Anatomy and pathophysiology of heart failure Flashcards
Where does the pulmonary artery go?
- to the lungs
Where does the aorta go?
- to the body
Where does the pulmonary vein go?
- the left atrium
Where does the superior vena cava go?
- the right atrium
Primary causes of heart disease
- congenital
- acquired
– chronic degenerative valve dz
– cardiomyopathy
– endocardial infection
– pericardial dz
– rate/rhythm abnormalities
What 3 things maintain perfusion?
- normal systemic arterial pressure
- cardiac output (HR + SV)
- venous pressures
What is vascular resistance?
- force exerted on the blood by the vasculature
What is pre-load?
- the volume of blood / hydrostatic pressure within the ventricles at the end of diastole
What is afterload?
= systemic vascular resistance
- the pressure the heart works against to open up the aorta in systole
- material bp is the primary factor
Acute vs chronic heart failure
Acute
- rare
- vascular dz and AMI are rare
Chronic
- most common
- usually degenerative conditions
Pathophysiology of heart failure
- whatever the cause -> CO falls -> detected as a fall in BP
- chronic degenerative valve dz: regurgitation means fall in forward flow and CO
- DCM: systolic failure -> fall in stroke volume and therefore CO
- HCM/RCM: ventricle can’t fill -> fall in CO
- congenital dz: if develop failure because CO fall
- mechanisms activated to restore bp:
– sympathetic ns activation
– RAAS
– cardiac enlargement
Sympathetic nervous system - action in heart failure
- increases rate
- vasoconstriction
- causes the kidney to release renin
RAAS - action in heart failure
- systemic vasoconstriction
- increased blood volume
- renal sodium and fluid retention
Consequences of CO & BP fall
Increased sympathetic activity ->
- increased rate & force of myocardial contraction
- peripheral venoconstriction
- renin secretion and activation of RAAS
- peripheral vasoconstriction
Renin secretion & activation of RAAS ->
- retention of salt & water
Retention of salt & water + peripheral venoconstriction ->
- increased venous return
Increased rate & force of myocardial contraction + increased venous return ->
- increased CO
Peripheral vasoconstriction ->
- increased peripheral resistance
Increased peripheral resistance + increased CO -> increased systemic blood pressure
Effect of compensatory mechanisms
- HR increases
- vasoconstriction
- contractility goes up
- salt & water retained
- (cardiac enlargement)
- hence CS
Effect of vasoconstriction
Of arteries
- increased after load -> CO falls more -> increased after load -> valves leak more
Of veins
- increased volume returning to heart
- increased atrial pressures
- increased likelihood of oedema
Effect of salt & water retention
- volume returned to heart goes up
- volume of fluid in vessels goes up
- pressure in capillaries goes up
- oedema develops
Effect of cardiac enlargement
- AV valves leak more
- oxygen needs go up
- oxygen supply goes down
- cells die -> not replaced, scar tissue forms
- contractility falls further
Effects of chronic stimulation of SNS
Heart
- increased oxygen demand by myocardium -> heart weakened further
- increased venous return -> circulatory congestion
Arteriole
- vasoconstriction -> increased afterload
Skin & muscles
- vasoconstriction -> weakness & fatigue
Kidney
- release of renin
-> activation of RAAS
How do we tx heart failure?
Most pts present with oedema
- typically pulmonary oedema -> due to left-sided dz
- oedema is a consequence of the compensatory mechanisms
So we manipulate those mechanisms
1. reduce fluid build up - diuretics
2. antagonise RAAS - ACE inhibitors ± aldosterone antagonists
3. vasodilator - pimobendan
