Physiology: Cardiovascular, High Yield Topics (First Aid, p. 308)

 

1.  Basic electrocardiographic changes

. also see Lilly p. 89 for effects of hyper/hypokalemia and hyper/hypocalcemia

Description

EKG changes

Notes

Q wave (transmural) MI

Q wave (persists)

ST segment elevation (acutely)

 

Non-Q wave (nontransmural) MI

ST segment depression (acutely)

 

Angina

ST segment depression (usually) or

T wave flattening/inversion

(rare: transient ST segment elevation)

Both indicate sub- endocardial ischemia

1st Degree AV Block

Prolonged PR (>.2 sec (1 big box))

Site of delay = AV node

Every pulse gets through

2nd Degree AV Block

 

Type I (Wenkebach)

 

Type II (Mobitz)

 

Not every P followed by QRS

 

PR prolonged until no QRS (dropped beat)

Sporadic “drop” of QRS complex

PR fixed, QRS widened

Intermittent failure of AV conduction

Block at AV node

 

Block at His-Purkinje

3rd Degree AV Block

P waves dissociated from QRS complexes

Complete AV Block (failure of conduction from atria to ventricles)

Sinus Tachycardia

PR shorter than at rest

100-180 bpm

Atrial Tachcardia

RP variable

150-250 bpm

No coupling between P and QRS

Atrial Flutter

Inverted sawtooth appearance

300 bpm

Macro re-entrance circuit in RA

Atrial Fibrillation

Undulating baseline (on V1)

400-600 bpm

Most impulses blocked in AV node, leading to erratic conduction

Ventricular Tachycardia

P waves dissociated,

QRS regular and wide

100-250 bpm

Ventricular impulses invade AV node retro/ anterogradely, creating physiologic interference and block

Torsades de Pointes

Twisting of points (spiraling)

Polymorphic VT with prolonged repolarization

Ventricular Flutter

Sine wave appearance

>250 bpm

Ventricular Fibrillation

Chaotic

Chaotic rapid ventricular rhythm precipitated by ventricular tachycardia

 

 

2.  Effects of electrolyte abnormalities (I apologize for the lousy job on this one – this is all I found in Lilly and I didn’t know what else to do with it)

 

Electrolyte-related causes of dilated cardiomyopathy (Lilly, p 219):

· chronic hypocalcemia

· chronic hypophosphatemia

 

Electrolyte-related factors that precipitate symptoms in compensated heart failure (Lilly, p. 207):

· Excessive sodium content in diet

· Excessive fluid administration

 

Electrolyte-related causes of secondary hypertension (Lilly, p. 275):

· Renal parenchymal disease (2-4% of HTN cases): damaged nephrons are unable to excrete normal amounts of sodium and water, leading to a rise in volume, elevated cardiac output, and increased BP

· Adrenocortical hormone excess: mineralocorticoids cause increased sodium absorption, increased intravascular volume, and hypokalemia; glucocorticoids also cause blood volume expansion, leading to HTN

 

hypokalemia leads to EKG changes and arrhythmias

 

 

 

3.  Physiologic effects of the Valsalva Maneuver (Cecil’s 4th ed, p.18)

 

Valsalva Maneuver – expiring against a closed glottis (initial ­BP in phase I; followed by ¯ BP in phase II)

 

Physiologic effects:

¯ BP

¯ venous return

¯ LV size (phase II)

 

Useful auscultatory changes:

¯ aortic stenosis,

¯ mitral regurgitation

­ hypertrophic obstructive cardiomyopathy

mitral valve prolapse click occurs earlier in systole and its murmur prolongs

 

 

 

 

 

 

 

 

 

4. Cardiopulmonary changes with pregnancy (Cecil’s, p. 108-109)

 

Increases in:

Decreases in:

· Cardiac output (by end     of 1st trimester)

· Stroke volume

· Heart rate

· Blood volume

· Oxygen consumption

· Minute ventilation

· Systolic BP

· Systemic and pulmonary vascular resistances

 

 

· Easy fatigability, decreased exercise tolerance, dyspnea, peripheral edema, a third heart sound, and a mid-systolic murmur may be normal in pregnancy.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

5. Responses to hemorrhage (Saunder’s Physiology, p. 157-158)

Parameter

Compensatory Response to Hemorrhage*

Carotid sinus nerve firing rating

Decreased

HR

Increased

Contractility

Increased

CO

Increased

Venous volume

Decreased (produces incr in venous return)

TPR

Increased

Renin

Increased

Angiotensin II

Increased

Aldosterone

Increased

Circulating Epi and NE

Increased (from adrenal medulla)

Antidiuretic Hormone

Increased (stimulated by decr blood volume)

* Compensatory responses are compared to values immediately after hemorrhage, NOT to pre-hemorrhagic levels.

 

Other responses to hemorrhage

· if hypoxemia ® chemoreceptors in carotid and aortic bodies sense the decr in PO2 ® incr symp outflow to heart and blood vessels.  This mech augments the baroreceptor reflex.

· if cerebral ischemia ® local incr in PO2 and decr in pH ® chemoreceptors in medullary vasomotor center activated ® incr symp and parasymp outflow to heart and blood vessels

 

 

 

6. Responses to changes in position (Saunder’s, p. 158-159)