Physiology Block I: Heart

Front 1

Why is the ventricular ejection time shorter on the left side of the heart?

Back 1

Because the time that the left ventricle pressure is greater than the aortic pressure is shorter that the time that the right ventricular pressure is greater than the pulmonary arterial pressure.

Front 2

This heart sound is heard during isovolumic contraction and is the result of ventricular contraction and closure of the AV valves:

Back 2

S1

Front 3

This heart sound is only heard when there is lower ventricular compliance and is heard during rapid ventricular filling:

Back 3

S3

Front 4

Decreased ventricular compliance may be caused by which two things:

Back 4

Fibrosis and hypertrophy

Front 5

This heart sound is only heard when there is severely decreased ventricular compliance:

Back 5

4th heart sound

Front 6

This systolic murmur is associated with an ejection click

Back 6

Aortic Stenosis

Front 7

This systolic murmur causes left ventricular hypertrophy, high ventricular pressure, low aortic pressure and left axis deviation:

Back 7

Aortic Stenosis

Front 8

This mid-diastolic murmur causes reduced cardiac output, high atrial pressure (PWP), right heart hypertrophy and right congestive heart:

Back 8

Mitral Stenosis

Front 9

This diastolic murmur causes low diastolic pressure, large pulse pressure, and high end diastolic volume resulting in left ventricular hypertrophy:

Back 9

Aortic insufficiency

Front 10

This systolic murmur causes high atrial pressure (PWP), high EDV and pressure, leads to left ventricular hypertrophy:

Back 10

Mitral insufficiency

Front 11

The EDV or preload of the heart is a determinate of __________.

Back 11

Cardiac Output

Front 12

The ionotropic state of the heart is the intrinsic contractility of the muscle regardless of EDV and is related to ________.

Back 12

Intracellular Concentration of Ca++.

Front 13

This positive ionotrope works by inhibiting the Na-K pump and raising the intracellular concentration of Na+. This slows the Na-Ca Exchanger and maintains higher calcium.

Back 13

Cardiac Glycosides

Front 14

These negative ionotropes inhibit the L-Type Calcium channels:

Back 14

Ca++ channel blockers

Front 15

What are the two primary effects of Beta-1 agonists?

Back 15

1) the open ROC channels and act via cAMP-PKA pathway to phosphorylate DHPR and RYR to increase Ca++ entering the cell and exiting the SR
2) The increased Ca++ leads to greater phosphorylation of the MLCK

Front 16

Cardiac glycosides such as digitalis inhibit _________. Why?

Back 16

Na-K ATPase- reduces the electrochemical gradient for Na-Ca++ exchanger and resulting in less Ca++ being removed.

Front 17

A paradoxical S2 split suring expiration is caused by _____.

Back 17

Left bundle branch block

Front 18

Which sympathetic system has more influence on the heart at rest?

Back 18

Parasympathetic > Sympathtic

Front 19

The resting membrane potential is unstable in the cardiac nodal cells because of what?

Back 19

The decay in conductance of K+ channels and the opening of funny cation channels that permit Na+ to enter the cells.

Front 20

The AP of non-pacemaker cardiac cells is caused by the opening of which channels:

Back 20

Fast Na+ channels - just like skeletal muscle

Front 21

Calcium channel blockers block both T-type and L-type calcium channels, what effect does this have on the pacemaker AP?

Back 21

Blocked T-Type channels cause it to take longer to reach threshold and decreased L-type sensitivity decreases conductance and decreases the amplitude of the AP

Front 22

Calcium channel blockers have what two main effects?

Back 22

Decreased heart rate and conduction rate in pacemaker cells.- decreased slope of phase 4 and 0- DECREASED CONTRACTILITY

Front 23

NE has what effect on the slope of phase 4? Why?

Back 23

Increases the slope by increasing Ca++ permeability

Front 24

ACh has what effect on the slope of phase 4? Why?

