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92 Cards in this Set

  • Front
  • Back
Frank-Starling Law of the Heart
When the heart is filled more, it will automatically contract more strongly
Capacitance Vessels-- structure and function
Another name for the veins with valves that hold 60% of the body's total blood at any given time. These have muscles that are activated by SNS--> increased tone/ constriction and hold less blood, e.g., following hemorrhage
Function of atria
Fill the ventricles with one-third MORE blood than they would otherwise contain-- however, atrial contraction is usually not essential, as a-fib patients can be fine.
Autonomic innervation of the heart
PSNS: right vagus --> slows SA node
left vagus --> slows AV node
little, if any, effect on ventricular contractility

SNS: Increase firing rate of SA node, ventricular contractility, conduction velocity through AV node, and coronary blood flow
Location of SA, AV nodes
SA node: where the SVC joins the RA

AV: at the septum between the tria near the tricuspid valve. the fibrous tissue around tricusp./mitral valves that separates A/V's forms an electrically tight seal, making AV node a regulated gate of impulses
Describe capillaries and gas exchange in tissues
Thin, single layer of endothelial cells on a basement membrane.
No Muscle.
No Elastic Fibers.
Allows 250ml/min O2 and 200 ml/min CO2 to exchange between tissues and capillaries at rest on average
Right ventricle and left ventricle: comparison in structure and function
RV little muscle compared to LV-- RV needs to generate only 25mmHg during systole, whereas LV needs to generate 120 mmHg during systole and thus has very muscular walls
Aorta: tissue composition and function
Lots of elastic tissue, some muscle--withstands high pressure generated by LV.
Expands during systole, storing just under 2/3 of SV. As LV relaxes, Aorta recoils, forcing rest of blood into system. BP = 120/80 in these large muscular vessels (e.g. brachial)
Arterioles: tissue composition and function
AKA Resistance Vessels
All Muscle, no elastic tissue, innervated by SNS --> NE --> α1 --> constriction --> resistance ^^ --> BP in large arteries increases
Pre-capillary sphincter
Sphincters that are autoregulated by waste products of metabolism: CO2 opens sphincters
Describe electric pathways and velocities of autorhythmic tissues of the heart
SA Node generates impulse at 60-80/min. These travel along the atria at 0.5 m/sec to the AV node. Here, traveling at 0.02m/sec, there is a 0.1s delay to allow atria to contract and fill ventricles. Then the impulse spreads down the bundle of His, R/L bundle branches, to Purkinje fibers. In the PKF the impulse travels at 3 m/sec to travel almost simultaneously to LV, RV.
Wolff-Parkinson-White Syndrome
Normally, atria and ventricles are electrically insulated from one another, with the AV node acting as the gatekeeper of impulses. This insulation can be broken by abberant conduction through the Bundle of Kent in WPW syndrome.
Why is conduction of impulses through the AV node slow?
1) fibers are small
2) there are fewer gap junciton between fibers
3) conduction occurs via slow Ca2+ ion diffusion (rather than fast Na+ ion diffusion) during phase 0
Why is conduction of impulses through the Purkinje fibers fast?
1) high permeability of gap junctions
2) few contractile fibers
3) rapid movement of Na+ ions across membrane via fast Na+ channels during steep phase 0 of AP.
Describe the AP of Ventricular Muscle
Phase 4: Resting potential = -90mV maintained by K+ leak channels

Phase 0: arriving impulse from PKFcauses Na+ channel to open, depolarizing cell to +20 mV

Phase 1: fast Na+ channels closed causing transient repolarization (20mV --> 0mV). Inward Cl- may also contribute.

Phase 2: Plateau created by opening of L-type Ca2+ channels (Ca2+ influx when D-gates open during phase 0) and K+ channels, (K+ efflux).

