Disclaimer: Not covered on this page: GI Physiology

CARDIOVASCULAR

Q: What is the ion distribution across the ventricular myocyte cell membrane at resting membrane potential?
A: high potassium on the inside. High calcium and sodium on the outside.

Q: What type of channels are responsible for establishing the resting membrane potential of a ventricular myocyte?
A: K+ leak channels, Na/K ATPase.

Q: What are the five types of ion channels you find in cardiac sarcolemma?
A: K+ leak channels, voltage-gated Fast Na channels, voltage-gated transient K+ channels, voltage-gated slow Ca channels, Pacemaker Funny Channels.

Q: What voltage does the depolarization of ventricular myocytes reach?
A: +20mV

Q: Which phase is the “plateau” in the action potential of ventricular myocytes?
A: Phase 2

Q: What causes the “Plateau” of Phase 2?
A: relative balance between outward K+ flux and inward Ca flux

Q: What causes the temporary “spike” at Phase 1 during action potential of ventricular myocyte?
A: transient (fast, voltage-gated) K+ channel opening, then closing.

Q: What happens during Phase 3 in the ventricular myocyte?
A: K+ flux from inside increases dramatically. Ca channels inactivate, leading to depolarization.

Q: How is potassium returned to the ventricular myocyte after the action potential?
A: via Na/K ATPase.

Q: How is calcium eliminated from the ventricular myocyte after the action potential?
A: via Na/Ca exchange (primary) and Ca ATPase

Q: How does increasing extracellular potassium affect resting membrane potential of ventricular myocytes?
A: The K+ concentration gradient across membrane is reduced. Less K+ will move from inside to outside, and resting membrane potential will therefore become more positive.

Q: How does decreasing extracellular potassium affect resting membrane potential of ventricular myocytes?
A: Potassium Concentration gradient will increase. More K+ will move from inside to outside, and resting membrane potential will therefore become less positive.

Q: What is the protective purpose of the Effective Refractory Period (ERP) in a ventricular myocyte?
A: It prevents multiple, compounded action potentials from occuring, and limits heart rate. At very high heart rates, heart would unable to adequately fill with blood. Blood ejection from ventricles would be reduced. ERP also ensures conduction proceeds in forward manner.

Q: What do arrhythmic drugs prolong?
A: prolongs ERP in ventricular myocytes, so ensures conduction does not reverse backwards direction.

Q: Can an action potential be elicited during a relative refractory period (RRP) in ventricular myocytes?
A: Yes, but you need a larger-than-normal stimulus to induce it.

Q: When does the relative refractory period occur in a ventricular myocyte?
A: Middle to end of phase 3.

Q: The Total Refractory Period (ERP + RRP) lasts almost the entire contraction-relaxation cycle. What problem does this prevent?
A: fusion of individual twitch contractions.

Q: Cell membranes of SA node fibers are naturally leaky to what two ions?
A: Sodium and Calcium.

Q: Funny channels are responsible for what phenomenon?
A: slow diastolic depolarization, or pacemaker potential.

Q:What ion fluxes through the funny channels?
A: Sodium

Q: When the cardiac autorhythmic cell reaches threshold, what channel opens to cause depolarization?
A: Slow Calcium channels.

Q: What channel causes the repolarization in autorhythmic cells?
A: Potassium

Q: Funny channels open again when membrane potential reaches what voltage?
A: -60

Q: In What kind of cells will you find funny channels?
A: SA node, AV node, Purkinje fibers.

Q: Why do pacemaker cells have a longer refractory period than ventricular myocyte cells?
A: because they are depolarized by slow Ca+ channels rather than fast sodium channels. Slower channel = longer refractory period.

Q: What does Ach do to the SA and AV nodes?
A: It increases K+ outflux during repolarization, hyperpolarizing the maximum membrane potential during Phase 4. It also deactivates slow Ca channels (depolarization). Takes longer to reach threshold for action potential.

Q: What heart cells do Ach (parasympathetic) innervate? NE (sympathetic)?
A: Ach innervates SA and AV node. NE innervates all heart muscles.

Q: Does Sympathetic innervation affect resting membrane potential in heart?
A: no, instead it increases the depolarization.

Q: What are 3 things that sympathetic stimulation do in autorhythmic cells?
A: Increases inward movement of Na channels, Ca channels, and K currents. All of these speed up the action potential, and therefore the heart.

Q: How do AV and SA node compare in terms of diastolic depolarization speed?
A: AV is slower than SA.

