Heart Failure Flashcards
Hemodynamic profiles in acute heart failure
“Buckets” of pathophysiologic insults that may lead to heart failure
- Impaired ventricular contractility
- Increased afterload
- Impaired ventricular relaxation and filling
When thinking of heart failure, it is helpful to think in terms of ___.
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).
RV is quite susceptible to failure in situations that present ___.
RV is quite susceptible to failure in situations that present a sudden increase in afterload, such as acute pulmonary embolism.
The most common cause of right-sided heart failure is ___.
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.
Isolated right heart failure
Usually reflects increased RV afterload owing to diseases of the lung parenchyma or pulmonary vasculature (cor pulmonale)
Compensatory mechanisms that buffer the fall in cardiac output in heart failure
- Frank-Starling mechanism
- Neurohormonal alterations
- Ventricular hypertrophy and remodeling
Natural compensation of reduced stroke volume by Frank-Starling mechanism
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 Lmax. This mechanism also increases EDP, putting you at risk for pulmonary edema.
Neurohormonal compensation in heart failure
Adrenergic activaiton in heart failure
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.
Renin-Angiotensin-Aldosterone in heart failure
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).
Vasopressin in heart failure
Presumably stimulated via baroreceptors and angiotensin II detection. Increases water (but not salt) retention at distal nephron.
Vasopressin increases intravascular volume and vasoconstricts systemically.
Why are neurohormonal alterations good and bad?
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 Gi GPCRs, leading to reduced catecholamine sensitivity and reduced contractility.
In addition to vascular effects, chronically elevated angiotensin II and aldosterone provoke. . .
. . . increased type 2 cytokine production and activation of heart remodeling and fibrosis.
Natriuretic Peptides in heart failure
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.
Endothelin-1 in heart failure
Negative prognostic factor. Potent vasoconstrictor. Drugs that antagonize endothelin-1 function are currently under development.
Wall stress is often increased in developing heart failure because of either . . .
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
Decreased wall stress from hypertrophy comes at the cost of ___, and thus ___.
Decreased wall stress from hypertrophy comes at the cost of decreased compliance, and thus increased diastolic ventricular pressures.
Cellular mechanismsconsidered the most important contributors to dysfunction in heart failure include:
- Reduced ability to maintain calcium homeosatsis
- Changes in production, availability, utilization of high-energy phosphates
Tachyarrhythmias precipitate heart failure by. . .
. . . decreasing diastolic ventricular filling time and by increasing myocardial oxygen demand
An increase in salt ingestion, renal dysfunction, or failure to take prescribed diuretic medications may increase the circulating volume, thus promoting ___
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.
A large pulmonary embolism results in both ___ and ___.
A large pulmonary embolism results in both hypoxemia (and therefore decreased myocardial oxygen supply) and a substantial increase in right ventricular afterload.
L sided heart failure physical findings
- Dyspnea
- Sweating
- Tachycardia
- Tachypnea
- Pulmonary crackles
- S3 gallop (in systolic dysfunction)
- S4 gallop (in diastolic dysfunction)
- Orthopnea (difficulty breathing when lying supine)
R sided heart failure physical findings
- Jugular venous distention
- Peripheral edema
- Weight gain (from fluid retention)
- Hepatomegaly (often w/ R upper quadrant discomfort)
Juxtacapillary receptors
Receptors in the lung that are triggered by fluid during pulmonary edema and stimulate rapid, shallow breathing. Afferent signal communicated via the vagus nerve
Cheyne–Stokes respiration
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.
Pulsus alternans
Alternating strong and weak contractions detected in the peripheral pulse
May be present as a sign of advanced ventricular dysfunction
Cardiac asthma
Compression of conduction airways by pulmonary congestion may produce coarse wheezinig
Why are inspiratory crackles of cardiogenic pulmonary edema best heard at the base of the lungs?
