CVPR 03-27-14 08-09am Heart Failure-Pathophysiology - Allen Flashcards
Poor forward blood flow in HF
= Low flow (decreased cardiac output) = Key requirement of HF
Backward buildup of pressure in HF
= Congestion (increased filling pressures; retention of salt/fluids –> swelling); typically a response to low flow; almost always present as well
Heart Failure – definition
A constellation of signs & symptoms caused by many possible abnormalities of heart function (i.e., it is a junk term); Inability of heart to pump blood forward at a sufficient rate to meet metabolic demands of the body (forward failure – low flow), or the ability to do so only if the cardiac filling pressures are abnormally high (backward failure - congestion)
The Heart as a Displacement pump – function & dysfunction
Displacement pumps Squeeze (contraction/systole) and Relax (filling /diastole); Failure of either systole or diastole causes HF
The heart as double pumps – function & dysfunction
The heart is a double pump, with right (body to lungs; less work) and left (lungs to body) sides in series; In HF, the left, right or both can fail
Electrical coordination of the heart - – function & dysfunction
Heart rate & contraction is coordinated in the heart; In HF, it can be too slow, too fast, or asynchronous, all of which decrease the efficiency of the heart & dysfunction
Valves of the heart – function & dysfunction
The heart contains 4 valves (inflow valve + outflow valve for each ventricle) to ensure a unidirectional flow of blood through; In HF, a pt may have regurgitation (backflow) or stenosis (resistance), which both stress the heart
Coronary arteries of the heart – function & dysfunction
The heart is supplied by coronary arteries; In HF, myocardium will die in minutes w/out adequate blood flow (very metabolically active); cause ex: atherosclerotic coronary artery disease
Pericardium – function & dysfunction
The pericardium encases the heart; If there is fibrosis or other pericardial problems that compress the heart, there may be HF
Key mediators of Blood Flow
Inotropy (contraction), Preload increase Stroke Volume, while Afterload decreases SV…..SV (100mL/squeeze) and HR (60 bpm) increase Cardiac Output (6L; which is the job of the heart = to pump blood)… in real pts, all of these factors can be changing at the same time (Pt has MI —> stiffer walls = can’t squeeze or fill as well, at the same time)
Preload & the Force Tension Relationship
Greater filling (Increased Preload) —> Greater stretch of cardiac myocytes (diastolic pressure) —> Greater ventricular output; Frank Starling Curves show Left Ventricular End-Diastolic pressure (LVEDP, i.e. filling) vs. Stroke Volume (contraction/output); Thus increased Preload produces increased SV (& thus CO) for the same inotropic state.
Inotropy and SV/CO
Aka contractility; Same filling (preload) of left ventricle produces greater squeeze of contraction (determined by catecholaminergic/adrenergic stimulation & Ca2+); Thus, greater Inotropy produces increased SV (& thus CO) for the same level of preload
Major divisions of HF
Systolic HF (Dilated heart – increased space inside) vs. Diastolic HF (Hypertrophied heart – increased wall muscle mass); Left-sided vs. Right-sided
Loss of contractility (inotropy) – mechanism & type of HF
Weak/damaged myocardium —> systolic failure (heart isn’t squeezing as well and so volume has gotten bigger/dilated)
Systolic dysfunction – basic problem & hallmarks
A problem with squeezing (decreased contraction/inotropy); To solve, try to make up for it by increased filling (preload; via salt/water retention) Hallmark = decreased ejection fraction (“HF with reduced ejection fraction,” HFrEF, or “left ventricular systolic dysfunction,“ LSVD) AND Ventricular enlargement/dilation (“dilated cardiomyopathy,” DCM)
Primary causes of systolic HF
- Direct destruction of heart muscle cells (MI, viral myocarditis, alcohol, etc.)…….2. Overstressed heart muscle (Tachycardia-mediated HF, Meth/Cocaine, Stress-provoked or tako-tsubo cardiomyopathy, etc.)…….3. Volume overloaded heart muscle (Mitral regurgitation, High CO – shunting of blood, wet beriberi [thiamine B1 deficiency], etc.)