Q: What are Characteristics of Bundle of His action potential?
A: rapid upstroke, very prominent Phase 1, longer plateau, very slow diastolic depolarization (phase 4).

Q: What is the normal sinus rhythm?
A: normal heart rhythm driven by SA node… normally it has a rhythmic discharge rate faster than all other parts of the heart.

Q: What is the intrinsic frequency of SA node (without autonomic nervous system)?
A: 100 beats/min

Q: If the SA node fails, the AV node can take over. If the AV node becomes the pacemaker, what is this called?
A: Nodal rhythm. You can diagnose this with ECG.

Q: What is the intrinsic rate of AV node?
A: 40-55 beats/min

Q: If the signal from SA node to AV node is blocked, then the Purkinje can take over. What is the resulting heart rhythm called?
A: Complete Heart Block, Complete AV block, or Complete AV Dissociation.

Q: what is the intrinsic rate of Purkinje Fibers?
A: 25 to 40 beats/min

Q: What is associated with a large dV/dt (voltage/time) during phase one in a cardiac rhythmic cell?
A: Fast cell-to-cell conduction

Q: Rank His-Purkinje, AV node, and Atrial/Ventricular muscles in terms of conduction velocity.
A: His-Purkinje conducts the fastest, followed by Atrial/Ventricular muscle, then the slowest is AV node. So in terms of conduction velocity, AV node is the slowest, but in terms of pacemaker tempo, AV node is the fastest.

Q: How do depolarization of autorhythmic cells (SA, AV, His, Purkinje) spread to contractile muscle cells in the heart (atrial and ventricular muscle cells)?
A: via gap junctions. Na+ pass through.

Q: Where do atrial muscle fibers get direct electrical activity from?
A: spreads from SA node to atrial muscle fibers via gap junctions, and then to AV node.

Q: Where is the AV node located?
A: right atrium

Q: what electrically isolates the atria from the ventricles?
A: connective tissue of the mitral and tricuspid valve annulus.

Q: What does the ventricular conducting system consist of?
A: Bundle of His, left/right bundles, Purkinje fibers.

Q: Purkinje fibers innervate 75% of ventricular muscle mass. How is the remaining 25% innervated?
A: via gap junctions.

ELECTROCARDIOGRAM

Q: What does P wave represent?
A: electrical potential spreading from SA node during atrial depolarization (before atrial contraction)

Q: What does the PR interval represent
A: From initiation of SA node to ventricular depolarization (phase 0)

Q: What is another name for the PQ segment?
A: The isoelectric line… used as a baseline when measuring wave amplitudes.

Q: What phase of ventricular cells does ST segment represent?
A: phase 2 “plateau”

Q: What phase of ventricular cells does the T wave represent?
A: Phase 3 repolarization

Q: What is the J point?
A: point at which R or S wave return to baseline.

Q: The R-R interval represent the length of the cardiac cycle. What is the average adult human R-R interval at rest?
A: 0.83 seconds.

Q: What kind of cardiac muscle does the ECG mainly represent?
A: electrical activity in ventricular and atrial muscle.

Q: Correlate the phases to the ECG waves.
A: 0 – P, rise in QRS; 1 – drop in R; 2 – ST; 3 – T; 4 – post-T baseline

Q: What two planes do the 12 ECG detect in the torso?
A: 6 limb leads to project frontal plane of torso and 6 chest leads to project horizontal plane of torso.

Q: In the Einthoven triangle, which trunk has -/-? +/+? +/-?
A: -/- Right hand; +/+ Left Foot; +/- Left Hand (actually, it doesn’t matter if its hand, wrist, or shoulder, as long as the direction’s correct)

Q: In the axial reference system, which bipolar limb lead is 60 degrees clockwise from horizontal? 120 degrees?
A: 60 degrees = Lead II. 120 degrees = Lead III. 0 = Lead 1

Q: What are the three augmented (unipolar) limb leads?
A: aVR (on right hand, -150 degrees); aVL (on left hand, -30 degrees); aVF (on left foot, 90 degrees).

Q: In augmented limb leads, what is used as the zero reference point?
A: heart. The (+) electrodes are at the limbs.

Q: In the horizontal unipolar chest leads, what is used to act as the electrical ground (zero reference point)?
A: A ground is formed by connecting right arm, left arm, and left leg.

Q: How are the chest leads named?
A: V1-V6. V1/2 correspond to the anteroseptal region. V3/4 correspond to anteroapical region. V5/6 correspond to anterolateral region.

