Cardiac Physiology

Front 1

Ion channels present in the heart

Back 1

Ungated K, voltage-gated fast Na, voltage-gated calcium, inward rectifying iK1, delayed rectifying iK

Front 2

Voltage-gated Na channels of the heart

Back 2

Open and close fast upon depolarization of the membrane

Front 3

Voltage-gated calcium channels of the heart

Back 3

Open upon depolarization, close more slowly than sodium channels. Partly responsible for the plateau (phase 2)

Front 4

Inward rectifying iK1 channels of the heart

Back 4

Open under resting conditions, depolarization closes them, they reopen during repolarization phase.

Front 5

Delayed rectifying iK channels of the heart

Back 5

Very slow to open with depolarization (late plateau), and close very slowly. Partly responsible for repolarization

Front 6

Phase 0 of the ventricular action potential

Back 6

Fast Na channels open, ↑ gNa causes depolarization. Inward rectifying iK1 channels close.

Front 7

Phase 1 of the ventricular action potential

Back 7

Slight repolarization due to transient potassium current and the closing of sodium channels

Front 8

Phase 2 of the ventricular action potential

Back 8

Slow Ca channels open, ↑ gCa, ↓ gK. Plateau phase is due to slow calcium current and decreased K current

Front 9

Phase 3 of the ventricular action potential

Back 9

Slow Ca channels close, the delayed rectifier iK reopen, ↑ gK. K efflux causes repolarization.

Front 10

Phase 4 of the ventricular action potential

Back 10

Voltage-gated and ungated potassium channels are open, ↑ gK. The delayed rectifiers close but are responsible for the relative refractory period.

Front 11

Why can't the heart be tetanized?

Back 11

A long absolute refractory period extends through most of the contraction. Short relative refractory period.

Front 12

How do premature ventricular depolarizations occur?

Back 12

Action potential develops during the relative refractory period, but the earlier the potential, the shorter in amplitude and duration it will be

Front 13

Funny current

Back 13

In specialized cells of the heart. It's a voltage-gated sodium channel the opens during repolarization and closes during depolarization. The sodium influx during phase 3 slowly depolarizes the cell towards treshold.

Front 14

Phase 0 of SA nodal cells

Back 14

Depolarization due to opening of voltage-gated slow Ca channels.

Front 15

Phase 3 of SA nodal cells

Back 15

Repolarization due to ↑ gK.

Front 16

Phase 4 of SA nodal cells

Back 16

Gradually depolarizes cell towards threshold due to funny current - ↑ gNa

Front 17

Effects of sympathetics on pacemaker cells

Back 17

Slope of phase 4 increases due to ↑ funny current and ↑ gCa. Action via β1 receptors.

Front 18

Effects of parasympathetics on pacemaker cells

Back 18

↑ gK causing hyperpolarization and ↓ sodium funny current decreasing slope of phase 4. Effect via M2 receptors.

Front 19

Fastest conducting cells of the heart

Back 19

Purkinje cells

Front 20

Slowest conducting cells of the heart

Back 20

AV node cells

Front 21

PR interval

Back 21

Due to conduction delay of AV node. 0.12 - 0.2 seconds or 120 to 200 miliseconds

Front 22

QRS complex

Back 22

Ventricular depolarization - should be less than 0.12 seocnds.

Front 23

QT interval

Back 23

Indicated ventricular refractorieness. Normal between 0.35 - 0.44 seconds.

Front 24

Effect of hypercalcemia in ECG

Back 24

Shortened QT interval (< 0.35 seconds).

Front 25

Effect of hypocalcemia in ECG

Back 25

Prolonged QT interval (> 0.44 seconds)

Front 26

Drugs that shorten QT interval

Back 26

Digitalis

Front 27

Drugs that prolong QT interval

Back 27

Quinidine, procainamide

Front 28

Effect of intracerebral hemorrhage in ECG

Back 28

Inverted T waves with prolonged QT interval

Front 29

ST segment

Back 29

Indicates conduction through ventricular muscle. Corresponds to plateau phase of action potential.

