Heart Failure

Question 1

Hemodynamic profiles in acute heart failure

Answer 1

Question 2

“Buckets” of pathophysiologic insults that may lead to heart failure

Answer 2

1. Impaired ventricular contractility
2. Increased afterload
3. Impaired ventricular relaxation and filling

Question 3

When thinking of heart failure, it is helpful to think in terms of ___.

Answer 3

When thinking of heart failure, it is helpful to think in terms of ejection fraction.

There is heart failure with reduced EF (systolic dysfunction) and heart failure with preserved EF (diastolic dysfunction).

Question 4

RV is quite susceptible to failure in situations that present ___.

Answer 4

RV is quite susceptible to failure in situations that present a sudden increase in afterload, such as acute pulmonary embolism.

Question 5

The most common cause of right-sided heart failure is ___.

Answer 5

The most common cause of right-sided heart failure is the presence of left-sided heart failure.

The elevated pressures from the LV are transmitted backwards through pulmonary circulation and increased RV afterload.

Question 6

Isolated right heart failure

Answer 6

Usually reflects increased RV afterload owing to diseases of the lung parenchyma or pulmonary vasculature (cor pulmonale)

Question 7

Compensatory mechanisms that buffer the fall in cardiac output in heart failure

Answer 7

1. Frank-Starling mechanism
2. Neurohormonal alterations
3. Ventricular hypertrophy and remodeling

Question 8

Natural compensation of reduced stroke volume by Frank-Starling mechanism

Answer 8

Reduced stroke volume results in incomplete chamber emptying, so that the volume of blood that accumulates in the ventricle during diastole is higher than normal. This effectively increases preload, thereby increasing stretch on the myofibers and buffering the CO by the Frank-Starling mechanism.

Unfortunately, this won’t do any good if you are already on the Frank-Starling plateau, close to L_max. This mechanism also increases EDP, putting you at risk for pulmonary edema.

Question 9

Neurohormonal compensation in heart failure

Answer 9

Question 10

Adrenergic activaiton in heart failure

Answer 10

Sensed by baroreceptors and transmitted to the medulla via glossopharyngeal and vagus nerves. Medulla responds with increased sympathetic output and decreased vagal output. (increased contractility, compliance, and HR, along w/ vasoconstriction via alpha receptors. Venous constriction increases preload, arteriolar constriction increased BP but also afterload)

Note that this response only occurs in resonse to blood pressure change.

Question 11

Renin-Angiotensin-Aldosterone in heart failure

Answer 11

Juxtaglomerular cells detect decreased pressure and decreased salt delivery to macula densa. May also respond to beta2 receptor stimulation from sympathetics. Renin is released, downstream angiotensin II is formed. Vasoconstriction increased BP, stimulation of thirst at hypothalamus, increased aldosterone secretion (increased water/salt reabsorption at distal convoluted tubule).

Question 12

Vasopressin in heart failure

Answer 12

Presumably stimulated via baroreceptors and angiotensin II detection. Increases water (but not salt) retention at distal nephron.

Vasopressin increases intravascular volume and vasoconstricts systemically.

Question 13

Why are neurohormonal alterations good and bad?

Answer 13

At first, they increase circulating volume and preload, and prevent BP from falling too low.

Later on though, the high BP, excess fluid, and high preload may lead to worsening pulmonary edema through increased volume and LVEDP. Also, if BP becomes too high, SV may be lowered further by afterload, net decreasing CO. And, of course, with adrenergic stimulation comes increased myocardial oxygen demand, increasing risk of CAD. Finally, continuous sympathetic activation downregulates beta1 receptors at the heart and upregulates antagonizing G_i GPCRs, leading to reduced catecholamine sensitivity and reduced contractility.

Question 14

In addition to vascular effects, chronically elevated angiotensin II and aldosterone provoke. . .

Answer 14

. . . increased type 2 cytokine production and activation of heart remodeling and fibrosis.

Question 15

Natriuretic Peptides in heart failure

Answer 15

Secreted in response to increased intracardiac pressures. Blood levels are a positive prognostic factor in HF.

