Heart Failure Flashcards
Stage A of HF
High risk of HF without structural heart disease or sx.
Risk factors: HTN, atherosclerosis, DM, obesity, metabolic syndrome, family history of cardiomyopathy
What are the tx for dry and cold acute HF patients?
These are usually the end stage HF patients
Inotropes if low BP
vasodilators if BP ok
How does pressure-volume loop change with changes in afterload?
WIth increases in afterload (with no change in preload or contractility), stroke volume decreases due to increased systemic vascular resistance. While the EDV doesn’t change, more ventricular work is needed to overcome the afterload, and as a result, less fiber shortening takes place. This results in an increased ESV. The ESPVR line slope doesn’t change; however, it goes up inearly as afterload increases because at the fully contracted state from control, think of it as more volume being added (increase in ESV) and the pressure that results (End systolic pressure).
Sx of Left sided HF
Due to
1) decreased CO: decreased flow to kidneys leads to activation of RAAS → fluid retnetion exacerbates CHF
2) Pulmonary congestion: dyspnea, orthopnea/ PND, intra-alveolar hemorrhage (due to burst of congested capillaries in lungs)
What are the tx for wet and cold HF pts?
1) IV inotopes- warm them up first by improving perfusion
2) Diuretics- treat the congesiton
What is the goal of neuro-hormonal activation compensatory mechanisms in HF?
Neuro-hormonal activation (SNS, RAAS, ADH) serves to maintain perfusoin to vital organs (e.g. brain and heart) by increasing SVR to nonvital organs and increasing intravascular volume.
What role do natriuretic peptides play in compensatory mechanisms of HF?
Natriuretic peptides (e.g. ANP and BNP) are released when they sense that the ventricle is getting overstretched (too much volume). ANP and BNP opposes the RAAS system by increasing Na+ and water excretion and inhibiting renin secretion. They also promote vasodilation.
What are the tx for dry and warm acute HF pts?
stable chronic HF pts- just monitor
What is ESPVR a function of?
Contractility; when contractility increases, ESPVR slope increases while when contractility decreases, ESPVR slope decreases.
Physical findings in right sided HF
1) RV heave
2) Right sided S3/S4
3) Increased JVD
4) hepatosplenomegaly
5) Ascites, leg edema
Components of neuro-hormonal compensatory mechanisms in HF and their effects
1) SNS activation (and decreased PSNS activity) to heart and periphery. To the heart, it increases HR and contractility. To the periphery, it induces peripheral vasoconstriction (via alpha receptors) in order to maintain perfusion to the heart and brain.
2) RAAS- ATII constricts arterioles (increase SVR) and induces Aldosterone release, leading to Na+ retnetion by kidneys and increased volume (increased preload).
3) ADH/vasopressin: secreted by posterior pituitary; increases water retention in distal nephron.
Stage D of HF
End-stage HF. Refractory HF sx that require special intervention including inotropes, LVAD, Transplant, hospice.
Causes of left sided HF
Ischemia, HTN, dilated cardiomyopathy, MI, restrictive cardiomyopathy
Sx of right sided heart failure
All sx are due to congestion of vessels that feed into right side of the herat.
1) Jugular venous distention
2) Painful hepatosplenomegaly/ with “nutmeg” liver- venous system from liver and spleen feeds into right side of heart. (leads to abdominal discomfort/ ascites)
3) Pitting leg edema- due to increased hydrostatic pressure; since lower extremities drain into right side of heart
P-V loop in HFrEF due to decreased contractility
The ESPVR line (dependent on contractility) slope decreases. As a result, there is an increased ESV. When blood from pulmonary venous system returns to the LV, it adds onto the increased ESV left from systole, which increases preload. This shifts the whole P-V loop to the right. While there is a compensatory increase in SV due to increase in preload, overall SV and EF goes down.
Main tx of left sided heart failure
ACE inhibitors- decrease RAAS
What is ESPVR in a P-V loop?
It is the straight line that tells the relationship between pressure and volume when all the muscle fibers have completely contracted (at the end of systole). It tells you what will happen to the pressure when volume is added or subtracted from a contracted myocardial cell. This essentially tells you elastance, which is P/V.
What does this show?
Increasing preload within physiologic limits (while afterload and contractility are held constant) increases myocardial fiber stretch, which increases LV EDV and increases SV (via Frank-Starling mechanism) so that the same ESV is achieved. This means that when preload is increased without changes in afterload and contractility, heart can compensate and empty to match its end diastolic volume. However, after a certain point, an increase in preload (EDV) will not change SV much because the myocardial fibers have stretched beyond the optimal limits (falling off frank-starling curve)
How does P-V loop change with changes in inotropy?
Increases in inotropy (w/o changes in preload or afterload) increases the slope of the ESPVR line and shifts it to the left. As a result, for a given preload and afterload, the ventricle empties more completely. SV increases and end systolic volume decreases.