Front 30

First-degree block in ECG

Back 30

Slowed conduction through AV node. PR interval > 200 msec

Front 31

Second-degree block in ECG

Back 31

Some impulses not transmitted through AV node. Missing QRS complexes following P wave.

Front 32

Third-degree block in ECG

Back 32

No impulses conducted from atria to ventricles. No correlation between P waves and QRS complexes.

Front 33

Sinus rhythms

Back 33

Normal, bradycardia or tachychardia

Front 34

Atrial flutter

Back 34

Repeated succession of atrial depolarizations. Continuous P waves. Saw-tooth appearance.

Front 35

Atrial fibrillation

Back 35

No discernable P waves, irregular QRS

Front 36

Ventricular fibrillation

Back 36

No identifiable waves. Chaotic, erratic rhythm.

Front 37

Causes of left axis deviations

Back 37

Left ventricular hypertrophy or dilation, conduction defects of left ventricle, AMI on right side

Front 38

Causes of right axis deviations

Back 38

Right ventricular hypertrophy or dilation, conduction defect of right ventricle, AMI on left side

Front 39

Initial AMI in ECG

Back 39

ST segment depression, prominent Q waves, T wave inversion

Front 40

AMI in ECG

Back 40

ST segment elevation, T wave inversion, prominent Q waves

Front 41

Resolving AMI in ECG

Back 41

Baseline ST, inverted T waves, prominent Q waves

Front 42

Stable infarct in ECG

Back 42

Prominent Q waves

Front 43

Indices of left ventricular preload

Back 43

LVEDV, LVEDP, left atrial pressure, pulmonary venous pressure, pulmonary wedge pressure (swan-ganz)

Front 44

Sarcomere legth in skeletal muscle Vs. heart muscle

Back 44

In skeletal muscle it's close to L0. In heart muscle, sarcomere length is below optimal, therefore increased preload moves sarcomere length towards optimal for maximal cross-bridge linking

Front 45

Factors that increase slope of cardiac function curve

Back 45

↑ inotropy, ↑ heart rate, ↓ afterload

Front 46

Factors that decrease slope of cardiac function curve

Back 46

↓ inotropy, ↓ heart rate, ↑ afterload

Front 47

Factors that shift vascular function curve up and to the right

Back 47

↑ blood volume, ↓ venous compliance

Front 48

Factors that shift vascular function curve down and to the left

Back 48

↓ blood volume, ↑ venous compliance

Front 49

Factors that increase slope of vascular function curve

Back 49

↓ SVR

Front 50

Factors that decrease slope of cardiac function curve

Back 50

↑ SVR

Front 51

What is contractility and what influences it?

Back 51

Contractility is the force of contraction at a given preload or sarcomere length. Due to changes in intracellular calcium induced by hormones

Front 52

Indices of contractility

Back 52

dp/dt (change in pressure/change in time); ejection fraction (stroke volume/EDV)

Front 53

Changes to the action potential induced by increased contractility

Back 53

↑ slope (↑ dp/dt), ↑ peak left ventricular pressure, ↑ rate of relaxation, ↓ systolic interval

Front 54

Changes to the action potential induced by heart rate

Back 54

↓ diastolic interval

Front 55

Cardiac function curve in hemorrhage

Back 55

↓ preload (down); ↑ contractility to partially compensate (left)

Front 56

Cardiac function curve in excersice

Back 56

↑ contractility (up, same preload)

Front 57

Cardiac function curve in volume overload

Back 57

↑ preload (right); ↓ contractility (slightly down)

Front 58

Cardiac function curve in CHF

Back 58

↓ contractility (down); ↑ preload (right)

Front 59

Afterload

Back 59

Force that must be generated to eject blood into aorta. ↑ afterload in hypertension, ↓ afterload in hypotension. Acute ↑ in afterload - ↓ stroke volume, ↑ EDV, ↑ preload

