Cardio physiology Flashcards

1
Q

Mechanism of contraction in cardiac myocytes

A

Myocytes contain myofibrils

Myofibrils are made up of sarcomeres

Sarcomeres contain thin actin filaments and thick myosin filaments

In the absence of calcium –> troponin/tropomysin complexes block cross-bridging

Calcium binds topronin –> allows cross-bridging and contraction

ATP required to detach myosin and actin

Myocytes have two systems of intracellular
membranes:
■ T-tubules
■ sarcoplasmic reticulum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Cardiac action potential cycle

A

Phase 0
-Rapid increase in sodium permability
-Rapid depolarisation

Phase I
-Rapid repolarisation
-Rapid decrease in sodium permeability
-Small increase in potassium permability

Phase 2
-Slow repolarisation
-Plateu effect due to influx of Ca2+
-Plateau lasts about 200 ms.

Phase 3
-Rapid repolarisation
-Increase in potassium permability
-Inactived Ca2+ influx

Phase 4
-Resting membrane potential,
for ventricular muscle -90mV
-SA noode and conduction system do not have resting potential, continual rhythmic firing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Action potential: Phase 0

A

Na fast gates open, increase Na permability

Na fast influx

Cell becomes most positive it can be away form resting potential –> depolarisation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Action potential: Phase 1

A

Na permability reduces, fast Na gates closed

Rapid repolarisation begins, electrical potential moves more negatively away from positive Na peak

Small increase in K permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Action potential: Phase 2

A

Slow repolarisation – plateau effect due to inward
movement of calcium

Plateau lasts about 200 ms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Action potential: Phase 3

A

Rapid repolarisation – increase in potassium permeability

Inactivation of slow inward Ca++ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Action potential: Phase 4

A

The resting membrane potential of the ventricular
muscle is about −90 mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Location of AV node

A

Atrioventricular node

Located in atrioventricular fibrous ring on the right side of atrial septum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Vagal stimulation to heart

A

Vagal innervation to the SA node

Increased activity slows firing of SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Phases of the cardiac cycle

A

Phase I: Isovolumetric contraction

Phase II: Ejection

Phase III: Diastolic relaxation

Phase IV: Filling phase of diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Phase I: cardiac cycle

A

Isovolumetic contraction

Atroventricular valve closes

Aortic and pulmonary valves closed

Volume remains constant but presssures dramatically increases as ventricles contract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Phase IIa: cardiac cycle

A

Ejection

Pressure in ventricles exceeds that in the aorta and pulmonary artery

Aortic and pulmonary valves open, blood ejected from ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Phase IIb: cardiac cycle

A

Ejection - equal pressures

Aortic and pulmonary artery pressures now equal to that of the ventricles - flow reduces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Phase III: cardiac cycle

A

Diastolic relaxation

Isovolumetric relaxation, volume in ventricles remains the same and the resting ventricular pressure forms as pulmonary and aortic valves close

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Phase IVa: cardiac cycle

A

Passive filling during diastole

Atrioventricular valve opens

Low atrial pressure due to suction effect of ventricle

Rapid ventricular filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Phase IVb: cardiac cycle

A

Decline in rate of filling as atrial volume increases

Atria now full, flow rate reduced

85% of final diastolic ventricular volume reached

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Phase IVc: cardiac cycle

A

Atrial contraction

SA node depolarises

Atrial muscle contracts

Provides an additional 15% to ventricles (at-rest)
At higher HR and stroke volumes this is significantly more
–> Failure of atrial contraction therefore at higher heart
rates, e.g. fast atrial fibrillation (AF); exercise may be life-threatening.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Normal right atrial pressures

A

0-4 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Normal right ventricular pressure

