351 Exam 3

Front 1

Atrioventricular valves

Back 1

- open at the beginning of diastole, allow blood to fill the ventricles

- close at the beginning of ventricular contraction to prevent backflips of blood to the atria

-mitral and tricuspid

Front 2

Semilunar valves

Back 2

-open at the end of ventricular contraction when the pressure in the ventricles exceed the pressure in the pulmonary artery and aorta

-close at the beginning of ventricular relaxation as the pressure in the chambers drops below the pressure in the pulmonary artery and aorta to prevent back flow into the ventricles

-aortic and pulmonic

Front 3

Chordae tendinae

Back 3

Connect valve leaflets or cusps to papillary muscles

Front 4

Papillary muscle

Back 4

Extension of the myocardium that pull cusps together and downward at the beginning of ventricular contraction to prevent backward expulsion of the AV valves into the atria

Front 5

Tricuspid valve

Back 5

- av

- has three cusps

- largest diameter of all valves

Front 6

Mitral valve

Back 6

-has two cusps (bicuspid)

-resembles a cone shaped finnel

Front 7

Pulmonic and aortic valves

Back 7

Have 3 cup shaped cusps

Behave like one way swinging doors

Pulmonic slightly thinner than aortic

Front 8

Great vessels

Back 8

Superior and inferior vena canvae- veins to r atrium

Pulmonary artery- artery to lungs

Pulmonary veins- to left atrium

Aortic artery- to body

Front 9

Coronary artery

Back 9

Blood to the myocardium of the heart

Front 10

Coronary artery

Back 10

Blood to the myocardium of the heart

Front 11

Diastole

Back 11

Relaxation, blood fills ventricles

Front 12

Coronary artery

Back 12

Blood to the myocardium of the heart

Front 13

Diastole

Back 13

Relaxation, blood fills ventricles

Front 14

Systole

Back 14

Contraction, blood pumped out of the ventricles

Ejection of right ventricle slightly earlier than left due to pressure differences

Front 15

atrial contraction

Back 15

Right- blood enters from vena cave and coronary sinus

Left- blood enters from 4 pulmonary veins

Atria fills and distend-->opens AV valves

Blood passively fills ventricles

Atrial contraction provides the atrial kick - actively pumps additional blood into the ventricle

Front 16

Atrial kick

Back 16

Active pump of approx 25 mls of blood to ventricles

Front 17

Cardiac phase 1

Back 17

Isovolumetric contraction

Ventricular volume is constant

Increase in ventricular pressure closes Av Valves

Front 18

Cardiac phase 2

Back 18

Increase in ventricular pressure opens semilunar valves and blood is ejected into circulation

Intraventricular volume and pressure deceea

Front 19

Cardiac phase 3

Back 19

Isovoulmetric relaxation

Decrease in ventricular pressure close semilunar valves

Ventricles continue to relax

Front 20

Cardiac phase 3

Back 20

Isovoulmetric relaxation

Decrease in ventricular pressure close semilunar valves

Ventricles continue to relax

Front 21

Cardiac phase 4

Back 21

Decrease in ventricular pressure opens av valves

Permits ventricular filling from the atria

Front 22

The cardiac cycle

Back 22

Front 23

Diastole

Back 23

Isovolumetric ventricular relaxation and filling (.4 sec)

Front 24

Systole

Back 24

Isovolumetric ventricular contraction and ejection (.3 seconds)

As the pressure in the ventricles becomes greater than atria, av valves shut

There is an isovolumetric contraction of the ventricles

As the pressure increases and becomes greater than the arteries, the semilunar valves open and blood is ejected into circulation

Front 25

S1

Back 25

Closure of av valves (the sound is the turbulence of blood rushing against heart wall)

Front 26

S1

Back 26

Closure of av valves (the sound is the turbulence of blood rushing against heart wall)

Front 27

S2

Back 27

At the end of systole , semilunar valves shutting

Front 28

Physiologic split

Back 28

Lub b dub

Because aortic valve has a bigger opening than pulmonic, the pulmonic valve opens sooner and closes later

Split s2- normal

Front 29

Valve closure and cardiac cycle

Back 29

Front 30

S3

Back 30

If ventricular wall compliance is decreases (not stretching like it should), structures in ventricular wall vibrate

