Exam 1: Lecture 8: Heart Failure I Flashcards
What is heart failure?
Chronic, typically progressive condition in which cardiac output is too low for the needs of the body
can result from inadequate systole (SV) or diastole (ventricular filling)
generally fatal disease unless something else kills you first
Signs of heart failure
chest pain Swelling in extremities, sometimes abdomen (Ascites) Shortness of breath Arrhythmia Persistent cough High BP Decreased energy Weight gain Frequent urination Decreased appetite, increase nausea or vomiting Difficulties focusing or concentrating Decreased exercise tolerance
Stages of heart failure
Stage A,B,C,D
Stage A
Prefailure
No symptoms but risk factors present
Treat obesity, hypertension, diabetes, hyperlipidemia,etc
Stage B
I
Symptoms with severe exercise
ACEi/ARB, B-blocker, diuretic
Stage C
II/III
Symptoms with marked (class II) or mild (class III) exercise
Add aldosterone antagonist, digoxin, CRT,hydralazine/nitrate
Stage D
IV
Severe symptoms at rest
Transplant, LVAD (left ventricular assist device)
Risk factors for heart failure
Coronary artery Disease Diabetes High blood pressure Obesity Valvular Heart disease Unhealthy behaviors Smoking tobacco Eating foods high in fat, cholesterol and sodium not enough physical activity excessive alcohol intake
Heart failure can be diagnosed by imaging…
Ultrasound or Chest Xray
Two groups of heat failure
Systolic and Diastolic
Systolic Heart Failure is….
LV doesn’t squeeze well enough
reduced ventricular contractility, ejection fraction and CO
50% of younger patients
progressive disease, may involve changing in set point of baroreceptors
increase in angiotensin II, aldosterone, apoptosis of myocytes
Systolic Heart failure can occur due to….
getting inadequate blood supply to LV muscle (atherosclerosis, fat in arteries)
Ischemia means…
less blood supply
Hypoxia means….
decreased oxygen supply
Diastolic Heart failure is…
decreased filling of LV, and leading to decreased CO
from hypertrophy and stiffening of cardiac muscle, heart muscle gets bigger and bigger
seen in people starting out with symptoms later in life
does not respond well to positive inotropic drugs
Extrinsic (neuro-hormonal) compensation
Has to do with Catecholamines/SNS and RAAS Crete a spiral progression of heart failure…
Happens due to resetting of the baroreceptor reflex, the changes then drive further adjustments in RAAS
Reseting of baroreceptor reflex causes…
decrease sensitivity to atrial BP, increasing sympathetic activity leading to tachycardia, increase contractility, increase PVR, and release of proteins and hormones that increase BP
Further RAAS changes due to changes in baroreceptor reflex include….
Increase renin = increase angiotensin II
Increase angiotensin II = increase afterload, decrease ejection fraction and CO
Increase aldosterone = increase Na/H20 retention = increase BP
Increase Sympathetic activity = decrease in B1 receptors
Intrinsic compensation
Myocardial hypertrophy
At 1st, heart compensates for heart failure by increasing muscle mass. Increasing hypertrophy = heart ischemia and “cardiac remodeling”, including changes in ventricular geometry
Ultimately, mycoses die, further stressing those alive
Cardiac performance depends on 4 factors
Preload (increases in HF)
After load (increases in HF, SNS/RAAs compensations)
Contractility (reduced in HF)
Heart rate (increases as a compensatory mechanism)
Cardiac contractility
Trigger Ca = enters cell during AP
Activator Ca = released from SR during systole
once high enough Ca conc, it will sensitize and initiate contractions
contraction intensity = trigger + activator
What does SERCA2a do?
Its a protein in SR membrane.
Bring ca back into SR reticulum, PLN sensitizes and modulates activity of SERCA2a