Phase 3: Repolarization: Ca2+-sensitive-K+channels open, with voltage gated K+ channels, repolarizing the membrane potential. Inactivation gates of fast Na+, slow Ca2+ channels begin to open.
Compare the membrane potentials at which f-gates of slow Ca2+ channels and h-gates of fast Na+channels open. Why is this important?
Voltage of f-gate opening is higher than the voltage of h-gate channels. In ischemic heart cells, the membrane potential is more positive and the fast-channels are not functional. Phase 0 is thus carried by Ca2+ slow channels, and is prolonged-- slowing conduction of impulses through ischemic tissue
How is Phase 4 of the Ventricular Action Potential maintained?
1) Passive outward diffusion of potassium ions
2) Na+/K+ exchange by Na+K+ ATPase
3) Active extrusion of Ca2+ by Ca2+ ATPase 5%
4) Active extrusion of Ca2+ by Na+/Ca2+ exchanger: 15%
5) SRCa2+ pump: 80%
Describe the Action Potential of a SA Node Pacemaker cell
Phase 4) Resting potential ~ -60mV. Depolarization caused by lowered K+ efflux, increased funny current (If, Na+ influx), then Ca2+ influx at -55mV.

Phase 0) At threshold -50mV, T-type Ca2+ channels open, causing a spike (although Ca2+ influx slow, so spike not as sharp as, say, ventricles).

Phase 3) Ca2+ channels close, Outward K+ current rapidly repolarizes the membrane.
What effects the rate at which impulses are carried through the AV node? What drugs can affect this?
The rate of AV impulse conduction depends on the steepness of the slope of Phase 0 (Ca2+ influx). Calcium channel blockers such as Nifedipine can slow conduction-- useful for PSVT, A-fib
How does parasympathetic stimulation affect the SA node? Mechanism?
PSNS stimulation...
ACh --> M-receptors --> K+ permeability ^ --> hyperpolarizes
1) lowers the max diastolic potential by opening GIRK channels that increase K+ efflux --> hyperpolarizes the resting potential
2) diminishes If, decreasing Na+ influx
3) diminishes ICa/calcium influx
How does sympathetic stimulation affect the SA node? Mechanism?
SNS stimulation...
Epi, NE --> β1-Adr.Receptors --> [cAMP] increases --> opens funny channels!
1) increases If: Na+ influx
2) Increases ICa: Ca2+ influx
What can block the effect of PSNS stimulation of the heart?
Atropine blocks the effect of ACh --> Muscarin Receptors, and can speed up the heart rate of patients with vagally-induced bradycardia. Note: Athletes have high parasympathetic tone, and their bradycardia is probably normal.
What can block the effect of SNS stimulation of the heart?
β1-receptor blockers block the effects NE, Epi --> β1-Adr. Receptors, preventing sudden HR increase. Good for Pts recovering from an MI.
Describe the action potential of an AV Node pacemaker cell.
Like an SA Nodal Cell, except the maximum diastrolic potential is lower: -70mV.
Describe the refractoriness of heart muscle cells.
Cardiac muscle cells have a long refractory period. This prevents spasming or tetanus that can occur in skeletal muscle. The effective refractory period is QT interval of 0.4 seconds.
Period of hyper-excitability
When the membrane repolarizes below -70mV (threshold), there is a brief period of hyper-excitability, where a lesser than normal stimulus will evoke an impulse. Oscillations in baseline membrane potential may increase sensitivity by bringing the membrane potential closer to threshold.
How does one slow cardiac impulse conduction?
Inhibit phase 0 through sodium channel blockers (Lidocaine, etc) in Ventricular Muscle, and Ca2+ channel blockers (Nifedipine, etc) in the AV node.
What determines the speed at which an impulse will move along a membrane?
The Slope of Phase 0
-Permeability of the membrane to sodium ions (Purkinje Fibers, Ventricular Muscles) or calcium ions (atrial muscle, AV Nodal cells).
Which drugs selectively target different cardiac tissues, and how to they work?
Drugs that target slow channels (Ca2+ channels in the atria) affect the SA and AV nodes-- e.g. Verapamil.
Drugs that target fast channels (Na+ channels) affect the ventricles-- e.g. Lidocaine.
Why does repolarization of ventricular muscle cells occur in the opposite direction of repolarization?
Because the impulses-- specifically, the plateaus in phase 2 of the epicardium, are shorter than those of the endocardium
What happens to the T-wave in ischemic heart tissue? Why?
Ischemia causes T-wave inversion. This is because the endocardium repolarizes before the epicardium, generating a dipole away from the positive lead. Ischemia affects endocardial tissues first. As a consqeuence,
1) the endocardial resting potential is elevated in phase 4 (no ATP for Na/K ATPase)
2) Phase 0 depolarizes largely through T-type Ca2+ channels, slope is less steep, conductance is slower, epicardium depolarization delayed.
3) the plateau of the endocardium is shortened in phase 2
PVC
Premature Ventricular Contraction: when a ventricle depolarizes spontaneously and prematurely.
Sign: Large upward (LV unopposed contraction) and large downward deflections (RV unopposed contraction) spread out over time (slow ventricular muscle conductance).
What is the significant of P-R interval? What is its normal length? What does a long P-R interval imply?
P-R interval defines the time it takes for an impulse to travel over the atria and through the A-V junction. P-R interval is normally 0.12 to 0.20 seconds (less than 1 large box). A long P-R interval (>0.2s) implies an AV block.
What can delay an impulse at the AV junction?
Parasympathetic stimulation, digitalis, calcium channel blockers can all delay an impulse at the AV junction.
What does the Q-T interval signify?
The QT interval is an approximate measure of the duration of systole.
What is the length of time measured by a big block on ECG paper? A small block?
Big Block: 0.2 Seconds