Excretion of sodium and water, vasodilation, inhibition of renin secretion, antagonism of angiotensin II effects on aldosterone and vasopressin levels.

Question 16

Endothelin-1 in heart failure

Answer 16

Negative prognostic factor. Potent vasoconstrictor. Drugs that antagonize endothelin-1 function are currently under development.

Question 17

Wall stress is often increased in developing heart failure because of either . . .

Answer 17

Wall stress is often increased in developing heart failure because of either LV dilatation (increased chamber radius) or the need to generate high systolic pressures to overcome excessive afterload

Question 18

Decreased wall stress from hypertrophy comes at the cost of ___, and thus ___.

Answer 18

Decreased wall stress from hypertrophy comes at the cost of decreased compliance, and thus increased diastolic ventricular pressures.

Question 19

Cellular mechanismsconsidered the most important contributors to dysfunction in heart failure include:

Answer 19

1. Reduced ability to maintain calcium homeosatsis
2. Changes in production, availability, utilization of high-energy phosphates

Question 20

Tachyarrhythmias precipitate heart failure by. . .

Answer 20

. . . decreasing diastolic ventricular filling time and by increasing myocardial oxygen demand

Question 21

An increase in salt ingestion, renal dysfunction, or failure to take prescribed diuretic medications may increase the circulating volume, thus promoting ___

Answer 21

An increase in salt ingestion, renal dysfunction, or failure to take prescribed diuretic medications may increase the circulating volume, thus promoting systemic and pulmonary congestion.

Question 22

A large pulmonary embolism results in both ___ and ___.

Answer 22

A large pulmonary embolism results in both hypoxemia (and therefore decreased myocardial oxygen supply) and a substantial increase in right ventricular afterload.

Question 23

L sided heart failure physical findings

Answer 23

• Dyspnea
• Sweating
• Tachycardia
• Tachypnea
• Pulmonary crackles
• S3 gallop (in systolic dysfunction)
• S4 gallop (in diastolic dysfunction)
• Orthopnea (difficulty breathing when lying supine)

Question 24

R sided heart failure physical findings

Answer 24

• Jugular venous distention
• Peripheral edema
• Weight gain (from fluid retention)
• Hepatomegaly (often w/ R upper quadrant discomfort)

Question 25

Juxtacapillary receptors

Answer 25

Receptors in the lung that are triggered by fluid during pulmonary edema and stimulate rapid, shallow breathing. Afferent signal communicated via the vagus nerve

Question 26

Cheyne–Stokes respiration

Answer 26

Breathing characterized by periods of hyperventilation separated by intervals of apnea (silent breathing). May also be present in advanced heart failure.

Related to the prolonged circulation time between the lungs and respiratory center of the brain in heart failure that interferes with the normal feedback mechanism of systemic oxygenation.

Question 27

Pulsus alternans

Answer 27

Alternating strong and weak contractions detected in the peripheral pulse

May be present as a sign of advanced ventricular dysfunction

Question 28

Cardiac asthma

Answer 28

Compression of conduction airways by pulmonary congestion may produce coarse wheezinig

Question 29

Why are inspiratory crackles of cardiogenic pulmonary edema best heard at the base of the lungs?

Answer 29

Hydrostatic forces are greatest in the vessels at these positions, owing to gravity and to distance traveled inside vessels from the heart

Question 30

S3

Answer 30

Early diastolic gallop

Heard in adults with systolic heart failure and is caused by abnormal filling of the dilated chamber

Question 31

L sided heart sounds in systolic failure

Answer 31

1. S3 gallop
2. S4 gallop
3. Mitral murmur

Question 32

R sided heart sounds in systolic failure

Answer 32

• R sided S3 gallop
• R sided S4 gallop
• Tricuspid murmur

Question 33

A normal mean left atrial (LA) pressure is __

Answer 33

A normal mean left atrial (LA) pressure is ≤10 mm Hg.

If the LA pressure exceeds approximately 15 mm Hg, the chest radiograph shows upper-zone vascular redistribution, such that the vessels supplying the upper lobes of the lung are larger than those supplying the lower lobes. This is due to combined effects of gravity and hypoxic pulmonary vasoconstriction.

