Physiology of the heart 3 Flashcards

1
Q

Where do the coronary arteries come from and how do they supply the heart?

A

First branch off the aorta

coronary arteries run over the surface of the heart- blood perfuses into the myocardium

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2
Q

Whats does coronary blood flow =

A

coronary blood flow= perfusion pressure/ resistance

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3
Q

What is perfusion pressure?

A

Pressure at either end of the coronary circulation

pressure gradient that drives coronary blood pressure

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4
Q

What does resistance depend on?

A

flow going down the tube
length of the tube
viscosity of the contents
diameter of the artery

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5
Q

When does coronary blood flow occur?

A

In diastole- when the heart is not contracting

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6
Q

How does the perfusion pressure differ from the top of the coronary arteries to the bottom?

A
Top= equivalent to the arterial diastolic pressure 
bottom= hard to measure as its small capillaries at the bottom- equates to the pressure in the ventricles
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7
Q

What is the oxygen consumption of an arrested heart, resting and active?

A

arrested (alive but not contracting)= 2ml/min/100g
resting= 8
heavy exercise= 70

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8
Q

Whats the perfusion of the heart like?

A

One of the worst perfused organs

uses all the oxygen it can get

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9
Q

What does oxygen delivery =?

A

arterial oxygen concentration x coronoary blood flow

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10
Q

What are the characteristics of arterial oxygen concentration?

A

mainly determined by oxygen bound to haemoglobin

generally maximised- theres little change

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11
Q

What are the characteristics of coronary blood flow?

A
controlled by :
neural factors
hormones
local metabolites
mechanical factors
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12
Q

What does the left ventricle to aorta pressure trace look like?

A

use a catheter to get the measurements
systolic BP is the same
arterial diastolic pressure is higher than the LVEDP due to the aortic valve closing
difference between ADP and LVEDP= perfusion pressure

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13
Q

Why is the window between systoles important?

A

This is the time for perfusion to occur

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14
Q

Which events affect perfusion and why?

A
  1. Tachycardia- reduces diastole and thus time for perfusion
  2. Raised LVEDP (due to heart failure, hypertension etc.)- decreases perfusion pressure
  3. Reduced arterial diastolic pressure- decreased perfusion pressure
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15
Q

How does the heart exhibit autoregulation of coronary blood flow?

A

If arterial pressure dropped and thus blood flow through the capillaries dropped-
heart goes into autoregulation mode
resistance of vessels decreases- maintains the coronary flow
maintained flow despite the pressure remaining reduced
*only within a certain range of pressures- if pressure is way too high or low- autoregulation is overridden

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16
Q

What is autoregulation of blood flow?

A

Ability of an organ to maintain constant blood flow despite changes in perfusion pressure for example

17
Q

How do they know that metabolites are important in vascular control?

A

Hypoxia causes marked coronary vasolidation in situ
but not in an isolated coronary artery
there is something in the heart responding to hypoxia and causing vasodilation

18
Q

Which receptors cause vasodilation and vasoconstriction?

A

Alpha receptors on the larger coronary arteries cause vasoconstriction
Smaller beta 2 receptors on smaller arteries- cause vasodilation
*resistance is all in the small vessels
big vessels matter pathologically- tight stenosis in the coronaries needs fixing

19
Q

Why is the heart technically an endocrine organ and happens as a result?

A

Secretes natriuretic peptides
atrial natriuretic peptide
brain natriuretic peptide
-released due to stretching of atrial and ventricular muscle cells/ raised atrial or venticular pressure = overload
Main effects:
increases renal extraction- natriuresis and diuresis
relax vascular smooth muscle (apart from efferent arterioles of renal glomeruli- maintain filtration pressure to get rid of na and water)
increased vascular permeability
inhibit the release/ actions of:
aldosterone (retain na and h20), angiotensin 2 (vasocontrictor), endothelin and ADH

20
Q

What is CNP and what inhibits its degradation?

A

Cardiac natriuretic peptides
broken down by neutral endopeptidases (neprilysin)
inhibits its breakdown- potentiates the effects of the CNPs- have longer lasting effects
drugs that do this:
sacubitril- neprilysin inhibitor
valsartan - angiotensin 2 blocker
both used as a novel therapy of heart failure- block angiotensin 2 and potentiate the effects of good CNPs