Small Block: 0.04 Seconds
What does the Q-wave signify? What does a normal Q-wave look like?
Q-wave (the first downward deflection after the P wave) is associated with Septal Depolarization when using Lateral Leads I, aVL, V5, or V6.

A normal Q wave is less than 0.04s (less than one small box).
What do large Q-waves signify?
Significant Q-waves (more than one small box wide and 1/4 of the succeeding R-wave) are a sign of myocardial infarction. This is because the LV's contributions to the septal depolarization vector is weakened, and the vector becomes more negative.
What is an R-wave? What influences its shape?
The R-wave represents the vector of depolarization in the direction of a lead.

Magnitude depends on the muscle mass and which of the 12 leads you are looking at.
What is an S-wave?
The S-wave is the downward deflection that follows the R-wave. If no R wave precedes it, it is a QS complex--> possible MI.
S-waves will be large on leads placed on right chest wall.
What does a T-wave signify?
T-wave signifies ventricular repolarization. Inverted T-waves suggest myocardial ischemia (except for lead V1). Tall (peaked) T-waves suggest hyperkalemia.
What do U-waves signify?
U-waves are only seen in patients with hypokalemia-- the wave is thought to be from repolarization of Purkinje cells whose phase 3 occur later.
What equation gives the duration of cardiac systole?
QTc = QT / (RR)^1/2

The corrected cardiac systole interval (QTc) equals the QT interval divided by the square root of the RR interval. If HR = 60/min, RR = 1, (RR)^1/2 = 1.

As HR increases, QTc decreases.
What is the normal value for the QT interval? How can different factors affect the QT interval?
The QT interval defines the duration of systole, and reflects the velocity of ventricular contraction and relaxation. Normaly QT = 0.40s. Hypercalcemia can shorter the QT interval, hypocalcemia can lengthen it. Pts with CHF can have longer QT intervals, which can be shortened with digitalis treatment.
What does a normal ST segment look like? What can it tell you?
The ST segment extends from the end of the S-wave (the J point) to the beginning of the T-wave. This segment is normally flat and has the same voltage as the baseline just before QRS. Depression or elevation of this segment is often associated with myocardial ischemia, but can be altered by other factors; e.g. raised in pericarditis, depressed in digitalix tx.
What does the QRS complex signify? What does a normal QRS complex look like?
A QRS complex runs from the beginning of the Q-wave (often the R-wave) through the end of the S-wave. It signifies the time required for the ventricles to depolarize. Its normal length is 0.05 - 0.10s (less than 2.5 small boxes). This interval is prolonged to more than 0.12s in bundle branch blocks.
What are the standard limb leads? What dipoles are measure by each?
Lead I: 0 degrees
Lead II: +60 degrees
Lead III: +120 degrees
What are the augmented limb leads? What dipoles does each measure?
aVR: -150 degrees
aVL: -30 degrees
aVF: +90 degrees
What is the mean QRS angle? What is its normal value? What lead will pick it up strongly?
The mean QRS angle is the average vector during ventricular depolarization of an average, normal heart. This is towards +60 degrees, and will be picked up strongly by Lead II.
What are the lateral limb leads?
Leads I (0 degrees) and aVL (-30 degrees) are the lateral limb leads, and they examine the electrical activity of the heart from the lateral aspect.
What are the inferior limb leads? What vectors do they measure?
Leads II (+60 degrees), III (+120 degrees), and aVF (+90 degrees) are the inferior limb leads.
leads on the lateral wall of the left ventricle
I, aVL, V5, V6
leads on the inferior wall of the left ventricle
II, III, aVF
leads on the anterior wall of the left ventricle, interventricular septum
V1 - V4
Sign of Injury
Elevated ST segment made by current of injury
Sign of Infarct
Significant Q wave
Sign of Ischemia
Inverted T wave
Acute vs Subacute vs Chronic MI
Acute: infarct + injury + ischemia

