19 Pathophysiology of Heart Failure Flashcards
Q: Define heart failure.
A: A clinical syndrome caused by an abnormality of the heart and recognised by a characteristic pattern of haemodynamic (bp is low, HR is increased, renal (renal perfusion is decreased-> hormonal changes), neural (PNS and SNS is out of balance) and hormonal responses
Q: What are the causes of heart failure? (5) Which is most common?
A: Arrhythmias - mainly tachycardias
Valve Disease - mitral or aortic regurgitation or valve stenoses
Pericardial Disease - if the pericardium becomes inflamed and fibrotic then the heart can’t relax and pump as well
Congenital Heart Disease - if there are holes or misconnections then there is an increased risk of heart failure
Myocardial Disease - commonest cause of myocardial disease in this country is coronary heart disease
Q: What are the types of myocardial disease? (6)
A: Cardiomyopathy
- Dilated Cardiomyopathy (DCM) - specific or idiopathic
- Hypertrophic Cardiomyopathy (HCM or HOCM or ASH)
- Restrictive Cardiomyopathy
- Arrhythmic Right Ventricular Cardiomyopathy (ARVC) - congenital
- Coronary artery disease
- Hypertension
Q: Which drugs can cause myocardial disease? (3)
A: Overdosing on beta blockers can decrease the heart rate so much that you get heart failure type syndrome
All the anti-arrhythmics can cause dysfunction of the heart
Calcium antagonists
Q: What is the leading cause of death in europe? Survivors are left with? but they have a chance of?
A: Coronary heart disease
Survivors are left with a damaged heart
50% of all survivors develop heart failure
Q: What’s the relationship between deaths due to heart attacks and heart failure? Population is?
A: Deaths due to heart attacks are declining but due to heart failure are increasing (as they’re surviving)
The population is ageing and heart failure is commoner in old age
Q: What is an MI?
A: acute obstructive occlusion of coronary artery
sudden onset
Q: Describe a transmural MI. (4)
A: full thickness of heart wall
- part that has dies: thin and fibrotic so it will NOT be contracting
- get infarct expansion - the fibrous tissue expands and the rest of the heart tries to remodel to maintain normal pumping activity
- This is called MYOCARDIAL REMODELLING which takes place over months or years
- The rest of the heart tries to remodel itself to cope with the damage that has occurred
Q: Draw 3 diagrams show myocardial remodelling. Describe.
A: REFER
BASELINE 1. area at risk before infarction
HOURS 2. infarct expansion
DAYS 3. late ventricular enlargement
- thinning due to cell slippage
Hypertrophy (outer part where infarct is) - Thinning: cell stretch, loss of cells, decreased ECS, fibrosis (where infarct is)
Q: What is cardiomyopathy? Occurs in what percentage of the heart failure population? What’s the most common cause for young athletes to die?
A: heart disease in the absence of a known cause and particularly coronary artery disease,
valve disease, and hypertension
5%
Hypertrophic cardiomyopathy
Q: What can cause dilated cardiomyopathy? (10)
A: Idiopathic
Genetic and/or Familial cardiomyopathies
Infectious causes eg Viruses & HIV
Toxins and poisons eg Ethanol and Carbon dioxide or hypoxia
Drugs eg Chemotherapeutic agents (could have a detrimental effect on myocardial cells leading to heart failure)
Metabolic disorders eg Nutritional deficiencies
Collagen disorders
autoimmune cardiomyopathies
Peri-partum cardiomyopathy
neuromuscular disorders
Q: What are the causes of restrictive cardiomyopathy? (4)
A: Associated with fibrosis eg Diastolic dysfunction eg Elderly
Infiltrative disorders eg inborn errors of metabolism
Storage disorders eg glycogen storage disease
Endomyocardial disorders eg radiation damage
Q: What are the causes of death in heart failure? (5)
A: 1. Progression of heart failure
- Increased myocardial wall stress
- Increased retention of sodium and water
- Sudden death
- Opportunistic arrhythmia
- Acute coronary event (often undiagnosed) - Cardiac event eg myocardial infarction
- Other cardiovascular event eg stroke, PVD
- Non cardiovascular cause eg pneumonia (Patients with pulmonary oedema in their lungs can get infections which cause metabolic shut down and death)
Q: What are the 3 types of hormonal mediators in heart failure? Where are these factors also activated?
2 other molecules?
A: constrictors
dilators
growth factors
(a lot are also activated in cancer)
cytokines and oxygen radicals
Q: Name 5 constrictor molecules that are released in heart failure.
A: -noradrenaline (increase in adrenaline drive because the body thinks that it’s bleeding to death so you switch on the sympathetic drive and get an increase in noradrenaline)
- renin/angiotensin II (kidney tries to retain salt and water so the RAS system is switched on in the kidney)
- endothelin (potent)
- vasopressin
- NPY (neuropeptide Y)
Q: Name 5 dilator molecules that are released in heart failure. Which is a marker for heart failure identification and severity?
A: -ANP (Atrial natriuretic peptide) *****
- prostaglandin E2 and metabolites
- EDRF
- dopamine
- CGRP
Q: Name 4 growth factors that are released in heart failure.
A: -insulin
- TNF alpha
- growth hormone
- ang II (potent vasoconstrictor)