Heart as a Pump

Question 1

Chronotropic

Answer 1

speed of contraction (affect opening of channels)

Question 2

Ionotropic

Answer 2

strength of contraction (where the Ca goes)

Question 3

Describe contraction of cardiac muscle

Answer 3

(2 ways Ca increases)
Action potential causes influx of Ca via L-type dihydropyridine (DHP) channels

DHP activation causes conformational change in ryanodine R in SR
causes Ca to flood out

Rise in intracellular Ca (influx and sarco release) is insufficient to cause max contraction force

Question 4

Plateau on myocardial AP caused by what

Answer 4

the influx of Ca

Question 5

How do you increase HR via f-type Na channels?

Answer 5

by increasing their probability of opening (chronotropic effects)

Question 6

2 functions of the plateau phase

Answer 6

1. avoiding summative contraction (otherwise whole muscle would contract, no pulsatile force to push blood/ time to fill the heart)
2. Is the Absolute Refractory Period: keeping depolarised to prevent another AP from occurring

Question 7

What causes the refractory period of cardiac muscle?

Answer 7

inactivation of Na channels

Question 8

Refractory period of skeletal muscle vs cardiac muscle (times)

Answer 8

Skeletal: absolute 1-2ms, contraction 20-100ms

Cardiac: ARP ~245ms, RRP, SNP (period of supranormal excitability), period of contraction 250ms

Question 9

What happens in the SNP?

Answer 9

Supranormal period of excitability:
majority of Na channels reset, but not quite at low enough levels to have same change in membrane R required for threshold. You are starting closer to the threshold than normal, so if another AP tried to propagate, there’s an increased chance of this happening.

Question 10

Calcium levels in ischaemic damage

Answer 10

excessive Ca released extracellularly, more available to influx into cells, cause weird fluxes in RRP, SNP.

Question 11

difference between end diastolic volume and end systolic volume is

Answer 11

stroke volume (80ml)

Question 12

Is diastolic filling passive or active?

Answer 12

2/3rds of it is passive opening of mitral valve (as pressure in pulmonary greater than in ventricles)

last 1/3rd the atria contract. Atria contribution increases with exercise.

Question 13

Why is the pressure in the ventricles low when its filling?

Answer 13

compliance of ventricles: slight bulge in pressure when the atria contract for the last 1/3rd of blood to come in

Question 14

What causes first heart sound

Answer 14

contraction of the ventricles pushes against the mitral valve - causes AV VALVE SHUT CLOSED

Question 15

How do we get the aortic valve to open?

Answer 15

need to build force in ventricle to exceed what’s in aorta
need ventricular pressure > aorta to open it.
Push blood out of ventricle

Question 16

Isovolumic period of contraction

Answer 16

Contraction: rapid ejection 1/3rd when 70% SV ejected

Period of slow ejection (2/3) when 30% ejected

Question 17

Blood pressure in systemic vs pulmonary circulation

Answer 17

Much lower in pulmonary! Systolic 30mmHg, diastolic 12mmHg.

Shorter distance, resistance is lower, don’t need same MABP to generate flow around it.

Question 18

Describe Frank Starling mechanism?

Answer 18

the ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return.

There comes a point where stretching the heart reaches an optimum/max capacity for sarcomeres, after that it plateaus and you are causing damage to heart.
If you stretch too far: heart failure.

Question 19

Where do we get cardiac sympathetic and parasympathetic innervation?

Answer 19

Sympathetic: throughout entire heart exerting a positive ionotropic effect (noradrenaline)

Parasympathetic: mostly to SA node. Mainly effect to decrease rate.

Question 20

What effect does noradrenaline have on Beta1 receptors in the heart?

Answer 20

enhances Ca influx
Promotes storage and release of Ca from sarcoplasmic stores
–> increased contractility and speed of relaxation

Question 21

What could cause a positive ionotropic effect on length-tension relationship?

Negative ionotropic effect?

Answer 21

Sympathetic innervation (greater stroke volume achieved)

Pathophysiology (altering ventricle wall function)

Question 22

ESV/EDV refers to volume where?

Answer 22

in the ventricle

Hence EDV-ESV=SV (quantity of blood expelled per beat)

Question 23

What happens at same time point as ESV? (valve)

Answer 23

the aortic valve closes

Question 24

What happens at same time point as EDV? (valve)

Answer 24

mitral valve closes

Question 25

What is Fick’s principle?

Answer 25

to determine cardiac output

CO= rate of O2 consumption/arteriovenous O2 difference

Question 26

Three things that increase the SV

Answer 26

1. increase end-diastolic volume (Frank Starling)
2. increase sympathetic nerve activity
3. increase adrenaline

This will then increase the CO.

Question 27

4 ways to increase venous pressure & return to the heart

Answer 27

1. increased sympathetic innervation
2. increased skeletal muscle
3. increased blood volume (eg. haemorrhage, fluid challenge)
4. increased inspiratory movements (caused by increased pressure diff between peripheral veins and heart)

Question 28

What effect does sympathetic innervation have on veins

Answer 28

increases venous return to heart and therefore increases CO