Cardiac physiology

• 4
• low and high

• - 0-25mmHg on the right side
• - 0-120 mmHg on the left.

2/3

• Cardiac output = HR x SV (stroke volume) 
• 5-6L per minute

Yes, due to intrinsic myogenic rhythm within cardiac myocytes

the cardiac impulse is generated in the sino atrial node in the right atrium & 

conveyed to the ventricles via the atrioventricular node.

• Yes
• 100x per minute 
• Thus, higher resting heart rate found in cardiac transplant cases.

In the SA and AV nodes the resting membrane potential is lower than in surrounding cardiac cells and will slowly depolarise from -70mV to around -50mV at which point an action potential is generated.

Differences in the depolarisation slopes between SA and AV nodes

Refractory period - during which cells cannot be re-stimulated and this period allows for adequate ventricular filling.

• In pathological tachycardic states this time period is overridden -> inadequate ventricular filling -> cardiac output falls & syncope may ensue.
•  

Parasympathetic fibres project to the heart via the vagus and will release acetylcholine. 


Sympathetic fibres release nor adrenaline and circulating adrenaline comes from the adrenal medulla.

Noradrenaline binds to β 1 receptors in the SA node and increases the rate of pacemaker potential depolarisation. 

(Sympathetic fibres release nor adrenaline)

• Mid diastole - AV valves open 
• Late diastole - Atria contract 
• Early systole - AV valves shut 
• Late systole - ventricular muscles relax
• Early diastole - all valves are closed

- Mid diastole: AV valves open. Ventricles hold 80% of final volume. Outflow valves shut. Aortic pressure is high.

- Late diastole: Atria contract. Ventricles receive 20% to complete filling. Typical end diastolic volume 130-160ml.

- Early systole: AV valves shut. Ventricular pressure rises. Isovolumetric ventricular contraction. AV Valves bulge into atria (c-wave). Aortic and pulmonary pressure exceeded- blood is ejected. Shortening of ventricles pulls atria downwards and drops intra atrial pressure (x-descent).

- Late systole: Ventricular muscles relax and ventricular pressures drop. Although ventricular pressure drops the aortic pressure remains constant owing to peripheral vascular resistance and elastic property of the aorta. Brief period of retrograde flow that occurs in aortic recoil shuts the aortic valve. Ventricles will contain 60ml end systolic volume. The average stroke volume is 70ml (i.e. Volume ejected).

- Early diastole: All valves are closed. Isovolumetric ventricular relaxation occurs. Pressure wave associated with closure of the aortic valve increases aortic pressure. The pressure dip before this rise can be seen on arterial waveforms and is called the incisura. During systole the atrial pressure increases such that it is now above zero (v- wave). Eventually atrial pressure exceed ventricular pressure and AV valves open - atria empty passively into ventricles and atrial pressure falls (y -descent )

• Air embolization to occur if the neck veins are exposed to air.
• -> This patient positioning is important in head and neck surgery to avoid this occurrence if veins are inadvertently cut, or during CVP line insertion.

• Preload = end diastolic volume
• Afterload = aortic pressure

• For hollow organs with a circular cross section: the total circumferential wall tension depends upon the circumference of the wall, multiplied by the thickness of the wall and on the wall tension.
• The total luminal pressure depends upon the cross sectional area of the lumen and the transmural pressure.
• Transmural pressure is the internal pressure minus external pressure and at equilibrium the total pressure must counterbalance each other.
• In cardiac physiology: the rise in ventricular pressure that occurs during the ejection phase is due to physical change in heart size. Also why a dilated diseased heart will have impaired systolic function.

• Increase in end diastolic volume will produce larger stroke volume.
• Up to a point beyond which cardiac fibres are excessively stretched and stroke volume will fall once more.
• It is important for the regulation of cardiac output in cardiac transplant patients who need to increase their cardiac output.

• Baroreceptors located in aortic arch and carotid sinus.
• Aortic baroreceptor impulses travel via the vagus and from the carotid via the glossopharyngeal nerve.
• They are stimulated by arterial stretch.
• Even at normal blood pressures they are tonically active.

• *Increased parasympathetic discharge to the SA node.
• *Decreased sympathetic discharge to ventricular muscle causing decreased contractility and fall in stroke volume.
• *Decreased sympathetic discharge to venous system causing increased compliance. 
• *Decreased peripheral arterial vascular resistance