Pathophysiology of Heart Failure Flashcards
how are the following parameters affected by systolic vs diastolic heart failure?
a. ejection fraction
b. cardiac output
c. morphology of cardiomyocytes
systolic heart failure: reduced ejection fraction, reduced CO, eccentric hypertrophy (sarcomeres added in series)
diastolic heart failure: preserved ejection fraction but lower CO, concentric hypertrophy (sarcomeres added in parallel)
mitral valve regurgitation and congenital heart defects can develop into what kind of heart failure?
systolic heart failure - ventricle is stressed by increased volume (eccentric hypertrophy) —> decreased contractibility
in what kind of heart failure might you observe a lateral shift of PMI, S3 heart sound, and mitral regurgitation?
lateral shift of PMI: point of maximal impulse
S3 heart sound: due to ventricle filling more than it should
mitral regurgitation: back-flow of blood from ventricles into atria
these are all possible findings of systolic heart failure: volume overload —> eccentric hypertrophy —> decreased contractibility —> reduced ejection fraction / cardiac output
how is the LV pressure-volume loop affected by systolic heart failure?
systolic heart failure = volume overload, eccentric hypertrophy, decreased contractibility
pressure volume loop shows lower ESPVR (end-systolic pressure-volume relationship): slope of graph, representing maximal pressure developed by the LV at any given volume, measure of contractibility
right shift due to higher ventricular volume, upward shift due to higher ventricular pressure
systolic heart failure is due to ______overload, while diastolic heart failure is due to ______ overload
systolic HF = volume overload
diastolic HF = pressure overload
what kind of heart failure can be caused by HTN and aortic valve stenosis?
diastolic heart failure: pressure overload —> concentric hypertrophy (sarcomeres add in parallel) —> reduced compliance —> reduced SV/CO (but preserved ejection fraction)
in what kind of heart failure might you observe sustained PMI, S4 heart sound, and RV heave?
sustained PMI: point of maximal impulse
S4 heart sound: due to stiff ventricle
RV heave: right ventricle heave, due to RV hypertrophy, feels like heavy beating against chest wall
these can all be observed in diastolic heart failure (pressure overload)
how is PMI (point of maximal impulse) affected by systolic vs diastolic heart failure? what pathogenic heart sounds would you heart with each?
systolic HF = volume overload, eccentric (sarcomere in series) hypertrophy —> lateral shift in PMI, S3 heart sound (too much filling)
diastolic HF = pressure overload, concentric (sarcomere in parallel) hypertrophy —> PMI unchanged, S4 heart sound (stiff ventricle)
how would diastolic heart failure affect the LV pressure-volume loop?
diastolic HF = pressure overload, reduced compliance, reduced SV/CO (but maintained ejection fraction)
increased end-diastolic pressure volume relationship (slope on the bottom of the loop)
left shift due to decreased ventricular filling (volume), upward shift due to higher ventricular pressure
how would systolic vs diastolic heart failure affect the left-ventricle pressure-volume loop?
systolic HF = volume overload —> right/upward shift (more filling, higher pressure)
diastolic HF = pressure overload —> left/upward shift (less filling, higher pressure)
what 3 compensatory mechanisms occur to maintain homeostasis in the case of reduced cardiac output?
- sympathetic nervous system activation
- RAAS activation (renin-angiotensin-aldosterone system)
- increased vasopressin/ADH (anti-diuretic hormone) synthesis
where in the brain do high pressure baroreceptors in the carotid sinus and aortic arch signal to? how do they get there?
carotid sinus —> glossopharyngeal nerve (CN IX) —> solitary tract nucleus (medulla)
aortic arch —> vagus nerve (CN X) —> solitary tract nucleus
solitary tract nucleus then signals to cardioinhibitory center in vasomotor area (A1, C1) of medulla , which sends out efferent PNS fibers to the heart
describe how the SNS is activated to increase cardiac output
baroreceptors in carotid sinus and aortic arch usually provide inhibitory input to the CNS (to solitary tract nucleus)
but when arterial filling drops, baroreceptors stop firing, and SNS tone increases (disinhibition)
explain why excessive SNS stimulation in a state of decreased CO is counter-productive
SNS activates beta1 receptors (heart) and peripheral alpha1 receptors
beta1 —> increased inotropy/chronotropy (—> increased oxygen demand, ventricular remodeling), increased RAAS activity (—> increased blood volume)
alpha1 —> vasoconstriction (—> increased afterload —> increased oxygen demand)
overall, SNS causes an increase in oxygen demand and afterload in a heart that is already struggling to maintain CO
where in the kidney are changes in blood sodium detected? which cells respond to decreases in plasma sodium?
