17 - The Cardiovascular System: The Heart

Front 1

PMI.

Back 1

Point of Maximum intensity. The easiest place to feel the heart where the apex contacts the chest wall between the 5th and 6th ribs just below the left nipple.

Front 2

Pericarditis.

Back 2

Inflamation fo the pericardium. The serous membrane roughens and the heart rubs it as it beats causing a creaking sound. Leads to chest pain and adhesions.

Front 3

Cardiac Tamponade.

Back 3

Fluid builds up and compresses the heart from pericarditis. Can be drained by inserting a needle.

Front 4

Epicardium.

Back 4

The superficial heart layer of the serous pericardium, infiltrated wih fat in elderly.

Front 5

Myocardium.

Back 5

The middle layer of the heart layer, composed of cardiac muscle, the layer that contracts.

Front 6

Fibrous skeleton of the heart.

Back 6

The networks of connective tissue that reinforce the myocardium.

Front 7

Arrangment of myocardium muscle cells.

Back 7

These cells are tethered by connective tissue fibers and arranged in spiral bundles.

Front 8

Endocardium.

Back 8

The inner layer, a glistening white sheet of endothelium that rests on a thin layer of cennective tissue, continuous with vessels leaving and entering the heart.

Front 9

Interatrial septum.

Back 9

Seperates the right and left atria.

Front 10

Interventricular septum.

Back 10

Seperates the right and left ventricles.

Front 11

Auricles.

Back 11

Small wrinkles apendages that extend off the atria that increase the atria volume.

Front 12

Fossa Ovalis.

Back 12

A shallow depression in the interatrial septum, the remains of the foramen ovale from the fetal heart.

Front 13

Foramen Ovale.

Back 13

This was a shunt in the fetal heart to keep blood out of the lungs in utero. It is now the fossa ovalis.

Front 14

Atria.

Back 14

The recieving chambers.

Front 15

Through which blood enters the right atrium.

Back 15

Blood enters here through the inferior and superior vena cava and the coronary sinus.

Front 16

Through which blood enters the left atrium.

Back 16

Blood enters here through the four pulmonary veins.

Front 17

The _____________ are the only veins to carry oxygenated blood.

Back 17

The right and left pulmonary veins are the only veins carrying __________.

Front 18

Papillary muscles.

Back 18

These muscles are involved in valve function.

Front 19

The thickest walled chamber is the _____.

Back 19

The _____ walled chamber is the left ventricle.

Front 20

The ventricles are ________ walled than the atrium are.

Back 20

The _______ are thicker walled than the _______ are.

Front 21

Through which blood leaves the right ventricle and travels to the lungs.

Back 21

The blood leaves here through the left and right pulmonary arteries and travels to the lungs.

Front 22

The ________ are the only arteries to carry deoxygenated blood.

Back 22

The left and right pulmonary arteries are the only arteries to carry _________ blood.

Front 23

Through which blood leaves the left ventricle and travels to the body.

Back 23

The blood leaves here through the aorta and travels to the rest of the body.

Front 24

Coronary circulation.

Back 24

This is the shortest circulation system and supplies blood to the heart muscles. It contains anastomies in case one gets blocked.

Front 25

Angina Pectoris.

Back 25

A blockage of the coronary arterial circulation. This is always serious and can be fatal. There is crushing chest pain due to inadequate myocardium blood supply.

Front 26

Myocardial Infarction (MI).

Back 26

This is commonly caused by prolonged lack of blood flow to the myocardium. It causes cell death, cells are replaced with scar tissue. This interferes with the heart's ability to pump.

Front 27

Atrioventricular valves.

Back 27

These are located between the atria and vetrincles.

Front 28

Tricuspid valve.

Back 28

The valve between the right atrium and right ventricle.

Front 29

Bicuspid valve (mitral).

Back 29

The valve between the left atrium and left ventricle.

Front 30

Chordae Tendineae.

Back 30

These keep the valves closed during ventricular contraction to prevent backflow.

Front 31

Semilunar valves.

Back 31

The valves for the blood enterance into the aorta and the pulmonary artery.

Front 32

Semilunar valve function.

Back 32

These valves have three cusps that open in response to pressure of blood, their closure makes the second beat of the heart.

Front 33

Incomplete valve.

Back 33

A valve that does not close properly and forces the heart to pump the same blood over and over.

Front 34

Stenotic valve.

Back 34

A narrowing of the valve sue to scar tissue from an infection that causes the valve to become stiff. This causes the heart the work harder. Surgical interventions required.

Front 35

Cardiac muscle cells.

Back 35

These cells have one or two central nuclei, are striated, use a sliding filament mechanism for contraction, are branching with intercalated discs, and have desmosomes and gap junctions.

Front 36

How the heart muscles produce energy and prevent fatigue.

Back 36

These muscle cells have large mitochondria for this purpose

Front 37

Automaticity (autorhythmicity).

Back 37

The ability of the node cells to stimulate their own action potentials.

