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
Stage C of HF
Structural heart disease who have HF sx now or in the past; once pt develops HF sx, they are in stage C.
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.
Physical findings in left sided HF
1) Rales: due to pulmonary edema in lung interstitial space
2) Weak pulses: due to decreased CO
3) S3/S4, MR murmur
4) Tachycardia
What is the tx plan for wet and warm patients?
Diurese, diurese, diurese + vasodilators (decreases afterload and increases perfusion)
What are some causes of decreased inotropy that lead to HFrEF and what are some conditions associated with this?
Decreased contractility results from myocyte loss and/or increased fibrosis, which leads to abnormal systolic function. Some conditions that lead to decreased contractility and ultimately HFrEF is CAD and chronic volume overload leading to dilated CM.
What are some conditions that cause HF with preserved EF?
Anything that impairs diastolic filling (stiffness or relaxation) e.g. myocardial ischemia (transient inhibition of energy delivery and diastolic relaxation), LVH + fibrosis (chronic stiffening)
How is SV affected in cases of stiff ventricles or impaired relaxation?
SV goes down because pressure abruptly rises in the ventricle even for small amount of volume that enters (shifting up of diastolic pressure-volume curve); as a result, aortic valve opens quicker + aortic valve closes sooner.
How does the heart suffering from decreased contractility (HRrEF) try to maintain its SV? How does this lead to problems?
It accepts more blood, increasing preload (and end diastolic volume). According to frank-starling curve, as a result of preload, there will be greater tension and therefore greater SV; however, as the heart keeps failing, it will try to accept more and more blood, increasing it’s preload beyond the optimal amount. Then the heart falls off the starling curve and stroke volume actually decreases, which exacerbates the disease process and the extra blood gets transmitted to the lungs.
Causes of HF with reduced EF (2)
1) Impaired contractility
2) Increased afterload
Normal EF of heart
50-60%
Cor pulmonale
Cause of right sided heart failure> occurs due to chronic lung diseases (e.g. COPD, PE, etc.). As a result of lung disease, develop hypoxia since blood vessels in the lungs constrict in response to hypoxia. The right side of the heart tries to pump against the contricted blood vessels and eventually develops heart failure.
Why are IV vasodilaotrs added to wet and warm patients?
Decrease afterload, increase perfusion. Useful for congestion (pumonary edema) + severe HTN
General cause of HF with preserved EF
Impaired diastolic filling (failure to relax due to stiffness)
What is the most common cause of right sided heart failure and why?
Left sided heart failure is the most common cause. This is because when LV fails, pressure goes up to LA → lungs (pulmonary HTN) → right sided heart failure.
What are signs and sx of low perfusion?
Cool extremities
Hypotension with ACEI
Narrow pulse pressure
Sleepy/ Obtunded
Determinants of SV
Increased preload
Increased contractility
Decreased afterload
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)
Causes of right sided HF
Most commonly due to Left sided heart failure. Other important causes include left to right shunt and chronic lung disease (cor pulmonale).
How does ventricular remodeling/ hypertrophy a compensatory mechanism for HF? What are the problems with this?
the body tries to ease up wall tension on ventricle by hypertrophy (inc wall thickness). This is because Wall stress= Pxr/2h. However, by increasing thickenss over time, it increases stiffness which increases diastolic pressure, which promotes back up of blood into the lungs.
P-V loop for HFpEF
Diastolic pressure-volume curve is shifted upward due to stiffness of ventricle, resulting in higher pressures at a given volume during diastole. This results in a decreased EDV due to reduced filling of stiffened ventricle at a higher-than-normal end diastolic pressure. SV goes down because pressure abruptly rises in the ventricle even for small amount of volume that enters; as a result, aortic valve opens quicker + aortic valve closes sooner.
What are BNP levels useful for?
Used in diagnosis of HF
What are the initial vs. chronic effects of neuro-hormonal compensatory mechanisms of HF?
Initially, it is beneficial since it increases SVR and intravascular volume, serving to perfuse vital organs. However, in the lung run as the heart fails it is detrimental in the following ways:
1) Increased volume → increased pulmonary congestion
2) Increased vasoconstriction → increased afterload → decreased CO
3) RAAS- inflammatory responses induces cardiac fibrosis.
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.
4 compensatory mechanisms in HF
1) Frank-Starling Mechanism
2) Neuro-hormonal activation (SNS, RAAS, ADH)
3) Natriuretic peptides
4) Ventricular hypertrophy and remodeling
Stage B of HF
Structural heat disease w/o development of HF
Examples: Prior MI, depressed LV EF, LVH, asymptomatic valvular heart disease
What are the various presentations/classifications (4) of acute decompensated heart failure and what 2 factors are looked at to determine this?
Warm + wet, Warm + dry, Cold + wet, Cold + dry.
Determined by whether pt has low perfusion at rest and if patient has congestion at rest.
Signs and sx of congestion: Orthopnea/PND, JVD, ascietes, edema, rales
Signs and sx of low perfusion: narrow piulse perssure, sleepy, cool extremities, hypotension with ACEI