Congestive heart failure or valvular regurgitation

May be normal <30 years

Lub dub dub

Front 31

S4

Back 31

During atrial kick, If there is resistance to ventricular filling

De lub dub

Cardiac hypertrophy, disease or injury to ventricular wall

Front 32

Coronary vessels

Back 32

Coronary circulation

Part of systemic circulation, branch off aorta via coronary Ostia (to coronary arteries )

Coronary veins Return to the right atrium through ostium called the coronary sinus

Front 33

Right coronary artey

Back 33

Conus- supplies upper r ventricle

Right marginal branch - transverses r ventricle to apex

Posterior descending- supplies smaller branches to both ventricles

Front 34

Right coronary artey

Back 34

Conus- supplies upper r ventricle

Right marginal branch - transverses r ventricle to apex

Posterior descending- supplies smaller branches to both ventricles

Posterior septum

Posterior heart

SA and AV node

Front 35

Left coronary artery

Back 35

Left anterior descending (Aka anterior interventricular artery aka the widow maker) - blood to portions of the left and right ventricles and much of the interventricular septum (bundle of his, electrical)

Circumflex artery- blood to left atrium and lateral wall of left ventricle

Front 36

Collateral arteries

Back 36

Anastomoses (connection) between two branches of the coronary that develop over time

Epicardium contains more collateral vessels than endocardium

Collateral circulation protects the heart

Front 37

Coronary capillaries

Back 37

3300 capillaries per sq mm

One capillary per muscle

Where exchange of oxygen and nutrients takes place

In ventricular hypertrophy, the capillary network doesn't expand--> same number of capillaries must perfuse a larger area--> decreases exchange of o2 and nutrients

Front 38

Cardiac action potentials

Back 38

Electrical impulse--> fibers shorten--> muscle contraction--> systole

After action potential--> fibers relax --> return to resting length --> diastole

Front 39

Qualities of heart muscle cells related to conduction

Back 39

Intercollated discs

Automaticity- can generate and discharge an electrical impulse

Excitability - can respond to an electrical impulse

Conductivity - ability to transfer an electrical impulse from one cell to another

WITHOUT STIMULATION FROM THE NERVOUS SYSTEM

Front 40

Automatic inputs into the heart

Back 40

Back (Definition)

Front 41

Cardiac conduction

Back 41

Back (Definition)

Front 42

Cardiac conduction

Back 42

Front 43

P wave

Back 43

Atrial contraction

Av node

Front 44

QRS complex

Back 44

Ventricular contraction (Purkinje fibers)

Front 45

T wave

Back 45

Repolarizarion phase

Electrical changes during relaxation phase of the ventricles

Front 46

T wave

Back 46

Repolarizarion phase

Front 47

Depolarization

Back 47

Activation , inside of the cell becomes less negative (positive ions entering the cell)

Front 48

T wave

Back 48

Repolarizarion phase

Front 49

Depolarization

Back 49

Activation , inside of the cell becomes less negative (positive ions entering the cell)

Front 50

Repolarization

Back 50

Deactivation

Front 51

T wave

Back 51

Repolarizarion phase

Front 52

Depolarization

Back 52

))Activation , inside of the cell becomes less negative (positive ions entering the cell)

Voltage sensitive Na channels open and and allow rapid influx of Na then rapidly close (phase 0-1)

K channels close then reopen slowly

Voltage-sensitive Ca channels have delayed at slower opening relative to Na (phase 2)

Ca responsible for contraction of cardiac muscle

Normal circumstances : < max Amt of Ca released which permits modulation of contractile strength

Front 53

Repolarization

Back 53

Deactivation

Return to resting membrane potential is delayed (phase 3)

Makes it impossible to fire a second action potential before the first is complete

Prevents summation and tetany

Front 54

Membrane potential

Back 54

Electrical (voltage) difference across the cell membrane

R/t changes in permeability of cell membranes (Na & K)

Front 55

Threshold

Back 55

Point at which cells selective permeability to Na & K is temporarily disrupted = depolarization

When the cell fires

Front 56

Hyperpolarization

Back 56

I.e. With hypokolemia (low potassium)

Cell becomes more and more negative

Front 57

Cardiac action potentials

Back 57

Back (Definition)

Front 58

Fast response

Back 58

Occurs in atrial and ventricular muscle cells and the purkinje conduction systems

Uses the fast sodium channels

Front 59

Fast response

Back 59

Occurs in atrial and ventricular muscle cells and the purkinje conduction systems

