CVS: Action Potentials and Cardiac Cycle Flashcards
Where does initiation of the heartbeat begin?
Begins at sino-atrial node (SAN)
SAN generates a.potentials called pacemaker potentials sin external stimulation, e.g. nerves/ hormones
Firing rate and rhythm of these action potentials= heart rate and rhythm
SAN cells are not contractile- their job is to produce electrical activity
How does the SAN produce pacemaker potentials?
The SAN has an unstable resting membrane potential so wants to continually depolarise:
Phase 0- Activation of vgcc!!! Ca2+ influx causes depolarisation
Phase 3: overtime, vgccs start to switch off, K+ channels open. K+ efflux causes repolarisation
Phase 4: as the cell gets more negative, IF channels get activated. This causes Na+ influx–> depolarisation
So IF channels are crucial to allow continual depolarisation sin external stimulation.
Why is conduction between atrial and ventricular cells so fast?
Low resistance pathways between atrial and ventricular cells called intracalated discs allows fast conduction
Describe electrical activity and conduction through the heart
Conduction across both atria to atrial-ventricle node (AVN)
AVN is non-contractile tissue which slows conduction between atria and ventricles. This allows atrial ejection to correctly fill ventricles before ventricular conduction and contraction
Electrical activity then spreads to the Bundle of His, to L+R bundle branches, to purkinje fibres. This is fast conduction to allow both ventricles to be stimulated + contracted juntos
Describe, draw and explain the Atrial/ventricular action potential
A.potentials in atrial/ventricular cells need to be stimulated from electrical activity arising in SAN
Phase 0: Opening of vg Na+ channels. Na+ influx= depolarisation
Phase 2: Na+ channels switch off, vgccs activate. Sustained Ca2+ influx= sustained depolarisation (the plateau phase)
Phase 2-3: VGCCs switch off, K+ channels switch on. Phase 3: K+ efflux= repolarisation
Phase 4: hyperpolarisation of -90mV
What is the function of the plateau phase?
Tissue is unexcitable or REFRACTIVE – CANNOT fire more action potentials in this timeframe
Voltage-gated Na+ channels are inactivated
No twitching from many a.potentials - One action potential produces ONE contraction, ESSENTIAL for proper ejection of blood from heart
How do atrial and ventricular action potentials couple to contraction?
Outline general principles of the cardiac cycle
Blood flows from high to low pa, unless flow is blocked by a valve
Valves open/close depending on pa changes in chambers
Events on the right and left sides of the heart are the same and are simultaneous- they just occur at different pa (lower on the right)
Describe the flow of blood through the heart
Venous return from SVC, IVC into RA
Tricuspid valve opens, blood flows into RV
Pulmonary semilunar valve opens, blood flows into pulmonary arteries and then lungs
Pulmonary veins bring 02 blood to the LA
Bicuspid (Mitral) valve opens, blood flows into LV
Aortic semilunar valve opens, blood is pumped to the body
Explain the 4 numbered phases shown
1: Atria contraction: tri/bi valves open. Ventricles are empty, open and have very low Pa
2: Isovolumetric contraction: tri/bi valves close. Ventricle walls start to contract, which increases Pa
3: Ejection: Aortic and pulmonary valves open. Blood flows out of heart.
4: Isovolumetric relaxation: Aortic/pulmonary valves close. Closed ventricle relaxes
Describe heart sounds. What are the 2 main heart sounds?
Vibrations induced by closure of cardiac valves.
Turbulent blood flow through valves can cause murmurs
S1 - “lubb”. Closure of tricuspid/mitral values at beginning of ventricular systole
S2 - “dupp”. Closure of aortic/pulmonary valves at beginning of ventricular diastole
What are some occasional heart sounds?
S3. Turbulent blood flow into ventricles, detected near end of first 1/3 diastole – common in young who have more aggressive/turbulent ventricular filling
S4 - pathological in adults. Forceful atrial contraction against a stiff ventricle causing turbulent flow – potentially abnormal
Draw and describe the left ventricle pressure-volume loop
x axis= volume of blood. y axis= LV pa. The cardiac cycle goes in a clockwise direction
eg: during the filling phase volume of blood goes from 40-120 but pa does not change much. This is bc the ventricle is elastic and increases in size to accomodate more blood.
Area inside loop = amount of stroke work done
Relates to the amount of energy consumption used to produce stroke volume
Changes in left ventricular pressure-volume loop explain problems associated with valve disease. What is valve stenosis?
Valve stenosis – narrowing of valve, doesn’t fully open, restricts blood flow
Describe aortic stenosis
Aortic valve not fully open bc it has been stenosed. Therefore hay build up of high pa in left ventricle. Poor ejection
If you exercised, you coudnt increase your SV bc its been clamped by stenosis- fatigue and breathlessness, fainting
Describe mitral stenosis
Mitral valve not fully open bc it has been stenosed
Poor filling of left ventricle
Low End Diastolic Vol (EDV), so reduced ejection and thus SV
Explain pressure changes in the RA during the cardiac cycle
A wave: SVC and IVC fill the atria, atria contract, high pressure
X descent: blood is ejected to ventricles. V little blood is left in atria so pressure decreases
V wave: atria starts to fill up again from systemic circulation, so pressure rises again
Y descent: tricuspid valve opens, atria empties into ventricles, pressure drops slightly before A wave happens again
What is the clinical relevance of right atria and jugular venous pressures changes?
If right atria pa increases, so does height of venous pulsatile distension (raised JVP)
This occurs in right sided heart failure: atria and RV fills, but hay poor ejection from right ventricle. More blood volume remains in right ventricle, so RV BP increases