Hydrostatic forces are greatest in the vessels at these positions, owing to gravity and to distance traveled inside vessels from the heart
S3
Early diastolic gallop
Heard in adults with systolic heart failure and is caused by abnormal filling of the dilated chamber
L sided heart sounds in systolic failure
- S3 gallop
- S4 gallop
- Mitral murmur
R sided heart sounds in systolic failure
- R sided S3 gallop
- R sided S4 gallop
- Tricuspid murmur
A normal mean left atrial (LA) pressure is __
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.
When the LA pressure surpasses ___, ___ appear on radiographs.
When the LA pressure surpasses 20 mm Hg, Kerley B lines appear on radiographs.
When LA pressure exceeds ___, ___ will develop.
When LA pressure exceeds 25-30 mmHg, alveolar pulmonary edema will develop.
In patients with chronic heart failure, chest radiographs tend to be. . .
. . . 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.
Azygos silhouette sign
A high right atrial pressurecauses enlargement of the azygous vein silhouette, detectable on X-ray.
___ is an especially useful, available, and noninvasive test for heart failure diagnosis.
Echocardiography is an especially useful, available, and noninvasive test for heart failure diagnosis.
Treating heart failure with reduced ejection fraction
- 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)
The intent of diuretics in heart failure with reduced ejection fraction
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.
Most important furosemide or thiazide side effect for heart failure patients
Electrolyte disturbances (namely hypokalemia and hypomagnesemia) contribute to arrhythmias.
Best initial management plans for a heart failure w/ reduced ejection fraction patient
- 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
Chronic management for heart failure with reduced EF
- First line, ACE inhibitor or ARB
- If not tolerable (cough, renal insufficiency, or hyperkalemia), hydralazine-isosorbide dinitrate (arteriolar vasodilator-venodilator)
Nesiritide
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
Digitalis
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
Paradoxical effects of β-blockers in heart failure
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
Cardiac Resynchronization Therapy
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).
Treating heart failure with preserved ejection fraction
- Relief of pulmonary and systemic congestion
- Address correctable causes of impaired diastolic function
Unlike patients with impaired systolic function, ___ have no demonstrated mortality benefit in patients with heart failure with preserved EF
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
Profile A patients: Warm and Dry
Healthy!
Profile B patients: Warm and Wet
Acute pulmonary edema, but preserved tissue perfusion
Profile C patients: Cold and Wet
Acute pulmonary edema and impaired cardiac output resulting in systemic vasoconstriction (through adrenergic activation) and poor peripheral perfuion
Profile L patients: Cold and Dry
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.
Treating acute pulmonary edema
- Seat upright (permit blood pooling in feet, decrease venous return)
- Supplemental oxygen
- Morphine sulfate to reduce anxiety and as venous dilator (decrease venous return)
- IV Furosemide (rapid diuretic)
- IV nitrates (venous dilator, decrease venous return)
- Treat precipitating cause
LMNOP mnemonic for pulmonary edema management
Lasix (furosemide)
Morphine
Nitrates
Oxygen
Position (upright)
How can one measure left atrial pressures via a R heart catheterization?
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.
How can one detect a left ⇒ right shunt via right heart catheterization?
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.
Fick equation for cardiac output
Fick method for calculating PVR
PVR = (Parterial - PSVC) / CO
Parterial can be measured just via sphyngomanometer
PSVC is obtained in R heart catheterization
CO may be obtained via the Fick method during R heart catheterization
S3 sound cadence
S1 . . . S2 S3
Ken tu cky
S4 sound cadence
Where do you hear gallops best?
Over the cardiac apex, with the bell
The two things you should think when hearing S4 on physical exam are. . .
- Ventricular hypertrophy
- Myocardial infarction (dead muscle can’t relax)
If a patient comes in with angina from cocaine-induced vasospasm, what do you do?
Pump that sucker full of nitrates
Nondihydropyridines are like __ in their effects.
Dihydropyrimidines are like __ in their effects.
Nondihydropyridines are like beta blockers (negative inotropes) in their effects.
Dihydropyrimidines are like ACE inhibitors (vasodilators) in their effects.
CXR shows hyperinflated lungs with extremely flat diaphragm on lateral. What is the likely diagnosis?
Emphysema