Q: In ECG, if an electrical wavefront sweeps past a positive electrode, how would the ECG deflection look?
A: It will first have a postive peak as it sweeps toward the positive electrode and then a negative peak as it passes the electrode.

Q: What does direction and length of the depolarization vector (net dipole) represent?
A: The direction of the vector is the average direction of the depolarization wave. The head of the vector points towards positive (towards non-depolarized part of myocardium). The length(height) is the magnitude of the electrical field.

Q: A wavefront of depolarization is traveling +60 degrees would produce the greatest positive deflection in which lead?
A: Lead II.

Q: What two factors determine the strength (length) of the depolarization vector (dipole)?
A: 1. how many cells simultaneously depolarized at that moment. 2. how many dipoles are oriented the same/opposite directions. Additive effect if same direction. Canceling if opposite.

Q: When is the mean depolarization vector largest?
A: When one-half of the atrial myocardium is depolarized. When all cells are depolarized, there will be no vector.

Q: Where is the AV node depolarization represented in the ECG?
A: It magnitude of the vector for AV node is too small for it to show up on surface recording.

Q: Which side of the interventricular septum is normally depolarized first?
A: left side.

Q: Why is there no Q wave in Lead III?
A: Because the vector is traveling towards the positive end at Lead III during septal depolarization (at the interventricular septum). It just begins the R wave.

Q: When the depolarization goes from apical to ventricular, what layers of the myocardium does the electric wave pass through?
A: subendocaridal to subepicardial layers.

Q: Which side of the ventricle is the last to depolarize?
A: Left, because it is thicker than the right.

Q: What happens to the ECG after all the ventricular cells depolarize?
A: Flat line. (ST segment)

Q: What direction will the T wave be facing in relationship to the QRS?
A: same direction

Q: What areas are the first to be repolarized?
A: subepicardial myocardium. They are the last to depolarize and the first to repolarize. This is because they have the shortest action potentials because they are the thinnest (compared with mid-myocardial (longest) and subendocardial myocytes)

Q: At what angle would T wave vector be positive in all three leads?
A: between 30 to 90 degrees downward from the horizontal.

Q: What is strange about the vector arrow during repolarization?
A: The arrow head does not point toward the direction of repolarization. It simply just points towards whatever part of the heart has positive cells.

Q: If depolarization is moving from left to right at +150 degrees, which lead will show the greatest negative deflection?
A: Lead aVL

Q: In a depolarization wave front, is it positive or negative in front of the wave?
A: positive, because you are looking at the charge of what is immediately outside the cell. So at depolarization, since Na goes into the cell, all the outside past the depolarization is negative.

Q: Why do V1 and V2 show a negative R wave but V3-6 show a positive wave?
A: because depolarization moves from left to right across septum, V3-6 are in more “direct view.” V1-2 are looking from the other side.

Q: If all three of your leads have the same direction, what can you look at to estimate the mean electrical axis?
A: Look at which of the leads have the greatest magnitude. If they are the same size, then look for a lead that is equiphasic and choose it’s parallel.

Q: What direction is the mean QRS vector in a normal human ventricle? What range is considered normal?
A: +60 degrees, which corresponds greatest to Lead II. -30 to +90 are considered normal.

Q: Divergence beyond normal QRS vector causes right or left axis deviation. Beyond what degrees do these occur?
A: Beyond -30 degrees (aVL) leads to Left Axis Deviation. Beyond +90 degrees (aVF) leads to Right axis deviation.

Q: When the heart moves to the right or left, like when breathing, it can temporarily alter the heart’s angulation, shifting the electrical axis of the heart. What causes rightward angulation?
A: when you breathe in, when you stand up, and in tall, lanky people. The opposite, leftward angulation happen when you breathe out, lie down, and in stocky fat people whose diaphragm press upwards against heart.

Q: How will Pulmonary Valve Stenosis affect the ventricular electrical axis?
A: Pulmonary valve stenosis leads to right ventricular hypertrophy, which leads to right axis deviation of mean QRS vector.

Q: How does Left Bundle Branch Block affect the vector of the QRS?
A: left bundle branch block leads to a very slow depolarization on that side (now can only depend on gap junctions). Outside of these left-side cells stay positive much longer than the right side. So the vector points (with arrowhead at the positive) extremely to the left side (electropositive). This results in a positive axis deviation of -50 degrees. In addition, QRS is also a lot longer because depolarization is prolonged.

Q: What is the normal time duration of QRS?
A: 60-100 msec.