Front 38

The refractory perios is 250ms.

Back 38

This refractory perios prevents tetanic contractions which would interfere with the hearts pumping ability.

Front 39

Node cells locations.

Back 39

These are found in the Sinoatrial node (SA node), atrioventricular node (AV node), atrioventricular bundle, purkinjie fibers, and the AV bundle branches.

Front 40

SA node.

Back 40

The pacemaker of a healthy heart that causes electrical impulses.

Front 41

The heart muscle action potential.

Back 41

1. Resting potential (-70mV)
2. Depolarization (Na+ channels open)
3. Plateau (K+ channels open-small conductance, Ca2+ channels open and enter cell.
4. Repolarization (Ca2+ channels close, K+ channels open and K+ leaves cell)

Front 42

The Node cell action potential.

Back 42

1. Resting potential (-70mV)
2. Depolarization (these cells have pace maker potentials-spontaneous depolarizations where Na+ influxes. Ca2+ channels open and Ca2+ enters cell.
3. Repolarization (K+ channels open, Ca2+ channels close)

Front 43

Pacemaker Potential.

Back 43

Spontaneous resting potentials where slow depolarization occurs toward the threshold and triggers action potentials.

Front 44

The Sequence of heart excitation.

Back 44

1. signal starts in SA node
2. Depolarization wave travels through the internodal pathway via gap junction to the AV node. .1 second delay to allow atria to contract and totally fill ventricles before they contract.
3. Depolarization wave travels through AV bundle (bundle of His) down to the purkinji fibers which go to the apex of the ventricular septum then turn upwards.

Front 45

Purkinji fibers.

Back 45

These are depolarized after the AV bundle and signal to the papillary muscles to contract before the rest of the atria to help prevent backflow.

Front 46

Arrhythmais.

Back 46

The uncoordinated atrial and ventricular contractions caused by a defect in the conduction system.

Front 47

Fibrillation.

Back 47

A rapid and irregular (usually out of phase) contractions where the SA node is no longer controlling the heart rate.

Front 48

Atrial Fibrillation.

Back 48

This fibrillation can cause clots and ineffecient filling of the ventricles.

Front 49

Ventricular Fibrillation.

Back 49

This fibrillation is more life threatening. The ventricles pump without filling and if the rhythm is not rapidy reestablished then circulation stops and brain death occurs.

Front 50

Defibrillation.

Back 50

The application of an electrical stimulus to shock the heart back into a normal SA rhythm.

Front 51

Electronic Pacemaker.

Back 51

This is a device surgically placed to diliver the stimulus instead of the SA node.

Front 52

Ectopic focus.

Back 52

An abnormal pacemaker that takes over the conduction system usually because it goes faster then the SA node.

Front 53

SA node damage.

Back 53

In this instance the AV node can take over and deliver adequate circulation, although lower then normal.

Front 54

Extrasystole.

Back 54

Premature contraction.

Front 55

PVCs (prematureventricular contractions).

Back 55

Most common type of extrasystole.

Front 56

Damaged AV node.

Back 56

Heart Block.

Front 57

Total block.

Back 57

No impulses get through the heart due to damages AV node so the ventricles beat at their intrinsic rate (purkinji fibers) but this is too slow to maintain circulation.

Front 58

Partial Block.

Back 58

The impulse in the heart is slow due to AV node damage, but still works. A pacemaker treats this condition.

Front 59

Electrocardiogram.

Back 59

A graphic composite record of the heart's electrical activity.

Front 60

The P wave.

Back 60

The wave indicates depolarization from the SA node to the AV node. Atria Contract.

Front 61

QRS Complex.

Back 61

This wave indicates the ventricular depolarization and precedes ventricular contraction.

Front 62

T Wave.

Back 62

This wave indicates ventricular repolarization.

Front 63

This wave is obscured by the QRS complex.

Back 63

This wave indicates atrial repolarization.

Front 64

P-Q Interval.

Back 64

This space on an EKG indicates the time from the beginning of atrial excitation to the beginning of ventricular excitation.

Front 65

S-T Segment.

Back 65

This wave segment is when the entire ventricula myocardium is depolarized.

Front 66

G-T interval.

Back 66

This wave interval indicates the beginning of ventricular depolarization through repolarization.

Front 67

Enlarged Ventricle seen on EKG.

Back 67

Enlarged R Wave.

Front 68

Cardiac Ischemia seen on EKG.

Back 68

A depressed S-T segment.

Front 69

Repolarization problems (increase risk for ventricular arrhythmias) seen on EKG.

Back 69

A prolonged Q-T interval.

Front 70

Heart murmurs.

Back 70

Abnormal heart sounds. Usually caused by valve problems.

Front 71

Swishing sounds.

Back 71

Sound indicating an incomplete valve.

Front 72

High pitched or clicking sound.

Back 72

Sounds indicating a stenoic valve.

Front 73

Systole.

Back 73

Contraction.

Front 74

Diastole.

Back 74

Relaxation phase.

