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HSS 3305 > Lecture 14 > Flashcards

Lecture 14 Flashcards

1
Q

Cardiac Function

A

Muscular pump; propels blood through the lungs to the tissues and transports nutrients, oxygen, carbon dioxide, hormones, and blood cells (immunity, hemostasis)

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2
Q

Location of heart

A

Within mediastinum; extends obliquely about 5 inches from second rib to fifth intercostal space; rests on the diaphragm; anterior to vertebral column and posterior to sternum

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3
Q

Pericardium

A

Double-walled fibrous sac, outer layer of tough connective tissue (mesothelial cells)

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4
Q

Epicardium (mesothelial)

A

Visceral layer of pericardium covering myocardium

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5
Q

Epicardium

A

Outer layer of connective tissue, coronary arteries

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6
Q

Myocardium

A

Middle layer, muscular, thickest layer, workhorse of the heart

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7
Q

Endocardium

A

Thin endothelial layer- Innermost layer, smooth membrane, covers heart valves - part of endocardium

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8
Q

Function of the layers of the heart wall

A

Form fibrous framework tissue which provide support and divides atria/ventricles so they can function independently

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9
Q

T/F: There is direct communication between right and left halves of the heart

A

False, no direct communication (divided by septum)

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10
Q

Atria function

A

Receive blood returning to the heart

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11
Q

Ventricle function

A

Pump blood away to lungs/aorta

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12
Q

Right half

A

Right atrium (RA) and right ventricle (RV), Pulmonary pump, circulates blood into the pulmonary artery, and lungs

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13
Q

Left half

A

Left atrium (LA) and left ventricle (LV), Systemic pump, circulates blood into the aorta, organs, and tissues

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14
Q

Systole

A

During contraction of Ventricles, no tension, blood flow forces closure

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15
Q

Diastole

A

During relaxation as ventricle refill, causes tension on valves through chordae, causing them to open

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16
Q

Atrioventricular (AV) valves (Lub)

A

Flap-like valves between atria and ventricles; prevent back flow of blood into atria when ventricles contract (4 valves keeping blood flow in one direction) attached and supported by chordae

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17
Q

Tricuspid valve (AV)

A

Three flexible flaps; directs blood flow from RA to RV, prevents backflow to RA when RV contracts

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18
Q

Bicuspid valve or mitral valve

A

Directs blood flow from LA to LV; prevents backflow to LA when LV contracts

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19
Q

Semilunar valves – dub (Aortic/Pulmonary)

A

Prevent backflow of blood into ventricles during diastole; Cup shaped – 3 cusps on both

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20
Q

Ventricular contraction

A

Coordinates valve functions – Closure of AV valves and opening of semilunar valves

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21
Q

Pulmonary valve

A

From RV to pulmonary trunk

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22
Q

Aortic valve

A

From LV to aorta

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23
Q

Coronary arteries

A

Main blood supply of the heart, Shortest circulation in the body

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24
Q

Aorta branches (aortic sinus)

A

Carry arterial blood to the heart when relaxed

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25
Q

Right coronary artery (RCA)

A

Supplies posterior wall and posterior part of interventricular septum with blood

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26
Q

Left coronary artery (LCA) and branches

A

Supplies anterior wall, anterior part of interventricular septum

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27
Q

Anastomoses

A

Connections that terminal branches of coronary arteries communicate through (compensatory mechanism if there is blockage of an artery)

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28
Q

Do heart muscles/cells proliferate?

A

No, they do not proliferate to replace damaged muscle fibers. Areas of cell death are repaired with noncontractile scar tissue

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29
Q

Heart conduction system

A

Electrical impulses through depolarization in the sinoatrial (SA) node in RA near the opening of the superior vena cava; intrinsic; does not depend on the nervous system

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30
Q

Sinoatrial (SA) node

A

Controls normal cardiac rhythm - “cardiac pacemaker” Initiates atrial contraction

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31
Q

Where does conduction system terminate

A

Perkinje fibers that activate heart muscle contraction

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32
Q

How does the autonomic NS influence the depolarization rate?

A

Sympathetic – increase, Parasympathetic - decrease

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33
Q

Cardiac cycle

A

Atrial systole → atrial diastole → ventricular systole → ventricular diastole

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34
Q

Cardiac output

A

Typically 5L/min pumped out by each ventricle

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35
Q

How many veins does blood enter each atrium from?

