Lecture 4 Flashcards
How is a pressure gradient set up in the coronary arteries?
- Pressure at top end of coronary arteries (closest to aorta) = pressure that’s in aorta – drives blood flow down coronary arteries
- Some arteries finish in myocardium = pressure in ventricle determines pressure at end of coronary artery
- Pressure difference is diff between aortic pressure at the top and ventricular pressure at the bottom – drives blood flow
what is the equation for coronary blood flow ?
Coronary blood flow = Perfusion pressure / Resistance
what is perfusion pressure?
pressure difference between the top and the bottom
what is diastole?
when heart muscle relaxes and the heart fills with blood
when coronary blood flow occurs
what happens to the smaller arteries when the heart contracts?
Squeezes the arteries = no flow down them
Every time heart contracts it cuts off its own blood supply
Flow only occurs in diastole
Length of diastole important = time allowing for blood flow to occur
what are the features of cardiac oxygen consumption ?
- Metabolically the heart uses a lot of energy = v active
- Heart actually one of the worst perfused – not a lot of reserves – no wasted flow
- When we exercise our heart – perfusion goes up, flow goes up
what is the equation for oxygen delivery ?
Arterial oxygen concentration x Coronary blood flow
what is the oxygen concentration in the arteries like?
o Relatively little dissolved in plasma
o Mainly determined by oxygen bound to haemoglobin
o Anaemia will cause reduced oxygen delivery
o Ordinarily little change in oxygen content of arterial blood
o So primary determinant of oxygen delivery is coronary blood flow
what are the features of the left ventricular pressure trace?
- Each time heart contracts / QRS complex occurs and ventricles contract – get peak pressure and then fall in pressure in diastole
- If aortic valve opens fully, the pressure generated in ventricle in systole is exactly the same as the pressure generated in the aorta = systolic pressures are all the same
- Ventricles are proximal to the aortic valve – not influencing the diastolic pressure
- So when the ventricles stop contracting and relax – pressure drops pretty much to zero – as its upstream of aortic valve – not being supported in any other way
- Starts to fill again in diastole for the next cycle
- End point in diastole = left ventricle end-diastolic pressure – LVEDP
what are the features of the left ventricle to aorta pressure trace?
• Aortic valve now supporting blood pressure so you get the aortic trace
• Systolic pressures remain exactly the same
• Arterial diastolic BP – 70/80 – much higher than ventricular
• LVEDP – much lower – due to not being supported by aortic valve
• Perfusion pressure in diastole is dependent on the top end – aortic diastolic pressure, and bottom end = LVEDP
o Diff between the 2 is the diastolic pressure gradient – determines blood flow
when does perfusion occur?
during diastole
what can affect the length of diastole?
Tachycardia – increased heart rate – reduces diastole.
Systole is at a pretty much fixed length
o Raised LVEDP – decreases perfusion pressure – (occurs in heart failure) – stretches muscle
o Reduced diastolic pressure – decreases perfusion pressure
what is the definition of autoregulation of coronary blood flow?
Ability of an organ to maintain a constant blood flow despite changes in perfusion pressure
how does autoregulation occur in coronary blood flow?
- Fall in perfusion pressure:
- Arterial pressure drops
- Coronary blood flow drops
- Autoregulation comes in and alters resistance – drops resistance
- Coronary flow back up
- Does this despite the pressure staying low
what is the effect of metabolites in hypoxia?
o Causes marked coronary vasodilatation in situ but not in isolated coronary artery
o Suggests caused by local metabolite – adenosine
o Whole organ needs to be affected – whole organ releases metabolites - vasodilation
o If perfusion is happening anaerobically – get a collection of Potassium ions, Carbon dioxide, Hydrogen ions, Lactic acid
Products of anaerobic metabolism – cause coronary vasodilation
what are the effects of neural and humoral control of vascular control?
o Less important
o Large vessel α-adrenoceptor vasoconstriction
o Smaller vessel β2 vasodilatation
what are the 2 cardiac natriuretic peptides?
Atrial natriuretic peptide (ANP)
B-(Brain) natriuretic peptide (BNP)
what are the features of Atrial natriuretic peptide (ANP)?
Released from atria
Secretory granules in atrial tissue – when stretched (due to increased pressure) they release ANP into the blood
what are the features of -(Brain) natriuretic peptide (BNP)?
Found in brain but released by ventricles
what are the main effects of Cardiac Natriuretic Peptides?
o Increase renal excretion of sodium (natriuresis) and water (diuresis)
o Relax vascular smooth muscle (except efferent arterioles of renal glomeruli)
o Increased vascular permeability
o Inhibit the release or actions of: Aldosterone, angiotensin II, endothelin, anti-diuretic hormone (ADH)
what is the effect of Neutral Endopeptidase (NEP)?
metabolises cardiac natriuretic peptides
inhibition of NEP increases levels of natriuretic peptides
What drugs target Cardiac Natriuretic Peptides?
- Sacubitril – neprilysin inhibitor
* Valsartan –angiotensin II blocker
