitive and even slight changes in pressure will result in rapid firing of action potentials.

At blood pressures lower than 30 mm Hg, the chemoreceptors come into play. The chemoreceptors function by sensing the arterial concentration of carbon dioxide, oxygen, Ph and other metabolites . They do not detect changes in blood pressure.

Baroreceptor Reflex

The baroreceptor reflex like other reflex arcs is comprised of three units:

  • Afferent nerve carrying impulses from the receptors
  • Central processing unit
  • An efferent nerve that innervates the effector


Afferent impulses from the carotid sinus are carried by the Herring nerve, a branch of Glossopharyngeal nerve (CN-9). In the case of baroreceptors present on the arch of aorta, the Vagus nerve (CN-10) is the afferent nerve that carries impulses to the spinal cord. Both, the Vagus nerve and the Glossopharyngeal nerve, feed impulses from the baroreceptors into the nucleus of tractus solitarius. These nuclei are situated in the medulla of the spinal cord and their job is to process the incoming afferent impulses. Also within the Medulla and lower 1/3rd of the Pons, there are vasoconstricting center, the vasodilatory center and the cardio-inhibitory center. These centers receive processed impulses from the nucleus of tractus solitarius and from here efferent impulses in the form of sympathetic and parasympathetic nerves arise. Impulses are carried to the heart via the parasympathetic Vagus nerve. Sympathetic impulses travel down the intermedio-lateral segment of the spinal cord and give rise to efferent motor spinal nerves which enter the sympathetic ganglion running parallel to the spinal cord. Postganglionic sympathetic nerves ultimately supply the heart and the peripheral vasculature. Another preganglionic sympathetic nerve also supplies the adrenal medulla which results in the release of epinephrine and norepinephrine, which further contribute in enhancing the sympathetic activity. The end result is either an increase or decrease in the blood pressure, thereby correcting the disturbance in hemodynamics of the body. This phenomenon is also referred to as the buffering effect, since the change in pressure is buffered back to normal. The Vagus and Glossopharyngeal nerves, because of the same reason, are therefore known as the buffering nerves.

Factors Responsible For Change in Mean Arterial Pressure

MAP = Heart Rate x Cardiac Output

Whereas, CO = SV (stroke volume) x TPR (total peripheral resistance)

Therefore, MAP = HR x SV x TPR

The stroke volume is altered by altering the force of contractility of the heart muscles. The sympathetic nerves supplying the heart muscles affect the stroke volume. The parasympathetic nerves supplying the SA and AV node are responsible for producing changes in heart rate. The TPR can be increased or decreased by changing the diameter of peripheral vasculature which is under the control of the sympathetic nervous system.

Effects of Baroreceptors in Various Conditions

Due To Changes In Blood Pressure

  • Reduced Blood Pressure: Reduction in blood pressure will result in a decrease in the number of afferent impulses from the baroreceptors. The sympathetic activity will increase and as a result, the TPR, HR and the stroke volume will all increase. At the same time, the parasympathetic input will taper down. All these changes will result in increasing the blood pressure back to normal.
  • Increased Blood Pressure: This happens in situations like exercise or stress. Increased blood pressure will result in stretching of the stretch receptors. This increases the frequency of afferent impulses. Sympathetic supply will decrease and the parasympathetic system will take over. Finally, the blood pressure is decreased back to normal.

 Due To Changes In Cardiac Output

  •  Decreased Cardiac Output: Occurs in situations of vomiting, diarrhea, hemorrhage etc. As a result of these, both the volume, and therefore pressure of the blood decreases. Afferent impulse firing of the baroreceptors decreases. As a consequence, there’s a sympathetic overflow which causes an increase in HR, TPR and SV. Due to an increase in these parameters, the blood pressure is raised back to normal.
  • Increased Cardiac Output: There’s an increased impulse generation from the baroreceptors due stretch caused by increased volume of blood. This increased afferent input from the baroreceptors results in activation of the PANS. Once activated, the parasympathetic nervous system decreases the blood pressure back to normal.

Massaging The Carotid Sinus

Massaging the carotid sinuses physically increases the pressure on the baroreceptors present there. The carotid baroreceptors respond by increasing the rate of afferent impulse firing. The sympathetic system will be shut down and the parasympathetic system is activated. This results in decrease in blood pressure of the body.

Carotid massage by activating parasympathetic nervous system increases AV nodal refractory period, thereby decreasing AV node conduction and finally decreasing Heart Rate. This is the reason Carotid sinus massage is the initial menuever used in the treatment of paroxysmal supra-ventricular tachycardia.

Stenosis Of The Carotids

Stenosis of carotids proximal to the sinus or obstruction of the carotids due to atherosclerosis will cause the baroreceptors to register a decrease in pressure. Therefore, sympathetic system activation follows. Increased sympathetic activity causes a resultant increase in blood pressure. This increase in blood pressure may cause hypertension in an otherwise normal person.

Baroreceptor responses are summarized in the table below


It’s important to understand that control of BP by baroreceptor is a short term regulation of blood pressure. Any short term derangements are dealt via the baroreceptor response, whereas long term control of the BP is controlled via the RAAS (Renin Angiotensin Aldosterone System).

The baroreceptors also have the ability to adapt to chronic changes in blood pressure. If the mean pressure is changed over time to a new value, the baroreceptors will start using that MAP as the baseline. Any subsequent blood pressure changes will then be rectified keeping in view the new baseline value of MAP.

CVS - Clinical/Cardiology

Congestive Heart Failure (Part 2) – Labs

Read part 1 here

Laboratory Findings

  • Blood Count
    • Blood count may show anemia. Poor prognosis.
    • High red cell distribution width (RDW). Poor prognosis.
  • Kidney functions may show reduced renal perfusion.
  • Electrolytes
    • Hypokalemia (risk of arrhythmias)
    • Hyperkalemia (limits the use of ATN inhibitors.) Poor prognosis.
  • Thyroid Function Tests
    • Occult thyrotoxicosis
    • Myxedema
  • Iron Studies
    • Figure out hemochromatosis

Presence of the chronic kidney disease (CKD) limits the treatment options.

Need for Biopsy

In unexplained cases cardiac biopsy can be performed. It can help figure out conditions like amyloidosis. Keep in mind, however, that the biopsy will be more helpful to rule out than to diagnose a cause of the heart failure.

Labs to help differentiate between the dyspnea due to the heart failure vs non-cardiac causes

Serum BNP is produced in the ventricles. It elevates when the filling pressure in the ventricle is high. It is less specific in women, older patients, and COPD patients.

Acute Setting

In the emergency room triage to diagnose acute decompensated heart failure serum BNP less than 100 ph/mL or NT-proBNP less than 300 pg/mL with normal ECG makes heart failure unlikely.

Chronic Setting

BNP in chronic patients is less sensitive and specific; and hence less useful. One utility in the chronic setting is to assess worsening breathlessness and/or weight gain with increased BNP can help prompt you to increase the dose for diuretics. This is not yet added to the practice guidelines. (2016)

ECG Changes

  • May show arrhythmias secondary to the heart failure
  • MI may be detected with conduction defect changes (if any)

Chest X-Ray

  • Cardiomegaly is an important finding. Poor prognosis.
  • Signs indicating pulmonary venous hypertension may be observed. These include dilation of the upper lobe veins, and hazy vessel outlines due to perivascular edema resulting from the hypertension.
  • Interstitial edema
  • Alveolar fluid


Considering that most patients of heart failure will have abnormalities of the EKG, Chest X-Ray, and serum studies, clinically the pressing need is to figure out the LV failure and the type of the failure (systolic vs diastolic).

Echocardiogram can be the most useful to identify the LV function and state. As you may know, echocardiogram will provide information about the size and function of each cardiac chamber. It will also show pericardia effusion, valvular defects, any intracardiac shunts, and most importantly segmental wall motion abnormality – which in turn helps you identify an old MI.

Is Catheterization Indicated/Useful?

Most of the times the non-invasive studies above should provide you sufficient information to manage the patient. In some cases the state of coronary artery disease (CAD) may be needed. In such cases an LV catheterization maybe done.

Patients not responding to standard therapy may need right heart catheterization to choose and to monitor therapy.


Management will be the next topic.


CVS - Clinical/Cardiology

Congestive Heart Failure (CHF) Part 1

Inability of heart to pump blood out, resulting in the fluid build up in lungs and other body tissues is called heart failure or congestive heart failure. This condition usually is attributable to the left heart failure but it can occur due to left, right, or failure of both sides. Remember as a rule the fluid will build up behind the heart that is failing. Lungs are behind the left heart and rest of the body tissue is behind the right heart.

Heart failure is a disease of aging. 75% of new cases occur in individuals over 65 years of age.

Some conditions leading to the CHF can be reversed while many conditions can only be slowed down in their progress.

