Flashcards in First Pass Miss Deck (39):
What is the purpose of Ik1 channel? How does it's activity change?
It is the inward rectifier potassium channel. It's activity decreases during the plateau phase to prevent rapid repolarization
Where do IKur channels exist and why?
Atrial myocytes. (ultra rapid) They shorten the atrial action potential so the plateau phase isn't is long since it is a thinner wall and is not as necessary for them to contract as long
Where is the IKach channels vs IKatp?
IKach - atrial myocytes + SA/AV nodes, opens to shorten action potentials in atrial myocytes only
IKatp - atrial and ventricular myocyes - opens to shorten both atrial and ventricular in response to low ATP levels. (unbinds when the ATP/ADP ratio is low)
Why is there always a slow diastolic depolarization in slow fibers?
There is no Ik1 inward rectifier channel to keep the membrane hyperpolarized
What is the sequence of events leading to a cardiac slow fiber contraction?
If = Ifunny, nonspecific channels respond to membrane hyperpolarization when membrane potential goes below -50 mV. This is a nonspecific channel.
Inward flux from If causes a depolarization via the voltage gated calcium channels (slower AP rise than sodium channels)
K+ outward current via Ik starts immediately and ensures no plateau phase to re-hyperpolarize the membrane to start next cycle
What channels mediate the activity of positive and negative chronotropic effects on pacemakers?
Positive - Sympathetic - increased activity of If + Ica channels to produce a higher sloping and thus quicker diastolic depolarization (phase 4). Ik activity is decreased
Negative - Parasympathetic - IKach channels keep the membrane more hyperpolarized so it takes longer to reach threshold potential. Also reduces Ica and If activity.
What causes an early afterdepolarization (triggered activity)?
Typically at low HRs or altered electrolyte levels.
Due to another depolarization in relative refractory period since Ca+2 is no sufficiently cleared from the cytoplasm and repolarization via Iks is not as good at slow heart rates (we are sitting much closer to Ca+2's threshold, giving enhanced automaticity)
What causes a delayed afterdepolarization?
Typically with high heart rates / sympathetic activity, may occur due to genetic mutations causing increased intracellular concentrations and RyR dysfunction.
What is depolarization-induced automaticity?
Something that occurs in ventricular or atrial myocytes that can be induced by never reaching resting potential (i.e. ischemia). Membrane potential sits close enough to Na+ or Ca+2 threshold to trigger a depolarization.
What is first degree heart block characterized by?
PR intervals longer than 200 msec (slowed AV conduction)
What are the two types of second degree AV block characterized by?
Mobitz I - gradually lengthening PR intervals so that a ventricular beat will be dropped
Mobitz II - normal PR intervals and random dropping of a beat
What characterizes third degree AV block?
Complete dissociation between PR intervals and ventricular contraction, an ectopic pacemaker distal to the block of the AV node will cause the ventricular contraction
What is atrial fibrillation vs atrial flutter?
Atrial flutter - a single ectopic firing that is propagated through a re-entry circuit. May not lead to a ventricular tachycardia if physiological AV block is good
Atrial fibrillation - One or more ectopic foci are firing causing to chaotic, discoordinated atrial depolarization and random conductions to the ventricles. May lead to clotting since blood is net not moved.
What is the most common cause of Ventricular Tachycardia?
Re-entry, especially due to areas of slowed conduction (ischemic tissue during myocardial infarction)
How can ventricular tachycardia be caused by the AV node?
AV nodal re-entrant tachycardia:
alpha-pathway is refractory due to premature atrial contraction
beta-pathway is slow-travelling but lower refractory period, stimulated on next normal AV rhythm.
beta to alpha pathway stimulates re-entry loop and Vtach ensues
What causes WPW syndrome and does not lead to Vtach? What is the ECG finding?
Bundle of Kent -> area of reduced resistance in cardiac skeleton to bypass AV node.
PR interval will be slightly shortened and a delta wave will appear
How can long QT syndrome lead to ventricular arrythmias? How is it diagnosed?
Diagnosed as QT interval greater than 0.46 seconds, due to failure to repolarize properly (decreased activity of Ikr or Iks. Also the sodium channels H gates may not be closing)
Can lead to arrythmias due to failure to fully repolarize and subsequent EADs.
What is the difference in the appearance of the T wave between subendocardial and transmural ischemia?
