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)
Q: What does the heart release as an inflammatory marker? (2)
A: -troponin I
-troponin T
Q: What do vessel walls release as inflammatory markers? (4)
A: ICAM-1
VCAM-1
(E-selectin
P-selectin)
Q: What is the most effective drug for chronic heart failure? 2 other drugs.
A: beta blockers which block the sympathetic drive
ACE inhibitors block the RAS system
Aldosterone receptor antagonists block the aldosterone receptors which are high in heart failure
Q: What are the main 2 symptoms of heart failure? 5 others experienced by patient?
A: -breathlessness
-fatigue
=> main but are vague
- ankle swelling
- weightloss
- anorexia
- orthopnoea (shortness of breath lying down)
- nocturia (having to wake up at night to pee)
Q: Clinical signs of heart failure? (7)
A: -tachycardia
- decrease in pulse volume
- increase in venous pressure
- oedema
- rales (abnormal rattling sound heard when examining unhealthy lungs- sign of LV failure)
- increase in liver size (increase in blood in it-> from increased pulmonary pressure)
- ascites (end stage- belly full of fluid)
Q: Summarising heart failure. Symptoms? (3) Heart is? (2) QoL? LE?
A: Patient is breathless, tired and retains fluid
- Heart is damaged
- Heart less effective as a pump
Quality of life is poor
Life expectancy reduced
Q: What does a chest X ray look like for heart failure?
A: -no fluid retention in lungs but heart is dilated
-There is an increase in the cardio-thoracic ratio
Q: How do you measure the cardio-thoracic ratio in an X ray? Normal value?
A: You measure the widest part of the heart and the distance between one inside rib and the opposite one at the greatest diameter and compare the two
In normal people, the width of the heart should NOT be more than 50% the width of the thorax
Q: Describe the functional classification of heart failure? (4) Main reason for it? (2)
A: 1 = virtually no symptoms - the heart is dysfunctioning but most things are fine
2 = slight limitation of physical activity
3 = marked limitation of physical activity
4 = the patient can’t get out of a chair or is in bed // out of breath from minimal exertion
so that you can tell whether a patient has got better or not after treatment // in clinical trials
Q: Draw a graph to show the progression of heart failure. Describe.
A: -often okay for a while then go down
REFER
-onset of heart failure
- > loss of myocardium
- > fall of BP - baroreceptors ergoreflexes and chemoreflexes activated
- > maintains hormone activation
- sudden death
- coronary events
-progression
mild
- > bacterial invasion
- > immune and inflammatory response
- > onset of cachexia
- > hastens demise
moderate
severe
“There is a plateau and then it suddenly drops off
The last downwards bit can happen in weeks or months
An event can happen (e.g. an infection) which leads to rapid progression and death”
Q: What are the 3 syndromes of heart failure? Describe.
A: Acute Heart Failure
-Associated with pulmonary oedema usually occurs after acute MI
Circulatory collapse
- Associated with cardiogenic shock (poor peripheral perfusion, oliguria, hypotension)
- heart is so badly damaged it can’t maintain circulation
Chronic Heart Failure
-Untreated, congestive, undulating, treated, compensated
Q: If there is a blockage in a coronary artery and the heart muscle dies, what will the patient look like? (5)
A: -look very sick
- tachycardic
- sweating
- sitting upright in bed, very breathless
- coughing up frothy sputum
Q: What does pulmonary oedema look like on a chest x ray? Treatment? (3)
A: lots of white
You need to give intravenous diuretics very quickly to try and get rid of the fluid in the lungs and give small amount of dimorphine
-> get them to cath labs and get coronary artery open quickly
Q: What are the key investigations if you think someone has heart failure? (5) Main way to determine there is an abnormally functioning heart?
A: - chest X ray
- cardiac catheter
- Coronary Angiography - can show where there is a stricture
- 2D echocardiogram - you can see how the heart is actually pumping *******
- MRI scanning - this has revolutionised how we look at the heart and may replace chest X-rays
Q: What’s the management algorithm for heart failure? (8)
A: 1. Establish that patient has heart failure
- Determine aetiology of heart failure-> is it CHD or too much alcohol
- Identify concomitant disease relevant to heart failure -> eg comorbities
- Assess severity of symptoms
- Predict prognosis
- Anticipate complications -> risk assess patients if they’re likely to have acute/life threatening arrhythmias
- Choose appropriate treatment
- Monitor progress and tailor treatment
Q: What are the 4 objectives of treatment in chronic heart failure? Describe each. (3,3,3,1)
A: 1. Prevention (prevent progression)
- Myocardial damage
-Occurrence
-Progression of damage
-Further damaging episodes
- Reoccurrence
-Symptoms
-Fluid accumulation
Hospitalisation
- Relief of symptoms and signs
- Eliminate oedema and fluid retention
- Increase exercise capacity
- Reduce fatigue and breathlessness - Prognosis
- Reduce mortality
Q: Beta blockers are main therapy for acute heart failure. T or F?
A: F
never for acute (need to wait for heart failure to be stable)
Q: Management I. What are the general lifestyle measures that should be taken? (4)
A: Weight reduction
Discontinue smoking
Avoid alcohol excess
Exercise
Q: Management II. (6) Main? Which 3 drug classes should be taken by all patients? Which is good for those with atrial fibrillation?
A: -Diuretics**
-ACE Inhibitors* / ARAs
-Beta-Blockers*
-Aldosterone Antagonists (Spironolactone)
=> Mineralocorticoid receptor antagonist (MRA) *
-Digoxin *A
-Devices (cardiac resynchronisation, ICD)
Q: Management I. Medical interventions. (4)
A: -Treat hypertension, diabetes,
arrhythmias
-Anticoagulation (since their chances are producing clots are increased) -> decrease risk of stroke
-Immunisation-> severe influenza could kill them
-Sodium / fluid restriction (more fluid= more chance of peripheral or pulmonary oedema)
Q: What are the possible treatments for severe heart failure? (4)
A: Intravenous drugs
Fluid control
Devices
Surgery
Q: Name 3 intravenous drugs that can treat severe heart failure.
A: - Diuretics or combination of diuretics
- Nitrates
- Positive inotropes - dopamine/dobutamine
Q: Name 2 forms of fluid control in severe heart failure treatment.
A: Haemofiltration
Peritoneal dialysis or haemodialysis
Q: Name 3 devices that can treat severe heart failure.
A: ICD or pacing
Intraaortic balloon pump
Ventricular assist device, total artificial heart
Q: Name 4 forms of surgery that can treat severe heart failure.
A: CABG for “hibernation”
Valve surgery
Cardiomyoplasty, volume reduction/restriction
Transplantation
Q: What is destination therapy?
A: use to VADs (ventricular assist device) as intermediary to heart transplantation