Diagnostic Essentials

For the left heart fluid build up in the lungs leading to dyspnea and symptoms of the low cardiac output to body tissues.

Right hear failure is usually due to the left heart failure. Fluid overload is predominant cause of clinical signs and symptoms.

It is said that left heart failure has symptoms (dyspnea for example) and right heart failure has signs (ankle edema for example). This is a quick aid for approaching the patient, but not the whole story.

Clinical Signs and Symptoms

Left Heart Failure

  1. Dyspnea due to fluid build up (edema) in the lungs.
    • Exertional dyspnea -> Othopnea -> Proxysmal Nocturnal Dyspnea -> Rest Dypnea.
    • Dyspnea during conversation.
  2. Persistent non-productive Cough. (J receptors in the lungs irritated due to the edematous exudate.)
  3. Nocturia due to fluid pressure on the kidneys at night.
  4. Fatique and exercise intolerence
  5. Elevated pulmonary venous pressure. (Same reason as point 1.)
  6. Crackles at the base of the lungs.
  7. Listen for murmurs to exclude other heart conditions.

Right Heart Failure

  1. Can be primary (without left heart failure) 50%, or secondary (due to the left heart failure.) 50%.
  2. Gravitational edema is common sign. (Ankle or lower back.)
    1. Ankle edema
    2. Hepatic congestion
    3. Lower-back Edema at nigh
    4. Edema of the gut causing anorexia and nausea
    5. Ascites
  3. When right heart failure is due to the left heart failure then distinguishing between the two can become difficult.
  4. High jugular venous pulse.
  5. May have tender liver.
  6. Tricuspid regurge.
  7. Listen for murmurs to exclude other heart conditions.

Common Signs


  1. Observe neck, lungs, trunk and extremities for signs.
  2. Cachexia
  3. Tachycardia with hypotension and reduced pulse pressure
  4. Crackles


NYHA Classification

  • Class I: Asymptomatic
  • Class II: Symptomatic after moderate activity
  • Class III: Symptomatic after mild activity
  • Class IV: Symptomatic even at rest


Common causes are

  1. Systolic Dysfunction

    1. Systemic Hypertension
    2. Coronary Artery Disease
    3. Alcoholic Cardiac Myopathy
    4. Viral Myocarditis including HIV
    5. Idiopathic Cardiomyopathy
    6. Persistent Tachycardia due to Atrial Arrythmia
  2. Diastolic Dysfunction

    1. Aging
    2. Hypertension leading to Left Ventricular Hypertrophy (LVH)
    3. Restrictive/Hypertrophic Cardiac Myopathies
    4. Diabetes

We will continue Labs, ECG changes, and Treatment in the next parts




CVS Pathology



light bulbDrbeen Study Tip: Syphilis is an extremely important topic for all board and NBME examinations. As far as the cardiovascular lesions are concerned, 10-15% are late syphilitic lesions which are often progressive, disabling and even fatal.

Involvement usually starts as an arteritis in the supra cardiac portion of the aorta and progresses to the following:

  • narrowing of coronary ostia; resulting in decreased coronary circulation
  • angina and acute myocardial infarction
  • scarring of the aortic valves; producing aortic regurgitation and eventually Congestive Heart Failure  
  • weakness of the wall of the aorta with saccular aneurysm formation.

Note: There are associated pressure symptoms of dysphagia, hoarseness, brassy cough, back pain (vertebral erosion is characteristic) and occasionally rupture of the aneurysm.
Recurrent respiratory infections are common as a result of pressure on the trachea and bronchi.





light bulbDrbeen Test Taking Tip:  Normal Electrocardiogram (ECG or EKG) is a concept driven topic and USMLE and FSMB will probably not test normal ECG directly. However, it is imperative that you start with knowing the components of a normal ECG wave in order to identify the deviated and abnormal ECGs (covered in part 2). These skills will be inevitable in diagnosing conditions like Arrhythmias, Myocardial infarction, Hypertrophy of various cardiac chambers and Electrolyte disturbances. Here, we cover the high yield components on the ECG wave as these are the most commonly tested topics on Board exams.


ECG refers to the the process of recording potential fluctuations during the cardiac cycle. As a result of sequential spread of excitation in the atria, the interventricular septum and the ventricular walls and finally repolarization of the myocardium, a series of positive and negative waves designated as P, Q, R, S, and T are recorded during cardiac cycle. Depolarization moving towards an active electrode in a volume conductor produces a positive deflection, whereas depolarization moving in the opposite direction produces a negative deflection.


EKG Wiki Public Mod



  • P WAVE
    +P wave is a positive (upright rounded) deflection caused by the depolarization of atrial musculature also known as the atrial complex.
    +Duration of P wave is not more than 0.1 second and Amplitude of P wave is from 0.1 to 0.12 mV.
    +Clinical significance of P wave is the extrapolation in diagnosing conditions related to the functional activity of atria.
    +QRS complex consists of three consecutive waves. Q wave is a small negative wave which may be normally absent quite often. It is continued by a tall R wave followed by a small negative S wave. QRS complex is a result of ventricular depolarization.
    +Duration of QRS complex is normally less than 0.08 second, it is a measure of interventricular conduction time.
    +Amplitude of Q wave is 0.1 to 0.2mV, R wave is 1mV and S wave is 0.4mV (Total being 1.5-1.6mV)
    +Clinical significance of QRS complex from precordial leads are more important than limb leads.
  • T WAVE
    +T wave is the last, positive, dome shaped deflection. Normally, it is in the same direction as that of QRS complex, because ventricular repolarization follows a path opposite to that of depolarization. T wave represents ventricular repolarization.
    +Duration of T wave is approximately 0.27 seconds and Amplitude is about 0.3mV.
    +Clinical significance of T wave involves in diagnosing the following;
  • U WAVE
    +U wave is a small and positive round wave representing slow repolarization of papillary muscle.
    +The duration of U wave (when present) is 0.08 seconds and the amplitude is about 0.2mV.
    Note: Since atrial repolarization coincides ventricular depolarization, so it is merged with QRS complex and thus not recorded as a separate wave.




+It is measured from the onset of P wave to the onset of the QRS complex. Functionally, it is the PQ interval.
+This interval is the measure of AV conduction time, including the AV nodal delay.
+The duration varies from 0.12 to 0.21 second depending on the heart rate.
+A prolonged PR interval is helpful in diagnosing AV conduction block. First degree AV block is produced when PR interval is between 0.2-0.3 second and the second degree block is produced when the PR interval is increased to 0.3-0.45 second.

  • J point
    +Point on ECG that coincides with the end of depolarization and start of repolarization of ventricles, i.e. it occurs after the end of QRS complex.
    +Since all parts of the ventricle at this point are depolarized, no current is flowing around the heart. Thus, J point is a ZERO VOLTAGE point. It is the time from the start of the QRS complex to the end of T wave.This indicates total systolic time of ventricles, i.e. ventricular depolarization and repolarization.
    +The duration of QT interval is about 0.4 second.



+An iso-electric period between the end of QRS complex and the beginning of T wave.
+The duration is about 0.32 second
+ST segment corresponds to the period of ventricular repolarization phase of cardiac cycle.


12leadECG wiki Public


CVS Questions Uncategorized

CVS Question

What disease/condition doubles the risk of CVS diseases?

  • A. Diabetes
  • B. Smoking
  • C. Hypertension
  • D. Alcoholism
  • E. Liver cirrhosis
CVS Hemodynamics

General Principles of Hemodynamics

Organization of Cardiovascular System

The human heart has 4 chambers which are the two atria and the two ventricles. These 4 chambers are divided into 2 functional units referred to as the left heart and the right heart. These atria and ventricle are single functional unit, separated by the atrioventricular valves. These AV valves are one way valves and allow blood flow in the forward direction only.

Right heart is formed by the right atrium and the right ventricle, and it forms one functional unit. The right atrium receives the venous deoxygenated blood from three following sources

  1. Superior vena cava: brings deoxygenated blood from the head, neck and upper limb region.
  2.  Inferior vena cava: brings deoxygenated blood from the lower extremities, the abdominal region and the rest of the body except the heart itself.
  3.  Coronary sinus: brings deoxygenated blood from the veins of the heart itself.

During diastole when the atria contract, this deoxygenated blood is pumped into the right ventricle. During systole, the right ventricle pumps this deoxygenated blood out of the heart and into the pulmonary circuit via the pulmonary artery.

The right heart plus the pulmonary arteries, capillaries and veins together form the pulmonary circulation.

The right side of the heart deals with deoxygenated blood only and it functions to send this deoxygenated blood to the pulmonary circulation to get oxygenated.