Subendocaridal 1. Peaked T wave - due to shortening of plateau phase due to activation of Katp channels in subendocardium, bringing the transmural repolarization closer together (Lasley says the opposite)
Transmural 2. Inverted T wave - due to failure of Ito1 channels, so that repolarization happens the same way as depolarization (endocardial to epicardial), normally happens epicardial to endocardial
What causes ST depression?
Subendocardial ischemia - A type of systolic injury current in which the healthy tissue is the epicardium so it depolarizes more. Positive charge flows from the epicardium to endocardium in plateau phase. V5 is a positive electrode that sees positive charge moving away from it, thus causing a depression.
What causes ST elevation?
Transmural ischemia - positive charges flowing towards the injured epicardium results in a positive deflection
What does LV necrosis cause on ECG?
Abnormally large Q waves because RV depolarization seems more significant whenever the LV wall is dead (no electrical profile).
RS complex not really seen, often has inverted T wave as well.
What does hyperkalemia cause on ECG? this is counterintuitive
Peaked T wave - Increased rate of depolarize across entire ventricular wall -> increased extracellular K+ increases the conductance of Ikr channels.
Also makes sense -> slower phase 0 membrane is already slightly depolarized. Leads to longer QRS complex and thus longer QT interval.
What does hypokalemia cause on ECG?
Opposite of hyperkalemia - shallow T waves, appearance of U waves
What does left atrial hypertrophy cause in ECG?
A split P wave in V1. The second part is negative due to the large depolarization of the left atrium moving away from it (V1 is next to RV).
What are the causes of the A, C, and V peaks of the venous pulse?
A = atrial systole - right atrial contraction (increases jugular backflow)
C = isovolumic Contraction - increase in RA pressure due to bulge of tricuspid valve into RA
V = increased Venous return due to pressure from systole
Which of the semilunar valves opens earlier and closes later and why?
Pulmonic valve opens earlier and closes later due to less afterload from pulmonary artery.
When is physiological splitting of S2 heard and why?
During inspiration, since there is a greater volume ejected in the lungs during inspiration and the P valve must stay open even longer (long difference between aorta and pulmonic valves).
Lungs want more blood because of negative intrathoracic pressure from increasing the volume of the thoracic cavity, and increased venous return from IVC and SVC during inspiration.
What is the function of PKA in cardiac muscle contractility?
Stimulated by B-adrenergics, it phosphorylates:
1. L-type Ca+2 channel for greater influx
2. Phospholamban -> increases SERCA activity
3. Troponin I -> reduces affinity of TnI for TnC
2/3 decrease the time of contractions at fast HRs.
How is stroke work defined?
Stroke work = stroke volume * mean arterial pressure
How does Pulmonary Capillary Wedge Pressure approximate pre-load?
It is the pulmonary artery diastolic pressure, which is a good estimation for LA pressure = LV end diastolic pressure
Why does left atrial hypertrophy often happen during aortic stenosis?
LV hypertrophy decreases the compliance of the ventricle, causing the same volume of blood to exert a greater pressure on the wall (greater stiffness, less give from the wall). This forces the left atrium to push harder to meet that end diastolic pressure.
Why might mitral insufficiency not actually decrease cardiac output significantly?
Backflow into left atrium leads to greater volume and pressure, which allows for more diastolic filling. This increases the preload and negates most of the losses during ventricular systole
How does aortic insufficiency affect blood pressure and size of heart?
More blood backflowing after ejection -> left ventricular dilation and eccentric hypertrophy
This increases preload -> greater systolic blood pressure max. Backflow decreases systolic pressure. Overall, blood pressure is higher.
What receptor is normally affected by norepinephrine but is only affected by epinephrine at high concentrations?
alpha-adrenergic, for vasoconstriction
What is the sympathetic neurotransmitter causing vasodilation in the fight or flight response?
What neurotransmitter controls skin blood vessel dilation during hyperthermia?
How does decreased inhibition of the vasomotor center by baroreceptors increase blood volume in the longterm?
1. Vasomotor center stimulates vasopressin release which increases thirst, kidney reuptake, and vasoconstriction
2. SANS stimulates renin release, the ratelimiting step in angiotensin conversion. Angiotensin II also stimulates thirst
How do O2 vs CO2 chemoreceptors differ?
O2: SANS response does not occur unless there are large drops in PO2
CO2: very tonically activity normally, and will increase more with higher CO2 / H+ levels