Heart Failure and Cardiomyopathy Flashcards
What is heart failure?
The inability of the heart to properly fill or empty the ventricle
What usually causes heart failure?
CAD Cardiomyopathy Valve abnormalities (esp mitral and aortic) HTN Pericardial diseases Pulmonary HTN
Forms of ventricular dysfunction
Systolic and diastolic HF
Acute and chronic HF
Left and right sided HF
Low output or high output HF
Adaptive responses to HF
In the failing heart, these mechanisms are initiated to help improve CO:
Frank-Starling Relationship
SNS activation
Alterations in contractility, HR, and afterload
Humoral responses
When these mechanisms become maladaptive, it leads to myocardial remodeling.
What is myocardial remodeling?
Changes in size, shape, structure and physiology of the heart after injury to the myocardium
Initially, the body tries to compensate for HF in this manner
Activation of the SNS
Why does the body activate the SNS in HF?
It’s all about maintaining BP and CO**
1) Arteriolar constriction
- Maintains BP (increases SVR) despite decrease in CO
- Redirects blood flow to coronary and cerebral systems (shunt to important systems!)
2) Venous constriction
- Increase preload
- Attempt to increase CO via frank starling
3) RAAS
- Activated d/t decrease in RBF from shunting to important organs
- Causes increase in blood volume and ultimately CO
4) HR is increased (trying to increase CO)
Eventually this system will poop out because the increase in SVR increases workload
Patho of HF
Pressure overload- aortic stenosis, HTN
Volume overload – mitral or aortic regurgitation
Myocardial ischemia/infarction
Myocardial inflammatory disease
Restricted diastolic filling – constrictive pericarditis, restrictive myocarditis
Other adaptive mechanisms to increase CO
Increase in contraction velocity Reduction in afterload Increase in HR Release of BNP - Function is to decrease SVR and cause natriuresis
Myocardial remodeling that can occur
Hypertrophy
Dilation and wall thinning
Increased interstitial collagen deposition
Fibrosis and scar formation
Remodeling leads to increased O2 requirements (more at risk for ischemia)
S/S of HF
Dyspnea - Orthopnea/ orthopneic cough - Paroxysmal noctural dyspnea Fatigue Weakness at rest Tachycardia Oliguria Edema Atrial fibrillation due to dilation Tachypnea Lung Rales S3 gallop Hypotension JVD
Diagnosis of HF
CXR
Cardiac Echo
Elevated levels B-type natriuretic peptide
MRI
Management of HF
ACE Inhibitors/ ARBs
- Decrease afterload by interfering with RAAS to cause peripheral vasodilation
Aldosterone antagonists
- Aldosterone production is increased in HF d/t activation of the RAAS. Causes Na+ retention and K+ excretion.
Diuretics
- Decrease preload (thiazide and loop)
Digoxin
- Increases contractility and treats a-fib
Inotropes
- Increase contractility (dobutamine and milrinone)
Beta blockers
- Inhibit the SNS. Slow HR and lowers BP. Shown to reverse remodeling.
Vasodilator therapy
- Decreases afterload (hydralazine and isosorbide)
Biventricular pacing
- improves ventricular function and reverses remodeling
Nesiritide
- Synthetic BNP. Decreases preload by stimulating natriuresis, and decreases afterload via vasodilation
Assist devices
- IABP
Transplant
The presence of __ is the single most important risk factor for predicting perioperative cardiac morbidity and mortality
HF
Patho of HF in a nutshell
Decreased contractility
Ventricle is dilated to increase contractility from stretched muscle fibers
Increased radius of ventricle increases cardiac work
Increased work and O2 demand
CO falls
SNS outflow to increase HR and SVR
SV falls