A

Blood enters RA via three veins, Superior vena cava (from body regions above diaphragm), Inferior vena cava (from body areas below diaphragm), Coronary sinus (collects blood that drains from myocardium), Blood enters LA via four pulmonary veins (Blood that is low in oxygen returns to the heart)

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36
Q

Pulmonary circulation

A

Oxygen-poor blood enters RA → RV through tricuspid valve → pulmonary artery → lungs

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37
Q

Systemic circulation

A

Freshly oxygenated blood leaves lungs through pulmonary veins → LA → LV through mitral valve → aorta → rest of the body

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38
Q

Blood Pressure

A

Blood flow in the arteries results from the force of ventricular contraction, Pressure is decreased due to elasticity of blood vessels

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39
Q

Systolic pressure

A

Pressure is highest when ventricles contract

40
Q

Diastolic pressure

A

Pressure is lowest when ventricles relax

41
Q

Atherosclerosis

A

Loss of elasticity of blood vessels which leads to increased BP

42
Q

ECG

A

Measures electrical activity of heart; diagnostic tool

43
Q

P wave

A

Atrial depolarization, atrial systole

44
Q

QRS complex

A

Ventricular depolarization, ventricular systole

45
Q

T wave

A

Ventricular diastole

46
Q

PR interval

A

Time for depolarization to pass from atria to ventricles via AV bundle

47
Q

Echocardiogram

A

Ultrasound imaging of heart and helps to Identify valve/chamber/blood flow abnormalities

48
Q

Congenital Heart Disease cause

A

German measles (viral infections), Down syndrome, drugs, genetic factors, undetermined causes (Fetal bypass channels fail to close normally)

49
Q

Ductus arteriosus (pulmonary artery-aorta)

A

Redirects blood from lungs

50
Q

Foramen ovale

A

Maintains blood flow between RA to LA(one way valve) while heart is developing

51
Q

Abnormalities/diseases obstructing blood flow in heart

A

Pulmonary stenosis, aortic stenosis, coarctation of the aorta

52
Q

Abnormal formation of aorta and pulmonary artery or abnormal connection of vessels

A

Tetralogy of Fallot, transposition of great vessels

53
Q

Patent ductus arteriosus

A

shunts blood from aorta into pulmonary artery

54
Q

Atrial and ventricular septal defects

A

Usually cause by non-closure of foramen ovale

55
Q

Pulmonary or aortic valve stenosis

A

Obstructed/narrowed valve

56
Q

Tetralogy of Fallot

A

Ventricular septal defect

57
Q

Myocarditis (what is it, its cause, and treatment)

A

Inflammation; injury and necrosis of individual muscle fibers
Cause: Viruses, parasites (Trichinella), fungi (Histoplasma), or hypersensitivity (acute rheumatic fever); abrupt onset; may lead to acute heart failure
Treatment: underlying cause, most time subsides without permanent damage

58
Q

Cardiomyopathy

A

No evidence of inflammation, 2 types (Dilated cardiomyopathy and hypertrophic cardiomyopathy)

59
Q

Dilated cardiomyopathy (what is it, cause, and treatment)

A

Enlargement of heart and dilatation of chambers; impaired ventricular action leads to chronic heart failure; cause uncertain
Treatment: None

60
Q

Hypertrophic cardiomyopathy (what is it an treatment)

A

Hereditary, transmitted as a dominant trait, muscle fibers in disarray with marked hypertrophy of heart muscle; reduces the size of ventricles
Treatment: Genetic screening, use beta blockers to slow the heart, calcium channel blockers to reduce contractions, or surgical resection of blocking septum

61
Q

Rheumatic Fever

A

Commonly encountered in children, A response to a bacterial infection; an immunologic reaction that develops weeks after the initial streptococcal infection (group A beta-hemolytic streptococcal)

62
Q

Rheumatic heart disease

A

Scarring of heart valves following rheumatic inflammation; Causes inflammation in connective tissues throughout the body especially the mitral and aortic valves and joint tissues; eventually leads to heart failure

63
Q

Rheumatic heart disease prevention

A

Treat beta strep infection promptly and Prophylactic penicillin throughout childhood and young adulthood to prevent strep infections and reduce the risk of recurrent rheumatic fever and further heart valve damage (Surgical removal and replacement of valve if severely damaged)

64
Q

Aortic Stenosis (what is it, outcomes, prevention, and treatment)

A

Strain on heart valve which can lead to heart failure, Occur due to aging, coronary atherosclerosis
Prevention: Control risk factors (high cholesterol, diabetes, hypertension)
Treatment: Surgical repair/replacement

65
Q

Valvular Heart Disease (What is it, diagnosis, and treatment)

A

Common, but only a few patients develop problems; One or both leaflets enlarge, stretch, and prolapse into LA during ventricular systole, clicking sound on systole followed by a faint systolic murmur, can cause chordae rupture
Diagnosis: echocardiogram
Treatment: surgical repair/replacement

66
Q

Infective Endocarditis

A

Inflammation and causes severe symptoms of infection and valve destruction; affects normal heat valves; is Caused by organisms of low virulence (bacterial - Staphylococci) and is a complication of any valvular heart disease. Platelets and fibrin may deposit on abnormal or damaged valves then serve as sites for bacteria to implant or for thrombi to form

67
Q

Who are at risk of infective endocarditis and how does it affect them?

