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Flashcards in Cardiac Cycle Deck (52)

What is the effect of B1-adrenoceptor activation? (Sympathetic stimulation)

Adenylate cyclase is activated, which produces cAMP from ATP. cAMP activates protein kinase A which phosphorylates the L-type Ca2+ channels (dihydropyridine receptors) so they stay open longer. This means there is a bigger release of Ca2+ into the sarcoplasmic reticulum, so more cross-bridges are formed between myosin heads and actin so there is positive inotropy.
Also, phospholamban is phosphorylated so it stops inhibiting SERCA so more Ca2+ is sequestered in the sarcoplasmic reticulum so more is released next time. This also increases relaxation rate (positive lusitropy). Positive lusitropy means there is more time for ventricular filling.


What is the effect of parasympathetic stimulation (Ach released from vagus nerve)?

Acetylcholine binds to muscarinic receptors, which activates GIRK channels.
GIRK (G-protein inwardly rectifying K+ channel), pump K+ out of cell to repolarise it and decrease the force of contraction.
Also, T-type calcium channels are inhibited to stop Ca2+ entry from extracellular fluid.


What is positive dromatropy?

Increased frequency of action potentials.


What is the effect of cardiac glycosides (e.g digitoxin)?

Inhibit Na+/K+ pump, which causes Na+ inside cell to increase, so that the Na+/Ca2+ exchanger doesn't work and intracellular Ca2+ increases.
Calcium-induced calcium-release causes more calcium to be released. This causes positive inotropy.
The inhibition of Na+/K+ ATPase reduces atrioventricular node conduction, so negative chronotropy.


Name the autorhythmic fibres in the heart.

Sinoatrial node (spontaneous depolarisation = pacemaker potential)
Atrioventricular node
Atrioventricular bundle (Bundle of His)
Right and left bundle branches
Purkinje fibres
Ventricular myocardium


How is the resting membrane potential maintained?

Na+/K+ ATPase
Negatively charged proteins in cytosol
K+ leak channels make membrane much more permeable to K+


What is the difference between fast-response action potentials and slow-response action potentials?

Slow response action potentials are in sino-atrial node and atrioventricular node and give the atria enough time to empty completely.
Slow-response action potentials are in the atrial and ventricular myocardial fibres and the Purkinje fibres.


What happens in a slow response action potential?

Resting membrane potential = -60mV
Phase 4 = pacemaker potential (spontaneous depolarisation), funny channels (slow inward Na+ channels) open, T-type Ca2+ channels open.
Phase 0 = depolarisation of membrane above threshold.
Phase 3 = potassium ion channels open and membrane is repolarised.


What happens in a fast response action potential? (Happens in contractile fibres rather than autorhythmic fibres)

Phase 4 = Resting membrane potential = -90mV
Phase 0 = voltage gated fast Na+ channels open transiently to depolarise membrane
Phase 1 = transient K+ channels open so K+ rapidly diffuses out of cell
Phase 2 = depolarisation is maintained by voltage-gated slow L-type Ca2+ channels opening in sarcolemma to balance outflow of K+ and maintain depolarisation - Ca2+ released from sarcoplasmic reticulum and tension develops
Phase 3 = Ca2+ channels in sarcolemma and sarcoplasmic reticulum close. Additional voltage gated K+ channels open so there is an outflow of K+ which repolarises the membrane


What is the effect of increased Ca2+ concentration in the sarcoplasm?

Increased inotropy


Why can't tetanus occur in cardiac muscle like it can in skeletal muscle?

In cardiac muscle the refractory period lasts longer than the contraction itself, so the muscle is relaxing before the refractory period has finished. This means another contraction can't begin until relaxation is well under way, so prevents tetanus which would cease blood flow as the ventricles would be unable to refill.


What is the resting membrane potential and the threshold for a fast action potential in a cardiac myocyte?

Resting membrane potential = -90mV
Threshold = -70mV
Depolarised = +20mV


What is the resting membrane potential in a pacemaker cell?



What is the difference between the relative refractory period and absolute refractory period of a cardiac myocyte?

Absolute/effective refractory period = another action potential can't be generated, it is during the period of prolonged depolarisation (phase 2) and means there can be no action potential whilst the muscle is still contracting, so tetanus is prevented
Relative refractory period = an action potential can only be generated under specific conditions e.g a particularly large stimulus


What effect do the sympathetic and parasympathetic nervous systems have on the gradient of the pacemaker potential (phase 4)?

Sympathetic nervous system increases the gradient (duration) of the pacemaker potential, parasympathetic nervous system decreases the gradient (duration) of the pacemaker potential.


What is the P-Q interval on an ECG?

The conduction of the nerve impulse from the sino-atrial node to the atrio-ventricular node.


What is the P wave on an ECG?

Atrial depolarisation.


What is the QRS complex on an ECG?

Ventricular depolarisation (phase 0)


What is the T wave on an ECG?

