7 Heart Failure (pathology) Flashcards
What is CHF?
- 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)
What is the pathogenesis of CHF?
- 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)
What are some examples of acute/chronic abnormal load on the heart that can result in CHF?
- acute
- fluid overload
- MI
- valve dysfunction
- chronic
- ischemic heart disease
- dilated cardiomyopathy
- hypertension
What are some examples of acute/chronic impaired ventricular filling that can result in CHF?
- acute
- pericarditis
- cardiac tamponade
- chronic
- restrictive cardiomyopathy
- severe left ventricular hypertrophy
What is systolic dysfunction? What are 3 possible causes?
- Progressive deterioration of cardiac (contractile) function
- Causes:
- ischemic heart disease
- pressure or volume overload
- dilated cardiomyopathy
What is diastolic dysfunction? What are 4 possible causes?
- 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
What are 2 rapid compensatory mechanisms in CHF?
-
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
Describe the renin-angiotensin-aldosterone system (RAAS)
- 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
What is ANP?
- Atrial natriuretic peptide
- secreted by atrial myocytes when the atrium is dilated
- causes:
- vasodilation
- diuresis
- **think: opposite effects as the RAAS
Describe cardiac hypertrophy. What determines the extent of hypertrophy?
- 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
What are the two types of hypertophy?
- 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.
What is often the result of sustained cardiac hypertrophy?
**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
What is the pathogenesis of left heart failure? What are 4 common causes?
- 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)
What are the clinical symptoms of left heart failure?
-
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
What are the clinical symptoms of pulmonary congestion?
- heart failure cells on histology
-
dyspnea, orthopnea (dyspnea lying down), paroxysmal nocturnal dyspnea
- when supine, venous return increases and diaphragm elevates
- rales on exam
What are 2 systemic systems affected by left heart failure?
- Kidneys
- decreased renal perfusion activates RAAS -> increased blood volume
- severe perfusion deficit -> prerenal azotemia (impaired kidney function)
- Brain
- cerebral hypoxia
- encephalopathy
Describe right heart failure. What are 4 possible causes?
- Effects are primarily due to engorgement of systemic and portal venous systems
- Causes:
- usually secondary to left sided failure
- pulmonary HTN
- primary myocardial disease
- tricuspid or pulmonary valvular disease
What is the heart’s response to right heart failure?
Right ventricle responds to increased workload with hypertrophy and often dilation
What are 4 systemic systems affected by right heart failure?
- liver/portal system
- increased pressure in portal vein -> congestive hepatosplenomegaly, cardiac cirrhosis, ascites
- “nutmeg liver” from centrilobular congestion
- kidneys
- congestion, fluid retention, peripheral edema, azotemia (more marked with R failure than L)
- brain
- venous congestion and hypoxic encephalopathy
- lung
- pleural effusion, atelectasis (lung collapse)
Describe the edema seen in right heart failure
- systemic/peripheral edema
- at ankle (pedal)
- presacral
- pleural and pericardial effusion
- eventual anasarca (generalized massive edema)
Compare and contrast left/right heart failure
What is azotemia? How is it different in left and right heart failure?
- abnormally high levels of nitrogen-containing compounds (e.g. urea) in the blood from insufficient filtering by the kidneys
- left HF causes low arterial flow to kidneys
- less severe impairment
- decreased nutrient supply
- right HF causes venous congestion in the kidneys
- more impairment of function
- secondary to lack of metabolite/waste removal (and when severe, stasis on arterial side)
- Think: it’s worse when the supplies build up in the factory than if they don’t get there in the first place