Left heart forms another functional unit and consists of the left atrium and left ventricle. The left atrium receives oxygenated blood from the pulmonary circuit via the  four pulmonary veins, two from each lung. When the atria contract, the left atrium pumps this oxygenated blood into the left ventricle. During systole, this oxygenated blood is pumped out of the heart via aorta, when the left ventricle contracts. The aorta then carries this oxygenated blood into the systemic circulation.

The left heart plus the systemic arteries (starting at the aorta), capillaries and veins together form the systemic circulation.

The left heart deals with the oxygenated blood and sends it to the systemic circulation via the aorta.


Arteries conduct blood away from the heart towards the tissues. Arteries normally carry oxygenated blood away from the heart, but an exception to this rule are the pulmonary arteries and the umbilical arteries(during fetal life only) which carry deoxygenated blood away from the heart and toward the lungs & placenta respectively. Veins normally carry deoxygenated blood, except the pulmonary veins in adults and the umbilical vein (during fetal life only) which bring back oxygenated blood to the heart from the lungs and the placenta respectively.


Systemic Tissue

As part of the systemic perfusion, the oxygenated blood in the aorta is eventually transported to the following six major systemic tissues. These systemic tissues receive blood via a parallel system of arteries which originate at various levels from the aorta itself.

  1. Cerebral: The CNS plus the head & neck region. 15% of the cardiac output enters the cerebral arteries.
  2. Coronary: The myocardium itself which receives oxygenated blood during diastole in contrast to the rest of the body which receives oxygenated blood as part of systole. 5% of the total cardiac output is designated for the myocardial perfusion via the kidneys.
  3.  Splanchnic: The gastrointestinal system and its accessory organs such as the liver, spleen, pancreas and the biliary system. 25% of the total cardiac output reaches the GIT system via the splanchnic arteries.
  4. Renal: The kidneys and the genitourinary system. Kidneys, as part of the renal system, receive 25% of the total cardiac output.
  5. Skeletal: Roughly 25% of the total cardiac output is reaches the skeletal system. Exercise increases the percentage of cardiac output which is made available for the skeletal system. Bones and the musculature of the body form part of this system.
  6.  Cutaneous: The skin and its associated structures (sebaceous glands, hair follicles). Around 5% of the total cardiac output reaches the cutaneous circulation.


Direction of Blood Flow and chemical composition of Blood

There are four pulmonary veins which bring back oxygenated blood from the lungs to left atrium. This blood is rich in oxygen (PaO2=100 mm Hg) and low in carbon dioxide (PaCO2=40 mm Hg). The mitral valve which forms the left atrioventricular valve, allows passage of blood from the left atrium into the left ventricle during the diastole phase. When the left ventricle begins to contract and its pressure rises more than the left atrial pressure, the mitral valve closes to prevent backflow of the blood. This ensures anterograde flow of blood in to the aorta i.e., the forward direction of blood flow. Backflow from the aorta back into the left atrium is prevented by the semilunar aortic valve. It’s important to remember that all the valves of the heart are tricuspid i.e., having three cusps, except the mitral valve which is bicuspid i.e., having two cusps. However, only the right atrioventricular valve is referred to as the tricuspid valve.

From the aorta, the blood is transported to the systemic tissues which are mentioned above. The aorta divides into large and medium sized arteries, which eventually give arise the arterioles. The arterioles continue to form capillaries, and these capillaries merge together to form venules at their venous ends. The venules eventually end up forming the veins. The veins are low pressure vessels which return the deoxygenated blood back to the right heart via the three above mentioned sources of venous return to the heart. This deoxygenated blood is low in oxygen (40 mm Hg) and rich in carbon dioxide (47 mm Hg). The right atrioventricular valve, which is also referred to as the tricuspid valve, allows this deoxygenated blood to flow from the right atrium into the right ventricle. During ventricular systole when the left ventricle contracts, this deoxygenated blood is pumped out of the right side of the heart via the pulmonary artery. The backflow of this deoxygenated blood into the right side of the heart during ventricular diastole is prevented by the semilunar pulmonary valve. This deoxygenated blood reaches the lungs and enters the pulmonary circuit to get deoxygenated. At this point the blood completes its route both around the pulmonary and systemic circuits.

Series and parallel Circuits

The right and left sides of the heart are connected in a series circuit to both the pulmonary and systemic tissues respectively. By series circuit, what’s meant here is that quantitatively, the blood flow through the lungs is equal to the blood flow through the rest of the body. For simplicity in understanding, it should be considered that the lungs are connected to the rest of the body in a series circuit. During a single cardiac cycle, the right and left ventricular outputs are the same.

However, the blood supply of the systemic tissues is connected in a parallel circuit. This means that each organ system is supplied by an artery which originates as a branch of the aorta. This ensures that the blood which reaches a particular organ system is perfused at the same partial pressure of oxygen, as that of the site at which the branch originated from the aorta. If the organ systems were connected and perfused via a series circuit, by the time the blood reached the last organ system, it would have been completely depleted of oxygen and nutrients. The sum of blood flow to these individual systems adds up to the total left ventricular output (the cardiac output).

Pressures in cardiovascular system


Systole is time interval when the ventricles are contracting. Systolic BP therefore is the pressure in the systemic arteries when the left ventricle is contracting. Therefore, SBP is the highest blood pressure in the systemic arteries during a cardiac cycle.

Average SBP in healthy adults is 120 mm of Hg.


Diastole is the time interval when the ventricles are relaxing and therefore receiving blood from the atria. Diastolic BP is the pressure in the systemic arteries when the left ventricle is relaxing. DBP therefore is the lowest pressure in systemic arteries during a cardiac cycle. Average DBP in healthy adults is 80 mm of Hg.


This is the difference between the systolic blood pressure and the diastolic blood pressure in the systemic arteries at any given time. Pulse pressure can therefore be calculated as following:

Pulse pressure (PP) = Difference between the systolic & diastolic blood pressures.


PP = 120-80= 40 mm of Hg

Variations in pulse pressure can be in anemia, fever, blood loss etc. Narrow pulse pressure can be seen when there is blood loss, aortic regurgitation. Pulse pressure widens during exercise.


MAP is the average arterial pressure of the systemic arteries. However, quantitatively it’s not an arithmetic mean of the SBP & DBP. Since the ventricular muscle spends 2/3 of the time of a cardiac cycle in diastole, the MAP is closer to the DBP, than it’s to the SBP.

MAP signifies the perfusion pressure of the tissues. If the MAP of the patient decreases below 60 mm of Hg, then it should be a cause of concern for the doctor. What this signifies is that a perfusion pressure below 60 mm of Hg would not be able to meet the nutritional needs of the systemic tissues. So, the MAP, which is easier to calculate quantitatively, can be used in lieu of systemic perfusion pressure.

MAP = (CO x SVR) + CVP {CVP is negligible, so it can be ignored}

MAP = (CO x SVR)

CVP= central venous pressure

SVR (systemic vascular resistance) is the sum of resistance of all the vessels in the systemic circuit. However, the major component of systemic vascular resistance is the arteriolar resistance.

Also, MAP can be calculated by using the following formula if the SBP and DBP are known:

MAP = DBP + 1/3 (SBP – DBP)

For a normal healthy adult, SBP = 120 & DBP = 80

So, MAP = 80 + 1/3 (120 – 80)

MAP = 80 + 1/3 (40)

MAP = 80 + 13.33

MAP = 93 mm of Hg (After rounding off)

Alternatively MAP can also be calculated by the following formula:

MAP= 2/3 DBP + 1/3 SBP

MAP= (2/3 x 80) + (1/3 x 120)

MAP= 53.33 + 40 = 93 mm of Hg

The Mean Arterial Pressure is necessary pressure to bring blood supply to the systemic tissues to ensure their nutritional needs.



CVS Hemodynamics

Overview of Blood Flow

This overview begins with major steps found in blood circulation throughout the cardiovascular system. Remember this process is continuous allowing the:

1) maintenance of cell-level metabolism by the transportation of nutrients, hormones, metabolic wastes, O2 and CO2 throughout the body; 2) regulation of pH, osmotic pressure and temperature of the whole body; 3) protection from microbial and mechanical harms

Tracing Blood Flow 

There are two main functional units:

A. Right heart consisting of both the Right atrium and Right ventricle

B. Left heart consisting of both the Left atrium and Left ventricle.

Pulmonary_CircuitFrom each lung, you can trace blood being transported to the Left atrium via four pulmonary veins, which contain high O2 and low CO2 concentration. Blood flows from the Left atrium through the Left atrioventricular valve (also called Mitral valve or Bicuspid valve) reaching the Left ventricle. (Because the Left ventricle is the chamber that pumps blood from the heart, it is the most muscular and powerful of the four chambers). From the Left ventricle, blood is then pumped through the aorta to supply all systemic tissues:

1.Cerebral   2.Coronary heart  3.Splanchnic  4.Renal system 5.Musculoskeletal 6.Skin



Arteries split into arterioles, capillaries, draining into venules and then veins drains into either the Superior vena cava, Inferior vena cava, or Coronary sinus,  opening into the right atrium.