Q: What time duration of QRS would indicate incomplete bundle branch block?
A: 100-120 msec

Q: What time duration of QRS would indicate complete bundle branch block?
A: over 120 msec

ELECTROCARDIOGRAM ABNORMALITIES

Q: What is the normal range of heart rate? Tachycardia? Bradycardia?
A: 60-100 beats/min. Anything above 100 is tachycardia. Anything below 60 is bradycardia.

Q: What is the normal PR interval?
A: 120 to 200 msec, which shows proper conduction delay through the AV node.

Q: What is carotid sinus syndrome?
A: When the baroreceptors in the carotid sinus are excessively sensitive. Mild pressures can lead to discharge of parasympathetic nerves, causing bradycardia.

Q: How much does the heart rate increase per unit temperature?
A: Increases 10 beats/min per °F (or 18 for °C). Beyond 105°F, heart rate would decrease because of heart muscle debility.

Q: What causes Respiratory Sinus Arrhythmia?
A: When you breathe in, lung stretch receptors and right atrium stretch receptors (Bainbridge Reflex) decrease parasympathetic activity, and heart beats faster. More pronounced in athletes and children.

Q: What are the most common arrhythmias?
A: atrial fibrillation and atrial flutter. arrhythmias are related to age and heart disease.

Q: What is Altered Impulse Formation?
A: changes in automacity of pacemaker cells, or ectopic foci (when non-SA node form the beats)

Q: What is Altered Impulse Conduction?
A: block in the electrical conduction in the heart. This can lead to impulse reentry, which leads to tachyarrhythmias.

Q: What are 5 Categories of the causes of arrhythmias?
A: abnormal pacemaker rhythm, ectopic foci, blocks, abnormal pathways, spurious impulses.

Q: What are ectopic foci?
A: Abnormal sites in the heart that act as pacemakers (outside of SA node). However, their activity is usually overdriven by SA node. They can cause additional beats, or completely take over. They can cause tachycardia or bradycaria. Slower than normal.

Q: In a third degree AV nodal block, how do the ventricles still beat?
A: via an ectopic foci in the Purkinje system in the ventricle.

Q: What are three causes of “Reentry Arrhythmias”?
A: Impulse pathway is longer than the refractory period (i.e. dilated hearts). Decreased velocity of conduction, passing refractory period (block in Purkinje or ischemia). Shortening of the refractory period (i.e. epinephrine).

Q: Normally during a beat, all muscle cells depolarize, causing a refractory period. How do “Reentry Arrhythmias” lose part of their refractory period?
A: If there is a conduction block, not all the myocardium is depolarized. So while excited cells go through the refractory period, some of their impulses can be transmitted to the non-depolarized cells, causing those to excite cells over and over, independent of the rhythm set by the SA node.

Q: What are two causes of Paroxysmal Atrial Tachycardia (PAT) (aka “supraventricular tachycardia”)?
A: Ectopic focus in the atrium. Reentry phenomenon in the atrium. Both of these abnormally excite ventricles. Since abnormality in the atrium, their P waves look abnormal. Sometimes the P and T are superimposed because heart rate is increased.

Q: How risky is Paroxysmal Atrial Tachycardia (PAT) compared with Ventricular Tachycardia?
A: It is not life threatening like ventricular tachycardia. However, the decrease in cardiac output could cause drop in blood pressure or fainting.

Q: What are paroxysms?
A: sudden bursts

Q: What happens in first degree heart block?
A: There’s just a slow conduction through the AV node. Hence, PR interval is longer than normal. 1:1 relationship between P waves and QRS is preserved

Q: There are two types of Second Degree Heart Blocks: Mobitz Type I (Wenckebach) and II. What does it mean when the heart has a 6:5 sequence?
A: 6 P waves to 5 QRS waves.

Q: Unlike Mobitz Type I, what is the pattern of AV conduction loss for Type II?
A: Sudden and unpredictable.

Q: What are some causes of Heart Block?
A: medication, ischemia, inflammation. Disturbed onduction in Bundle of His or Purkinje also a possibility for Type II block (which is more serious).

Q: Why is Mobitz Type II AV block a concern?
A: Because there can be more than 2 P waves per QRS. There is a chance that 3:1 can become 4:1 and so forth until a complete AV block.

Q: What happens in a complete AV block?
A: Since no signal from SA node is reaching the ventricles, the ventricles develop its own impulses (ectopic foci).

