7 Heart Failure (pathology) Flashcards
1
Q
What is CHF?
A
- congestive heart failure
- the inability of the heart to pump blood at a rate to meet the needs of active tissues
- not enough blood to perfuse the body
- ischemic heart disease= not enough blood to heart
- common, poor prognosis (symptomatic= 45% 1 year mortality)
2
Q
What is the pathogenesis of CHF?
A
- usually results from a slowly developing intrinsic deficit in contraction (occasionally occurs acutely)
- mechanisms;
- abnormal load
- impaired ventricular filling
- obstruction due to valve stenosis (e.g. chronic rheumatic mitral valve disease)
3
Q
What are some examples of acute/chronic abnormal load on the heart that can result in CHF?
A
- acute
- fluid overload
- MI
- valve dysfunction
- chronic
- ischemic heart disease
- dilated cardiomyopathy
- hypertension
4
Q
What are some examples of acute/chronic impaired ventricular filling that can result in CHF?
A
- acute
- pericarditis
- cardiac tamponade
- chronic
- restrictive cardiomyopathy
- severe left ventricular hypertrophy
5
Q
What is systolic dysfunction? What are 3 possible causes?
A
- Progressive deterioration of cardiac (contractile) function
- Causes:
- ischemic heart disease
- pressure or volume overload
- dilated cardiomyopathy
6
Q
What is diastolic dysfunction? What are 4 possible causes?
A
- Inability of heart to relax, expand, and fill sufficiently during diastole
- Causes:
- massive LVH
- amyloidosis (protein deposits in the myocardium, decreasing compliance)
- myocardial fibrosis (primary or after MI)
- constrictive pericarditis
7
Q
What are 2 rapid compensatory mechanisms in CHF?
A
-
Frank-starling
- increased preload dilation
- helps sustain cardiac performance by enhancing contractility
- however increases wall tension and oxygen demand
- Neurohumoral activation
- NE released by cardiac nerves -> increased HR, contractility and vascular resistance
- Renin-angiotensin-aldosterone system
- ANP secreted from atrial myocytes
8
Q
Describe the renin-angiotensin-aldosterone system (RAAS)
A
- decreased renal perfusion -> increases renin release
- renin converts angiotensinogen to Ang I
- ACE converts Ang I -> Ang II
- Ang II= increased vasoconstriction
- Ang II stimulates aldosterone release
- Aldos= increased Na and water resorption
- Vasoconstriction and Na/H2O resorption increases/maintains cardiac output
9
Q
What is ANP?
A
- Atrial natriuretic peptide
- secreted by atrial myocytes when the atrium is dilated
- causes:
- vasodilation
- diuresis
- **think: opposite effects as the RAAS
10
Q
Describe cardiac hypertrophy. What determines the extent of hypertrophy?
A
- CHF compensatory response to increased load over weeks to months
- increased numbers of sarcomeres makes fibers visibly bigger
- NO HYPERPLASIA (same amount of cells)
- extent of hypertrophy varies with underlying cause
- mild: pulmonary HTN, IHD
- moderate: systemic HTN, aortic stenosis, mitral regurg, dilated cardiomyopathy
- severe: aortic regurg, hypertrophic cardiomyopathy
11
Q
What are the two types of hypertophy?
A
- concentric
- from pressure overload (increases systole wall stress)
- parallel sarcomeres remodel
- e.g. HTN, aortic stenosis
- eccentric/hypertrophy accompanied by dilation
- from volume overload (increases diastole wall stress)
- series sarcomeres remodel
- e.g. mitral or aortic regurg.
12
Q
What is often the result of sustained cardiac hypertrophy?
A
**cardiac failure
- increased myocyte size -> decreased capillary density -> increased intercapillary distance -> increased fibrous tissue
- higher cardiac oxygen consumption
- altered gene expression and proteins
- loss of myocytes due to apoptosis
13
Q
What is the pathogenesis of left heart failure? What are 4 common causes?
A
- Effects due to progressive damming of blood within the pulmonary circulation and diminshed peripheral blood pressure and flow
- Causes:
- IHD
- HTN
- aortic and mitral valve disease
- non-ischemic myocardial diseases (cardiomyopathies/myocarditis)
14
Q
What are the clinical symptoms of left heart failure?
A
-
LVH and often dilation
- can result in mitral valve insufficiency
- Secondary enlargement of the left atrium
- Can cause atrial fibrillation -> stagnant blood in atrium -> thrombus, emoblic stroke
- Pulmonary congestion and edema
15
Q
What are the clinical symptoms of pulmonary congestion?
A
- heart failure cells on histology
-
dyspnea, orthopnea (dyspnea lying down), paroxysmal nocturnal dyspnea
- when supine, venous return increases and diaphragm elevates
- rales on exam
21
Q
Compare and contrast left/right heart failure
A
