HMA - CV Physiology

Nutrient delivery, waste removal, signalling, thermoregulation, immunity

Name 5 ways in which the cardiovascular system achieves homeostasis.

Diffusion

how substances move between the plasma and interstitial fluid, requiring permeable capillary walls and a concentration gradient.

Convection

carrying of dissolved substances, suspended in plasma through circulation to move substances between organs.

Pressure gradient

difference in pressure between 2 points in the cardiovascular system driven by the pumping action of the heart.

Pressure gradient over resistance

Give formula for flow.

Pulsatile pressure

blood pressure in the aorta and large arteries varies according to the contractile state of the heart (i.e. systole or diastole).

120 over 80 mmHg

Recall normal aorta/systemic systolic and diastolic blood pressure.

25 over 8 mmHg

Recall normal pulmonary systolic and diastolic blood pressure.

Systolic minus diastolic BP

Give formula for pulse pressure.

Cardiac output (CO)

amount of blood the heart pumps per minute.

Heart rate times stroke volume

Give formula for cardiac output.

5 L/min

Recall normal stroke volume at rest.

Dilution method

method for measuring cardiac output by determining the dilution of a known substance as it passes through the heart.

Fick principle

method for measuring cardiac output using the body’s oxygen consumption and the difference in oxygen content between arterial and venous blood.

Pressure reservoirs

large arteries distend to absorb blood surge, and recoil during diastole = downstream non-pulsatile flow and propels blood forward, functioning as WHAT?

Large arteries

conduit vessels with large internal diameter (4mm) and thick, fibrous, elastic walls to withstand high, pulsatile pressure, distending and collapsing with pressure changes (compliance).

Capillaries

exchange vessels, with walls of only endothelial cells and a basement membrane to maximise permeability and a small interior diameter (5-10um) for slow flow.

Venules, veins

capacitance vessels, thin walled with some muscle, very distensible and compliant with a large lumen (70 um - 5mm) allowing storage of blood.

65%

What proportion of blood is in the venous system at rest?

Sinoatrial (SA) node

located in the right atrium, undergoes spontaneous, rhythmic depolarisation to initiate an electrical signal (action potential), setting the heart rate.

Internodal pathways

specialised bundles of atrial muscle cells conducting the electrical impulse from the SA node rapidly through both atria.

Atrioventricular (AV) node

where the action potential passes from the atria to ventricles, signal moves slowly (0.1 sec delay) to delay contraction of ventricles.

AV bundle, purkinje fibres

specialised conducting cells facilitating extremely rapid conduction of the action potential from the AV node, down the septum, and into the ventricular muscle for coordinated contraction of muscle cells.

Functional syncytium

contraction and relaxation of all cardiac muscle cells simultaneously, as cells are electrically coupled.

Intercalated discs

specialised cell junctions between cardiac muscle cells containing desmosomes and gap junctions.

Desmosomes

firm mechanical attachments within intercalated discs aiding in function syncytium as the contraction of a cell pulls on the next.

Gap junctions

low-resistance electrical connections within intercalated discs, channels between cells allowing rapid spread of action potentials between cells.

Electrically excitable cells

cells with membranes capable of depolarising and generating an action potential, including all cardiac cells.

Membrane potential

electrical potential across membranes due to concentration differences between ions inside and outside the cell, and selective permeability of these ions.

Ion equilibrium potential

membrane potential at which chemical and electrical forces are balanced, meaning there is no net movement of the ion.

-90 mV

Recall potassium equilibrium potential.

+70 mV

Recall sodium equilibrium potential.

+100 mV

Recall calcium equilibrium potential.

-90 mV

Recall resting membrane potential, considering most excitable cells are far more permeable to K+ compared to Na+ and Ca2+.

Action potentials

rapid changes in the membrane potential facilitated by the movement of ions spreading quickly along the cell membrane and between cells, generating an electrical current.