Q: How does QRS and P wave relate in a complete AV block?
A: They don’t. P waves from atrial rhythm is completely dissociated from QRS. If new QRS impulse is from AV node, then QRS is 40-60 beats/min. If new QRS is from Purkinje, then QRS is 30-40 beats/min.

Q: What causes complete AV block?
A: damage to AV node, Bundle of His, heart attack, drugs.

Q: You see a T wave that looks way too tall… what caused it?
A: Premature Atrial Beat. The P wave occurs too early, often but not always, fusing with the T wave.
Q: What causes Premature Atrial Beat?
A: emotional stress, alcohol, fatigue, caffeine, fever. You don’t need therapy.

Q: Where does the electrical impulse of a junctional premature beat come from? How can you tell from looking at the ECG?
A: from the junction between atria and ventricle. Since the wave is coming from the AV upward to the atria, there is a retrograde P wave (upside down).

Q: Atrial flutter is an example of…
A: Reentry arrhythmia. The impulse begins in the right atrium, and flutters round and round the heart.

Q: There are QRS waves but not in a regular pattern. Everything between is chaotic. The P waves are not discernable. What is the Diagnosis?
A: Atrial Fibrillation. The depolarization happens in all directions. Some get to ventricle, hence the irregular QRS.

Q: How would Atrial Fibrillation cause a stroke?
A: without organized atrial contraction, blood can be static in certain areas like the left atrial appendage. Blood clot forms, which can lead to a stroke.

Q: How can a valve lesion cause Atrial Fibrillation?
A: a valve lesion can cause atrial enlargement. Dilated atria walls increase length of conduction, and further irregularities, leading to A-Fib.

Q: Why is Wolff-Parkinson-White Syndrome called a pre-excitation syndrome?
A: Because an abnormal muscle lets the impulse bypass the AV node, causing an abnormally early ventricular activation. At the same time, you still have the normal connection as well. Hence, you get tachycardia.

Q: How can you tell by looking at an ECG that someone has Wolff-Parkinson-White Syndrome?
A: Look for the Delta Wave. This is due to the pre-excitation ventricular wave combining with the normal QRS wave.

Q: What are Premature Ventricular Contractions (PVC) caused by?
A: action potentials initiated by ectopic focus in ventricular muscle… causes ventricles to contract early, without P wave.

Q: What is a compensatory pause?
A: It is a pause that follows a premature ventricular contraction (PVC). This is because ventricular muscles conduct slower than Purkinje fibers.

Q: What can Long QT Syndrome lead to?
A: Torsades de Pointes (multifocal ventricular tachycardia). Looks like a party streamer in ECG. Can lead to V-Fib, then death.

Q: What causes Long QT Syndrome?
A: defect in Na+ channel or K+ channels during the action potential.

Q: What causes Ventricular Tachycardia?
A: Abnormal pacemaker from ectopic focus in ventricle, like PVC. Since the depolarization is from ventricular muscle, there are no P waves. The P waves from the atria are obscured by the close proximity of the ventricular waves.

Q: Why is ventricular tachycardia bad?
A: When the hearts beating this fast, there isn’t enough time for ventricular filling. Causes hypotension and fainting. Can lead to V-fib, then to death.

Q: Describe Ventricular Fibrillation
A: depolarization wave so disorganized, leaving patches of refractory muscle everywhere.

Q: In Myocardial ischemia, if you increase the O2 supply to the heart, does it help supply an increased O2 demand?
A: No.

Q: How can you tell the difference between subendocaridal ischemia and transmural ischemia on an ECG?
A: subendocaridal ischemia shows ST depression or T wave inversion. Transmural ischemia shows ST elevation.

Q: How do you do an exercise stress test?
A: Tell patient to run on treadmill. Tell them to keep running until the ECG show signs of myocardial ischemia (ST depression). Record the heart rate.

Q: How much stenosis would cause coronary arteries to stop supplying enough O2 during exercise stress test?
A: 70%

Q: How much stenosis would cause coronary arteries to stop supplying enough O2 during rest?
A: 90%… Bypass surgery needed immediately!

Q: How can you tell there has been a myocaridal infarction over a certain region of the heart?
A: If you detect a greater downward reflection of the Q wave. This is because the region under the electrode is necrotic, so the electrode detects the healthy tissue on the other side of the ventrical, away from the infarct.

Q: What is the difference between ischemia and infarction?
A: Well obviously, ischemia is restriction of blood supply while infarction is necrosis of heart cells. Ischemia is reversible, but once your heart cells are dead during infarction, they are dead.