4 Questions with answers on note-
feb-15-2025pdf
You'll find the list of questions at the end of the document
1. What is the primary effect of adenosine on coronary arteries, and
how is this effect mediated?
Adenosine causes mild dilation of coronary arteries. This effect is mediated
through parasympathetic innervation and muscarinic receptors. Activation
of these receptors leads to increased blood flow.
2. Describe the relationship between myocardial oxygen
consumption and myocardial perfusion. What is the clinical
significance of this relationship?
Myocardial perfusion is directly dependent on myocardial oxygen
consumption. This means that as the heart muscle's need for oxygen
increases (e.g., during exercise), the blood flow to the heart muscle must
also increase to meet that demand. Clinically, this relationship is crucial
because inadequate perfusion relative to oxygen demand can lead to
ischemia and angina. Conditions like coronary artery disease impair this
relationship.
3. Explain the Frank-Starling mechanism and its role in regulating
cardiac output. How does preload influence this mechanism, and
what are the limitations of increasing preload?
The Frank-Starling mechanism states that within physiological limits, the
heart will eject all the blood that returns to the right atrium. This means
that increased venous return leads to increased stretch of the ventricular
myocardium (preload), which in turn increases the force of contraction and
stroke volume, ultimately increasing cardiac output. Preload is the volume
of blood in the ventricles at the end of diastole. As preload increases, so
does stroke volume, up to a point. Beyond a certain point (around 16
mmHg), further increases in preload lead to overstretching of the
myocardium, which reduces the force of contraction and can lead to heart
failure.
4. Describe the sequence of electrical conduction in the heart,
starting from the sinoatrial (SA) node and ending with the Purkinje
fibers. Include the approximate conduction velocities or relative
speeds at each stage.
The sequence of electrical conduction in the heart begins with the SA node,
which initiates the impulse at a rate of 60-100 bpm. The impulse then
travels through the atrial internodal pathways to the AV node. The AV node
slows the impulse to allow for atrial contraction (atrial kick). From the AV
node, the impulse travels through the Bundle of His, which separates into
the right and left bundle branches. The left bundle branch further divides