A

25 / 0-4 mmHg

20
Q

Normal left atrial pressures

21
Q

Normal left ventricular pressures

A

12 / 0-10 mmHg

22
Q

Third heart sound

A

Rapid ventricular filling

23
Q

Fourth heart sound

A

Atria contracting against a stiff ventricle

LVH or HF

24
Q

a-wave JVP

A

First peak: Atrial contraction

Absent in AF

Cannon waves in complete HB as atria contract against a closed tricuspid valve

Giant waves in pulmonary hypertension, tricuspid and pulmonary stenosis

25
c-wave JVP
Small peak on approach to x-descent This is tricuspid valve bulging during isovolumetric contraction of ventricles Timed with carotid artery pulse wave
26
x-descent JVP
First valley Due to tricuspid valve moving down during ventricular systole.
27
v-waveJVP
Second peak Rise in atrial pressure as atria fills prior to opening of tricuspid valve
28
y-descent JVP
Second valley Tricuspid valve opens and blood enters ventricle cuasing pressure in atria to drop
29
JVP waveforms
ACX VY At CX Vascular Yunit
30
Coronary flow is lowest...
During isovolumetric contraction - Phase II Compression of the intramyocardial arteries Conditions resulting in low diastolic BP or increased intramyocardial tension during diastole (e.g. an increased end diastolic pressure) may compromise coronary blood flow
31
Tissue with least coronary flow
Subendocardial muscle where the tension is highest
32
Coronary flow is highest...
Diatole when there is an adequate diastolic BP Increased when there is adequate time between beats - i.e. at slower HRs
33
Factors increasing afterload
Raised aortic pressure Aortic valve stenosis Ventricular cavity size, great volume, requires greater tension to achieve same pressure (Laplace's law)
34
Techniques to measure cardiac output
Thermodilution Dye test Doppler USS
35
Definition of MAP
= diastolic blood pressure + 1/3 of pulse pressure
36
Factors increasing diastolic blood pressure
Total peripheral resistance Arterial compliance (distensibility - stores elastic energy that means diastolic BP higher) Heart rate
37
Factors increasing the systolic blood pressure
Stroke volume Ejection velocity (without an increase in stroke volume) Diastolic pressure of the preceding pulse Arterial rigidity (arteriosclerosis)
38
Definition of systematic vascular resistance
SVR = MAP - mean right atrial pressure / CO Resistance to flow of blood through arterioles. By constricting and dilating, arterioles control the blood flow to capillaries according to local needs.
39
PAOP
~ Left atrial pressure Normally 6-12 mmHg >15 --> pulmonary oedema Flotation balloon catheter is passed through the right heart into the pulmonary artery The major advantage of the catheter is that it can be used to measure CO
40
Adrenaline
Alpha + Beta Ionotrope Chronotrope Vassopressor β2-effect at low doses causes vasodilatation in skeletal muscle, lowering SVR. α-vasoconstrictor effect at higher doses increases SVR and myocardial oxygen demands, with adverse effect on cardiac output
41
Noradrenaline
α-effect. Vasopressor Indicated in septic shock when hypotension due to peripheral vasodilatation persists despite adequate volume replacement
42
Isoprenaline
Exclusively β-effect Ionotrope Chronotrope Vasodilatation in skeletal muscle; therefore reduces SVR Tachycardia limits clinical use Used to increase rate in heart block while awaiting pacing
43
Dopamine
Low dose causes vessel dilataion of: Renal Cerebral Coronary Splanchnic via D1 and D2 receptors and β1 receptors, resulting in increased cardiac contractility and heart rate High dose stimulates α-receptors, causing vasoconstriction
44
Dobutamine
β1 β2 Inotrope Vasodilator β1 effect increases heart rate and force of contraction Mild β2 effect causes vasodilatation First choice inotrope in cardiogenic shock due to left ventricular dysfunction. Dobutamine and low-dose dopamine in conjunction used in cardiogenic shock to increase BP via increased cardiac contractility and urinary output (UO; via increased renal perfusion)
45
Dopexamine
β2 and D receptors. Inotrope, chronotrope. Peripheral vasodilatation, increased splanchnic blood flow and increased renal perfusion (increased UO)
46
Vasodilator therapies
Nitrates -Vendilatation reducing pre-load Nitroprusside -Arterial vasodilator with short t1/2- -Infusion Hydralazine -Arterial vasodilator -Reduces afterload
47
Phosphodiesterase inhibitors
Prevent breakdown of cyclic AMP by phosphodiesterase III Ionotropic and vasodilator -little chronoctropic Increased myocardial contractility (increased CO) with reduced PAOP and SVR No significant rise in heart rate or myocardial oxygen consumption