Voltage-sensitive, ion-selective channels

membrane channels enabling increased membrane permeability to Na⁺ and Ca²⁺ and decreased membrane permeability to K⁺ an action potential.

Rapid depolarisation (phase 0)

reaching threshold potential opens fast Na⁺ channels, allowing rapid influx of Na⁺, with decreased permeability of K⁺, bringing membrane potential to +20 mV.

End depolarisation (phase 1)

at peak depolarisation (+20 mV), fast Na⁺ channels inactivate.

Plateau phase (phase 2)

unique to cardiac ventricular muscle, Ca²⁺ channels that are slower to inactivate open, prolonging depolarisation.

Repolarisation (phase 3)

K⁺ channels open and permeability increases, allowing K⁺ influx, decreasing the membrane potential, aided by the closing of slow Ca²⁺ channels.

Rest (phase 4)

resting membrane potential returns, close to K⁺ equilibrium potential (-90 mV).

-60 to -55 mV

What is the unstable resting membrane potential of an SA node cell, which slowly raises until the threshold potential.

Slow leaking of sodium

Describe how the threshold potential is spontaneously reached in SA node cells.

Slow calcium influx

Describe what achieves depolarisation in SA node cells.

Calcium spark

localised release of concentrated Ca²⁺ ions from the sarcoplasmic reticulum as small Ca²⁺ occurring with cardiac muscle depolarisation entry opens Ca²⁺-sensitive ryanodine receptors (RyRs).

Calcium sensitive ryanodine receptors

channels in the sarcoplasmic reticulum triggered to open by influx of Ca²⁺ via slow voltage-sensitive Ca²⁺ channels in depolarisation.

ATP-dependent pump (SERCA)

What pumps Ca²⁺ back into the sarcoplasmic reticulum during muscle relaxation?

Sodium-calcium exchanger

What removes Ca²⁺ from the cell during muscle relaxation?

Refractory period

cardiac muscle cannot respond to stimulus during the action potential.

Absolute refractory period (200 ms)

following depolarisation, fast Na⁺ channels inactivate, meaning contraction cannot be caused regardless of stimulus strength.

Relative refractory period (50 ms)

following ARP, during repolarisation, a strong stimulus can cause contraction.

Tetanus

maximal, sustained contraction of a muscle receiving high frequency action potentials disallowing relaxation between stimuli, so individual contractions fuse together.

Prevent tetanic contraction

Why is the refractory period in cardiac muscle fibres long?

Premature Ventricular Complex (PVC, extrasystole)

extra contraction earlier than the next regular beat occurring when electrical impulses originate from outside the heart’s pacemaker outside the absolute refractory period.

Compensatory pause

diagnostic interval following a PVC, as the PVC’s own refractory period interferes with the signal firing from the pacemaker, so the next beat occurs at the subsequent, correctly timed impulse from the SA node.

Electrocardiogram

use of electrodes placed on the chest and limbs to record electrical signals in the heart, as they spread to surrounding tissue and skin.

Lead

graphical representation of the heart's electrical activity, calculated by measuring the difference in electrical potential between specific electrodes placed on the body.

P wave

pattern on the ECG representing atrial depolarisation.

Delay at AV node

What does the plateau between the P wave and QRS complex represent on an ECG?

QRS complex

pattern on the ECG representing ventricular depolarisation.

T wave

pattern of the ECG representing ventricular repolarisation.

Plateau phase in action potential

What does the plateau phase between the QRS complex and T wave represent on an ECG?

P-R interval

time for conduction of action potential through the atria and AV node, to the ventricles, normal 0.12-0.2 secs.

1st degree heart block (AV damage)

What does a prolonged P-R interval indicate?

Another conduction pathway

What does a short P-R interval indicate?

S-T segment

period when ventricles are fully depolarisation (is isoelectric, i.e. no current).

Ischaemia/infarction

What does a current present at the S-T segment indicate?

