Cardiovascular Physiology 2-3 Flashcards
Electrocardiogram 3 leads
-/- right arm
+/+ left leg
+/- left arm
P wave
Beginning of atrial contraction (systole), wave of depolarisation travels from the SA node towards the AV node
QRS complex
Beginning of ventricular contraction, the time for depolarisation to spread. Covers the wave that would be atrial repolarisation.
T wave
Ventricular repolarisation
P-Q interval
The time for the electrical excitation of the atria to reach the ventricles, usually slows through the AV node due to thicker fibers. (0.16 sec normal).`
Q-T interval
Duration of ventricular contraction (0.35 sec normal)
Einthoven’s triangle
Heart at the center, 3 electrodes from arms to legs.
Causes of cardiac arrhythmias
abnormalities in the rhythmicity conduction system of the heart:
- abnormal pacemaker activity
- ectopic pacemakers
- blocks
- abnormal pathways for impulses
- spontaneous generation of spurious impulses.
Sound 1
Closure of the AV valves
Sound 2
Closure of the pulmonary and aortic valves
S3 and S4
Early ventricular filling and atrial contraction
Atrial systole
From P-Q, atrial pressure remains low and ventricular pressure increases until the mitral valve closes.
Ventricular systole
Isovolumic contraction as blood volume remains constant until the pressure is greater than that of the aorta, opening the aortic valve.
Isovolumetric phases
Contraction - when the mitral valve has closed, until the aortic valve opens.
Relaxation - when the aortic valve closes, until the mitral valve reopens.
Stroke volume
amount of blood pushed into systemic circulation by ventricular contraction.
EDV - ESV, usually = 70mL
Cardiac output
= heart rate x stroke volume
Ejection fraction
The fraction of blood that was ejected during cardiac systole.
= (EDV - ESV) / EDV ~ 50-70% but goes up with exercise.
Indicates cardiac contractility.
Parasympathetic innervation of the SA/AV node
Sparse by releasing ACh on to muscarinic receptors.
Increases K efflux, and decreases Ca influx to HYPERPOLARISE the cell.
Sympathetic innervation of the SA/AV node
Rich by release NE on to β1 adrenergic receptors.
Increases both NA and CA influx to DEPOLARISE the cell.
Resting condition
Parasympathetic discharge dominates because ACh suppresses sympathetic activity and the release of NE from nearby nerve endings.
Atropine
Muscarinic receptor antagonist - blocks parasympathetic effects and increases heart rate.
Propranolol
β-adrenergic receptor antagonist that blocks sympathetic effects and decreases heart rate.
Extrinsic control of cardiac output
Sympathetic innervation that increases[ both contractility and venous return.
Frank-Starling law
Force (indicated by stroke volume) generated by cardiac muscle is proportional to initial length of the cardiac muscle fibers.