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