macula dense: senses changes in NaCl
JG (juxta-glomerular) cells: synthesize renin, which converts angiotensin (liver) to angiotensin I
*note that beta1 adrenergic stimulation causes increase in renin secretion from JG cells
what are the basic steps of the RAAS pathway?
- angiotensin (liver) is converted to angiotensin I via renin (JG cells, kidney)
- angiotensin I is converted to angiotensin II via ACE (lung) OR ACE-independent pathway
- angiotensin II induces vasoconstriction, aldosterone secretion (adrenal), AVP (vasopressin/ADH) secretion
overall, causes increase in BP through increased blood volume (fluid retention) and vasoconstriction
how does SNS activation affect the LV pressure-volume loop of a heart with systolic HF?
systolic HF LVPV loop - right shift (increased filling), decreased width (decreased SV/ increased ESV)
after SNS activation - left shift (positive inotropy), increased width (increased preload via RAAS/AVP)
*note that compensation mechanisms will ultimately cause harm via increased afterload (not sustainable)
what are the counter-hormones produced in heart failure to reduce the harmful effects of compensatory mechanisms?
HF induces compensatory mechanisms (SNS, RAAS, ADH/AVP) that will ultimately cause harm via increased afterload and cardiac oxygen demand
in response to volume stress/LV dilation, ANP (atrial natriuretic) and BNP (B-type natriuretic - ventricles) hormones are secreted —> natriuresis (salt excretion, water follows), vasodilation, inhibition of SNS
*however, as HF worsens, ANP/BNP become less effective (not sustainable)
which symptoms of congestive heart failure are related to pulmonary congestion, and which symptoms are related to decreased CO?
pulmonary congestion (LV problem) —> dyspnea w/ exertion, orthopnea, paroxysmal nocturnal dyspnea, and Cheyne-Stokes (“chain smoker”) respirations
decreased CO —> fatigue
*remember that LV causes pulmonary problems, RV causes systemic problems (think about where the backup of blood goes from each of these places)
describe why dyspnea with exertion occurs in congestive heart failure
impaired LV function —> increased pulmonary capillary pressure/ hydrostatic pressure —> pulmonary edema (blood gets backed up, fluid collects in alveoli and around bronchioles) —> impaired gas exchange —> hypoxemia/ dyspnea
what are the signs of dyspnea as seen with the early stages of congestive heart failure?
dyspnea w/ exertion - exercise intolerance, nocturnal cough (non-productive), pink/frothy sputum (acute)
caused by pulmonary edema - note that acute pulmonary edema is a medical emergency (can progress quickly)
what is a key histological finding in the lungs of a patient with congestive heart failure?
“heart failure cells”: hemosiderin-laden macropahges
increased hydrostatic pressure —> increased fluid in alveoli and around bronchioles —> capillary damage —> RBC leak
[recall that hemosiderin indicates breakdown of hemoglobin, and this will get taken up by macrophages]
explain why congestive heart failure causes orthopnea and paroxysmal nocturnal dyspnea, and contrast these 2 symptoms
orthopnea: dyspnea while supine, associated with nocturnal cough (while falling asleep), patients sleep with many pillows to elevate - due to redistribution of fluid from splanchnic circulation/lower extremities to central circulation —> increased pulmonary capillary pressure
paroxysmal nocturnal dyspnea: SOB that wakes patient from sleep, associated with wheezing/cough, persists after patient is upright - due to intestinal edema causing airway resistance/compression
explain why congestive heart failure causes Cheyne-Stokes respiration
Cheyne-Stokes respiration (“chain smoker respirations): cyclic changes in depth of respiration
common in advanced CHF, associated with low cardiac output
due to increased sensitivity of respiratory centers to arterial pCO2