Why don’t we want tetany of the heart?
The heart would remain contracted so no matter how many stimulants there are there is only 1 response
What develops tension in the heart?
Entry of calcium into cardiac muscle
How do we prevent tetany?
Have a long refractory period so a new action potential cant be initiated until the last one is over
Why does the SAN demonstrate spontaneous electrical activity?
It has an unstable resting membrane potential
How do the action potentials of the heart differ?
SAN doesn’t start from -90 like the others
The purkinje fibres, ventricles and atria also all have differing curves
Why does the SAN have a more positive resting membrane potential?
It has fewer potassium ions
Describe the differences between the SAN and ventricular action potentials? (3)
Varying resting potentials
Increases faster
Ventricular lasts longer
Describe SAN ions in the action potential
Na doesn’t really have any channels in the SAN
Ca channels are long acting so make a slow rising action potential
Ka channels allow for repolarisation
What blocks SAN K channels?
Barium
What blocks SAN Ca channels?
Verapamil
Nifedipine
What blocks SAN Na channels?
Ivobrodine
What is a long acting Ca channel?
Stay open for a long time but let fewer in at a time
What is a transient Ca channel?
Doesn’t stay open for long but let loads in at a time
What is the pacemaker potential?
The gradual depolarisation after the last action potential has finished, giving it its resting potential, this time decides heart rate (decay)
Chronotrophic
Something affecting heart rate
Give examples of chronotrophic agents
Noradrenaline
Acetylcholine release
What NS releases noradrenaline?
SNS
What does noradrenaline do?
Increase ion conductance
How are myocytes coupled?
Intercalated disc with desmosome, connexion and hen a gap junction
What does rate of conductance depend on? (2)
Resistance of gap junctions and membrane capacitance
Terminal cisterns
Enlarged areas of the sarcoplasmic reticulum surrounding the t tubules, storing calcium
Dyad
At the Z-line it is a t-tubule paired with a terminal cisterna of the sarcoplasmic reticulum. The diad plays an important role in excitation-contraction coupling by juxtaposing an inlet for the action potential near a source of Ca 2+ ions
What is the Treppe effect?
Increase in heart rate increases tension as there is a high amount of Ca present so there’s less time to remove it so contraction force increases
How do we get rid of Ca during repolarisation?
Put them back into stores
Where do you place the electrodes?
Red and black on clavicles and green on left rib
What controls CO and peripheral resistance? (2)
Neural and endocrine mechanisms
Mean arterial blood pressure =
Diastolic blood pressure + (systolic blood pressure-diastolic blood pressure)/3
How do you calculate pulse pressure?
SBP-DBP
CO=
SV x TPR
Inotropic agents
Alter heart contractility
3 positive inotrophic agents
Noradrenaline form the SNS
Increase Ca
B agonists
Negative inotrophic agents
Acidity
Positive chronotrophic agents
Noradrenaline from the SNS
4 negative chronotrophic agents
Acetylcholine from the PNS
B/B1 blockers
Glycosides increase vagus activity Activate K channels
How do we get the ECG shape?
It goes up or down depending on whether the muscle impulse is going towards or away from the electrode
The size of the line indicates how far the impulse travels
How is tension related to action potential?
No matter how much tension the same size action potential is always generated