Module 6 Study Guide - Physiology I

Everything above, compressed to what you should be able to reproduce without the slides in front of you.

Core ideas¶

Na⁺ and Ca²⁺ always want to flow into a cardiac cell and K⁺ always wants to flow out, because their Nernst potentials sit outside the −90 to +30 mV range of cardiac membrane potentials. The farther V_m is from E_X, the stronger the flow.
Potassium dominates resting potential because it is essentially the only ion crossing the membrane at rest, in both the chord conductance and GHK equations.
Three tissue roles: excitatory (pacemaker, slow waveform), conductive (fast conduction, little contraction, fast waveform), contractile (myocardium, slower conduction, fast waveform).
The impulse runs SA node, internodal tracts, atrial muscle, AV node, bundle of His, bundle branches, Purkinje fibers, ventricular muscle. Atria depolarize top down; ventricles bottom up.
Conduction velocity is proportional to action potential amplitude and phase 0 dV/dt: how many positive charges enter, and how fast.
The slow action potential has phases 4, 0, 3 only. Phase 4 creeps up spontaneously through falling I_K, then I_f, I_CaT, and I_CaL. Phase 0 is driven by calcium, not sodium.
Chronotropy changes heart rate by changing phase 4 duration: its slope (I_f and I_Ca through cyclic AMP), the maximum diastolic potential (parasympathetic I_K-ACh only), and threshold (I_Ca).
The AV node is the lone electrical gateway to the ventricles. It delays the impulse about 0.1 s by low dV/dt and low amplitude, and backs up the SA node at 40–50 bpm. Dromotropy changes its conduction velocity through I_CaL.
The fast action potential has five phases: I_K1 at rest, I_Na upstroke, I_to notch, I_Kr/I_Ks against I_CaL at the plateau, then unopposed K⁺ efflux once calcium-dependent inactivation closes the calcium channels.
The sodium channel’s conformation sets the refractory period. Absolute through the first half of phase 3; relative from about −50 mV until rest.
Internodal pathways are not insulated and depolarize the atria as they go. The His-Purkinje system is insulated so the ventricles depolarize from the apex up.
P wave is atrial depolarization, QRS is ventricular depolarization with hidden atrial repolarization, T wave is ventricular repolarization. The PR segment matches the atrial plateau and the ST segment the ventricular plateau.
Two-cell model: V_ECG ≈ V_m,A − V_m,B, the first region to depolarize minus the second. That difference behaves like a time derivative of the action potential.
The human T wave is upright because cell B (epicardium) has the shorter action potential: depolarization runs endocardium to epicardium, repolarization epicardium to endocardium.
The signal on a lead is largest when the heart’s electrical vector runs along that lead. The electrical axis is found by the geometric or inspection method; normal is 0° to 90°.

Key terms¶

Nernst potential: Membrane potential at which an ion’s concentration and electrical gradients balance, so there is no net movement of that ion.
Funny current (I_f): Mostly Na⁺ influx through HCN channels, opened by hyperpolarization and stimulated by cyclic AMP.
HCN channel: Hyperpolarizing cyclic nucleotide-gated channel. Carries the funny current.
I_K1: Inwardly rectifying K⁺ current. Active at very negative voltages, sets fast phase 4, finishes phase 3.
I_to: Transient outward K⁺ current. Produces phase 1.
I_Kr / I_Ks: Rapid and slow K⁺ currents of the plateau and early phase 3.
T-type / L-type Ca²⁺ channel: Tiny conductance, transient opening (pA) / large conductance, long-lasting opening (nA).
Excitatory tissue: Pacemaker cells that depolarize spontaneously. SA and AV nodes.
Conductive tissue: Fast conduction, little contraction. Internodal pathways and His-Purkinje system.
Contractile tissue: Myocardium of atria and ventricles. Contracts, conducts slowly.
Maximum diastolic potential (MDP): The most negative point of the slow action potential, about −60 mV, where phase 4 begins.
Pacemaker potential: Phase 4 spontaneous depolarization of the slow action potential. Source of autorhythmicity.
Autorhythmicity: The heart’s ability to depolarize itself and set its own rhythm.
Intrinsic heart rate: How often the heart beats with no neural input. About 100 bpm.
Chronotropy: Variable timing of depolarization in the heart; heart rate modulation.
Dromotropy: Variable conduction velocity in the heart; modulates AV delay.
I_K-ACh: K⁺ current through channels that open only with acetylcholine present. Deepens the MDP.
Overdrive suppression: The faster SA node rhythm suppressing the AV node’s own pacemaker activity.
Heart block (AV block): AV delay so long that the AV node fails to pass the action potential on.
Calcium-dependent channel inactivation: Rising intracellular Ca²⁺ closing L-type channels, ending the plateau.
Absolute refractory period: Na⁺ channels open or inactivated; no new action potential possible.
Relative refractory period: Some Na⁺ channels reset; a stronger-than-normal stimulus can fire the cell.
PR segment / ST segment: Flat ECG stretches matching the atrial and ventricular phase 2 plateaus.
Einthoven’s triangle: Triangle formed by leads I, II, III, used for vector analysis of propagation.
Augmented limb leads: aVR, aVL, aVF. Calculated leads with a phantom negative electrode averaged from two limbs.
Precordial leads: V1 to V6 on the chest, transverse plane, with the calculated heart center as negative.
Monophasic action potential (MAP): Extracellular recording that gives a scaled-down transmembrane action potential.
Monodomain assumption: Setting intracellular voltage of both cells to zero in the two-cell model.
Electrical axis: The main direction of the heart’s electrical depolarization in the frontal plane.
Isoelectric: A lead whose wave deflects up as much as down, so it is nearly zero. The axis is perpendicular to it.
Atrial kick: The atrium’s final squeeze of blood into the ventricle, protected by the AV delay.