Question 34

When the LA pressure surpasses ___, ___ appear on radiographs.

Answer 34

When the LA pressure surpasses 20 mm Hg, Kerley B lines appear on radiographs.

Question 35

When LA pressure exceeds ___, ___ will develop.

Answer 35

When LA pressure exceeds 25-30 mmHg, alveolar pulmonary edema will develop.

Question 36

In patients with chronic heart failure, chest radiographs tend to be. . .

Answer 36

. . . less helpful. This is because chronic heart failure is associated with enhanced lymphatic drainage as a compensatory mechanism. This means that high pulmonary capilary pressures will be accompanied by fewer radiologic signs.

Question 37

Azygos silhouette sign

Answer 37

A high right atrial pressurecauses enlargement of the azygous vein silhouette, detectable on X-ray.

Question 38

___ is an especially useful, available, and noninvasive test for heart failure diagnosis.

Answer 38

Echocardiography is an especially useful, available, and noninvasive test for heart failure diagnosis.

Question 39

Treating heart failure with reduced ejection fraction

Answer 39

• Identify and treat underlying condition (surgical valve repair, CBG, aggressive HTN management, cessation of alcohol, etc)
• Elimination of the acute precipitating cause in chronic patients
• Management of symptoms
  
  • For systemic/pulmonary edema, diuretic and sodium restriction
  • To increase forward CO, vasodilators and positive inotropes
• Modulation of neurohormonal response (to prevent remodeling and hypertrophy)
• Prolongation of long-term survival (evidence-based therapies shown to do so)

Question 40

The intent of diuretics in heart failure with reduced ejection fraction

Answer 40

If the patient is on the Frank-Starling plateau, which almost all HFw/REF patients with some form of edema are, diuretics may be used to reduce intravascular volume and EDP without substantially effecting stroke volume.

But, if the patient does not have systemic or pulmonary edema, this may be contra-indicated, as it would further lower stroke volume.

Question 41

Most important furosemide or thiazide side effect for heart failure patients

Answer 41

Electrolyte disturbances (namely hypokalemia and hypomagnesemia) contribute to arrhythmias.

Question 42

Best initial management plans for a heart failure w/ reduced ejection fraction patient

Answer 42

• If edema, furosemide (loop diuretic) and lisinopril
  
  • If unable to tolerate lisinopril, ARB or hydralazine plus isosorbide dinitrate
  • For persistent symptoms, digoxin and aldosterone antagonist
• If no edema, nitroglycerin (venodilator) and lisinopril
  
  • If stable, these patients should also get metoprolol
• Concurrent treatment of hypercoagulability and arrhythmias

Question 43

Chronic management for heart failure with reduced EF

Answer 43

• First line, ACE inhibitor or ARB
• If not tolerable (cough, renal insufficiency, or hyperkalemia), hydralazine-isosorbide dinitrate (arteriolar vasodilator-venodilator)

Question 44

Nesiritide

Answer 44

human recombinant B-type natriuretic peptide

Vasodilator and natriuretic

Still new and being evaluated for safety.

Currently used primarily in patients who have not responded to or cannot tolerate other intravenous vasodilators, such as intravenous nitroglycerin or nitroprusside

Question 45

Digitalis

Answer 45

Na+/K+ ATPase inhibitor, positive inotrope

Enhances contractility, reduces cardiac enlargement, and augments cardiac output in patients with systolic heart failure. Also increases baroreceptor sensitivity, decreasing adverse chronic adrenergic effects (lowering afterload).

Especially good for patients w/ concurrent Afib, as it also slows AV node conduction.

Note: Used for systolic heart failure, but not diastolic

Question 46

Paradoxical effects of β-blockers in heart failure

Answer 46

Historically contraindicated, but now proven to have important benefits in heart failure, including augmented cardiac output, reduced hemodynamic deterioration, and improved survival.

Well tolerated in stable systolic heart failure patients

carvedilol and metoprolol proven safe in this group, but should be used with caution due to their potential negative inotropy. Start at low doses and gradually ramp up

Question 47

Cardiac Resynchronization Therapy

Answer 47

Intraventricular conduction abnormalities with widened QRS complexes common in advanced heart failure. Can contribute to symptoms.

