The cardiovascular system - Physiology Flashcards
What is the 2 main role of the cardiovascular system?
- Rapid transport of nutrients (metabolic substrates) to tissues
- Rapid removal of metabolic waste products from tissues
Describe two challenges facing the coronary circulation?
Coronary blood flow occurs in diastole - 2/3 of the coronary arterial tree is intramural. These vessels get compressed during systole - therefore most (80%) of coronary blood flow occurs during diastole
The coronary arteries are function end arteries - they do not have effective anastomoses and therefor functional END arteries. This means a blockage has much more serious effects
The heart has a very high oxygen requirement even at rest. During extortion the oxygen requirements are even higher. Therefore, to meet these needs the coronary circulation has developed structural and functional adaptation.
a) Name 2 structural adaptations
b) Name 2 functional adaptations
a)
1. Myocardial capillary density is very high
2. Distance that oxygen and nutrient need to travel from blood to the myocyte is shorter
b)
1. Metabolic hyperaemia (release of cardiac metabolites e.g., adenosine) increases blood flow during exercise
2. Autoregulation - coronary circulation can maintain constant blood flow despite changes to blood pressure
a) Define cardiac output (CO)
b) Define stroke volume (SV)
c) What is the equation relating CO and SV
a) The volume of blood ejected by 1 ventricle in 1 minute
b) The volume of blood ejected from the ventricle in systole (1 heartbeat/contraction)
c) CO = SV x HR
Cardiac output is not evenly distributed between tissues. Myocardium does not receive much oxygen compared to other organs e.g., muscles, liver and GIT. What is the medical significance of this?
Coronary blood has little spare and so reserve oxygen
Cardiac pain due to oxygen lack (angina) can be triggered, by a relatively modest fall in coronary blood flow
What is heart rate controlled by?
Sympathetic and parasympathetic nerves which innervate the sinoatrial (SA) and atrioventricular (AV) nodes
What factors control stroke volume?
Preload - filling pressure (Starling’s law)
Contractility - sympathetic nerves, circulating factors
Afterload - pressure opposing ejection
a) What is preload?
b) Preload cannot be measured directly, therefore an indirect indices of preload is used?
a) The stretch of the ventricular fibres just before contraction (at end diastole)
b) End Diastolic Volume or End Diastolic Pressure
Describe the Frank-Starling mechanism
The greater the preload, the greater the force of contraction and so the greater the stroke volume
Describe the relationship between an increase venous return and cardiac output
Increase venous return –> increase end diastolic volume/pressure –> increase preload –> increase contraction –> increase cardiac output
Describe the relationship of central venous pressure (CVP) to the right ventricular preload
- CVP is the pressure in the vena cava at the entrance to the right atrium (so filling of blood in right atrium)
- During diastole the right atrial pressure is the same as the right ventricle pressure
- Therefore, CVP can be used as an estimate of the right ventricular end diastolic pressure/preload
- CVP determines right ventricular preload
What factors influence central venous pressure?
- Volume of blood in circulation
- Distribution of blood between central and peripheral veins
Describe 5 factors that influence the distribution of blood between central and peripheral veins (venous return - return of blood from the periphery back to the right atrium hence CVP and hence preload)
- Gravity - blood pools as we stand reducing CVP. Opposite effects occurs when we are supine
- Skeletal muscle pump - operate when we walk squeezing blood into the central circulation
- Sympathetic nerves- sympathetic nerves cause vasoconstriction of the peripheral veins, squeezing blood into the central veins back into heart
- Respiratory pump - when we breathe in the pressure inside our chest becomes mores negative, this encourages venous return to the right atrium and increases RV stroke volume
- Pumping ability of the heart - when the heart is beating faster it transfers blood more quickly from the central veins to the arteries
Why is fainting common among guards?
- This is due to venous pooling, lack of calf muscle pump activity and heat induced vasodilation
- This causes decreased CVP and therefore reduced filling of right side heart –> reduced filling of left side of heart –> reduced SV and CO
- This leads to cerebral hyoperfusion and fainting
Why is the most important role of Starling’s law?
To balance the outputs of the right ventricle and left ventricle
What is contractility?
Contractility is the force of myocardial contraction that is caused by neurohumeral factors (autonomic + blood borne factors or drugs which is independent of initial fibre length) (i.e., not dependent on the Frank Starling mechanism)
What is the key difference between filling pressure (Starling’s law) and contractility
Filling pressure (Starling’s law) - acts by stretch, not altering intracellular Ca2+ level
Contractility - acts by altering intracellular Ca2+ level, no stretch
Name 5 factors that cause an increase in contractility
- Raised extracellular calcium
- Increased preload
- Sympathetic stimulation
- Drugs e.g., inotropes, digoxin
- Hormones e.g., catecholamine, thyroxine, growth hormone, glucagon
Name 5 factors that cause a decrease in contractility
- Decreased extracellular calcium
- Decreased preload
- Parasympathetic stimulation
- Drugs e.g., beta-blockers, aesthetics, antiarrhythmics
- Hypoxia
- Hypercapnia (Increases CO2)
- Acidosis
What is after load?
