Cardiovascular Flashcards
What stimulates the baroreceptors?
Distension of the structures that contain these baroreceptors. More sensitive to pulsatile than constant pressure. Maximal firing at 150mm Hg at the carotid sinus
What are baroreceptors and where are they located?
Located in the adventitia of the aortic arch and also in the carotid sinus which is located in the internal carotid artery, immediately after the bifurcation from the common carotid artery. They are also located in low pressure area - atria at the entrance of IVC and SVC, pulmonary veins and pulmonary circulation
What are the effects after the baroreceptors are stimulated?
Increased blood pressure stretches the baroreceptors resulting in an increased firing in the afferent nerves. The afferent nerves are inhibitory to the vasomotor centre. Inhibition of the vasomotor centre reduces sympathetic drive and increases vagal drive.
These lead to vasodilation, venodilation, hypotension, bradycardia (tachycardia in low pressure baroreceptors), decreased cardiac output
What is the effect of chronic hypertension on the activity of the arterial baroreceptors?
They reset to maintain normal basal activity at the elevated blood pressure - reversible
What are the effects of sympathetic (noradrenergic) and vagal (cholinergic) stimulation on the membrane potential of the SA node?
Stimulation of the sympathetic cardiac nerves ⇒ increased depolarizing effect of the ‘h’ channels (Ih) and the rate of spontaneous discharge increases.
Noradrenaline secreted by the sympathetic endings bind to beta 1 receptors ⇒ increase in intracellular cAMP ⇒ facilitates the opening of L channels, increasing Ca influx and the rapidity of the depolarization phase of the impulse
Stimulation of the cholinergic vagal fibers to nodal tissue ⇒ hyperpolarization of the membrane and a decrease in the slope of the prepotentials. This is because the acetylcholine released at the nerve endings increases the K+ conductance of the nodal tissue. This action is mediated by M2 muscarinic receptors, which open a special set of K+ channels. Activation of M2 receptors also decreases cAMP in the cells, and hence slows the opening of L-type Ca2+ channels. The result is a decrease in firing rate.
Normal ECG intervals
PR interval - 0.12-0.20
QRS duration 0.08-0.10
QT interval - 0.40-0.43
ST interval - 0.32
Please describe the normal ECG waveforms in relation to the sequence of cardiac excitation
P wave - atrial depolarization
QRS - ventricular depolarization
T wave - ventricular repolarization
U wave - slow repolarization of the papillary muscles
What factors influence myocardial oxygen consumption?
1. Intramyocardial tension which is dependent on pressure, radius, and wall thickness (The Law of Laplace)
2. The contractility of the myocardium (Inotropy)
3. Heart rate
- Ventricular work per beat correlates with O2 consumption. Stroke work = SV x MAP
- Pressure load increases O2 consumption more than volume load, i.e. an increase in afterload causes a greater increase in O2 consumption than does an increase in volume.
Describe the phases the cardiac action potential
Phase 0 - Sharp, rapid depolarisation phase due to opening of the fast-opening voltage-gated Na+ channels (up to +20mv)
Phase 1 - Initial rapid repolarisation is due to closure of Na+ channels and opening of one type of K+ channel.
Phase 2 - Prolonged plateau is due to a slower but prolonged opening of voltage-gated Ca2+ channels.
Phase 3 - Final repolarization is due to closure of the Ca2+ channels and a slow, delayed increase of K+ efflux through various types of K+ channels.
Phase 4 - Resting membrane potential (-90mv)
What is the Frank-Starling law (or Starling’s law of the heart)?
What is the Frank-Starling curve?
The energy of contraction is proportional to the initial length of the cardiac muscle fiber.
For the heart, the length of the muscle fibers (i.e. the extent of the preload), is proportional to the end diastolic volume.
The relationship between the ventricular SV and the EDV is called the Frank-Starling curve.
What is long QT syndrome and what are the causes?
Prolonged repolarization ⇒ increased ventricular arrhythmias and sudden death
Causes - drugs, electrolyte abnormalities, myocardial ischaemia
Name two example of conditions with accelerated AV conduction.
Wolff-Parkinson-White (WPW)
- Presence of an additional aberrant muscular/nodal tissue connection between the atria and ventricles (bundle of Kent)
- Short PR interval, wide, slurred QRS complex, normal PJ interval*
Lown-Ganong-Levine (LGL)
- depolarization presumably passes from the atria to the ventricles via an aberrant bundle that bypasses the AV node but enters the interventricular conducting system distal to the node.
- Short PR interval, normal QRS complex, short PJ interval*
What are the renal effects caused by atrial natriuretic peptide (in the context of atrial stretch caused by CCF)?
- Decreased Na+ reabsorption in the DCT and collecting tubules
- Increased eGFR (dilatation of afferent arterioles and constriction of efferent arterioles)
- Inhibition of renin secretion ⇒ inhibiting RAA system
Define preload and afterload.
Preload - degree of stretch of cardiac muscle compared to resting length before it contracts. Equivalent to end-diastolic volume
Afterload - resistance against which blood is expelled
What factors affect preload (i.e. increase or reduce preload)?
