Cardio physiology Flashcards
Mechanism of contraction in cardiac myocytes
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.
Cardiac action potential cycle
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
Action potential: Phase 0
Na fast gates open, increase Na permability
Na fast influx
Cell becomes most positive it can be away form resting potential –> depolarisation
Action potential: Phase 1
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
Action potential: Phase 2
Slow repolarisation – plateau effect due to inward
movement of calcium
Plateau lasts about 200 ms.
Action potential: Phase 3
Rapid repolarisation – increase in potassium permeability
Inactivation of slow inward Ca++ channels
Action potential: Phase 4
The resting membrane potential of the ventricular
muscle is about −90 mV
Location of AV node
Atrioventricular node
Located in atrioventricular fibrous ring on the right side of atrial septum
Vagal stimulation to heart
Vagal innervation to the SA node
Increased activity slows firing of SA node
Phases of the cardiac cycle
Phase I: Isovolumetric contraction
Phase II: Ejection
Phase III: Diastolic relaxation
Phase IV: Filling phase of diastole
Phase I: cardiac cycle
Isovolumetic contraction
Atroventricular valve closes
Aortic and pulmonary valves closed
Volume remains constant but presssures dramatically increases as ventricles contract
Phase IIa: cardiac cycle
Ejection
Pressure in ventricles exceeds that in the aorta and pulmonary artery
Aortic and pulmonary valves open, blood ejected from ventricle
Phase IIb: cardiac cycle
Ejection - equal pressures
Aortic and pulmonary artery pressures now equal to that of the ventricles - flow reduces
Phase III: cardiac cycle
Diastolic relaxation
Isovolumetric relaxation, volume in ventricles remains the same and the resting ventricular pressure forms as pulmonary and aortic valves close
Phase IVa: cardiac cycle
Passive filling during diastole
Atrioventricular valve opens
Low atrial pressure due to suction effect of ventricle
Rapid ventricular filling
Phase VIb: cardiac cycle
Decline in rate of filling as atrial volume increases
Atria now full, flow rate reduced
85% of final diastolic ventricular volume reached
Phase IVc: cardiac cycle
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.
Normal right atrial pressures
0-4 mmHg
Normal right ventricular pressure
25 / 0-4 mmHg
Normal left atrial pressures
0-10 mmHg
Normal left ventricular pressures
12 / 0-10 mmHg
Third heart sound
Rapid ventricular filling
Fourth heart sound
Atria contracting against a stiff ventricle
LVH or HF
a-wave JVP
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
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
x-descent JVP
First valley
Due to tricuspid valve moving down during ventricular
systole.
v-waveJVP
Second peak
Rise in atrial pressure as atria fills prior to opening of tricuspid valve
y-descent JVP
Second valley
Tricuspid valve opens and blood enters ventricle cuasing pressure in atria to drop
JVP waveforms
ACX VY
At
CX
Vascular
Yunit
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
Tissue with least coronary flow
Subendocardial muscle where the tension is highest
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
Factors increasing afterload
Raised aortic pressure
Aortic valve stenosis
Ventricular cavity size, great volume, requires greater tension to achieve same pressure (Laplace’s law)
Techniques to measure cardiac output
Thermodilution
Dye test
Doppler USS
Definition of MAP
= diastolic blood pressure + 1/3 of pulse pressure
Factors increasing diastolic blood pressure
Total peripheral resistance
Arterial compliance (distensibility - stores elastic energy that means diastolic BP higher)
Heart rate
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)
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.
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
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
Noradrenaline
α-effect.
Vasopressor
Indicated in septic shock when hypotension due to
peripheral vasodilatation persists despite adequate
volume replacement
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
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
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)
Dopexamine
β2 and D receptors.
Inotrope, chronotrope.
Peripheral vasodilatation, increased splanchnic blood flow and increased renal perfusion (increased UO)
Vasodilator therapies
Nitrates
-Vendilatation reducing pre-load
Nitroprusside
- Arterial vasodilator with short t1/2-
- Infusion
Hydralazine
- Arterial vasodilator
- Reduces afterload
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