Blood from the head and neck region is drained by the Superior vena cava. Blood from the peripheral system is drained by the inferior vena cava. Blood from the heart is drained by the coronary sinus. Subsequently, all drain into the right atrium.

From the Right atrium, the deoxygenated blood (with decrease in O2 concentration, and increase in CO2 concentration) is pumped into the Right ventricle through the Right Atrium ventricular valve, also called Tricuspid valve. Finally, from the Right ventricle, blood is pumped through pulmonary arteries back to the lungs.


CVS EKG CVS Physiology

Ventricular Action Potentials


Na+ fast channels. Active briefly during the phase 0.

Slow and fast Ca++ channels. Active during the phase 2.

Leaky K+ channels. Always active.

Inward rectifying transient K+ channels. Active during the phase 1.

Inward rectifying delayed K+ channels. Active during the phase 2 early part and phase 3.

Inward rectifying K+ channels. Active during the phase 3. Primary channels to help restore resting potential.

Na+/K+ ATPase pump. Restores the ionic imbalance after an action potential has occurred. Moves K+ in and Na+ out of the cells.

CVS Embryology


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This lecture discusses about the structure, function and the differences in between the different components of the vasculature (arteries, arterioles, capillaries, venules, veins). Before delving into the details about individual components of the vasculature, an understanding about the general structure of the blood vessel will be discussed. A standard blood vessel is composed of three layers, which are discussed as following:

Click Here To Watch Video Lecture For This Topic

  1. TUNICA INTIMA forms the innermost layer of any vessel. Tunica intima itself is composed of three component layers. Endothelium forms the innermost aspect of the tunica intima. Surrounding the endothelium is a connective tissue layer called the subendothelial layer. Subendothelial layer has a varying amount of elastic and smooth muscle fiber depending on the type of vessel. In elastic arteries the density of elastic and smooth muscle fibers is higher compared to smaller arteries. Outermost component of the tunica intima is the internal elastic lamina.
  2. TUNICA MEDIAforms the middle layer of the vessel. It is mostly composed of the elastic and smooth muscle fibers which are arranged in a circular pattern. Tunica media is surrounded by the external elastic lamina.
  3. TUNICA ADVENTITIA forms the outermost layer of any vessel. Vasa vasorum are present in the tunica adventitia layer

In various types of vessels these above mentioned layers would be either present or absent. If present, the composition and thickness of these layers can slightly vary from one vessel type to another.

ARTERIES conduct blood away from the heart towards the tissues. Arteries normally carry oxygenated blood away from the heart. However, exceptions to this rule are the pulmonary arteries and the umbilical arteries which carry deoxygenated blood away from the heart.

Elastic arteries are larger in size and have a relatively thick tunica media. Examples of elastic arteries include the pulmonary arteries and aorta plus its 3 major branches (left brachiocephalic, right common carotid & the right subclavian arteries). Tunica media is so large in the case of aorta, that it has 50 layers of alternating elastic and smooth muscle fibers present in an alternating circular pattern. Elastic arteries are also referred to as the conducting arteries. Their main function is to receive high pressure blood from the heart and distend outwards keeping the blood there before they slowly return to their normal caliber and gently push the blood forward as the heart enters diastole phase. This is called the windcastle effect and it prevents any turbulence of the high pressure blood which leaves the heart. Hence, the elastic component allows the elastic arteries to recoil appropriately and serve their function as conducting vessels.  

Endothelium is the innermost layer of the tunica intima and this is surrounded by the subendothelial layer. In case of arteries, the subendothelial layer has a lot of elastic and smooth muscle fibers. Subendothelial layer is the part of the tunica intima that is most commonly involved in atherosclerosis. Atherosclerosis is an intimal disease which results in formation of atheromatous plaques within the subendothelial layer of the tunica intima. Atherosclerosis most commonly affects the medium and large sized arteries. This plaque formation tends to decrease the luminal size of the vessels and consequently the blood which flows across them. Arteries have abundant smooth muscle and elastic fibers in their tunica media, which gives them the recoil capability. Tunica adventitia forms the outermost layer. Small vessels called the vasa vasorum are located within the tunica adventitia, and they function to vascularize the wall of the walls of the elastic arteries.

Baroreceptors and chemoreceptor are present within the walls of carotid sinus and the arch of aorta. Baroreceptors are formed by the thinning of the wall of these arteries. This allows the increased blood pressure to have a more pronounced effect in distending the arterial wall in this region where the baroreceptors are located. There are nerves located in the adventitia of the baroreceptor region which sense this stretch of the vessel and send impulses if there’s a significant rise or drop in blood pressure. Similarly there are chemical receptors that are also present within the muscular wall of the arch of aorta. These chemoreceptors are formed by Glomus type 1 cells which are situated within the walls of the arch of aorta. These Glomus type 1 cells have channels for oxygen, carbon dioxide and hydrogen ions; this allows them to act as sensory receptors for the monitoring the concentrations of oxygen & carbon dioxide plus the pH of the arterial blood. Glomus type 1 cells are supported by the satellite receptors. These receptors respond to hypoxia, hypercapnia (increased arterial CO2 levels) and the pH changes in the arterial blood. Any derangements of these above mentioned parameters result in firing of the glomus cells thereby activating the corresponding control mechanism to ensure homeostasis within the body.

Muscular arteries arise from the larger elastic arteries. They are also referred to as the conducting arteries and they supply blood to various organs of the body. These muscular arteries mainly respond to sympathetic/adrenergic control because of the presence of alpha 1and beta 2 receptors. Sympathetic stimulation is responsible for the vasoconstriction effect in these arteries. They do have an endothelial and subendothelial layer. The smooth and elastic fiber layer in the subendothelium is not that dense. Their tunica media is composed of 3 to 10 layers of smooth muscle and elastic fibers. Outermost layer is formed by the tunica adventitia. Muscular arteries are also referred to as resistance vessels. This is because they exhibit vasoconstriction upon sympathetic stimulation; hence they can change their diameter. Upon decreasing their diameter, they can decrease the forward flow hence they are called resistance vessels. The volume of blood in the muscular arteries is referred to as stressed volume, since these arteries are always compressing upon the blood inside them to help maintain the blood pressure.  

The ARTERIOLES form the terminal arterial vessels and form a connection between the arteries and the capillaries. Arterioles form the major resistance site of the systemic vasculature and therefore, they are responsible for maintaining the blood pressure. The arterioles are also referred to as the functional sphincters of the arterial system. Within the tunica intima, they do have an endothelial and subendothelial layer. Subendothelial layer is not that dense in elastic and muscle fibers. Their tunica media has 1 to 3 layers of smooth muscle and elastic fibers. This tunica media responds to sympathetic and parasympathetic stimulation. Sympathetic stimulation achieves vasoconstriction of the arterioles and results in a decreased forward flow through them. In contrast, the parasympathetic stimulation achieves vasodilatation of the arterioles, which results in an increased forward flow across the arteriole.

In the case of skin, gastrointestinal system and the renal system; the sympathetic stimulation of their arterioles is modulated via the alpha-1 receptors. The arterioles leading to the skeletal muscles are controlled by beta 2 receptors.

CAPILLARIES have the smallest caliber in terms of luminal diameter. Though the capillaries have a small diameter, but they have the greatest cross-sectional area amongst all the vasculature. The total cross-sectional area of all the capillaries in the body can add up 2/3 of a meter. Also they have the largest surface area relative to all the blood vessels in the body. The tunica intima of capillaries is only composed of an endothelium and a basement membrane. The endothelium is formed by a single layer of endothelial cells which allows them to function as sites of exchange. Tunica media and adventitia are absent in the capillaries. Capillaries function as the exchange site of the vasculature because they exhibit selective permeability of substances across their walls. This permeability allows diffusion of oxygen, nutrients, signaling molecules and water from the blood to the tissues. Carbon dioxide and waste products diffuse in the opposite direction from the tissues into the capillaries.

When the capillaries merge together they end up forming VENULES. The venules have an endothelium and a broken subendothelium but they lack tunica media and adventitia. They are normally collapsed and have a low blood pressure. Venules are also involved in exchange of metabolites with the surrounding tissue. Another important function of venules is diapedesis which involves cellular trafficking across wall of the venules. This made possible by endothelial contraction which allows gaps to appear within the endothelium of the postcapillary venules. This diapedesis allows venules to function as sites of leukocyte extraction into the tissues. Inflammatory mediators released from the inflamed tissues allow leukocyte recruitment and via diapedesis leukocyte trafficking occurs into the tissue space. This allows leukocytes to take active part at the site of inflammation.

