Pathophysiology Of Heart Disease Flashcards
Give a definition of heart failure
A state in which the heart fails to maintain adequate blood supply to the body despite an adequate filling pressure
What is the primary cause of systolic heart failure?
Ichaemic heart disease
Describe the 4 classes of heart failure
Class I- asymptomatic, no limitation in physicial activity
Class II- Slight limitation of physical activity, comfortable at rest
Class III- Marked limitation of physical activity, comfortable at rest
Class IV- unable to carry on any physcial activity without discomfort, symptoms at rest
What is the approximate normal value for cardiac output?
5 l/min
What is the approximate normal volume for stroke volume?
75ml/beat
What is an approximation of a “normal” ejection fraction?
50%
What is Starling’s Law of the Heart?
Stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction i.e. the end diastolic volume
List some causes of heart failure
Coronary artery disease
Hypertension
AF
Valve disease
Cardiomyopathies
Infective endocarditis
Anaemia
Endocrine disorders
Cor pulmonale
How can heart failure be classified based on the cause of the inadequate cardiac output?
Left ventricular failure
Right ventricular failure
Congestive heart failure
Low output high output heart failure (excessive afterload, excessive preload, pump failure)- LVSD, HFpEF
Give some of the symptoms of LVF and RVF
LVF: paroxysmal nocturnal dysponea, wheeze, nocturnal coughing with pink sputum (caused by pulmonary oedema)
RVF: caused by LVF usually, peripheral oedema, ascites
What are the three broad methods of treating heart failure?
Give some examples of each.
Conservative - smoking cessation, weight loss, healthy diet, exercise
Medical - ABCDDS
ACE inhibitors, Beta blockers, Candesartan(if intol. for ACEi) Digoxin, Diuretics, Spironolactone
Surgical- heart transplant, valve replacement
What investigations might you want to carry out to test for heart failure?
FBC
U & Es
LFTs
TFTs
Lipid profile
BNP (suggests measure of stretch of cardiac myocytes)
CXR: “ABCDE”
Alveolar oedema, Kerley B lines, Cardiomegaly, Dilated upper lobe vessels, pleural Effusion
ECHO
ECG
Name some causes of LEFT sided heart failure
Coronary artery disease
Hypertension
Aortic valve disease
Mitral valve disease
Myocardial disease
Name some causes of RIGHT sided heart failure
*LEFT sided heart failure*
Tricuspid valve disease
Pulmonary valve disease
Pulmonary vascular disease (Cor pulmonale)
Briefly explain the pathophysiology of heart failure one LVF or RVF has been established
Ischaemic injury leads to reduced myocardial efficiency
Increases workload, decreased cardiac output, decreased contractility
COMPENSATORY MECHANISMS: Activation of RAAS, Activation of sympathetic nervous system, increased myocyte size
These worsen HF overtime + cardiac damage
How do chronically activated compensatory mechanisms such a RAAS and the sympathetic nervous system lead to worsening of heart failure?
RAAS activated: Increased Na+ and H20 retention
Increased PRELOAD
SNS activated: Increased HR and peripheral vasoconstriction
Increased AFTERLOAD
In HF, what is the cause of cardiac dilation?
Increased end-diastolic volume
In HF, what is the cause of raised JVP?
Right sided-heart failure and fluid overload
What causes hepatomegaly in right sided heart failure?
Congestion of the hepatic circulation
What is heart failure with preserved ejection fraction?
HF that is not caused by LV systolic dysfunction, but LV diastolic dysfunction i.e. not a problem with contraction but a problem with relaxation of the LV leading to reduced filling- caused by concentric remodelling of the LV
Explain how heart failure leads to peripheral oedema and ascites
Heart failure leads to increased capillary hydrostatic pressure at the venous end which pushes fluid out of the capillaries and into the interstitium
RAAS activation also leads to fluid retention
List some of the neuro-hormonal activation that occus due to heart disease
Sympathetic nervous system
RAAS
Natriuretic hormones
ADH
Endothelin
Prostaglandins/ NO
Kallikrien System
TNFalpha
Describe how the activation of the sympathetic nervous system attempts to improve cardiac output in HF and how this manifests in the long-term.
Increased cardiac contractility
Vasoconstruction
Tachycardia
Long- term:
Beta adrenergic receptors down-regulated
Cardiac hypertrophy, myocyte apoptosis and necrosis
Upregulation of RAAS
Reduction in HR variability
Why is RAAS commonly activated in HF?
Reduced renal blood flow
Sympathetic nervous system induction of renin from the macula densa (More AngI to AngII)
List some of the downstream effects of elevated angiotensin II
Vasoconstriction
LVH, myocyte dysfunction
Aldosterone release
Na+ and H20 retention
Thirst
Enhanced sympathetic activity
What is are the roles of natriuretic hormones: ANP and BNP?
Balance the effects of RAAS on vascular tone and Na/H20 balance
Constrict afferent and vasodilates efferent arterioles
Decrease Na+ reabsorption in the kidney
Decrease renin and aldosterone secretion
What important role does BNP have in the diagnosis of HF?
Used as a sensitive marker for HF (released from the ventricles in response to stretch)
What happens to ADH levels in a patient with HF?
Would you expect this? Explain.
Increased
No, not expected- increased atrial pressure and blood volume should decrease the production of ADH so the body can lose some fluid
RAAS and SNS seem to override this in HF and cause increased ADH
The hormone endothelin may be _______ in some patients with heart failure. Its role is to __________ systemic and renal blood vessels, thus _________ RAAS.
Increased
Constrict
Activate
What is the role of prostaglandin in HF?
Vasodilates Afferent renal arterioles–> increases the effects of NA/RAAS
How does NO relate to heart failure?
NO synthase is blunted in HF
Lose vasodilation –> contributes to HF
Is TNFalpha increased or decreased in HF?
Increased
List some causes of increased peripheral arterial resistance in HF
Sympathetic nervous system
RAAS
Reduced NO
Increased endothelin
What is cachexia and what is its relevance in HF?
Reduction in skeletal musle mass
Can be caused by HF due to reduced skeletal blood flow
Explain the renal effects of HF and how this changes throughout its progression.
Early HF: GFR maintained by haemodynamic changes at the glomerulus
Later: Increased Na+ and H20 retention, lose nephrons, kidney shrinks
Late HF: renal blood flow falls–> reduced GFR, rise in serum urea and creatinine
This can be exacerbated by inhibition of AngII (HF medication)