Numbers worth knowing¶

E_K	−94 to −84 mV
E_Na	+59 to +71 mV
E_Ca	+123 to +125 mV
Slow AP maximum diastolic potential	~−60 mV
Slow AP threshold	~−40 mV
SA node phase 0 dV/dt	~2 V/s
SA node cycle / intrinsic rate	0.6 s / 100 bpm
AV node phase 0 dV/dt	~5 V/s
AV node amplitude	~70 mV
AV node pacemaker rate	40–50 bpm
AV delay	~0.1 s (100–200 ms)
Fast AP phase 0 dV/dt	150–800 V/s
Fast AP amplitude	110–120 mV
Fast AP resting potential	−80 to −90 mV
Fast AP peak	~+30 mV
Plateau	0 ± 10 mV
Na⁺ channels begin resetting	~−50 mV
Atrial and ventricular muscle	0.5 m/s
AV node	0.05 m/s
Internodal pathways	1–1.5 m/s
Bundle branches	2 m/s
Purkinje fibers	4 m/s
Surface EKG signal	~1 mV
First-degree AV block	PR > 0.2 s
Normal axis	0° to 90°
aVL axis	−30°

Distinctions that get mixed up¶

Pair	How to keep them apart
Slow vs fast action potential	Slow: nodes, phases 4, 0, 3, sloping phase 4, Ca²⁺ upstroke at ~2–5 V/s. Fast: conductive and contractile tissue, five phases, flat phase 4, Na⁺ upstroke at 150–800 V/s.
I_f vs I_Na	Both sodium. I_f flows through HCN channels opened by hyperpolarization in slow phase 4. I_Na flows through voltage-gated Na⁺ channels in fast phase 0.
T-type vs L-type Ca²⁺	T is tiny and transient, only in slow phase 4. L is large and long-lasting, in slow phases 4 and 0 and the fast plateau.
Chronotropy vs dromotropy	Chrono is time: heart rate, set at the SA node through phase 4. Dromo is a race: conduction velocity, set at the AV node through dV/dt and amplitude.
Slope vs MDP vs threshold	Slope changes with both branches through I_f and I_Ca. MDP changes only with parasympathetic I_K-ACh. Threshold moves down with more I_Ca and up with less.
SA node vs AV node	SA: posterior high right atrium, primary pacemaker, ~100 bpm, purely excitatory. AV: low septal right atrium, conductive first, backup pacemaker at 40–50 bpm.
Phase 1 vs phase 3	Phase 1 is a brief notch from I_to. Phase 3 is full repolarization once Ca²⁺ channels inactivate, from I_Kr, I_Ks, then I_K1.
Absolute vs relative refractory	Absolute: Na⁺ channels open or inactivated, phases 0 through early 3. Relative: some channels reset, late phase 3, needs a stronger stimulus.
Internodal vs His-Purkinje	Internodal: 1–1.5 m/s, not insulated, atria top down. His-Purkinje: 2–4 m/s, insulated, ventricles bottom up.
PR segment vs ST segment	PR segment: His-Purkinje transit, and the atrial plateau. ST segment: the ventricular plateau, where ischemia shows.
Where atrial repolarization goes	Inside the QRS complex, swamped by the much larger ventricular depolarization.
Standard vs augmented vs precordial leads	Standard: two real limb electrodes. Augmented: one real positive limb electrode, phantom negative from two limbs. Precordial: real chest electrode, phantom negative at the heart’s center.
Cell A vs cell B	A depolarizes first: endocardium in humans, base in the frog. B depolarizes second: epicardium in humans, apex in the frog. V_ECG ≈ V_m,A − V_m,B.
Frog vs human T wave	Frog T is downward. Human T is upright because the epicardium has the shorter action potential and repolarizes first.
Hyper- vs hypokalemia	Hyper: more hERG current, tall peaked T. Hypo: anemic hERG current, flattened T.
Hyper- vs hypocalcemia	Hyper: more Ca²⁺-dependent inactivation, shorter action potential, short QT. Hypo: long QT.
Endocardial vs epicardial ischemia	Endocardial (cell A): ST depression. Epicardial (cell B): ST elevation.
First vs second vs third-degree AV block	First: PR > 0.2 s, every P conducted. Second: some P waves without a QRS. Third: P and QRS fully independent.