Front 75

The systemic circuit has _________ pressure and the pulmonary circuit has _________ pressure.

Back 75

The ______ circuit has higher pressure and the ________ circuit has lower pressure.

Front 76

Cardiac output.

Back 76

The amount of blood pumped out of each ventricle in one minute.

Front 77

CO = HR x SV

Back 77

Cardiac output formula.

Front 78

Normal cardiac output level.

Back 78

5.25 L per minute

Front 79

Stroke Volume.

Back 79

The difference between the end diastolic volume and the end systolic volume.

Front 80

SV = EDV - ESV

Back 80

Stroke Volume Formula.

Front 81

Normal stroke volume level.

Back 81

70 mL per beat

Front 82

Starlings law.

Back 82

This states that the critical factor controlling stroke volume is preload.

Front 83

Preload.

Back 83

The degree to which the cardiac muscle cells are stratched before they contract.

Front 84

Optimal Length/Tension relationship.

Back 84

The relationship is required for maximal force generation.

Front 85

EDV.

Back 85

The amount of blood that collects in a ventricle during diastole.

Front 86

ESV.

Back 86

The amount of blood that remains in the ventricle after systole.

Front 87

Preload.

Back 87

Proportional to the amount of ventricular myocardial fiber stretch just before systole.

Front 88

Afterload.

Back 88

The pressure that the ventricles must overcome to force open the aortic and pulmonary valves.

Front 89

Venous Return.

Back 89

The most important factor in causing stretch is the amount of blood in the ventricles, which is controlled by ________.

Front 90

Contractility.

Back 90

Defined as the contractile strength achieved at a given muscle length.

Front 91

Enhanced contractility is due to _____________.

Back 91

SNS stimulates NE/Epi release to initiate cAMP and release Ca2+ which enhances _____________.

Front 92

Stroke Volume is effected by:

Back 92

Extrinsic factors (hormones Epi and NE from the SNS) that increase contractility by Ca2+ influx. This contractility increase lowers ESV and therefore increases SV.

Front 93

Positive inotropic agents.

Back 93

Anything that increases contractility.

Front 94

Negative inotropic agents.

Back 94

Things that impair contractility.

Front 95

Positive Inotropic agent examples.

Back 95

1. Glucagon
2. Thyroxine
3. Digitalis
4. SNS release of NE and Epi to trigger cAMP and release Ca2+.

Front 96

Negative Inotropic agents examples.

Back 96

1. Acidosis
2. Increased intracellular K+
3. Calcium channel blockers.

Front 97

Positive chronotropic factors.

Back 97

Things that increase HR.

Front 98

Negative chronotropic factors.

Back 98

Things that decrease heart rate.

Front 99

Effects of PNS on HR.

Back 99

This system slows HR by releasing Ach which binds to muscarinic receptors and hyperpolarized node cells. Does not effect contractility, just innervates node cells.

Front 100

Effects of SNS on HR.

Back 100

This system releases NE which binds to beta1 adrenergic receptors of the heart which increase the rate at which SN node's fire potentials, therefore increasing HR. It also activates cAMP pathways to release Ca2+ which enhances crossbridge function and increases heart contractility.

Front 101

Baroreceptors.

Back 101

These sense changes in blood pressure and signal the opposing nervous system to bring pressure back to normal.

Front 102

Thyroxine's effect on HR.

Back 102

This hormone effects HR by increasing metabolic rate causing a slow and sustained increase in HR, it also enhances effects of Epi and NE.

Front 103

Hypocalcemia.

Back 103

Reduced blood calcium levels that depress heart function.

Front 104

Hyper calcemia.

Back 104

Increased blood calcium levels that prolong the plateau phase of the AP and cause irritability to the heart and may lead to spasms.

Front 105

Hyperkalemia.

Back 105

High K+ blood levels that interfere with the ability to depolarize. Leads to heart blocks and cardiac arrest.

Front 106

Hypokalemia.

Back 106

Low K+ blood levels that cause a weak heart beat and cause arrythmias.

Front 107

Tachycardia.

Back 107

Abnormally fast heart rate.

Front 108

Brady cardia.

Back 108

Abnormally slow heart rate.

Front 109

Congestive Heart Failure.

Back 109

This is a prograssively worsening disease in which the heart does not maintain blood flow to meet the tissue needs.

Front 110

Causes of Congestive Heart Failure.

Back 110

Coronary atherosclerosis, persistant high blood pressure, multiple MIs, and dialated cardiomyopathy are causes of this.

Front 111

Pulmonary Hypertension.

Back 111

This disease causes right ride issues and if left untreated pulmonary congestion will occur from the fluid leaking out of the capillaries into the tissues, causing the person to suffocate.

Front 112

Edema.

Back 112

Congestion of the peripheral tissues, usually a signs of CV.

Front 113

Treatment for Edema.

Back 113

Treatments for this disease include diuretics, BP lowering drugs to reduce afterload, and digitalis to conservse heat and energy by lowering HR.