VEINS are formed when the venules merge together. The veins function as a reservoir of the blood since 2/3rd of the total blood volume is present in the veins at any given time. Veins transport blood away from the tissues and return it to the heart. Veins normally carry deoxygenated blood, except the pulmonary veins in adults and the umbilical vein during fetal life which bring back oxygenated blood to the heart from the lungs and the placenta respectively. Veins as compared to arteries are thin walled, more compliant & distensible, have a greater luminal diameter and have valves which prevent the backward flow of blood. Veins lack the elastic and muscular component hence when the blood backflows under the influence of gravity, the valves tend to approximate and prevent the retrograde flow of blood. In contrast to venules, larger veins have more defined endothelium & subendothelium and they have a tunica media as well.


CVS Embryology


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  1. The fetus has a connection with the maternal blood supply at the site of placenta. This connection is formed by the two umbilical arteries and a single umbilical vein. The umbilical arteries carry deoxygenated blood from the whole body to the placenta which is the gaseous exchange site prenatally. On the other hand, the umbilical vein returns oxygenated blood from the placenta back to the fetus.
  2. The fetal heart has a right to left shunt in the form of a patent foramen ovale. This has extensively been discussed in the previous lectures. As part of interatrial septal development, the two septae (septum foramen and secundum) leave a defect in the interatrial septum which allows the shunting of the blood from the right to left atrium.
  3. The ductus arteriosus opens at the underside of the aorta and connects it with the pulmonary trunk. The role of ductus arteriosus and its situation just distal to the origin of the left subclavian artery will be discussed later into the notes.
  4. Ductus venosus connects umbilical vein to the inferior vena cava, allowing the blood to bypass the hepatic route in doing so.

Click Here To Watch Video Lecture For This Topic



Before birth, two umbilical arteries carry deoxygenated blood from the fetus to the placenta. Placenta allows gaseous exchange via diffusion to take place between the maternal oxygenated blood and the fetal deoxygenated blood.It’s important to remember that the fetal and maternal bloods don’t come into direct contact. Prenatally the fetal lungs are collapsed; hence placenta is the site of gaseous exchange before birth. Although the placenta has maternal deoxygenated blood but still it’s able to provide fetus with its oxygen requirements. This is made possible by the higher oxygen affinity of the fetal hemoglobin, HbF. HbF has 2 alpha and two gamma globin chains, which allows it to extract oxygen from a relatively deoxygenated maternal blood.

Ductus venosus connects umbilical vein (coming from the placenta) to the inferior vena cava, thereby forming a shunt that allows half of the placental blood to bypass the hepatic route. Hence 50% of the oxygenated blood from the placenta enters the hepatic sinusoids. This blood that enters the hepatic sinusoids is returned via the hepatic veins to the inferior vena cava. All of the oxygenated blood doesn’t enter the liver and the hepatic sinusoids because the passage through the hepatic sinusoids can take a very long time for the blood to reach the heart. The oxygenated blood in the IVC (80% oxygen saturation) at this point mixes with the deoxygenated blood from the hepatic veins (26% oxygen saturation). Before entering into the right atrium, the blood in the IVC has an oxygen saturation of around 67%.  

A hallmark of fetal circulation is that, the superior vena cava returns deoxygenated blood from the head, neck and upper extremities region to the right atrium. This deoxygenated blood reaching the heart via the SVC is directed into the right ventricle and subsequently into the pulmonary trunk. The inferior vena cava on the other hand brings relatively oxygenated blood (67% Oxygen saturation) to the right atrium, which due to flow dynamics passes through the patent foramen ovale into the left atrium. As discussed in earlier lectures, foramen ovale forms a right to left shunt which allows the oxygenated blood coming from placenta to bypass the pulmonary circuit. After birth, foramen ovale becomes obliterated and forms the fossa ovalis. Once it’s in the left atrium, this relatively oxygenated blood (coming from right atrium via foramen ovale) goes into the left ventricles and subsequently leaves the heart via the aorta. Most of this blood then leaves via the three large branches of aorta (brachicephalic trunk, left common carotid and the left subclavian arteries) towards the head, neck and upper extremities region. There’s no mixing of the blood coming from SVC and IVC, though they’re both received by the right atrium.

The deoxygenated blood (25% oxygen saturation) coming from the SVC entering the right atrium, is directed into the right ventricle and subsequently into the pulmonary trunk. The ductus arteriosus opens into the underside of the aorta, and connects the pulmonary trunk to the arch of aorta. Thus, ductus arteriosus forms a right to left shunt allowing the deoxygenated blood to bypass the pulmonary circuit. This shunting across the pulmonary circuit occurs because fetal pulmonary vascular resistance is very high resulting in just 10% of the right ventricular output goes to the lungs. The rest 90% of right venticular output is shunted from the pulmonary trunk to the aorta. This deoxygenated blood from the SVC which is in the aorta, now mixes with the relatively more oxygenated blood which came from the placenta and passed through the foramen ovale.

As mentioned earlier, only 10% of the fetal right ventricular output is directed to the lungs. This blood is brought back to the left atrium by the pulmonary veins and it leaves the left side of the heart via the aorta. The blood in the aorta after the opening of ductus arteriosus is at an oxygen saturation of 60%. This blood via the descending aorta is now directed to the abdomen and lower parts of the fetus and finally reaches the internal iliac arteries. Most of the deoxygenated blood now enters the two umbilical arteries and is taken to the placenta. The umbilical arteries on their route to the placenta touch bladder as well. Later on, the proximal parts of the umbilical arteries later form the superior vesical arteries.

Levels of oxygen saturation in different fetal vessels:

  1. Umbilical Vein = 80%
  2. Ductus Venosus = 75-80%
  3. IVC            = 67%
  4. Right Atrium   = 65-67%

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Ductus Arteriosus

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Foramen Ovale

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Ductus Venosus

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Earlier there was a brief mention of the high pulmonary vascular resistance and need for a shunt across the pulmonary circuit. Let’s touch that subject now in order to gain more clarity on this concept. Before birth the fetal lungs are collapsed. Since the fetus is inside the womb surrounded by amniotic fluid, the lungs are also filled with fluid and this keeps them collapsed. Since the lungs are collapsed as a result the pulmonary arterioles are also collapsed. This is because, the alveoli are filled with fluid at this point and the surrounding arterioles tend to exhibit vasoconstriction due to this resultant hypoxia (due to absence of oxygen in the alveoli). This hypoxic pulmonary arteriolar vasoconstriction results in a very high pulmonary vascular resistance and as a consequence the lungs remain in a collapsed state before birth. Since the right ventricle has to pump against a very high pulmonary vascular resistance, it results in the right ventricle being more hypertrophied than the left ventricle before birth. Fortunately only 10% of the right ventricular output flows to the lungs (other 90% is shunted across the pulmonary circulation by DA in the aorta) so the degree of hypertrophy isn’t that pronounced at the time of birth. This situation is reversed within one month after the birth.


After birth, the 3 above mentioned shunts tend to close because of changes in pressure gradients and in oxygen tension. Immediately after birth, as the newborn breathes the lungs become expanded. As the alveoli expand, the pulmonary vasculature also tends to expands due to decreased effects of hypoxic pulmonary vascular resistance. This results in an overall decrease in pulmonary vascular resistance and blood from the right ventricle is directed via the pulmonary trunk towards the pulmonary circulation. The increased pulmonary blood flow to the lungs also results in an increased pulmonary venous return to the left atrium. Consequently left ventricular output increases and the aorta receives more blood resulting in an increase in aortic blood pressure. Hence, the increased pressure in the aorta tends to reverse the shunt across the ductus arteriosus. Overall the pressure on the left side of the heart tends to increase more than the right side of the heart. As the lungs become functional, the following changes occur:

  1. Increased bradykinin levels
  2. Increased oxygen tension (more than 50mm of Hg)
  3. Decreased PGE2 and prostacyclin levels

Overall, there’s an increased oxygen tension due to expansion of lungs and an increased released of bradykinin from the lungs. Following this, there’s an immediate drop in PGE2 and prostacyclin levels which were being produced as a result of hypoxia. Prostaglandin E actually is an inhibitor of contracting response of ductus arteriosus to an increased oxygen tension. An oxygen tension above 50 mm of Hg promotes the closure of the ductus arteriosus. Therefore, all the above mentioned changes result in the contraction of specialized smooth muscle in the walls of ductus venosus and ductus arteriosus. Consequently, DV and DA become obliterated over the next couple of hours after birth. Failure of the ductus arteriosus results in a patent ductus arteriosus after birth. The closure of ductus arteriosus is a slow event and it’s summarized below:

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Within few hours

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Within 24 hours

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Within 48 hours

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Within 96 hours

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DA starts constricting

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Obliterated in 40% of newborns

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Obliterated in 80% of newborns

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Obliterated in 100% of newborns

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The umbilcal vein also closes upon birth as the umbilcus is clipped and the connection between the placenta and the fetus is severed. Closure of umbilical vein reduces the amount of blood flowing via the inferior vena cava into the right atrium. Hence the right atrial pressure tends to further drop relative to left atrial pressure. The increased left atrial pressure results in fusion of the septum primum and secundum and the foramen ovale is subsequently closed. Closed foramen ovale is referred to as fossa ovalis. The floor of the fossa ovalis is formed by the septum prium and its margin called the limbus ovalis is derived from the septum secundum. Closure of the foramen ovale means that the right heart is connected to the pulmonary circulation and the left heart is connected to the systemic circulation.

