CVS - Clinical/Cardiology Surgery

How Does the Impella Ventricular Assist Device Work?

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Impella is a ventricular assist device, that is FDA approved for short-term support of the left ventricle. There is also a version that can be used for the right ventricle as well. The device can support 2.5 to 5 L/min of blood flow, the latter of which is considered a normal cardiac output.

The device is minimally invasive and catheter-based, so it is usually placed by Interventional Cardiologists in the catheterization laboratory. It is an impeller driven, axial-flow pump (which derives its inspiration from the Archimedes pump from antiquity).

The device is positioned so that the intake of the pump sits in the LV cavity and the outflow in the aorta, just above the aortic valve. In this way, the pump replaces the work done by the left ventricle and sucks up the oxygenated blood as it returns from the left atrium and forcibly delivers it into the aortic root (beginning part of the aorta).

The oxygenated blood then feeds the coronary arteries and the rest of the body. By removing the blood from the LV cavity, the device reduces pre-load, and by ejecting it at a high velocity into the aorta, it reduces afterload. This has the net effect of “unloading” the left ventricle and thereby reducing the energy required by the LV to function. This, then, rests the LV and allows it to recover as the LVAD does the heart’s work. An impella placed in the RV works by the same principles, to help right ventricular function.


Impella Videos :

    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.

    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
    • CRT-P/CRT-D
    • 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 - 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