Back 24

Decreases the slope of phase 4 by increasing K+ permeability, hyperpolarizing the membrane

Front 25

Depolarization of the ventricles starts in the _____ and moves to the _______.

Back 25

Left and moves right.

Front 26

- this occurs fast, is coordinated by the purkinje system, and proceeds from endocardium to epicardium

Back 26

Ventricular Depolarization

Front 27

This occurs more randomly, is not fascilitated by the purkinjie system, and proceeds from epicardium to endocardium

Back 27

Ventricular Repolarization

Front 28

The mean electrical axis of the heart is usually between which two values?

Back 28

-30 - 120

Front 29

When the MEA is located between -30 - -90 , there has been a ______ shift

Back 29

Left Shift

Front 30

What are the values of the MEA for a left axis deviation?

Back 30

(-30) - (-90)

Front 31

When the MEA is located between 120-180, there has been a ______ shift.

Back 31

Right axis deviation

Front 32

Left ventricle hypertrophy, LBBB, high diaphragm (obesity, pregnancy, acites), and a right sided infarct, all cause what?

Back 32

Left Axis Deviation

Front 33

MEA shifts toward ______ and away from ________.

Back 33

Toward hypertrophy and away from infarct.

Front 34

Normal heart rate values:

Back 34

60-100 b/min

Front 35

Normal P-R interval

Back 35

0.12-0.20 seconds

Front 36

Normal QRS complex duration

Back 36

0.06-0.1

Front 37

This type of heart block occurs when conduction through the AV node is slowed and causes increased P-R interval

Back 37

First degree heart block

Front 38

This kind of heart block occurs when one or more atrial depolarizations are not conducted to the ventricles:

Back 38

Second Degree Heart Block

Front 39

This occurs when there is no conduction through the AV node and there are separate pacemakers and rates for the atria and ventricles:

Back 39

Third degree heart block

Front 40

This occurs when there is an ectpic focus in the ventricles that depolarizes at a rate faster than 150 beats/min.

Back 40

Ventricular Tachycardia

Front 41

What are the three inferior ECG leads?

Back 41

II, aVF, & III

Front 42

What coronary artery do the three inferior ECG leads (II, III, and aVF) show?

Back 42

Right Coronary

Front 43

What are the two lateral ECG leads? What coronary artery do they show?

Back 43

I and aVL, circumflex

Front 44

What are the times for a normal QT interval?

Back 44

0.36 - 0.43 seconds

Front 45

How do you measure HR on the ECG?

Back 45

60/ RR interval

Front 46

The lead perpendicular to the MEA is __________.

Back 46

Isoelectric (deflection is 0)

Front 47

This heart pathology comes from a rhythm originating in the ventricles independent of the SA node and displays a wide QRS

Back 47

Premature Ventricular Contraction (PVC)

Front 48

This type of heart block results in long PR intervals and a slower heart rate

Back 48

1st degree heart block

Front 49

Increased preload _________ stroke volume.

Back 49

Increases

Front 50

During this phase in the cardiac cycle there is increased pressure in the atria and ventricles, decreased aortic pressure, increased ventricular volume, and when pathological, S4 sound is heard:

Back 50

Atrial Systole

Front 51

During this phase in the cardiac cycle there is increased pressure in the ventricle, increased pressure in the atria, decreased pressure in the aorta and no change in volume (all valves are closed)

Back 51

Isovolumic Contraction

Front 52

During this phase in the cardiac cycle there is increased presure in the ventricle and aorta, decreased atrial pressure, decreased ventricular volume and increased aortic flow:

Back 52

Rapid Ejection Phase

Front 53

During this phase in the cardiac cycle there is decreased pressure in the ventricle, aortic pressure increases, increased atrial pressure and S2 sound is heard

Back 53

Isovolumic Relaxation

Front 54

During this phase in the cardiac cycle the mitral valve is open, the ventricular volume increases, aortic pressure decreases, and atrial pressure decreases:

Back 54

Rapid Filling Phase