Once the umbilical connection to the placenta is servered after birth, the ductus venosus also begins to start closing. The closure of ductus vensosus is a slow process and it can take a month after birth to completely become obliterated. In cases where the newborn is anemic, the ductus venosus can be cannulated from the outside to initiate a blood replacement therapy. Adult remanant of the ductus venosus is referred to as the ligamentum venosum.



Postnatal changes which occur after birth result in formation of some adult remnants from the fetal circulatory system. These remnants and the changes after birth which give rise to them are summarized in the table below:

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1. Fossa Ovalis

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2. Ligamentum Arteriosum

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3. Ligamentum Venosum

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4. Medial Umbilical liagmaents

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Closure of the foramen ovale

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Closure of ductus arteriosus

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Closure of ductus venosus

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Obliteration of the distal part of the two umbilical arteries, proximal part forms superior vesical artery

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5. Ligamentum Teres hepatis/ Round ligament of liver

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Obliteration of the umbilical vein

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The ductus arteriosus is formed from the 6th pharyngeal arch artery on the left side. It connects aorta to the pulmonary trunk just distal to the origin of the left subclavian artery and forms a right to left shunt. This right to left shunt enables most of the right ventricular output to bypass the pulmonary circuit because the lungs are collapsed at this time and as a result the pulmonary vascular resistance is quite high. The ductus arteriosus is composed of specialized smooth muscle which releases PGE2 and prostacyclins in response to low oxygen tension/ relevant hypoxia. The PGE2 and prostacyclins release tends to keep the ductus arteriosus open before birth. Normally, the ductus arteriosus closes within few hours after birth due to contraction of the smooth muscle in its wall and is referred to as ligamentum arteriosum.

Congenital condition which can cause hypoxia after birth can prevent the ductus arteriosus from closing. One such condition is erythroblastosis fetalis. As mentioned earlier, the low oxygen tension due to hypoxia can cause a release of prostaglandins and prostacyclins which will prevent the ductus arteriosus from closing. Other than that, babies born with a preductal coarctation of aorta tend to have a patent ductus arteriosus which should be kept open. In case of preductal coarctation, the ductus arteriosus remains patent and provides blood flow into the descending aorta and thereby the abdomen and lower parts of the body. In situations where a left to right shunt is important for the survival of the newborn, the ductus arteriosus is necessary to be kept patent. Congenital heart defects such as transposition of great vessels requires such an intervention to keep the ductus arteriosus open. Prostaglandin E analogues such as dinoprostone, are administered in such cases which helps in keeping the ductus arteriosus patent.

In preterm babies, the lungs aren’t fully developed, therefore after birth there is a decreased arterial oxygen tension and an increased prostaglandin E2 and prostacyclins synthesis in response to this relative hypoxia. Hence, the incidence of a patent ductus arteriosus is very high in preterm/premature infants. Patent ductus arteriosus results in a left to right shunt after birth, which is non-cyanotic and the newborn has a machine-like murmur audible upon auscultation. In such cases, prostaglandin E inhibitors such as indomethicin and ibuporfen are administered in order to promote the closure of ductus arteriosus.

The situation of ductus arteriosus just distal to the origin of left subclavian artery has great significance. Most of the oxygenated blood entering the right atrium is directed towards the head and neck region via the 3 branches large branches of the arch of aorta. Just distal to the origin of subclavian artery, the aorta is connected to the pulmonary trunk via the ductus arteriosus. At this point the deoxygenated blood (coming originally from the SVC) in the pulmonary trunk is shunted into the aorta (via DA) and is allowed to mix with the oxygenated blood which originally came from the placenta. Hence, most of the oxygenated blood from the placenta directed to the head and neck region which at that that point of development has greater oxygen demands. This remaining blood in the aorta, after it has mixed with the shunted deoxygenated blood from the pulmonary trunk, has an oxygen saturation of 50% and is now directed to the rest of the body (abdomen and lower limb).


CVS Embryology


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Atrial & Ventricular septum formation process begins at the same time by the start of the 4th week and wraps up by the 8th week. Though occurring simultaneously, however, atrial septation is a little ahead of ventricular septation. Common congenital cardiac anomalies mostly occur due to defects in the formation of these septae. In this lecture and its subsequent review, we discuss the high yield topic of atrial septation and development plus relevant congenital defect which can occur during this process.


  1. It divides the primitive atria into a right and left atria.
  2. During fetal life provides it provides a patent right to left shunt and ensures the shunt is not in the opposite direction of left to right shunt. During fetal life right to left shunts are essential for the survival of the fetus. A hallmark of the fetal circulation, which differentiates it from the adult circulation, is that the right atrium receives the oxygenated blood from the placenta via the inferior vena cava. In an adult heart, the right side deals with the deoxygenated blood!
  3. After birth, when there’s no need a right to left shunt since the lungs have become functional, foramen ovale tends to close. At this point interatrial septum divides adult left and right atria into separate non-communicating chambers.

    A small Reynolds number signifies that the blood is flowing in a smooth and laminar fashion. If the Reynolds number is high, the blood flowing through the blood vessel would be turbulent.

    Murmurs and bruits point to the presence of turbulence in blood flow. These can be appreciated upon auscultation at the relevant areas. Murmurs are sounds of blood splattering on the rest of the blood due to turbulence. These disturbances result in vibrations that resonate through the walls of blood vessels or the heart itself. These are picked up as distinct sounds upon auscultation.



    Embryonic timeline of Atrial Septation: Late 4th week to the middle of the 6th week.

    Initially the right and the left atria are actually one single chamber which is referred to Primitive Atrium. Sinus Venosus provides the Inflow in this primitive atrium. The primitive atrium is divided into two separate left and right atria following the process of atrial septation. Atrial Septation is actually a series of events which involves 2 septae (Septum Primum & Septum Secundum) and 2 foraminae (Foramen Primum & Foramen Secundum) forming within the primitive atria, thereby dividing it into a right and left atrium.



    1. From the roof of the primitive atrium a flexible and crescenteric shaped Septum Primum grows inferiorly towards the endocardial cushions. The initial defect in between the down growing septum primum and the endocardial cushions is referred to as foramen primum. Foramen Primum functions to allow shunting of blood from the right atrium to the left atrium. Endocardial cushion itself is a derivative of neural crest cells and gives rise to the following structures in a adult heart:
    2. Foramen Primum is eventually obliterated when the inferior edge of the septum primum fuses with the endocardial cushions. Just before the foramen primum closes, multiple small secondary defects form within the upper wall of septum primum as result of apoptosis. These multiple small defects in the upper wall of septum primum coalesce into forming a single defect called the foramen secundum. Foramen secundum is formed before the foramen primum is closed, and it serves to maintain the very important function of reinforcing a right to left shunt of the oxygenated blood entering the right atrium via the inferior vena cava.
    3. While the septum primum is undergoing these changes, from the roof of the atrium and just to the right of septum primum, a second crescentic shaped septum secundum starts developing. As the septum secundum grows downwards, it extends and obliterates most of the foramen secundum. The remaining part of foramen secundum which isn’t obliterated by the septum secundum is referred to as Foramen Ovale. The function of foramen ovale is the same as that of the foraminae primum and secundum, which was to maintain a right to left shunt.
    4. It’s important to remember that septum primum is a rather flexible structure compared to septum secundum which is a relatively rigid structure. This rather flexible property of the septum primum allows its inferior flap (which isn’t covered by the septum secundum) to function as valve for foramen ovale. This valve allows the flow of blood from the right to left side thereby reinforcing the shunt, but it tends to disallow the backflow of the blood from the left atria to the right atria.
    5. Septum Primum and Septum Secundum eventually fuse to form the interatrial septum. Most of the interatrial septum is formed from two septae (primum and secundum). However, the inferior part of the interatrial septum forms from a single septum (septum primum only), and hence this part is rather thinner compared to the rest of the atrial septae. This thinner part of the interatrial septum in the adult heart is referred to as Fossa Ovalis and is a major anatomical landmark of the adult right atrium. Fossa ovalis presents as a marked crescentic ridge on the medial wall of the right atrium.
    6. Immediately after birth Foramen Ovale tends to close. After birth there’s an increase in left atrial pressure due to decreased pulmonary vascular resistance which enhances pulmonary blood flow and subsequent return of blood to the left side of the heart. Also, closure of the umbilical veins tends to decrease the right atrial pressure with respect to left atrial pressure. The above mentioned decreased right atrial and increased left atrial pressure changes result in closure of the foramen ovale after birth.