Ventricular repolarisation


Which interval on the ECG is used to measure heart rate?

R-R duration.


Which part of the ECG shows the prolonged depolarisation of the ventricles?

Flat S-T segment


Is it diastole or systole that decreases in duration as heart rate increases?



What is the duration of the cardiac cycle? How much of that is systole and how much is diastole?

0.8 seconds total
0.1 seconds = atrial systole
0.3 seconds = ventricular systole
0.4 seconds = ventricular diastole


At which point do the ventricles contain end-diastolic volume and end-systolic volume?

EDV = After atrial systole.
ESV = Start of isovolumetric relaxation of the ventricles.


What is isovolumetric contraction?

When the semilunar valves and atrioventricular valves are shut and the ventricles are starting to contract to increase the pressure above afterload. Causes prolapse of the atrioventricular valves.


What is the dicrotic notch?

An increase in the pressure in the aorta after the semilunar valve shuts and there is a rebound of blood in the semilunar valve cusps.


What causes the first heart sound S1?

Closure of the mitral valve


What causes the second heart sound S2?

Closure of the semilunar valve.


What causes the third heart sound S3?

Blood turbulence during ventricular filling.


What causes the fourth heart sound S4?

Blood turbulence during atrial systole.


What is Stoke volume equal to?

End diastolic volume - end systolic volume


What is cardiac output?

Volume of blood ejected from one ventricle in one minute (CO = stroke volume x heart rate)


What is cardiac reserve?

The difference between the max cardiac output and cardiac output at rest.


What is ejection fraction, and what is its implication in heart failure?

Ejection fraction = (stroke volume/ end diastolic volume) x100
An ejection fraction less than 50% means heart failure


What are the events of the biphasic JVP?

a = atria contract
av = atria relaxes and tricuspid valve closes
c = isometric contraction of the right ventricle prolapse so tricuspid
x = ventricle contracts and shortens, pulling on the vein and elongating it and decreasing pressure
v = atrium filling against closed tricuspid valve
y = tricuspid valve opens


What are the three factors that regulate stroke volume?

Preload - the degree of stretch of the ventricles before contracting
Afterload - the pressure that has to be exceeded for ventricular ejection to occur
Contractility - the forcefulness of the contraction of individual ventricular muscle fibres (how many myosin heads have formed cross-bridges with the actin)


Why do athletes have higher resting stroke volumes?

Their heart rate is slower, so diastole is longer, so end diastolic volume increases and stroke volume increases.


What is the Frank-Starling relationship?

If the heart fills with more blood during diastole, the force of contraction during systole will be greater.
This means the heart can change stroke volume without influence from nerves or hormones, but due to the diastolic length of the myocardial fibres.
Increased stretch in myocardium increases the diastolic length which increases the tension developed and so increases contractility.


What happens according to the frank-starling relationship if there is increased vasoconstriction?

Increased vasoconstriction -> increased afterload -> decreased stroke volume -> increased end-diastolic volume with next beat -> increased preload -> increased force of contraction -> stroke volume increases again


What does increased preload and subsequently increased force of contraction do to the tension/[Ca2+] graph?

Shift it to the left.


What is the difference between autorhythmic fibres and contractile fibres?

Autorhythmic fibres have an unstable resting membrane potential of ~60mV
Contractile fibres have a stable resting membrane potential of ~90mV


What is an ECG?

The net sum of the depolarisations of all the myocardial cells.


What do the small and large squares on an ECG represent, and how can they be used for calculating heart rate?

Small squares = 0.04s
Large squares = 0.2s
300 large squares = 1 minute

Heart rate = (large squares between R-R interval)/300


Why is atrial fibrillation dangerous?

It can cause thrombo-embolism due to reduced stroke volume.


What 3 ways can atrial fibrillation be treated?

B1-adrenoceptor antagonists


What is mean blood pressure?

The difference between systolic and diastolic blood pressure (which represents the pressure in the capillaries).


What is the relationship between flow of blood per unit time and the pressure difference?

Q = change in pressure/resistance


What are pre-capillary sphincters?

Rings of smooth muscle in the walls of arterioles that determine the blood flow to the capillary bed.
The sphincters respond to changes in pH caused by metabolically active cells that release H+, K+ and adenosine, and so increase blood flow to active cells.


What do endothelial cells release to cause vasodilation?

Nitric oxide


What effect does hypoxia and high pCO2 have on blood vessel walls?

Cause vasodilation


What happens if the macula densa senses there is too much NaCl inside the tubule?

The glomerular filtration rate must be too high, so the macula densa releases adenosine to constrict the afferent arteriole and reduce glomerular perfusion.


What happens if the macula densa senses there is too little NaCl inside the tubule?

The glomerular filtration rate is too low, the macula densa triggers release of renin from the juxtaglomerular apparatus to increase blood pressure and increase glomerular filtration rate.