Difficulty filling – mechanism & type of HF
Stiff/noncompliant heart (decreased lusitropy/relaxation/filling) —> diastolic heart failure (heart can’t relax as well, so the heart muscle hypertrophies – size of wall increases, heart size may be normal, no dilation; must raise filling pressure to get blood in and fill)
Diastolic dysfunction – basic problem & hallmarks
Impaired filling (decreased lusitropy/relaxation); Hallmarks: Normal ejection fraction (“HF with preserved ejection fraction,” HFpEF, or “preserved systolic function,” PSF) AND Ventricular wall thickening (“left ventricular hypertrophy,” LVH)
PV Loop in Systolic HF
Loss of inotropy produces decreased SV and decreased generated systolic BP
PV Loop in Diastolic HF
Increased stiffness requires increased pressure to achieve same LV filling volume —> produces decreased SV
Primary causes of diastolic HF
- High afterload/pressure overload (long-standing HTN, aortic stenosis, dialysis w/inadequate volume removal)…….2. Myocardial thickening/fibrosis (Hypertrophic cardiomyopathy, Primary restrictive cardiomyopathy)…….3. External compression (Pericardial fibrosis/constrictive pericarditis, Pericardial effusion)
Normal Right-sided heart function vs Left (amount of work/pressure)
Normally, the right ventricle pumps the same amount of blood as the left ventricle, but does so against much lower pressure (normal systolic BP = 120/80; Normal pulmonary BP = 22/10)….RV work is much less and thus RV is a thin-walled structure
Right-sided heart failure - types
Stresses to the RV can cause it to fail to adequately pump blood through the lungs, which causes….1. Decreased circulating blood flow (forward RV HF)….2. Increased venous pressures (backward RB HF)
Primary causes of Right-Sided HF
- Left HF (backward HF from LV dysfunction stresses the right side by increases pulmonary venous pressures)…..2. Lung disease/pulmonary HTN/RV pressure overload (RV HF is called “cor pulmonale” when caused by primary lung disease– COPD, primary pulmonary HTN, sleep apnea)…..3. RV volume overload (shunt b/c of interarterial septal defect; tricuspid regurgitation)…..4. Damage to RV myocardium (isolated RV infarct, Myocarditis)
Clinical Coexistance of HF forms
Systolic dysfunction is typically accompanied by diastolic dysfunction and vice versa—Examples: Fibrosis (scar tissue can’t contract/relax); Ischemia (relaxation is energy dependent); …..LV failure often causes RV failure.
The cycle of heart failure – problem & body’s solutions
Problem: Decreased cardiac output…..Solution: Compensatory responses (Neurohormonal activation, Increased preload via Frank-starling mechanism, Ventricular hypertrophy & dilation)
The two types of Neurohormal responses to decreased CO
- Renin-Angiotensin-Aldosterone System (RAAS); 2. Autonomic NS / Adrenergic activation
Mechanism of normal neurohormonal response to decreased CO
Dehydration/Bleeding —> decreased LV filling —> decrease CO —> 1. Juxtaglomerular apparatus in kidney senses low flow & Renin-Angiotensin-Aldosterone system kicks in to cause Na+ retention & vasoconstriction….2. The carotid sinus / aortic baroreceptors sense low pressure and the autonomic nervous system / adrenergic system is activated to increase HR and cause vasoconstriction —> Both of these processes cause increase volume
Neurohormonal activation in Hear Failure
The body can’t distinguish between low blood flow from dehydration vs. from HF; goes through same mechanism in HF as it would w/dehydration –> Shorter gain for Long-term loss…RAAS causes Na+ retention & vasoconstriction, Carotid sinus / aortic baroreceptors activate ANS / adrenergic system to increase HR & cause vasoconstriction —> Both cause increased volume —> HOWEVER, in this case there are SUPRANORMAL FILLING PRESSURES added to the HF problems, causing high filling pressures that push fluid into lungs & cause pulmonary edema
Decreased Contractility in HF & Frank Starling Compensations
Stoke volume decreases in HF with decreased contractility; Frank Starling allows SV to be preserved by increasing End-Diastolic Filling/Pressure
Chronic Neurohormonal Activation Promotes HF
HF begets HF b/c short-term responses is causing long-term problem; Increased Cardiac workload or Metabolic demands, Ventricular hypertrophy/dilation, Myocardial damage/fibrosis —> Heart Failure —> 1. Adrenergic Activation leading to Vasoconstriction, Tachycardia, Inotropic augmentation….2. Renin-Angiotensin Activation leading to Vasoconstriction, Salt/Water Retention —> more HF
Cardiac Remodeling
Late: Mechanical stress & Neurohormonal activation (Norepi, Angiotensin, Aldosterone) on Cardiac muscle cells —> “Remodeling” Growth (Hypertrophy, Hyperplasia), Necrosis, Fibrosis —> Consequences: Decreased contractile force & dynamic function, Increased diastolic stiffness
Compensation for low CO – Decreased Contractility
Hypertrophy / Dilation
Compensation for low CO – Decreased Preload
Sodium/fluid retention
Compensation for low CO – Decreased Heart Rate
Tachycardia