Check yourself¶

Write the Nernst equation, name every constant, and explain why each ion’s Nernst potential is a range rather than a single value.
Using the four V_m against E_X principles, explain why Na⁺ and Ca²⁺ always flow in and K⁺ always flows out of a cardiac cell.
Why does potassium dominate both the chord conductance and GHK equations at rest?
Name the eight cardiac currents, their ion, and where each acts in the slow and fast action potentials.
Trace blood from the right atrium back to the right atrium, naming every valve, and relate each chamber’s wall thickness to its job.
Why must the atria depolarize from the top down and the ventricles from the bottom up?
Define excitatory, conductive, and contractile tissue and name the waveform each shows.
List the conduction pathway from SA node to ventricular muscle with the conduction velocity at each step.
Which two features of the action potential set conduction velocity, and what does each say about positive charge entering the cell?
Walk through the four currents of slow phase 4 in order, explaining what triggers each.
Why is the funny current called funny?
What drives phase 0 of the slow action potential, and why is that unusual?
Calculate the intrinsic heart rate from an SA node cycle length of 0.6 s.
Describe the three ways phase 4 duration can change, and say which autonomic branch can use each.
Trace sympathetic norepinephrine at the SA node from receptor to faster heart rate, naming both channel effects.
How does the AV node slow conduction to 0.05 m/s, and why is the delay necessary?
Explain overdrive suppression and when the AV node takes over as pacemaker.
Sketch positive and negative dromotropy against a baseline AV node waveform and explain each change through I_CaL.
Name the five phases of the fast action potential with the voltage and currents of each.
Why does the plateau hold steady, and what ends it? Name the mechanism.
Give two jobs of the calcium entering during phase 2 other than holding the plateau.
Map the three Na⁺ channel conformations onto the phases of the fast action potential, and mark the absolute and relative refractory periods.
Contrast the internodal pathways with the His-Purkinje system on speed, insulation, and direction of depolarization.
What does each ECG deflection represent, and where does atrial repolarization go?
Which cardiac structures are too small to appear on the ECG?
Match phase 0, phase 2, and phase 3 of atrial and ventricular action potentials to ECG features.
For leads I, II, and III, name the negative and positive electrode, and explain why lead II gives the most iconic waveform.
How are the augmented and precordial leads built, and which plane does each set view?
Derive V_ECG ≈ V_m,A − V_m,B from the two-cell model, stating each assumption.
State the three clues from comparing the frog MAP and frog EKG.
Predict the T wave after warming the frog base, and after warming the apex.
Why is the human T wave upright? State the directions of depolarization and repolarization across the ventricular wall.
Use the two-cell model to predict the EKG in hyperkalemia, hypokalemia, hypercalcemia, and hypocalcemia, with the channel mechanism for each.
Explain why endocardial and epicardial ischemia shift the ST segment in opposite directions.
Distinguish first-, second-, and third-degree AV block on the EKG, with one cause mentioned for first and third degree.
Using the inspection method, find the axis when aVL is isoelectric and lead II is positive.
Give the axis ranges for normal, right axis, mild and severe left axis deviation, with an example cause for each.