Front 60

Parasympathetic innervation of SA and AV nodes

Back 60

Left vagus predominates in AV node, right vagus predominates in SA node

Front 61

Effect of inspiration on heart rate

Back 61

Inspiration makes intrathoracic pressure more negative --> increase venous return --> Brainbridge reflex (stretch receptors in the right atrium) --> tachychardia

Front 62

Baroreceptor reflex

Back 62

Baroreceptors in the aortic arch send afferents via vagus nerve; baroreceptors in the carotid sinus via glosopharyngeal; baroreceptor center is in the medulla. ↑ firing of baroreceptors is sensed as ↑ blood pressure --> ↑ parasympathetic, ↓ sympathetic

Front 63

Acute reflex changes when blood pressure increases

Back 63

↑ afferent baroreceptors --> ↑ parasympathetic, ↓ sympathetic

Front 64

Acute reflex changes when blood pressure decreases

Back 64

↓ afferent baroreceptors --> ↓ parasympathetic, ↑ sympathetic

Front 65

Acute reflex changes with occlusion of the carotid

Back 65

↓ afferent baroreceptors --> ↓ parasympathetic, ↑ sympathetic, ↑ blood pressure, ↑ heart rate

Front 66

Acute reflex changes with a carotid massage

Back 66

↑ afferent baroreceptors --> ↑ parasympathetic, ↓ sympathetic, ↓ blood pressure, ↓ heart rate

Front 67

Acute reflex changes if baroreceptor afferents are cut

Back 67

↓ afferent baroreceptors --> ↓ parasympathetic, ↑ sympathetic, ↑ blood pressure, ↑ heart rate

Front 68

Acute reflex changes in orthostatic hypotension or fluid loss

Back 68

↓ afferent baroreceptors --> ↓ parasympathetic, ↑ sympathetic, ↑ blood pressure, ↑ heart rate

Front 69

Acute reflex changes in volume overload

Back 69

↑ afferent baroreceptors --> ↑ parasympathetic, ↓ sympathetic, ↓ blood pressure, ↓ heart rate

Front 70

S1 heart sound

Back 70

Closure of mitral and tricuspid valves; terminates ventricular filling, starts isovolumetric contraction

Front 71

S2 heart sound

Back 71

Closure of aortic and pulmonary valves; terminates ejection phase, begins isovolumetric relaxation

Front 72

Isovolumetric contraction

Back 72

Beginning of systole, ventricular pressure is increasing but aortic and mitral valves are closed. Most energy consumption occurs here

Front 73

Ejection phase

Back 73

Aortic valve opens when isvolumetric contraction generates high enough pressure; ventricular volume decreases. Most work done here.

Front 74

Isovolumetric relaxation

Back 74

Ventricular pressure decreases; volume is end-systolic volume; aortic and mitral valves are closed

Front 75

Filling phase

Back 75

Opening of the mitral valve passes volume to ventricle followed by atrial contraction

Front 76

Stroke volume

Back 76

EDV - ESV

Front 77

Ejection fraction

Back 77

Stroke volume / EDV

Front 78

a wave of the venous pulse

Back 78

Produced by contraction of the right atrium

Front 79

c wave of the venous pulse

Back 79

Bulging of the tricuspid valve into the right atrium during ventricular contraction

Front 80

v wave of the venous pulse

Back 80

Wave rises as the atrium is filled; terminates when the tricuspid valve opens

Front 81

y wave of the venous pulse

Back 81

Opening of tricuspid valve and atrial emptying

Front 82

Aortic stenosis

Back 82

Increase in afterload. Systolic murmur, concentric hypertrophy.

Front 83

Aortic insufficiency

Back 83

↑ preload, ↑ ventricular and aortic systolic pressures, ↓ aortic diastolic pressure, diastolic murmur, eccentric hypertrophy

Front 84

Mitral stenosis

Back 84

↑ pressure and volume in left atrium, enlargement of left atrium, diastolic murmur

Front 85

Mitral insufficiency

Back 85

↑ atrial volume and pressure; systolic murmur