Heart Failure Flashcards
Worsening dyspnea is a cardinal symptom of HF and is typically related to increases in cardiac filling pressures, but also may represent restricted cardiac output
related to increases in cardiac filling pressures,
Another cardinal symptom of HF is fatigue, generally held to be reflective of
f reduction in cardiac output a
Additional findings supporting amyloidosis include
deltoid muscle infiltration (leading to the “shoulder pad sign”), tongue hypertrophy, and bilateral thenar wasting from carpal tunnel syndrome.
A characteristic holosystolic murmur of mitral regurgitation is heard in many HF patients. Tricuspid regurgitation, which s also common, can be differentiated from mitral regurgitation by the location of the murmur at the left sternal border, an increased intensity of the murmur during inspiration, and the presence of prominent “V” waves in the jugular venous waveform.
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increased intensity of the murmur during inspiration, and the presence of prominent “V” waves in the jugular venous waveform.
The presence of a third heart sound is a crucially impo tant finding and suggests increased ventricula filling volume;
S3 increased ventricula filling volume;
s4 . A fourth heart sound usually indicates reduced ventricular compliance
The most definitive method for assessing a patient’s volume status by physical examination is by the measurement of
jugular venous pressure (JVP).
An elevated JVP has good sensitivity (70%) and specificity (79%) for
elevated left-sided filling pressure 13
Conversely, the JVP may be elevated without an increase in left ventricular filling pressures in patients with severe tricuspid regurgitation is present
pulmonary arterial hypertension, in those with isolated right ventricular pressure, or when isolated
(congested with normal perfusion, the most common combination found in decompensated heart failure),
“wet/warm”
acute coronary ischemia is a leading cause of acutely decompensated HF,
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Because of the differences in their clearance, BNP and NT-proBNP have considerably different half-lives (BNP: 20 minutes; NT-proBNP: 90 minutes),
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romising biomarkers bear mention.
Soluble concentrations of ST2, a member of the interleukin receptor family, have been shown to be strongly linked to progressive HF and death in patients across the four ACC/AHA stages of HF.
ST2 fibrosis of the heart
is a giant molecule, the largest protein yet described.
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Both Otto Frank and Ernest Starling observed that the more the diastolic filling of the heart, the greater the strength of the heartbeat. The increased heart volume translates into increased sarcomere length, which acts by a length-sensing mechanism
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The AT 2 receptor is localized more specifically in fibroblasts and the interstitium.
activation of the AT 2 receptor leads to vasodilation, inhibition of cell growth, natriuresis and bradykinin release
T 1 receptor leads to v tion, cell growth, aldosterone secretion, and catecholamine release
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In contrast, angiotensin III directly stimulates the zona glomerulosa of the adrenal glands to produce aldosterone, 2 which promotes sodium resorption in the distal collecting duct of the kidney
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he V 1a receptors mediate vasoconstriction, platelet aggregation, and stimulation of myocardial growth factors, whereas V 1b modulates adrenocorticotropic hormone (ACTH) secretion from the anterior pituitary. The V 2 receptor mediates antidiuretic effects by stimulating adenyl cyclase to increase the rate of insertion of water channel − containing vesicles into the apical membrane.
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Increased renal sympathetic activity leads to increased renin production by the kidneys, with a resultant sustained activation of RAS, despite an expanded extracellular volume.
Angiotensin II facilitates retention of sodium and water by multiple renal mechanisms, including a d rect proximal tubular effect, as well as through activation of aldosterone, which leads to increased sodium resorption in the distal tubule. Angiotensin II also stimulates the thirst center of the brain and provokes the release of AVP and aldosterone both of which can lead to further dysregulation of salt and water homeostasis.
Whereas ANP is secreted in short bursts in response to acute changes in atrial pressure, the activation of BNP is regulated transcriptionally in response to chronic increases in atrial/ventricular pressure
and short burts HL 3 min
BP chronic HL 20 min
The most powerful stimulus for peripheral vasoconstriction is sympathetic activation, which releases the potent vasoconstrictor
NE.
“concentric” hypertrophy
In pressure overload hypertrophy (e.g., with aortic stenosis or hypertension), increased systolic wall stress leads to the addition of sarcomeres in parallel, an increase in myocyte cross-sectional area, and increased LV wall thickening
linked with alterations in Ca 2+ /calmodulindependent protein kinase II–dependent signaling
eccentric” hypertrophy
volume overload hypertrophy (e.g., with aortic and mitral regurgitation),
increased diastolic wall stress leads to an increase in myocyte length with the addition of sarcomeres in series, thereby engendering increased LV ventricular dilation
protein kinase B (Akt) activation 2
n HF there is decreased uptake of Ca 2+ by the SR secondary to decreased SERCA2a protein levels and SERCA2a function.