Q-T interval

total time for which ventricles are depolarised, varying with heart-rate, age, and sex but should be 0.4s at 70 bpm.

Electrolyte imbalance, certain drugs

What does a prolonged Q-T interval indicate?

Ventricular arrhythmia, fibrillation

What does a prolonged Q-T interval cause?

Diastolic filling

mitral valve opens, allowing passive atrial and ventricular filling, followed by later atrial contraction driving final ventricular filling and causing ventricular pressure to exceed atrial pressure, closing the mitral valve (1st heart sound).

Isovolumetric ventricular contraction

mitral valve closes and ventricle contracts against the constant blood volume, causing ventricular pressure to exceeds aortic pressure, opening the aortic valve.

Ventricular ejection

aortic valve opens and blood is ejected into the aorta, followed by later ventricular repolarisation, causing ventricular pressure to fall below aortic pressure, closing the aortic valve (2nd heart sound).

Isovolumetric relaxation

aortic valve closes and ventricle relaxes with constant blood volume, causing ventricular pressure to fall below atrial pressure, opening the mitral valve.

Systole

involves isovolumetric ventricular contraction and ventricular ejection.

Diastole

involves isovolumetric ventricular relaxation and filling of atrium and ventricle.

End-diastolic volume (EDV)

the volume of blood in the ventricle at the end of ventricular filling and prior to contraction - i.e. the maximum volume in the ventricle during the cardiac cycle (120-130 mL).

120-130 mL

Recall typical end-diastolic volume.

50 mL

Recall typical end-systolic volume

End-systolic volume (ESV)

the volume of blood in the ventricle after ventricular contraction - i.e. the minimum volume in the ventricle during the cardiac cycle (50 mL).

Stroke volume (SV)

volume of blood ejected by one ventricle in one cardiac cycle (70-80mL), given by EDV - ESV.

Ejection fraction (EF)

the percentage of the EDV that is ejected from the ventricle during systole (55-70%), give by (SV/EDV) x 100%.

55-70%

Recall typical ejection fraction.

Cardiac index (CI)

method for evaluating heart function since cardiac output is generally proportional to body surface area (2.5-4 L/min/m^2), given by CO/m^2 of SA.

Heart rate, myocardial contractility

List extrinsic mechanisms altering cardiac output.

Preload, afterload

List intrinsic mechanisms altering cardiac output.

Heart rate

set by the frequency of pacemaker action potentials in the SA node, which travels to depolarise cardiac cells, causing contraction (60-100 bpm).

Preload

degree of pre-contraction tension on ventricular muscle at the end of diastole, determined by EDV, affects strength of contractile force upon stimulation.

Starling’s Law of the Heart

energy of contraction of ventricle is a function of the initial length of fibres in its walls.

Venous return

rate at which blood flows into the ventricle determining EDV, affected by blood volume, vasoconstriction or dilation, external venous pressure, and right atrial pressure.

Afterload

pressure the ventricle must overcome to eject blood during systole affecting ESV, largely determined by arterial blood pressure.

Myocardial contractility (inotropy)

strength of ventricular contraction independent of preload and afterload affecting ESV.

Bowditch effect

increased heart rate leads to increased contractile force.

Sympathetic stimulation (direct and Bowditch), cardiac drugs

List ways positive inotropy can be achieved.

Parasympathetic stimulation, heart disease, cardiac drugs

List ways negative inotropy occurs.

Phonocardiography

recording of the sounds and murmurs made by the heart, used to detect normal and abnormal heart sounds.

Aortic stenosis

stiffened aortic valve causing increased left ventricular pressure and turbulent flow as blood is forced through a smaller aperture.

Loud pan-systolic murmur

Describe phonocardiographic reading for aortic stenosis.

Mitral stenosis

stiffened mitral valve causing increased left atrial pressure and turbulent flow as blood is forced through a smaller aperture.

Slow developing rumble during diastole

Describe phonocardiographic reading for mitral stenosis.