    1. PROBE PATENCY OF FORAMEN OVALE: A probe is passed from the right atrium into the left atrium to check whether the foramen ovale has closed or not. In cases where the probe can pass through into the left atrium, it means that septum secundum & septum primum have not fused completely together and hence the foramen ovale is still patent. Patent foramen ovale is present in 25% of normal adults without any symptoms. Even if it’s patent, the foramen ovale remains functionally closed due to post birth increased left atrial pressure. However, transient increase in right atrial pressure above the left atrial pressure (such as during Valsalva manoeuvre) can lead to a right to left shunt via the patent foramen ovale. This can lead to paradoxical emboli, where venous thromboemboli cross into the systemic arterial circulation and can cause various clinical complications.
    2. FORAMEN SECUNDUM DEFECT/ SECUNDUM TYPE ASD: This is the most common type of ASD, which usually presents with delayed clinical symptoms after the age of 30, before the age of 30 it’s usually asymptomatic. Secundum type ASD presents with variable sized defects in between the right and left atria. These defects are present in the central part of the interatrial septum, just above the limbus. Secundum type defects may occur due to one of the following, or both:


      Excessive resorption of the Septum Primum can result in a very large Foramen Secundum being formed which couldn’t be effectively closed by the Septum Secundum.

      Alternatively Secundum type defects can occur when there’s an underdeveloped septum secundum which has a relatively smaller size and hence cannot efficiently obliterate the foramen ovale.

      Besides Secundum type defects, although much less common but there are also Primum type atrial septal defects. These primum type atrial septal defects result due to a failure of the septum primum to fuse inferiorly with the endocardial cushions. These Primum type defects can be located in the lower aspect of interatrial septum. Fossa ovalis tends to normal in primum type defects.

      Clinical signs of atrial septal defects include:

      Wide, fixed splitting of S2.

      Systolic ejection murmur best audible in the 2nd intercostals space along the left sternal border.

      Atrial septal defects can also lead to paradoxical emboli similar to those in case of patent foramen ovale.



    It’s basically a three chambered heart with one common atrium and two ventricles, thereby highlighting the situation where interatrial septum fails to develop.

    PREMATURE CLOSURE OF THE FORAMEN OVALE: As mentioned earlier that foramen ovale is supposed to remain patent until after birth. If however, foramen ovale closes early due to premature fusion of septae primum & secundum before birth, this can result in a hypertrophied right and left ventricles plus an underdeveloped left sided chambers.



    Heart tube with its dilatations undergoes an S-shaped bending which results in an orientation where the outflow tract (truncus arteriosus) lies most anteriorly. Behind the truncus arteriosus is the primitive ventricle and still behind is the primitive atrium. On the posterior surface of the primitive atrium opens the sinus venosus along with its branches. Branches of sinus venosus are anterior cardinal vein, posterior cardinal vein and the common cardinal vein. Two vitelline and umbilical veins also drain into sinus venosus. Initially the sinus venosus drains into the middle of the posterior wall of right atrium, however due to flow and hemodynamic changes, sinus venosus starts growing towards the right side. Ultimately sinus venosus ends up opening at the posterior right end of the right atrium. Hemodynamic changes responsible for this right side shifting of sinus venosus are as following:

    An anastomosis forms between the anterior cardinal veins of either side, and the blood starts flowing from the left to the right side.

    Umbilical and vitelline veins on the left side start degenerating. This results in an increased blood flow into the right side as blood from the caudal part of the fetus is also shunted to the right side of the right atrium.

    Eventually the right umbilical vein also degenerates, and the right vitelline vein starts increasing in calibre. End result of these hemodynamic changes is that sinus venosus shifts and starts growing on the right side.

    On the left side the remaining degenerating pieces of the sinus venosus become the coronary sinus. Right vitelline vein in future becomes the inferior vena cava. The common cardinal vein becomes the future superior vena cava. All these changes contribute to an increase in the size of right atrium since sinus venosus has also shifted there as part of its development. Anterior view of the right atrium shows that it’s divided by the crista terminalis into a smooth and rough or trabeculated part. The trabeculated parts of right atrium and the right auricle are derived from the primitive atria. The smooth parts are derived from the primitive inflow tract which was sinus venosus. Crista terminalis is the landmark where parts of sinus venosus were absorbed into right atrium as parts of right atrial development. The lower part of the sinus venosus marks the valve of the inferior vena cava. Also there is an opening of coronary sinus which actually is the degenerated left sinus venosus draining into the right atrium.



    Left atrial development is relatively not as complicated. Trabeculated part and the left auricle form a very small component of left atrium and they’re derived from the primitive atrium. Majority of the left atrium is its smooth part which is derived from the primordial pulmonary trunk which gets absorbed as part of left atrial development. Primordial pulmonary trunk is actually a budding off of the left atrium. The primordial pulmonary turn initially grows and forms four branches. However, so much of the primordial pulmonary trunk is absorbed into the making of left atrium that its four branches end up opening directly into the left atrium.

    CVS Embryology


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    The aorta arises from the left ventricle as its outflow tract. Aorta forms an arch before descending downwards as the thoracic/descending aorta. This arch of aorta gives rise to three arteries; from right to left these arteries are the brachiocephaic trunk, left common carotid and the left subclavian artery. On the right side the brachiocephalic trunk gives rise to right subclavian artery and then continues as the right common carotid artery which eventually divides into internal and external carotid arteries of the right side. The left common carotid artery is a direct branch of arch of aorta and it ends up dividing into external carotid and internal carotid arteries of the left side. Finally the left subclavian artery arises from the arch of aorta prior to the ductus arteriosus, after which the arch curves downawards and continues as descending or thoracic aorta.


    Click Here To Watch Video Lecture For This Topic


    As the embryo is developing, two dorsal aortae develop on either side and give off branches to oxygenate ventral and dorsal parts of the embryo. Simultaneously the pharyngeal arches develop along with their pharyngeal arteries. There are six pharyngeal arteries that develop. The first pair of pharyngeal arteries develops by the 3rd and 4th week and the sixth pair develops by the 6th or 7th week. By the time the last pair (6th pair) of the pharyngeal arteries develops, the first and second pair of pharyngeal arteries has degenerated. It’s important to remember that all six pairs of pharyngeal arch arteries aren’t present at the same time. The 1st and 2nd pharyngeal arch arteries give rise to part of Maxillary artery and Stapedial artery respectively. Other than that the first two pharyngeal arch arteries degenerate. The 3rd pharyngeal arch artery is of importance, as it combines with the adjacent part of dorsal aorta to form common carotid and proximal part of the internal carotid arteries. The 4th pharyngeal arch artery on the right side gives rise to proximal part of right subclavian artery while the left side it gives rise to the aortic arch. The 5th pharyngeal arch artery normally doesn’t develop in humans. However, in cases where it does develop, it tends to be rudimentary and degenerates soon. The 6th pharyngeal arch artery gives rise to ductus arteriosus on the left side and it regresses on the right side.

    On the right side, the 1st, 2nd, 5th and 6th pharyngeal arch ateries tend to regress (completely or partially) whereas, the 3rd and 4th are of importance in terms of giving rise to adult structures. On the left side 1st, 2nd and 5th pharyngeal arch arteries tend to regress (completely or partially), whereas the 3rd, 4th and 6th give rise to arterial structures. This above information is summarized in the table overleaf:

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    Aortic arch derivative

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    Arterial structure formed on the right side

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    Arterial structure formed on the left side

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    1st (Maxillary artery)*

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    2nd (Stapedial artery)*

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    3rd pharyngeal arch artery

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    Common carotid & proximal part of the internal carotid arteries

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    4th pharyngeal arch artery

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    Proximal part of the right subclavian artery

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    Aortic arch, rest of it degenerates

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    5th pharyngeal arch artery

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    6th pharyngeal arch artery

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    proximal parts of pulmonary arteries of both sides, rest of it degenerates

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    Ductus arteriosus

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    So what happens is, that the first two pharyngeal arch arteries degenerate and the third one ,as mentioned earlier, is directly connected to the dorsal aortae on either side. The parts of dorsal aortae connected to the 4th and 6th pharyngeal arches tend to degenerate as well. As a result the 3rd pharyngeal arch arteries on either side get directly connected in the middle to the aortic sac. Inferiorly, the aortic sac is connected to the truncus arteriosus which at this point is undergoing septation to form aorta and the pulmonary trunk.  So, the initial part of the pulmonary trunk is formed by the truncus arteriosus whereas the point where the pulmonary trunk bifurcates into two pulmonary arteries (proximal parts of pulmonary arteries) is formed by the 6th pharyngeal arch artery.

