Cardiac Physiology Flashcards
What are the main functions of the cardiovascular system?
Supply of oxygen and nutrients. Removal of CO2 and waste Regulation of pH of extracellular fluid Regulation of osmotic balance Signalling
Give examples of cardiovascular disease.
Heart attack
Angina
Heart failure
Arrhythmias
Describe the pump action of the heart.
Left and right heart acts as two pumps in series.
Output of the left and right heart is equal.
Left heart pumps blood into the body (systemic) tissue at high pressure.
Right heart pumps blood into the lungs (pulmonary circulation) at a relatively low pressure.
How do valves contribute to the cardiovascular system?
Ensure unidirectional flow. If the pressure beyond the valve is greater than before it - the valve closes to prevent backward flow.
Describe the way in which blood is pumped out from the ventricle through a valve.
Ventricular muscle contracts.
Ventricular pressure rises.
If ventricular pressure is smaller or equal to the pressure beyond the valve, the valve remains closed.
As soon as the ventricular pressure exceeds the pressure beyond the valve, the valve opens.
Describe stages of blood flow through the heart in a heart beat.
Systemic blood flows into the right atrium from the superior and inferior vena cava. Right atrium contracts causing the tricuspid valve to open and blood to fill the right ventricle. The right ventricle contracts causing the opening of the pulmonary valve. Blood flows from the right ventricle into the pulmonary vein which distributes it throughout the lungs. Blood returns to the heart from pulmonary circulation via the pulmonary vein. Pulmonary blood fills the left atrium which contracts causing the mitral valve to open and blood to fill the left ventricle. As the left ventricle contracts, the aortal valve opens allowing the blood to exit the heart throug the aorta into the systemic blood flow.
What is cardiac output?
Volume of blood pumped in a given time.
What are the units of cardiac output measurements?
L/min
How is cardiac output calculated?
Heart rate x Stroke volume
What is the normal cardiac output and the cardiac output of an athlete in exercise??
5L/min
20L/min
Using the value for normal cardiac output, calculate the normal stroke volume.
CO = HR x SV 5 = 72 x SV SV = 5/72 = 0.06944 ~ 0.07 = 70ml
What is the Fick principle used for?
Calculating cardiac output
Calculating flux of blood through organs
How is cardiac output measured using the Fick principle?
CO = VO2/(CV-CA)
Cardiac output = Rate of oxygen uptake / ([O2] in pulmonary artery - [O2] in pulmonary vein)
Why is measurement of cardiac output using the Fick principle difficult?
Requires catheterisation to obtain O2 concentration readings.
What methods, other than the Fick principle can be used to measure cardiac output?
Using indicators
Thermal dilution
Doppler ultrasound.
Echocardiography (ECG)
How is flux of blood in an organ calculated?
J = Q(Cin-Cout)
Flow rate x (concentration of fluid input - concentration of fluid output)
What is the Frank-Starling mechanism used for?
Ensures equal cardiac output from the left and right heart.
Contributes to increase in stroke volume during exercise.
How does the Frank-Starling mechanism increase stroke volume to balance cardiac output from both ?
If the cardiac output of the left ventricle increases, the venous return from the body will also increase. This causes an increase in stroke volume by increasing the ventriclular stretch of the left ventricle and an increase of end diastolic volume because a greater venous return requires a greater ventricular output to maintain the increased cardiac output.
What is the optimum sarcomere length of cardiac muscle and why?
1.9 micrometers. At lower lengths the actin filaments overlap, interfering with cross-bridge formation.
Higher sarcomere lengths cause increase in sensitivity of the contractile machinery
What is cardiac contractility?
Peak contractile force at a given initial fibre length.
Peak systolic pressure for the given end-diastolic volume.
What is the effect of increased contractility
Increased force and rate of contraction.
How can contractility be increased?
Sympathetic stimulation (NA) or adrenaline. Glycoside drugs.
How can contractility be calculated?
Contractility = Stroke Volume / End-diastolic volume
Why does increased central venous pressure increase cardiac output but decrease venous return?
Cardiac output is increased because of the increased stroke volume caused by increased central venous pressure.
Venous return decreases because the pressure gradient between veins and capillaries decreases.
Describe the structure of the cardiac muscle.
Composed of intercalated disks which separate cells
Many gap junctions enable conduction of electricity.
What is meant by myogenic electric activity?
Activity initiated within the muscle.
What effect do nerves have on the heart?
Modulate the heart beat.
Describe the events that occur within the heart muscle during a heart beat.
SA node initiates a pacemaker current.
Current spreads through the atrium causing atrial contraction.
Current reaches AV node where it is delayed to allow ventricular filling.
Current flows through the septum via the bundle of His.
Spreads across the purkinje fibres of the apex causing ventricular contraction.
What does the P-T labels on an ECG represent?
P - Atrial contraction
QRS - Ventricular contraction
T - Ventricular repolarisation
What is the pacemaker current caused by?
Calcium-induced depolarisation
Describe the changes in electrical currents during an impulse.