Refers to the amount of resistance that the heart overcomes to eject blood/degree of heart muscle stretching during systole
What is the relationship between after load and stroke volume
it is inversely related to stroke volume
Name 4 factors that increase afterload
- Raised aortic pressure
- Aortic stenosis
- Increased systemic vascular resistance such as hypovolemic shock
- Ventricular dilatation
Name 2 factors that decreas after load
- Vasodilator drugs e.g., nitrates calcium channel blockers
- Vasodilator metabolise in sepetic shock
What factors increase cardiac output during exercise
Increase stroke volume
- Increase pre load -> skeletal muscle pump and peripheral vasoconstriction
- Contractility –> increased sympathetic activity
Increase heart rate
- Decrease parasympathetic activity
- Increase sympathetic activity
Why does blood flow to active muscles increase during exercise?
Active muscles release metabolites that causes vasodilatation in the muscles thereby increasing the blood flow
a) There is a threat of hypotension during exercise. Explain why this is the case?
b) How is this avoided?
a)
- Vasodilatation occurs during exercise to increase blood flow to muscles. however, this vasodilation has the potential to cause problems because the systemic resistance reduces significantly
- BP = CO X SVR (systemic vascular resistance)
b) This is avoided by compensatory vasoconstriction in inactive tissue which prevents fall in SVR e.g., splanchnic, kidneys, inactive muscle
Vasodilatation occurs during exercise. This diverts blood away from the heart, so the preload is reduced but the heart maintains the cardiac output by increasing the heart rate.
During exercise in hot weather even more blood is diverted away from the heart and the cardiac output can’t be maintained despite the increased heart rate.
a) How is this prevented?
b) What is the disadvantage of this?
a)
- There are baroreceptors in the heart that detect the reduced cardiac output and activate the sympathetic nervous system
- This results in vasoconstriction of the skin blood vessels. While this means
b) While this means that more blood can now return to the heart it does so at the expense of rising core temperature and can lead to heat stroke
Explain the difference in how cardiac output is increased during upright and supine exercises
An increase in cardiac output during upright exercise is brought about partly by an increase in stroke volume and partly by an increase in heart rate.
During supine exercise (e.g., swimming), stroke volume is high even at rest, because central venous pressure and so pre-load and so stroke volume is high. Therefore there is less scope for stroke volume to increase during exercise. So, tachycardia is the main factor raising the cardiac output during supine exercise
The transplanted heart is enervated (there are no cardiac autonomic nerves). How do heart transplant patients increase cardiac output with exercise?
Heart transplant patients have circulating catecholamines that increase heart rate and the skeletal muscle pump acting via the Frank-Starling increases pre-load
Explain the difference in stroke volume and resting heart rate in the athletic heart vs non-athletic heart
The athletic heart is stronger and hypertophied. This leads to an increase in stroke volume and decrease in resting heart rate.
Name the 7 phases of the cardiac cycle
- Atrial systole
- Isovolumetric contraction
- Rapid ejection
- reduced ejection
- Isovolumetric relaxation
- Rapid ventricular filling
- Diastasis
Describe the 7 phases of the cardiac cycle including what part of the ECG the phases correspond to and any heart sound that occur
Atrial systole
- Causes rise in atrial pressure causing blood to move from the atria to the ventricles
- AV valves (mitral and tricuspid) are open
- P wave on ECG
- 4th heart sound generated = atrial gallop (extra heart sound during late diastole)
(Ventricular systole) Isovolumetric contraction
- Ventricles contract without any change in volume
- All valves are closed
- Initiated by ventricular depolarisation which corresponds to QRS complex on ECG
- 1st heart sound generated - due to closure of AV valves (mitral and tricuspid) from previous
Rapid ejection
- Ventricles pump out blood from the left ventricle to aorta and from right ventricle to pulmonary artery
- Pressure goes up until reaches peak
- AV valves remain closed preventing reflux of blood into atria
- Aortic and pulmonary valves open
- ST segment on ECG (Start of repolarisation which is then followed by relaxation)
Reduced ejection
- Soon will hear 2nd heart sound
Isovolumetric relaxation
- End of systole
- Ventricles relax without a change in volume
- Atria starts to fill with blood
- All valves closed
- Initiated by repolarisation which corresponds to T wave on ECG
- 2nd heart sound produced from semilunar (aortic and pulmonary closing)
- If 3rd heart sound is produced at this stage = can reflect of heart failure
Rapid ventricular filling
- AV valves open as ventricular pressure drops below atrial pressure
- Aortic and pulmonary vales remain closed
- Most blood flows passively from atria to ventricles
- 3rd heart sound produced
Diastasis
- Atria and ventricles filling
- Ventricles filling 70-80% passively during diastesis, rest 25% actively filling during atrial systole