    Eventually, the 3rd pharyngeal arch (which is directly connected to the aortic sac) starts dividing along with the aortic sac. This division eventually results in the brachiocephalic trunk developing on the right side. On the left side, part of the 3rd pharyngeal arch forms the aortic arch. Common carotid and internal carotid arteries on both sides are formed by the 3rd pharyngeal arch artery as well. However, distal part of internal carotid is formed by the dorsal aorta.

    The fate of dorsal aorta is different on either side. On the right side, the dorsal aorta ends up forming the right subclavian artery. On the left side however, the dorsal aorta forms a part of the descending aorta and the arch of aorta. Aorta primarily forms from the aortic sac. Although, part of aorta that is proximal to the commencement of the common carotid artery on the left side, is formed by the artery of the 4th pharyngeal arch. On the right side as well, the part just before the commencement of the common carotid artery from the brachiocephalic trunk is formed by the 4th pharyngeal arch artery. Right Subclavian artery forms from the dorsal aorta, whereas the left subclavian artery forms from existing vasculature as part of angiogenesis.

    On the right side, the right vagus nerve gives rise to right recurrent laryngeal nerve which passes under the the right subclavian artery to ascend towards the larynx region. On the left side, the left vagus nerve gives rise to left recurrent laryngeal nerve which hooks around the ligamentum arteriosum and further curves under the aortic arch to ascend and reach the larynx. On the right side, part of the 6th pharyngeal artery tends to degenerate hence the right recurrent laryngeal nerve has to pass behind the right subclavian artery on, as it courses upward.

    An important clinical correlate to remember is that, as the left recurrent laryngeal nerve curves under the arch of aorta, it can get damaged by aortic arch aneurysm or a malignancy. Left recurrent laryngeal nerve damage can result in paralysis of the left vocal cords. On the right side, since right recurrent laryngeal is unaffected by any aortic arch pathologies because it arises from the right vagus nerve in the root of the neck and subsequently passes under the subclavian artery (and not under the arch of aorta).

    Ligamentum arteriosum is the embryologic remanant of the ductus arteriosus. Ductus arteriosus itself arises from the left 6th pharyngeal arch artery. Ductus arteriosus opens into underside of the arch of aorta (distal to origin of the left subclavian artery) and it functions to form a shunt which allows the flow of deoxygenated blood from the pulmonary trunk to the aorta (right to left shunt). This right to left shunting allows the deoxygenated blood to complete bypass the pulmonary circuit.



    Coarctation of aorta is a constriction of the aorta just after it has given rise to subclavian artery. Post the coarctation site, the aorta becomes significantly narrowed and the blood supply to the lower limb and the abdomen is diminished which results in weak pulses of the lower limb. As compensation, over time collaterals develop around the chest wall and the abdomen to supply the lower body. Coarctation of aorta also affects the heart, which now has to pump against greater peripheral resistance and hence at a higher pressure in order to maintain peripheral circulation, thus it may lead to cardiac failure in severe cases.

    It’s important to understand the underlying cause for this coarctation of aorta. During development, the ductus arteriosus is composed of a specialized smooth muscular contractile tissue. This specialized contractile tissue at times makes its way into the arch of aorta. Hence, after birth when this migrated contractile tissue conracts and tends to narrow the aortic lumen (similar to obliteration of ductus arteriosus in response to increased oxygen and decreased PGE levels), there’s a resultant coarctation of the aorta. Alternatively, developmental alteration can also result in the coarctation of aorta.

    Clinically, coarctation of aorta manifests with the following:

    1. Brachial-femoral pulse delay.
    2. Blood pressure discrepancies between upper and lower extremities. These discrepancies normally present as hypertension in the upper extremities but feeble and delayed pulses in the lower limb.
    3. Associated with bicuspid aortic valve.

    Coarctation of aorta is divided into two types based on the location of the narrowing of aorta with respect to the position of ductus arteriosus:


      is also referred to as the infantile type, and it occurs prior to the site of ductus arteriosus. In this case the ductus arteriosus tends to remain patent. As part of compensation, the patent ductus arteriosus provides blood to the descending aorta and hence the lower parts of the body. Prostaglandin E analogues tend to keep the ductus arteriosus patent and they are administered to newborns in cases where DA patency is required. An important high yield point to remember is that preductal coarctation has a strong association with Turner’s syndrome.


      is the more common type and tends to occur in the adults. The narrowing of aorta in this case is distal to the origin of ductus arteriosus and hence DA tends to obliterate according to its normal timeline (immediately after birth). The compensatory collateral circulation in this case is provided by the intercostal arteries which link the internal thoracic artery (branch of the left subclavian artery) and the thoracic aorta to provide circulation to lower limb extremites. Over time, the collateral intercostal arteries enlarge resulting in erosion of the lower border of ribs which presents as notched appearance of ribs on the chest x-ray. This notched appearance of ribs on CXR is referred to as costal notching.


    CVS Embryology


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    Sinus venosus forms the inflow tract of the primitive heart tube. On each side of the sinus venosus, the common cardinal veins open into it. Anterior and posterior cardinal veins combine to form the common cardinal vein on each side of the sinus venosus. The common cardinal vein on the right side forms part of the superior vena cava. Besides the common cardinal veins, the umbilical and the vitelline veins also drain into the sinus venosus. On the left side, these veins undergo specific remodelling. This results in formation of specific anastamosis on the left side, giving rise to left to right shunts thereby causing most of the blood to be received by the right side of the sinus venosus. Consequently, the veins of the right side start maturing and increase in size relative to their left side counterparts. As the sinus venosus also grows and matures, it becomes incorporated into the right side of the primitive atrium. Eventually the vitelline, common cardinal and the umbilical veins of the left side degenerate. The blood received by the left side of sinus venosus is greatly reduced and as a result the left side of the sinus venosus shrinks.  Inferiorly the posterior cardinal veins anastamose together and form the iliac veins.


    Click Here To Watch Video Lecture For This Topic

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    The formation of the inferior vena cava is contributed by three set of veins:

    1. Anterior & posterior cardinal veins
    2. Subcardinal veins
    3. Supracardinal veins (develop a little latter)

    The anterior cardinal and the common cardinal veins on the left side give rise to brachicephalic and the left subclavian vein which drain into the SVC.  It is important to remember that, the umbilical vein on both sides and the vitelline vein on the left side, all tend to degenerate.  The vitelline vein on the right side along with the common cardinal vein of the right side together form parts of the SVC.

    The subcardinal veins have an anastomosis in the middle which is referred to as subcardinal venous anastomosis. These subcardinal veins are also connected to the posterior cardinal vein and form another anastomosis which is referred to as the mesonephric shunt. Later on the inferior part of posterior cardinal vein on the left side starts degenerating, however, it’s still connected to the subcardinal vein via the mesonephric shunt. Also, there are tiny buds arising from the subcardinal veins, these form parts of the future ovarian and spermatic veins.

    Subcardinal veins on the right side separate from the posterior cardinal veins and are joined in by the hepatic veins. This will later form the initial parts of the IVC. At this point it’s important to understand that an anastomosis forms between the supracardinal and the subcardinal veins, which is referred to as the supra-subcardinal anastomosis. This anastamosis becomes part of the IVC and later gives rise to the renal vein and parts of the spermatic veins. Over time the posterior cardinal vein on the right side also degenerates.

    As the IVC is formed, it is composed of the following parts:

    1. HEPATIC PART comes from the liver sinusoids and the hepatic vein. It also has a contribution from the sinus veonsus.
    2. PRERENAL PART of the IVC is contributed by the subcardinal veins. Primarily the right subcardinal vein has a greater contribution in forming this part.
    3. RIGHT AND LEFT SUPRARENAL VEINSare also parts of the IVC. They also develop from the subcardinal veins.
    4. RENAL SEGMENT OF THE IVC arises from the mesonephric shunt of the right side. The mesonephric shunt itself forms as a result of the anastamosis between the subcardinal and the posterior cardinal veins. Right renal vein also arises from this renal segment of the IVC. On the left side the mesonephric shunt becomes incorporated into the IVC and gives rise to the left renal vein. The spermatic/ovarian vein on the left side drains into the left renal vein which then opens into the IVC. However, on the right side, the right spermatic/ovarian vein opens directly into the IVC.
    5. POSTRENAL SEGMENT OF THE IVC is the region below the renal segment of IVC. Supracardinal veins contribute to the formation of the postrenal segment of the IVC.
    6. ILIAC VEINS form the most inferior parts of the IVC. The inferior anastomosis between the posterior cardinal veins is responsible for the formation of iliac veins.