Normal membrane potential of the SA node is -60mV. At this potential the I(f) channels (funny channels - Hyperpolarisation-activated cyclic nucleotide-gated channels) open causing an exchange of Na/K where a net influx of Na is observed. Influx of sodium causes an increase in membrane potential of the pacemaker cell. Potential reaches a threshold of ~-45mV causing opening of T-type calcium channels. Influx of calcium causes calcium-induced calcium release from L-type channels at a membrane potential of -30mV. L-type mediated influx of calcium causes an spike in membrane potential reaching 0mV. At 0mV the potassium VGCs open causing an efflux of the positive charge carried on potassium ions. Sodium-calcium exchanger (NCX) is also activate to pump calcium back into the sarcoplasmic reticulum. Once the membrane potentials goes below -45mV, the I(f) channels reopen to balance the concentration sodium in the cell. The Na/K-ATP pump restores the potassium concentration.
Which of the currents during an impulse is the true pacemaker current?
The funny current. Funny (HCN) channels.
Describe the phases of the ventricular action potential.
Phase 0 - Rapid depolarisation due to influx of sodium.
Phase 1 - Early partial repolarisation caused by a transient efflux of potassium (I(to)).
Phase 2 - Plateau. Inward calcium current of L-type channels balances with the non-transient efflux of potassium.
Phase 3 - Repolarisation caused by continued potassium efflux
Phase 4 - Resting potential established by influx of potassium to keep the potential near potassium’s E(K).
Describe how calcium-induced calcium release occurs.
Action potential travels over the sarcomere’s surface membrane and down the T-tubules that perforate the sarcomere.
Depolarisation activates L-type calcium VGCs causing entry of calcium into the sarcomere.
Calcium activates Ryanodine receptors which are coupled to calcium channels. Activation causes efflux of calcium from the sarcoplasmic reticulum into the sarcoplasm.
How is calcium removed from the sarcoplasm after an action potential?
Repolarisation of the action potential causes calcium VGCs to close.
SERCA - Sarcoplasmic and Endoplasmic Reticulum Calcium ATPase - pumps calcium back into SR.
Remaining calcium is removed by an antiporter of calcium and sodium on the plasma membrane.
How is the heart rate controlled?
Intrinsic:
SA node pacemaker control.
Extrinsic:
Parasympathetic modulation:
The vagus nerve of the ANS innervates the SA node enforcing a vagal tone which reduces the SA node’s firing rate to ~72BPM.
Sympathetic modulation by nerves:
Accelerator nerve causes an increase in heart rate during exercise.
Sympathetic modulation by adrenaline:
Adrenaline increases heart rate during the fight or flight response.
What is the SA node’s intrinsic firing rate?
80-100BPM
How is Stroke Volume controlled?
Intrinsically by the Frank-Starling mechanism.
Extrinsically:
Sympathetic stimulation, both neuronal and adrenal, increases SV.
Angiotensin II increases SV
Hormonal (Corticosteroids and thyroxine) increase in SV.
Describe the baroreceptor reflex control of the blood pressure.
Increase in arterial pressure stimulates baroreceptors. Leads to increase in activity of afferent (sensory) nerves which innervate the medullary centre.
Medullary centres decrease sympathetic activity and increase parasympathetic activity.
This causes reduction in cardiac output and reduction in contractile tone in blood vessels which reduces the peripheral resistance of blood vessels.
The fall in CO and PR causes a decrease in blood pressure of the artery.
Other than the baroreceptor reflex, what other receptors/reflexes control blood pressure?
Veno-atrial receptors
Chemoreceptors
Lung-stretch receptors
Skeletal muscle mechanoreceptors
How do Veno-atrial receptors decrease blood pressure?
Increased atrial volume causes a response in the atrial wall which leads to increased heart rate.
The response also causes diuresis to decrease the volume of plasma.
How do chemoreceptors regulate heart rate?
Respond to hypoxia (lack of oxygen)
Constrict blood vessels to increase the PR
Heart rate increases because of increased respiration
How do lung stretch receptors mediate heart rate?
Increase heart rate by inhibiting the vagus nerve.
Heart rate increases during each inspiration.
How do skeletal muscle mechanoreceptors regulate heart rate?
Inhibit vagal neurones during exercise to increase the heart rate.
Describe how the heart deals with exercise.
Blood flow through muscle increases in order to supply sufficient oxygen/glucose.
Pulmonary flow increases to increase oxygen uptake and CO2 excretion.
Cardiac output increases from 5 to 20L/min.
Heart rate increases from 72 to 180BPM by inhibition of vagus nerve and stimulation of accelerator nerve.
Contractility increases
Stroke volume increases from 70 to 105ml.
Diastole (ventricular filling + coronary blood flow) shortens proportionately more than systole.
How does the sympathetic system regulate cardiac action?
NA and adrenaline have similar effects.
Activate the GsPCR pathway that triggers action potential firing rate and contraction via PKA
What is meant by a positive chronotropic effect?
Increase in heart rate.
What is meant by a positive ionotropic effect?
Increase in contractility of the heart.
How does the sympathetic system increase heart rate?
Acts on the SA node to induce pacemaker depolarisation before threshold is reached.
I(f) channels open and close slowly.
NA stimulates Beta1-adrenergic receptors to produce cAMP and activate PKA via the GsPCR pathway.
PKA phosphorylates calcium channels to increase their activity and sensitivity (reduces threshold).
cAMP acts on I(f) channels to increase their activity.
How does the sympathetic system increase heart contractility?
Acts on the ventricle.
PKA increases activity of potassium channels which shortens the repolarisation and hence shortens the AP.
PKA phosphorylates L-type channels and increases their activity.
Increased ventricular AP plateau and calcium influx triggers a more elaborate calcium-induced calcium release which leads to increased contractile force.
