CVS. Lecture 2/3 Flashcards
What contributes to pacemaker potentials? (What are the three ion channel mechanisms?)
Pacemaker potentials are:
- Initiated by inward Na+
- Followed by inward Small transient Ca2+
- Gradual decrease in outward K+
Slow Na+ influx initiated during repolarisation/hyperpolarisation.
Unique set of channels, open when the membrane potential is at negative values.
F-type channels
T-type Ca2+ channels
Contributes inward Ca2+ current and an important final depolarising boost to the pacemaker potential.
(Progressive reduction in K+
permeability. The K+ channels that opened during repolarisation phase of the previous action potential gradually close due to the membrane return to negative potentials.)
The link between atrial depolarisation and ventricular depolarisation is which portion of the conducting system?
Atrioventricular node
For what reason is the propagation of action potentials through the AV node relatively slow. Approximately how long does it take for the impulse to actually pass through AV node?
- This delay allows atrial contraction to be completed before ventricular excitation occurs.
- Allows more time for ventricular filling before you get contraction of ventricles
(So it allows excitation of the atria; contraction of atria; sufficient ventricular filling)
Takes about 0.09 seconds for the impulse to actually pass through the AV node
What can cardiologists use the ECG to determine?
1) the anatomical orientation of the heart and the relative sizes of its chambers.
2) disturbances in cardiac rhythm and conduction
3) the extent and location of ischaemic damage to the myocardium
4) the effects of drugs or abnormal concentrations of various electrolytes on the heart
What are the major causes of cardiac arrhythmias?
1) Shift of the pacemaker from the sinoatrial node to other pacemaking regions
2) abnormal impulse formation in the sinoatrial node
3) blocking or delay of conduction of the impulse through the heart
4) spontaneous generation of abnormal impulse in any region of the heart. (E.g ventricular fibrillation)
At what rate do these regions of the heart pacemake?
1) SA node
2) AV node
3) Purkinje fibres
1) SA node
70-80 impulses/min
2) AV node
40-60 impulses /min
3) Purkinje fibres
15-40. impulses / min
SA node has the fastest intrinsic firing rate.
Therefore since SA node is normally the pacemaker of the heart it is called the sinus rhythm.
What is ectopic pacemaking?
When you are getting pacemaking in a region not associated with pacemaking, so in a non-pacemaker region.
This can occur in ventricular muscle.
Ventricular muscle cells when damaged can actually spontaneously start generating action potentials as well.
If purkinje fibres start firing at 140 beats/min. This can actually be dangerous- we get ventricular fibrillation.
Ventricular fibrillation.
Cause
What is damaged
Treatment
VF is a fatal consequence of myocardial ischemia and electrocution.
Ventricular muscle cells
Implantable defibrillator.
That will detect when ventricles go into fibrillation and then will shock her into normal sinus rhythm with an electrical shock
What heart rate defines tachycardia and bradycardia ?
Above 100bpm- tachycardia
Below 60bpm - bradycardia
How can we modulate Heart rate?
So we know in order to increase SA node pacemaking or increase heart rate during Exercise .
First of all:
Decrease in parasympathetic activity. Vagal withdrawal
Followed by increase in sympathetic activity.
Followed by increase in hormonal adrenaline
These all act on the SA node to increase pacemaking and this increase heart rate
How is the strength of cardiac muscle/stroke volume altered?
Two mechanisms:
1) changes in muscle cell length (End-diastolic volume; EDV)
2) changes in calcium release (contractility) (force of contraction)
What are the main determinants of End-diastolic volume ?
1) filling time
2) venous pressure
Increased venous return automatically causes an increase in stroke volume.
Matching input and output.
What is heart failure? What is happening to the heart
Heart failure= when the heart fails to pump Adequate CO (usually LV)
At normal EDV (135ml)
Ejection fraction of:
Failing heart ~ 30%
Normal heart ~ 52%
Tension on heart wall
= pressure in ventricle x radius of ventricle
Cardiomyopathy: ventricle becomes distended and the radius increases.
With increased radius, the muscle must generate more tension to maintain the pressure in the ventricle (to continue pumping the same amount of blood out of the heart as is entering it)
Ultimately the heart must work harder to get the same result it did before, leading to heart failure (i.e. The heart can no longer pump sufficient blood to the body)
Arterial blood pressure at rest:
What is hypertension?
What is hypotension?
Hypertension: high blood pressure
Higher than normal blood pressure
Consistently above 140/190
Hypotension (Low blood pressure)
Lower than normal
Consistently below 100/60
When do we get an increase in cardiac output and changes to the distribution of blood flow to organs changes?
During excercise