Subacute: infarct + Ischemia

Chronic: infarct only
What EKG sign would one expect for an Acute Posterior Myocardial Infarct? Why?
R wave and ST segment depression in Leads V1 V2.

Mirror images of signals for infarct/ischemia/injury will be created in opposing leads; thus the QS complex and ST segment elevation seen in an acute anterior infarct in V1-V4 becomes an R-wave and ST depression when the infarct is in the posterior wall.
What is the significance of a QS complex? What else signifies this?
The significance of a QS complex is the same as a large Q-wave: they signify transmural infarctions.
J-point
Place where ST segment begins-- good point to use to determine baseline voltage
What would you expect to see in various leads if a pt had an acute lateral myocardial infarction?
Lateral leads (I, aVL, V5, V6) would show a significant Q-wave, ST segment elevation, and T-wave inversion.

Inferior leads (II, III, aVF) would show an ST depression.
What would you expect to see in various leads in a pt. had an acute inferior myocardial infarction?
Inferior leads (II, III, aVF) would show a significant Q-wave, ST segment elevation,

Lateral leads (I, aVL) would show ST segment depression.
Premature Atrial Contraction (PAC)
PAC's always have a P-wave, and a compensatory pause following the T-wave.
Premature Nodal Contraction (PNC)
PNC's usually have no P-wave, or a small inverted P-wave just before (high focus) or after (low focus) the QRS complex.
Premature Ventricular Contraction (PVC)
PVC's have a wide QRS complex, which reflects the slow spread of impulses via gap junctions from the irritable focus in one ventricle to another. They possess high voltages because
What happens when the SA node fails to initiate an impulse (and a P-wave)?
An escape beat is initiated by an ectopic focus in the atria, AV node, or ventricles
Re-entry phenomenon
Where an impulse passing through two conduction paths is split and creates an aberrant retrograde conduction, resulting in multiple ventricular contractions. This results in PSVT.
Atrial Fibrillation
>350 bpm in the atria. S wave exhibits Ashman phenomenon: curving up through ST segment.
How to test for MI
EKG's, and cardiac enzymes: creatine phophokinase (CPK) and Troponins I and T
Most vulnerable part of the heart
Subendocardium of the left ventricle, where blood vessels are compressed by high intraventricular pressures during systole.
How to differentiate between angina and MI?
Stress test: "positive" if ST segment is depressed by > 2mm (0.2 MV) at relatively slow heart rates; if ST depression and angina are related to effort, the ECG returns to normal and the pain subsides on resting.
How would you recognize hypertrophy of the right of left ventricles on the ECG?
Left ventricular hypertrophy: V1: R/S > 1

Right ventricular hypertrophy:
S(V1) + R(V5) > 3.5mV or 35mm
What is meant by left and right axis deviations? What can cause each?
The mean QRS axis of a patient should be between -30 and +90. If it is less than -30 degrees then it is Left Axis Deviation, possibly caused by Left Bundle Branch Block or Left Ventricular Hypertrophy.

If the mean QRS axis is greater than +90 then it is a Right Axis Deviation, possibly caused by Right Bundle Branch Block or Right Ventricular Hypertrophy.
How to determine mean QRS angle.
1) Take summed R-S measurements (R minus S) of leads I, aVF.
2) Create a vector with I on the x-axis, aVF on the y axis (downward is positive!)
3) Calculate angle
4) Confirm by looking at the closest lead to that angle: e.g. 0 degrees --> lead I, 60 degrees ---> lead II. This lead should have the greatest deflections.
Why does a large Q-wave suggest myocardial infarction?
RV depolarization
What are escape beats?
heart beats that follow an abnormally long pause.
How you would suspect a Pt has A-fib even before taking the ECG?
Rapid pulse with irregular timed and strength of pulse from different filling time/contraction at different volumes.
How to distinguish between 1st, 2nd, and 3rd degree atrio-ventricular block?
1st degree: PR interval is lengthened beyond 0.20 seconds. In first-degree AV block, the impulse conducting from atria to ventricles through the AV node is delayed and travels slower than normal.