Placement of advanced placemakers that stimulate both ventricles at once may be implanted to prevent this.

Appropriate for advanced systolic dysfunction (LV EF < 35%) and prolonged QRS (>120 msec).

Question 48

Treating heart failure with preserved ejection fraction

Answer 48

1. Relief of pulmonary and systemic congestion
2. Address correctable causes of impaired diastolic function

Question 49

Unlike patients with impaired systolic function, ___ have no demonstrated mortality benefit in patients with heart failure with preserved EF

Answer 49

Unlike patients with impaired systolic function, β-blockers, ACE inhibitors, ARBs, and positive inotropes have no demonstrated mortality benefit in patients with heart failure with preserved EF

Question 50

Profile A patients: Warm and Dry

Answer 50

Healthy!

Question 51

Profile B patients: Warm and Wet

Answer 51

Acute pulmonary edema, but preserved tissue perfusion

Question 52

Profile C patients: Cold and Wet

Answer 52

Acute pulmonary edema and impaired cardiac output resulting in systemic vasoconstriction (through adrenergic activation) and poor peripheral perfuion

Question 53

Profile L patients: Cold and Dry

Answer 53

No pulmonary edema, but poor tissue perfusion due to low cardiac output and systemic vasoconstriction. Likely represents volume depleted patients or those with limited cardiac reserve in the absence of volume overload.

Question 54

Treating acute pulmonary edema

Answer 54

1. Seat upright (permit blood pooling in feet, decrease venous return)
2. Supplemental oxygen
3. Morphine sulfate to reduce anxiety and as venous dilator (decrease venous return)
4. IV Furosemide (rapid diuretic)
5. IV nitrates (venous dilator, decrease venous return)
6. Treat precipitating cause

Question 55

LMNOP mnemonic for pulmonary edema management

Answer 55

Lasix (furosemide)

Morphine

Nitrates

Oxygen

Position (upright)

Question 56

How can one measure left atrial pressures via a R heart catheterization?

Answer 56

By taking the pulmonary wedge pressure!

Occluding a pulmonary branch and all its subsidiaries down to the left atrium. This equalizes pressure in this column of blood and the left atrium, which may then be measured by the catheter. Using the waveform, one can also pick out the LVEDP from when the mitral valve closes.

So, catheterization gives you RA pressure, RV pressure, PA pressure, and ~LA pressure, and the ~LVEDP.

Question 57

How can one detect a left ⇒ right shunt via right heart catheterization?

Answer 57

By measuring oxygen saturation!

O2 sat in the SVC should be the same as that in the pulmonary artery. If it is not, then there is probably a L ⇒ R shunt.

Question 58

Fick equation for cardiac output

Answer 58

Question 59

Fick method for calculating PVR

Answer 59

PVR = (P_arterial - P_SVC) / CO

P_arterial can be measured just via sphyngomanometer

P_SVC is obtained in R heart catheterization

CO may be obtained via the Fick method during R heart catheterization

Question 60

S3 sound cadence

Answer 60

S1 . . . S2 S3

Ken tu cky

Question 61

S4 sound cadence

Question 62

Where do you hear gallops best?

Answer 62

Over the cardiac apex, with the bell

Question 63

The two things you should think when hearing S4 on physical exam are. . .

Answer 63

1. Ventricular hypertrophy
2. Myocardial infarction (dead muscle can’t relax)

Question 64

If a patient comes in with angina from cocaine-induced vasospasm, what do you do?

Answer 64

Pump that sucker full of nitrates

Question 65

Nondihydropyridines are like __ in their effects.

Dihydropyrimidines are like __ in their effects.

Answer 65

Nondihydropyridines are like beta blockers (negative inotropes) in their effects.

Dihydropyrimidines are like ACE inhibitors (vasodilators) in their effects.

Question 66

CXR shows hyperinflated lungs with extremely flat diaphragm on lateral. What is the likely diagnosis?

Answer 66

Emphysema