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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