CVS Flashcards
Pace making cells in heart
SA node, AV node, purkinje fibres
Describe a pacemaker action potential
- the membrane potential constantly depolarises until it reaches its own threshold (-40mV)
- this triggers L type calcium channels to open which causes a depolarisation as Ca enters the membrane, to +10mV
- at +10mV K gated channels open and it repolarises
- then T type calcium channels open, which creates a drift of calcium into the cell and depolarises it until it reaches threshold (-40mV) for it to begin again
Events occurring to its corresponding cardiac event (from ECG)
AD – P wave
VD – QRS wave
AR – QRS wave
VR – T wave
Where is Systole and Diastole on the ECG diagram
P-T = systole T-P = diastole
Explain why heart rate increases when we inhale (in sinus arrhythmia, but its fairly normal)
- Thoracic pressure decreases
- Baro stretch receptors detect this and increase venous return
- This increase heart rate because the heart doesn’t need as much time to fill because venous return is up
What is Left atrophy in the heart?
Heart conduction goes in the right axis
What is Left hypertrophy in the heart?
Heart conduction goes in the left axis
What valves are closing in during Lub and Dub
Lub – mitral and tricuspid
Dub – Pulmonic and aortic
Name the 5 classes of anti-hypertensive drugs and an example
A
a) ACE inhibitors – Perindopril
b) Ang II Receptor Antagonists – Losartan
c) a- adrenoreceptor antagonists – Prasosin
B - B – adrenoreceptor antagonists (Beta blockers) – Metoprolol
C - Calcium entry blockers – Nifedipine
D - Diuretics – Frusemide
E
a) Endothelin antagonists – Bosentan
b) Endopeptidase inhibitors – Omapatrilat
Explain how ace inhibitors and Ang 2 receptor antagonists decrease blood pressure
- ACE inhibitors They block the conversion of Ang 1 to o active Ang 2
- Ang 2 initiates vasoconstriction, so if this isn’t working then there is more vasodilation and a decrease in blood pressure
- Ang 2 receptor antagonists allow Ang 2 to be formed, but block its interaction with receptors