Uses the fast sodium channels

These don't normally initiate a cardiac impulse, if they do they are ectopic beats (generated outside of the designed electrical pattern of the heart)

Front 60

Slow response of the SA AND AV nodes

Back 60

Uses the slow calcium channels

Calcium has a role in generating cardiac impulse

Through the pacemaker nodes (SA and then AV)

Front 61

Absolute refractory period

Back 61

No stimuli can generate another action potential

Includes phases 0,1,2 and part of 3

The cell cannot depolarize again

Front 62

Absolute refractory period

Back 62

No stimuli can generate another action potential

Includes phases 0,1,2 and part of 3

The cell cannot depolarize again

Front 63

Relative refractory period

Back 63

Greater than normal stimulus response

Repolarization returns the membrane potential to below threshold, although not yet at the resting membrane potential

Begins when the transmembrane potential in phase 3 reaches the threshold potential level

Ends just before the terminal portion of phase 3

Front 64

Absolute refractory period

Back 64

No stimuli can generate another action potential

From the end of qrs to apex of t wave

Includes phases 0,1,2 and part of 3

The cell cannot depolarize again

Part of repolarization

Front 65

Relative refractory period

Back 65

Greater than normal stimulus response

After apex of t wave

Repolarization returns the membrane potential to below threshold, although not yet at the resting membrane potential

Begins when the transmembrane potential in phase 3 reaches the threshold potential level

Ends just before the terminal portion of phase 3

Where arrhythmias happeb

Front 66

Supernormal excitatory period

Back 66

A weak stimulus can evoke a response

Extends from the terminal portion of phase 3 until the beginning of phase 4

Cardiac arrhythmia a develop

Resting membrane potential (RMP)

Front 67

Summation

Back 67

Prevented by repolarization

Increase in frequency of muscle stimulation that increases strength of contraction which can relate to tetany

Front 68

Tetany

Back 68

So many firings the heart can't fill, the heart doesn't have blood to pump out, cardiac output declines

Front 69

Heart rate

Back 69

Nl: 60-100

Sinus tachycardia > 100

Less filling time

Sinus bradycardia <60

Increase in heart rate increases oxygen consumption and if it's too fast it gets used up before it gets to the brain and can lead to confusion

Front 70

SNS stimulation

Back 70

Occurs when there is a decrease in pressure detected

Norepinephrine released (+ hr, + av contractility, peripheral vasoconstriction)

Front 71

PNS stimulation.

Back 71

Occurs when an increase in pressure is detected

Releases acetylcholine (- hr, - av contractility & conductivity)

Front 72

St elevation

Back 72

Doesn't return to the line during ecg, MI

Front 73

ST Depression

Back 73

Goes below st line, ischemia

Front 74

Echocardiogram

Back 74

Ultrasound

Creates a 3D picture of the heart using a transducer

Takes 30-90 minutes

Evaluates how well heart is moving, how well valves are working, size is the heart and its pumping chambers (ventricles), and ejection fraction

Front 75

Stress test

Back 75

Treadmill or bike hooked up to ekg

Performed until ischemia, angina or dyspnea occur (or until optimal heart rate is reached and nothing happens)

Should not be performed with significant aortic stenosis, untreated hypertension, CHF, unstable angina

Persantine for pts unable to exercise (dilates coronary arteries)

Front 76

Stress test

Back 76

No smoking or alcohol or caffeine prior

No large meals prior

No hot shower/bath after (Vaso vagal response)

Front 77

Stress test

Back 77

No smoking or alcohol or caffeine prior

No large meals prior

No hot shower/bath after (Vaso vagal response)

Front 78

Hotter monitoe

Back 78

24 hour ecg

Diary of when they feel arrhythmia / swipe card or on cell phone

Front 79

Stress test

Back 79

No smoking or alcohol or caffeine prior

No large meals prior

No hot shower/bath after (Vaso vagal response)

Front 80

Hotter monitoe

Back 80

24 hour ecg

Diary of when they feel arrhythmia / swipe card or on cell phone

Front 81

Coronary arteriography

Back 81

Gold standard

Cardiac Catheterization (coronary angiography)

%%%%%

Most precise means of measuring CAD

Also gives measures of left ventricular function (LVF)

- left ventricular end diastolic pressure (LVEDP)

-left ventricular end diastolic volume (LVEDV)

