Cardiac Physiology: Electrical activity Flashcards
What are the walls of the heart made up of?
How are they connected?
-Contractile cardiac myocytes
- Intercalated disks:
1-Desmosomes: provide mechanical coupling between cells
2. Gap junctions provide a water-permeable pore which allows electrical communication between cardiomyocytes E.g. Ions
When do cardiac myocytes contract?
Relate this to the heart and what it can do….
- When stimulated electrically by the arrival of an action potential
>Heart is able to rhythmically generate its own cardiac action potential in the Sino-atrial node, which can spread through the heart and triggers its own contraction
How does the heart rhythmically generates its own action potential at the Sino-atrial node? (Heart beat)
- End of each action potential triggers a slow depolarisation of SAN. (PACEMAKER POTENTIAL)
» Bringing the nodal cell to threshold triggering next A.P
How is the pacemaker potential brought about to reach threshold?
- Open - HCN (activated by hyper polarisation and interaction of cyclic nucleotides)
- Close V.G K+
- Open T-type V.G Ca2+ ( Rapid > safety measure so we reach threshold, we don’t want it to be stable)
> Activates next depolarisation
- Upon reaching threshold how is action potential brought about in the heart?
- How does the cell polarise?
- Open L-type V.G Ca2+ (Large and Long lasting)
- V.G K+ channel opens / L-type V.G Ca2+ inactive
How does the cardiac action potential propagate between cells?
-Gap junctions
Describe the process of electrical conductivity.
- Action potential generated in Sinoatrial node
- Action potential rapidly proagates through atria triggering coordinated contraction of both atria – ATRIAL SYSTOLE
- Action Potential travels SLOWLY through atrioventricular node (This allows atrial systole to complete before ventricular systole begins )
- Action potential travels rapidly to the apex of the heart using the Bundle of His and Purkinje Fibres
- Bundle branches spread the action potential from myocytes at the apex upward to the base, triggering VENTRICULAR SYSTOLE
> helping to push blood up and out through the aorta and pulmonary artery
Why does the cardiac action potential propagate faster through myocytes than atrioventricular node cells?
- Differences in electrical resistance and potential difference between cells
Myocytes: Lower electrical resistance than nodal cells
> Larger diameter > less resistance so increased current so more depolarisation of next cell
>Longer > AP passes through gap junctions less often
> Increased density of gap junctions at intercalated disks , increases difference in potential difference , Electrical current travels faster
What else do ventricular mycoytes have to ensure faster propagation than nodal cells?
-Voltage gated Na+ channel which increases potential difference between myocytes
>Rapidly depolarise myocytes at higher level
>Increased current so increased voltage
Why does repolarisation appear to spread from the apex to the base of the heart during ventricular diastole?
** Action Potentials in the ventricular myocytes at the apex of the heart are shorter in duration than those at the base
How the cardiac action potential triggers contraction of the cardiomyocytes?
- (Troponin-Tropomyosin blocks crossbridge
forming in a Ca2+-dependent manner) When cytosolic Ca2+ concentration is high: Myosin-binding site is uncovered → Contraction
> > > The Cardiac Action Potential triggers a rise in cytosolic Ca2+ concentration through Calcium- induced Calcium release
1) Action potential propogates into t-tubules where it…
2) Opens L-type V.G. Ca2+ entry – allowing a tiny amount of calcium to enter
3) Calcium binds to and activate ryanodine receptors
4) Calcium leaves Ca2+ stores in the sarcoplasmic reticulum (SR)
5) Binds to troponin triggering contraction
6) Contraction terminated by Calcium being pumped back into the SR.
What is cross-bridge cycling?
- Myosin heads with ADP attached to them attach to binding sites forming an actinomyosin crossbridge (ATP)
- Myosin heads change angle pulling actin along myosin (ADP released) (ATP) (Powerstroke)
- ATP binds to myosin head (energy causes it to change shape) causing it to detach from actin binding site/ crossbridge
- Hydrolysis of ATP» ADP + Pi by ATPase (activated by Ca2+) releases energy for myosin heads to move back to their original position. (Recovery stroke)
- Myosin re-attaches to a different binding site further along actin, this continues as long as Ca2+ are present.
What do we use an ECG for? Why must patients rest?
What does a lead consist of?
-Measure electrical activity of the heart
> Generation of action potentials create extracellular potentials which we can be measured using surface electrodes placed on the skin
(skeletal electrical activity will interfere)
-2 Electrodes +/-
What is our test and reference electrode?
Reference : -
Test : +
Positive electrode relative to negative
Explain this.
2) Positive around positive electrode
-Positive number subtract negative number = +
4) Negative around positive electrode
-Negative subtract positive is negative
Why do we not get atrial repolarisation shown on ECG?
-Too slow and dyssynchronous
In an ECG what does 1 small box equal/1 big square ?
0.04 seconds / 0.2 seconds
Lead 2 ECG example
Leg relative to arm
What does an ECG detect?
-Extracellular potentials created by wave of depolarisation
What causes upwards/downwards deflections of ECG trace?
- What is an electrode and a lead?
- When do we get a maximum deflection?
1.
2. D/R travels in parallel to that lead (lead 2) thus perpendicular results in no deflection i.e isoelectric
Describe lead 2 ECG trace.
P wave = atrial depolarisation
- excitation pause at AV node , no P.D between 2 electrodes > isoelectric
QRS complex = ventricular depolarisation
- endocardium to epicardium outermost myocytes
- larger deflection as ventricular muscle is greater mass
- Pause where both ventricles fully depolarised > isoelectric > ST segment time between ventricular depolarisation to repolarisation
T wave = ventricular repolarisation
-Endocardial myocyte depolarise first , epicardial myocytes begin to repolarise first … wave of repolarisation travels in the opposite direction to ventricular depolarisation
How do you calculate instantaneous HR and Mean HR?
