Cardio Sim Lab

Meet our Sim. His name is Stan.

Stan's heart went through several racy scenarios for us this afternoon.
1) He started out in myocardial ischemia. As I was standing at his feet feeling his pedal pulse, it dropped off immediately, followed quickly by the remaining pulses (posterior tibial, radial, etc).
2) Next up, Stan quickly developed a pretty intense aortic stenosis as evidenced by a deafening pan-systolic murmur. (Don't forget, Liz, that on an EKG, the resulting left axis deviation from the hypertrophied left ventricle would show up as negative on Lead III. I need to go back over the axes again before my final on Thursday.)
3) 3rd Degree Heart Block was next on the agenda. He had a regular atrial rhythm but with a wide QRS complex. (QRS complexes completely dissociated from the P waves.) With 3rd degree heart block, you're going to have an increased EDV due to increased atrial depolarizations filling the ventricles before the ventricles themselves depolarize.
4) Stan deteriorated into congestive heart failure. He had sinus tachycardia, increased PCWP (pulmonary edema present = left-sided heart failure), increased BP, increased CVP (right-sided heart failure). Treat Stan with digitalis* to increase that contractility, increase stroke volume, and take some of the load off of that heart of his. (*At least for teaching scenarios, anyway.)
5) Two drugs were administered to Stan. The first drug increased Stan's heart rate initially, but then it tapered off. Both his systolic and diastolic BP increased. The drug was norepinephrine which hits those alpha-adrenergic receptors on his vasculature causing vasoconstriction. (If epinephrine would have been administered, it would have decreased his diastolic pressure due to its activity at beta-receptors causing vasodilation.)
The second drug caused an increase in HR (from 60 bpm to 117 bpm) and decreases in both systolic and diastolic pressure. So what would cause an increase in heart rate with a decrease in BP? An alpha-antagonist, of course. Phentolamine was given to block the increase in BP associated with norepinephrine at the alpha-1 receptors. This decrease in BP caused a baroreflex-mediated increase in HR. Key.
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Very cool day in the cardio sim lab. I wish we could learn more like this. More hands on. Though, I guess that's what we'll be doing for the rest of our lives once we're out of the classroom. I can live with that. Can you?

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