-ejection fraction (EF)

For patients with severe angina, recurrent idiopathic chest pain, survivors of cardiac arrest

If coronary artery stenosis >70%--> flow limiting and of clinical significance

Front 82

Blood vessel layers

Back 82

Tunica adventitia- outer, connective tissue

Tunica media- middle, smooth muscle, maintains basal tone (^tone= vasoconstriction;

Dec tone= vasodilation. )

Tunica intima- inner, smooth single layer of cells permits laminar blood flow

Controlled by SNS and local levels of O2 and CO2

Front 83

Resistance and capacitance vessels

Back 83

Front 84

Arterial blood pressure

Back 84

Front 85

Cardiac output and blood pressure

Back 85

Front 86

Stroke volume

Back 86

amount of blood ejected with ventricular contraction

70ml/beat nl

Front 87

Ejection fraction

Back 87

Percent volume of blood ejected with each ventricular contraction-- 55-75% of total ventricular volume

Ef = (sv/ edv) = 70ml/100 ml = 70%

Front 88

End- diastolic volume

Back 88

Total volume of blood in L ventricle at end of filling JUST PRIOR TO CONTRACTION

100ml

Function of : venous return to R atrium,

- strength of atrial kick during ventricular filling

-amount of blood pumped out of ventricle during last contraction

Front 89

Total peripheral resistance

Back 89

Aka systemic vascular resistance (svr) or peripheral vascular resistance (pvr)

Reflects the tone (degree of vasoconstriction) of resistance vessels (arteries and atrioles) as well as viscosity of the blood

Vasoconstriction = high bp

Vasodilation = low bp

Front 90

Aortic impedence

Back 90

Loss of elasticity of aortic wall (stiffens)

Increase with aging and functioning of aortic valve

Aortic narrowing -- left ventricle must generate higher pressure to get blood through , left ventricular hypertrophy

Front 91

Starlings law

Back 91

Back (Definition)

Front 92

Preload

Back 92

Degree of myocardial muscle stretch

Before the right atrium, the blood that comes back to the

Heart

Determined by blood volume

Increases preload , increased stretch, increased force of ventricular contraction (&stronger kick)

Related to degree of compliance of ventricular wall

-ischemic heart muscle-decreased compliance

-hypertrophied heart muscle- decreased compliance

Heart failure - increase in stretch without increase in force of ventricular contraction

Front 93

Preload

Back 93

Degree of myocardial muscle stretch

Before the right atrium, the blood that comes back to the

Heart

Determined by blood volume

Increases preload , increased stretch, increased force of ventricular contraction (&stronger kick)

Related to degree of compliance of ventricular wall

-ischemic heart muscle-decreased compliance

-hypertrophied heart muscle- decreased compliance

Heart failure - increase in stretch without increase in force of ventricular contraction

Front 94

Afterload

Back 94

What the left ventricle must push against to get blood out

Determined by:

Aortic and pulmonic impedence (aortic stenosis--- increased afterload)

Condition and tone of aorta and resistance offered by systemic and pulmonary arterioles (hypertension-- increases afterload)

Increased afterload = increased cardiac workload= increases o2 consumption

Front 95

Myocardial contractility

Back 95

Front 96

ANS REGULATION OF BP

Back 96

Front 97

Baroreceptors

Back 97

Front 98

Chemoreceptors

Back 98

Back (Definition)

Front 99

Renin Angiotesin aldosterone

Back 99

Back (Definition)

Front 100

Antidiuretic hormone (adh)

Back 100

Front 101

Atrial stretch receptors and ANP

Back 101

The heart can't rest

May be adverse reaction to anesthesia

Front 102

Brain natriuretic peptide (bnp)

Back 102

Discovered in brain of a pig

Less than 100 is normal

Front 103

Essential hypertension

Back 103

Front 104

Risk factors for HTN

Back 104

Front 105

Manifestations of HTN

Back 105

Back (Definition)

Front 106

Classifications of blood pressure

Back 106

Back (Definition)

Front 107

Causes of hypertension by age

Back 107

Back (Definition)

Front 108

Hypertension in the elderly

Back 108

Back (Definition)

Front 109

Secondary hypertension

Back 109

Front 110

Malignant hypertension

Back 110

Front 111

Target organ disease

Back 111

Front 112

Tx lifestyle modifications

Back 112

Back (Definition)