2nd Degree:There are two distinct types of second-degree AV block, called Type 1 and Type 2. In both types, a P wave is blocked; but, in Type 1, there are increasing delays in each cycle before the omission of a QRS complex, whereas, in Type 2, there is no such pattern.

3rd Degree: impulse generated in the SA node in the atrium does not propagate to the ventricles. Because the impulse is blocked, an accessory pacemaker in the lower chambers will typically activate the ventricles. This is known as an escape rhythm. Since this accessory pacemaker also activates independently of the impulse generated at the SA node, two independent rhythms can be noted on the electrocardiogram (ECG): a P-P rhythm and a R-R rhythm.
What is an important clinical sign of 3rd degree AV block?
A cannon-pulse of blood through the carotid arteries made when the Atria and Ventricles simultaneously contract.
How to detect (with ECG tracing) dangerously low or high serum potassium concentrations in a patient?
Normal concentration: 4mEq/L

Hypokalemia: Presence of a U-wave.

Hyperkalemia: Big T-waves at [K+] = 8mEq/L.

At 10 mEq/L --> slurring of QRS complex --> V-fib. Can result from crushing injury releasing intracellular K+ ketoacidosis, kidney failure, etc.
Explain paroxysmal supraventricular tachycardia.
Paroxysmal = sudden onset
caseud by re-entry phenomenon where an electrical pathway in a parallel pair is delayed long enough to propagate back up the other pathway (retrograde conduction) after its refractory period. This causes multiple ventricular contractions for each nodal beat.
You are a country doctor. You come across a fainted person, no pulse. You call 911, do CPR. What do you administer via IV? Why?
Epi, vasopressin --> alpha-1 receptors --> increase TPR, conserve blood for heart, brain.
Your attempts at defibrillating a patient fail. What drugs can you administer? Why?
Amioderone: decrease K+ permeability --> lengthens action potential, increases refractory period.

Lidocaine: blocks Na+ channels, slows phase 0/conduction.
How to read an EKG, step by step.
1) What is the rate?
2) Is the beat regular?
3) Check P-R interval: is it between 0.12 and 0.2s/fit in a box? --> 1st degree AV block
4) Check the QRS complex: does it fit in 2 small boxes/0.08s? wider --> RBBB: check V1: RR' complex?
5) Mean QRS complex: Check I, aVF: Between -30 and +90 degrees?
6) Is there hypertrophy? LAH: V1 downward P-wave. RAH: Big R-wave in V1. RVH: R/S >1 in V1. LVH: R(V1) + S(V5) > 35mm.
7) Is there ischemia? Look for inverted T-waves everywhere but aVR.
8) ST segment elevation? Current of Injury.
9) Any infarct? Significant Q-waves? Q-wave > 0.25* R-wave
Where does the R-wave in V1 come from?
From septal depolarization. Lack of R-wave, significant Q-wave could indicate anterior infarct.
Wandering pacemaker: description and what to expect on the ECG
Arrythmia from different foci in the atria generating P-waves, creating an irregular rhythm with different P-waves. At a fast rate, this condition is called Multifocal Atrial Tachycardia.
What change in the ECG would you expect when the posterior fascicle of the left bundle branch is blocked?
Right axis deviation from a hemiblock. Also, slight widening of QRS complex (0.10-0.12s)
What change in the ECG would you expect when the anteriorfascicle of the left bundle branch is blocked?
Left axis deviation. Also, slight widening of QRS complex (0.10-0.12s)
Why does the pulse rate of a patient with sinus arrythmia increase upon respiration?
Inspiration decreases PSNS tone to the SA node via activation of the Bainbridge and Baroreceptor reflexes.
Describe prolonged QT syndrome.
Several mutations of K+ channel responsible--> phase 3 repolarization hindered, so that PVCs may occur more easily.
sick-sinus syndrome
aka tachycardia-bradycardia syndrome, a variant of sick sinus syndrome in which slow arrhythmias and fast arrhythmias alternate.