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midrange ejection fraction” (generally considered as EF of)
40% to 49%
the difference between systolic and diastolic blood pressure) is a useful measure that is an indirect marker of cardiac output.
Pulse Pressure
High pulse pressure indicates
high-output state, including the possibility of unrecognized thyrotoxicosis, aortic regurgitation, or anemia
jugular venous pressure (JVP)
barometer of systemic venous hypertension
Right atrial pressure
indirect measure of LV filling pressures.
rales are often not heard in patients with a b ground of chronic HF and pulmonary venous hypertension, because of increased lymphatic drainage, reinforcing the important clinical pearl that the absence of rales does not necessarily imply normal LV filling pressures.
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estimated that a m nimum of ——-of extracellular fluid is accumulated to produce clinically detectable edema.
4 liters
peak early diastolic transmitral blood flow velocity (E) to the peak early-diastolic mitral annular tissue velocity (Ea) (E:Ea ratio)
An E:Ea ratio greater than 15 predicts a pulmonary capillary wedge pressure (PCWP) greater than 15 mm Hg
f the identified triggers,——— was associated with the highest in-hospital mortality (8%)
worsening renal function
inhaled oxygen (FiO 2 ≥0.4) may cause adverse hemodynamic effects (e.g., hyperoxia-induced vasoconstriction) in patients with systolic dysfunction
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AF with rapid ventricular response is the most common t rhythmia requiring treatment in patients with AHF.
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The most common cause of RV HF in AHF is left-sided failure.
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Cardiogenic Shock definitions
Cardiogenic shock is c ized by marked hypotension (SBP <80 mm Hg) lasting more than 30 minute
associated with severe reduction of cardiac index (usually <1.8 L/min/m 2 )
despite adequate LV filling pressure (PCWP >18 mm Hg)
resulting in organ hypoperfusion.
Cardiogenic shock is an unusual presentation of AHF, occurring in less than 4% of the patients in EHFS II,
commonly used practical definition is an increase in serum creatinine of more than 0.3 mg/dL (or 25% decreases in GFR) despite evidence of persistent clinical or hemodynamic congestion.
Cardiorenal Syndrome
Although a “transfusion threshold” for maintaining the Hct above 30% in patients with CV disease has been generally been accepted,
HFREFZ
IV iron replacement might be reasonable in patients with NYHA Class II and III HF and iron deficiency (ferritin <100 ng/mL or 100 to 300 ng/ mL if transferrin saturation < 20%) to improve functional status and quality of life. 10
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Patients should be advised to weigh themselves regularly to monitor weight gain and to alert a health care provider or adjust their diuretic dose in the event of a sudden unexpected weight gain of more than 3 to 4 pounds over a 3 day period
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ARTS-HF (Mineralocorticoid-Receptor Antagonist Tolerability Study). 17 ARTS-HF was a randomized, double-blind, comparator-controlled multicenter trial in 1066 patients with heart failure (LVEF ≤40%). The primary endpoint was the percentage of individuals with a decrease of more than 30% in plasma NT-p oBNP from baseline to day 90. When compared to eplerenone, finerenone was well tolerated and resulted in a 30% or greater decrease in NT-proBNP levels
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Triamterene and amiloride are referred to as potassium-sparing diuretics
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Triamterene is a pyrazinoylguanidine derivative, whereas amiloride is a pteridine
proximal tubule, where they block Na + reabsorption in the late distal tubule and collecting duc
EMPA-REG OUTCOME (Empagliflozin Cardiovascular Outcome Event Trial in Type 2 Diabetes Mellitus Patients) showed that empagliflozin reduced death from CV causes by 38%, hospitalization for HF by 35%, and progression to end-stage kidney disease in patients with type 2 diabetes and established CV disease 18
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Angiotensin Receptor Neprilysin Inhibitors
combines valsartan (an AT1 receptor antagonist) with sacubitril (a neprilysin inhibitor) in a 1 : 1 mixture
slows the degradation of natriuretic peptides, bradykinin, and adre nomedullin
inhibits renin and aldosterone secretion, while selectively blocking the angiotensin type 1 (AT1) receptor reduces vasoconstriction, sodium, and water retention and myocardial hypertrophy
Three beta blockers have been shown to be effective in reducing the risk of death in patients with chronic HF: bisoprolol and sustained-release metoprolol succinate both competitively block the β 1 receptor, and carvedilol competitively blocks the α 1 , β 1 , and β 2 receptors.
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Patients with HFpEF have normal LV end-diastolic volume and normal (or near-normal) EF and stroke volume (at rest) and usually exhibit concentric remodeling of LV chamber and/or cardiomyocyte
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