Physiology Flashcards by Britt Anders

CO =

Ficks Principle

CO= rate of O2 consumption / arterial O2 content - venous O2 content

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CO=

CO= SV X HR

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MAP=

MAP= CO X TPR

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MAP =

MAP = 2/3 diastolic pressure + 1/3 systolic pressure

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Pulse Pressure=

PP= systolic pressure - diastolic pressure

widened PP seen in aortic regurgitation

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SV=

CO / HR = EDV - ESV

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Stroke volume affected by

Contractility
Preload
Afterload (resistance in aorta to prevent blood from leaving the ventricle)

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Stroke volume increased when

Increased preload
Decreased afterload
Increased contractility

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Contractility increases with

Catecholamines (increase Ca from SR)
Increased intracellular Ca
Decreased extracellular Na (decreased Na/Ca exchanger)
Digitalis (blocks Na/K pump, increase intracellular Na, decrease Na/Ca exchanger, increase intracellular Ca)

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Contractility decreases with

B1 blockade (decrease cAMP)
Heart failure (systolic dysfunction)
Acidosis 
Hypoxia/ hypercapnea
Non dihydropyridine Ca channel blockers

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Myocardial oxygen demand is increased by

Increased afterload
Increased contractility
Increased HR
Increased heart size (increased wall tension)

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Nitroprusside

Decreases preload (venodilator) and decreases afterload (vasodilator)

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EF=

EF= SV / EDV = EDV -ESV / EDV

Normal is > 55%

EF decreases in systolic heart failure but is normal in diastolic heart failure

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Resistance

Directly related to viscosity

Inversely related to radius ^ 4

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Viscosity increases in …….. Thus causing more resistance and High Cardiac Output Failure

Polycythemia
Hyperproteinemic states
Hereditary spherocytosis

Viscosity depends mostly on hematocrit

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Viscosity decreases in

Anemia

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Total resistance in series

R1 + R2 + R3….

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Total resistance in parallel

1/R = 1/R1 + 1/R2 + 1/R3….

Remember to flip the answer to get R total

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Operating point of heart

CO and venous return are equal

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Decrease TPR

Curve shift up and right

Exercise, AV shunt/fistula

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Increase TPR

Curve shift down and left

Hemorrhage before compensation can occur

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Decrease contractility

Curve shifts down and right

Heart failure, narcotic overdose, B blockers

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X intercept of venous return curve=

Mean systemic filling pressures

AV shunts

Increase preload, decrease afterload

Pressure volume loop

"CAP" Shift left= increased Contactility Shift up= increased Afterload Shift right= increased Preload

A wave

Atrial contraction

C wave

RV contraction (closed tricuspid valve bulging into atrium)

X descent

Atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction

V wave

Increased right atrial P due to filling against closed tricuspid valve

Y descent

Blood flow from RA to RV

Mitral and tricuspid close, loudest at mitral area

Aortic and pulmonary valve close, loudest at left sternal border

Normal splitting

Delayed closure of pulmonic valve during inspiration

Wide splitting

Occurs in both I and E; seen in pulmonic stenosis, RBB block

Fixed splitting

ASD; left to right shunt causes extra blood to exit thru pulmonic valve so closure is greatly increased in both I and E

Paradoxical splitting

P closes before A, on I there is no split at all; due to aortic stenosis, LBB block

What determines HR

The slope of phase 4 (funny Na channels) which controls the SA node

PR interval

Conduction delay thru AV node (<200msec)

QRS

Normally <120 msec

Mechanical contraction of ventricles (systole)

T wave

Inversion may indicate recent MI

ST segment

Isoelectric, ventricles depolarized ****can be depressed or elevated with MI****

U wave

Hypokalemia, bradycardia

Speed of conduction

PavA Purkinke> atria> ventricles> AV node

Pacemakers

SA> AV> bundle of His/purkinke/ ventricles

Conduction pathway

SA node- atria- AV node- common bundle- bundle branches- purkinje fibers- ventricles

AV nodal delay

100 msec- Allows time for ventricular filling

Atrial fibrillation

Irregularly irregular with no discrete P waves

Atrial flutter

Sawtooth appearance | Rapid succession of identical back to back atrial depolarization

1st degree AV block

PR interval prolonged >200msec Bigger than 1 large square

2nd degree Mobitz type 1 (wenckebach)

Progressive lengthening of PR until a P wave is dropped

2nd degree Mobitz type 2

Normal PR intervals | No QRS following P wave

3rd degree heart block

P waves and QRS waves are independent of each other Can be caused by Lyme disease

PCWP = pulmonary capillary wedge pressure

Approximation of LA pressure In mitral stenosis, PCWP> LV diastolic pressure Measured with pulmonary artery catheter= swan-ganz catheter

Coronary arteries need more oxygen......what's the response

Increased blood flow.....they already extract 80% of oxygen......so only way to get more oxygen is to increase blood flow

Edema causes:

Increased capillary pressure (heart failure) Decreased plasma proteins (nephrotic syndrome, liver failure) Increased capillary permeability (toxins, infections, burns) Increased interstitial fluid colloid osmotic pressure (lymphatic blockage)

Net filtration pressure =

Pnet= ((Pc-Pi)- (colloid c- colloid i))