pathophys of CHF Flashcards
forward heart failure
The inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body
backward heart failure
the ability to pump blood forward at a sufficient rate only if the cardiac filling pressures are abnormally high
what is heart failure?
Syndrome, not a Disease!
At some time during the course of the illness, CHF is a principal manifestation of nearly every form of cardiac disease
can be forward, backward or both
can be acute or chronic
what are the 4 major determinants of cardiac performance
heart rate
preload
afterload
contractility
Role of Ca2+ in Cardiomyocyte Contractility
Calcium induced calcium release. the amount of calcium released from the SR determines the ionotrophy/contractility
how do you calculate ejection fraction
SV/EDV x 100
(SV = EDV-ESV) normal is greater than 50%
Frank-starling law
the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant
disorders of impaired contractility
Myocardial Infarction/Ischemic Cardiomyopathy
Chronic Mitral Regurgitation
Dilated Cardiomyopathy
disorders of increased afterload
Severe Aortic Stenosis
Uncontrolled Hypertension
Disorders with Impaired Ventricular Relaxation/Decreased Filling
Restrictive Cardiomyopathy
Acquired or Familial Hypertrophic Cardiomyopathy
Constrictive Pericarditis
Systolic Heart Failure’s affect on ejection fraction
reduces the ejection fraction
decreased contractility = decreased stroke volume
diastolic heart failures affect on ejection fraction
remains relatively the same - due to decreased compliance, EDV is decreased
differences of the RV compared to the LV
RV is much more “compliant” than LV
Wall Thickness
RV Developed Pressure
cardiac causes of right sided heart failure
LV Failure of any cause
Mitral Stenosis/Regurgitation
Acute MI with RV Infarction
Pulmonic Stenosis
pulmonary causes of right sided heart failure
Pulmonary Parenchymal Diseases
•COPD
• Interstitial Lung Diseases (silicosis, pulmonary fibrosis, etc.)
• ARDS
Pulmonary Vascular Diseases
• Pulmonary Embolism
• Primary Pulmonary Hypertension
compensation mechanisms to maintain CO in CHF
- Frank-Starling Mechanism - seconds (Length-Dependent Activation)
- Autonomic Nervous System - second (Baroreceptor Response)
- Renal Compensation – seconds to hours (Renin-Angiotensin-Aldosterone System)
- ` Ventricular Remodeling – weeks to years
all are acutely beneficial but can lead to worsening ventricular preformance
Post-MI Ventricular Remodeling definitions
LV enlargement and distortion of regional and global ventricular geometry occurring after myocardial infarction
or
Any architectural or structural change that occurs after myocardial infarction in either the infarcted or noninfarcted regions of the heart.”
Ventricular Remodeling in other forms of Heart Disease
Pre- and Post-Natal Cardiac Growth ( Cardiac Eutrophy)
Pressure-Overload LVH (Concentric LVH)
• Aortic Stenosis
• Systemic Hypertension
Volume-Overload LVH (Eccentric LVH)
• Mitral Regurgitation
• AV Fistula
• Hyperthyroidism
concentric hypertrophy vs. eccentric hypertrophy
Concentric hypertrophy is due to pressure overload (really thick walls), while eccentric hypertrophy is due to volume overload ( really big size)
what contributes to systolic and diastolic wall stress
volume overload pressure overload post-MI segmental dysfunction myocardial dysfunction myocardial hypertrophy
what does systolic and diastolic wall stress lead to
myocardial dysfunction
myocardial hypertrophy
wall stress equations
(pressure x radius)/ wall thickness
risk factors for developing post-MI ventricular remodeling
large infarct
anterior is greater risk than posterior
reduced EF 4 days after MI
vessel is occluded after the MI
when does remodeling occur
months to years before symptoms of CHF
how can congestive heart failure be prevented
by preventing or slowing the progression of ventricular remodeling
what causes remodeling
Remodeling is predominantly a growth-mediated response, and results from an interplay between mechanical factors, and systemic and locally derived neurohormonal factors.
Structural changes in the ventricular myocardium represent the disease process
drugs to prevent ventricular remodeling
ACE Inhibitors/ARBs/LCZ696
Beta Blockers
Aldosterone Antagonists
drugs to prolong survival with CHF
ACE Inhibitors/ARBs/LCZ696
Hydralazine + Nitrates
Beta Blockers (carvedilol, metoprolol, bucindolol)
Aldosterone antagonists (spironolactone,
eplerenone)
symptoms and clinical findings of right sided HF
peripheral edema
RUQ discomfort
JVD
hepatomegaly
symptoms of left-sided HF
dyspnea orthopnea (cannot lie flat) paroxysmal nocturnal dyspnea (shortness of breath while sleeping) cough fatigue
physical findings of left sided HR
diaphoresis tachycardia tachypnea pulmonary rales loud P2 *S3 gallop (systolic dysfunction) *S4 gallop (diastolic dysfunction)