A

Intravenous drug users; affect the tricuspid valve instead of mitral or aortic valves, Unsterile materials or contaminants (surgery) enter the right side of the heart, form large bacteria-laden growths on valves, can dislodge into pulmonary circulation and cause pulmonary infarct

68
Q

Cardiac Arrhythmias

A

Disturbances in heart rate or rhythm (Artial and ventricular fibrillation)

69
Q

Atrial fibrillation (AF)

A

Atria contract in irregular pattern: 400bpm- “quiver” versus normal contraction; Can also affect ventricular rate and Ventricles beat irregularly and fast (140-160), shortening diastole (pulse deficit due to inadequate ventricular filling), lack of P wave and variable QRS complex

70
Q

Ventricular fibrillation (VF) + treatment

A

Ventricles unable to contract normally, incompatible with life- no blood circulation, Heart block which is usually caused by arteriosclerosis
Treatment: Pacemaker to stimulate ventricular contraction at a determined rate

71
Q

Acute Coronary Syndrome

A

Sudden blockage of a coronary artery from a thrombus or atheromatous debris, hemorrhage, or arterial spasm - can trigger a heart attack (caused by sudden greatly increased myocardial oxygen requirements and arteriosclerosis of coronary arteries)

72
Q

Cardiac arrest may result from:

A

Arrhythmia (abnormal heart rhythm) from myocardial ischemia which disrupts ventricular contraction and asystole is the ending of cardiac contractions

73
Q

Stable angina

A

Temporary chest pain relieved by vasodilator (nitroglycerine) or rest

74
Q

Unstable angina

A

Needs anticoagulation and antithrombotic drugs

75
Q

Myocardial Ischemia

A

Heart attack, Caused by the inadequate blood supply to the heart muscle -precipitated by atherosclerosis, thrombosis

76
Q

Myocardial Infarction: Location

A

Left ventricle and septum (Thicker walls require rich blood supply; work harder to pump blood into systemic circulation; rarely involves atria or right ventricle)

77
Q

Clinical manifestations of Myocardial ischemia

A

Asymptomatic (free of symptoms), Angina pectoris (pain of the chest) bouts of oppressive chest pain that may radiate into neck or arms; caused by myocardial ischemia, Myocardial infarction: Actual necrosis of heart muscle, Cardiac arrest: Cessation of normal cardiac contractions

78
Q

NSTEMI

A

Complete occlusion of minor coronary artery or partial occlusion of major; Results in partial thickness damage to cardiac muscle

79
Q

STEMI

A

Complete occlusion of major coronary artery; Results in full thickness damage

80
Q

Cocaine-Induced Arrhythmias and Infarcts

A

Prolongs and intensifies effects of sympathetic nervous system (increased HR, muscle irritability, peripheral vasoconstriction and coronary artery spasm (High BP)

81
Q

Myocardial Infarction: Diagnosis

A

Medical history, Laboratory data
ECG, Cardiac imaging, Enzyme tests; enzymes leak out from necrotic cells after an infarct
- The larger the infarct, the longer for elevated levels to return to normal

82
Q

What Enzymes are present after an MI

A

Troponin T and Troponin I (Appears in 3h, peaks in 24 hours, remains high for 10 to 14 days)

83
Q

Myocardial Infarction: Treatment

A

Drug treatment (beta-blockers and nitro), Thrombolytic therapy (should not be used in stroke patients, hypertension, recent operation, or bleeding disorder), angioplasty (preferred method), bed rest, pacemaker, cardioverter-defibrillator, aspirin, control risk factors

84
Q

Myocardial Infarction: Complications

A

Arrhythmia, heart failure, intracardiac thrombi, and pericarditis

85
Q

Intracardiac thrombi

A

Mural thrombus forms on ventricular wall; bits of clot embolize into systemic circulation causing infarct in brain, kidneys, spleen

86
Q

Pericarditis

A

Infarct extends to epicardial surface, leads to inflammation and fluid accumulation in pericardial sac; may cause chest pain

87
Q

What does Aspirin do?

A

Interferes with platelet function by permanently inactivating thromboxane A2 that causes platelets to aggregate and start the clotting process, Reduces risk of cardiovascular disease and stroke, Increases risk of bleeding in the brain if person has stroke

88
Q

Cardiac rupture

A

Blood leaks into pericardial sac from perforation in necrotic muscle, prevents ventricular filling, and rupture may occur in ventricular septum or papillary muscle

89
Q

Papillary muscle dysfunction

A

Infarcted papillary muscle unable to control mitral valve leaflet, resulting in mitral valve prolapse and mitral insufficiency

90
Q

Ventricular aneurysm

A

Late complication; outward bulging of healing infarct during ventricular systole; reduces left ventricular function and cardiac output; rather than being ejected, blood fills aneurysm sac

91
Q

What are factors that affected survival of a MI?

A

Size of infarct, Age of patient, Complications, and Other diseases

92
Q

Heart Failure

A

No longer able to pump adequate amount of blood, can develop slowly (chronic) or rapidly (acute)

93
Q

Forward failure (Left)

A

Reduced blood flow to tissues → reduced renal blood flow → salt and water retention to increase blood volume and venous pressure → edema

94
Q

Backward failure (Right)

A

Blood backups in veins drain to the heart → increased venous pressure, congestion, edema

95
Q

Heart failure treatment

A

Diet/ lifestyle modification, Diuretic drugs (promotes excretion of excess salt), Cardiac/ Arrythmia Drugs, Angiotensin-converting enzyme (ACE) inhibitors, and pacemakers

HSS 3305 (21 decks)

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