Recorded on the computer, the EKG has PQRST components. P is atrial depolarization, QRS is ventricular depolarization, and T is ventricular repolarization. (Note, myocardial action potentials have long duration relative to nerve action potentials) Now you can appreciate the name of a well-known cardiac disorder (mentioned in your text) called "long Q-T syndrome."

Here is what happened to my peripheral pulse when I held my breath. (The rate did not change much, but the size did.)

Here is a PVC (premature ventricular contraction) [note the lack of a P-wave] followed by a compensatory delay.

In September, 2004, I obtained these results for a 4 s period.

To determine the mean electrical axis (M.E.A.) begin with a QRS complex from Lead 1 and count the number of millimeters that it projects above the base line. Add to this value the number of millimeters that it extends below the base line. If the QRS complex extends 7 mm above the baseline and 1 mm below the baseline, sum these values as 7+ (-1)= +6. Repeat the process for Lead 3. Then use the grid chart.

A previous student has a left ventricular hypertrophy from a heart murmur shows a left axis deviation.

A few years ago, I gave a quiz, and here are the answers:

Put your name here-> Key

The cardiac glycoside digitalis is most like
(a) acetylcholine. that's a neurotransmitter
(b) tetrodotoxin. that blocks the sodium channel
(c) atropine. that blocks muscarinic receptors
(d) ouabain. YES they're both cardiac glycosides blocking sodium pump
(e) anticholinesterases. like nerve gas, blocks acetylcholine breakdown

When taking the blood pressure with a sphygmomanometer,
(a) one records from the two wrists and left ankle. that's the EKG
(b) one needs to put a catheter into the aorta. that would measure pressure but not with a sphygmomanometer
(c) one listens for turbulent arterial flow. YES
(d) one listens for the "dup." you do not listen for heart sounds
(e) one listens for the "lub." you do not listen for heart sounds

If the EKG trace is very noisy
(a) use a low pass filter. YES
(b) substitute the peripheral pulse monitor since it tells you everything the EKG tells you. no it doesn't
(c) use lead II instead of lead I they would have the same noise
(d) get the paddles. not on me you won't
(e) use an inotropic agent. they change contraction strength not recording noise

Connections to both wrists and the left leg
(a) are used to measure blood pressure. no, EKG not pressure
(b) are named after Einthoven. YES Einthoven's triangle
(c) are described by Starling's law. more ventricular filling, more blood pumped
(d) originated with Paul Harvey in the 1600's. Paul Harvey? The "news" commentator? "Page 2"? Certainly you mean Sir William Harvey and they did not have electricity back then
(e) are used to start the pacemaker after fibrillation. paddles are connected to the chest

How come you can measure the EKG so far away from the heart?
(a) There is easy conduction through the salt water in the body. YES. Bode's exact wording and what I said in the handout
(b) Because of bradycardia. low heart rate is irrelevant
(c) Because of desmosomes in intercalated disks. structural cell connections are irrelevant
(d) The action potentials are many more mV than nerve action potentials. no they aren't
(e) You need different amounts of amplification for lead I, II or III. no you don't

What do you do to measure pressure from the brachial artery?
(a) Listen for the heart sounds. no, you listen for arterial sounds
(b) First administer beta blockers. blocking sympathetic heart influence is irrelevant
(c) Crank it up to the diastolic level and look for the veins to bulge. Need to inflate higher and listen
(d) Nonsense! Blood pressure has nothing to do with the arteries. Nonsense
(e) Inflate the cuff past the systolic pressure and slowly release the pressure. YES

The time between QRS and T might decrease during mild exertion. This would be indicative of
(a) dangerous pathophysiology. happens all the time
(b) the AV node controlling the heart beat instead of the SA node. not because of exertion
(c) a myocardial action potential of shorter duration. YES
(d) parasympathetic control. sympathetic influence
(e) Nonsense! The time would only increase. no it would decrease

If all parasympathetic and sympathetic inputs to the heart were instantly abolished while you were relaxed
(a) nothing would happen. The autonomic nervous system does not influence the heart. yes it does
(b) there would be an A-V conduction block. not from this intervention
(c) the heart would stop. heart is automatic
(d) the heart would speed up. YES. I ran that by you last week
(e) the heart would slow down. opposite

For the mean electrical axis, one measures
(a) the time between P and T at rest and after exertion. of interest but not for axis
(b) QRS above and below baseline for lead I and lead III. YES
(c) the average of the diastolic and systolic pressures. pressure is irrelevant to electrical
(d) the pacemaker potential from the bundle branches. they may have slow pacemaker activity but it never shows up
(e) stroke volume and heart rate. not relevant to electric axis

The arterial diastolic pressure is
(a) higher than the systolic pressure. systolic is higher
(b) the force that opens the A-V (bicuspid and tricuspid) valves. they are open because of low ventricular pressure in diastolic ventricular filling
(c) equal to the atrial pressure during diastole. very low, only from venous return
(d) usually higher than 180 mm Hg. hope not
(e) way higher than ventricular pressure during diastole. yes because ventricles are virtually zero in diastole

This page was last updated 2/19/08

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