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Asad > Chapter 12 - Cardiovascular System Disorders > Flashcards

Chapter 12 - Cardiovascular System Disorders Flashcards

1
Q

What is the parietal pericardium?

A

the outer fibrous percardium that attached the heart to the diaphragm.

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2
Q

Epicardium

A

i.e. visceral pericardium, serous membrane that provides small amount of lubricating fluid within pericardial cavity between the two membranes. Facilitates heart movement.

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3
Q

Myocardium

A

middle layer. Cardiac muscle cells. L ventricular wall thickest.

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4
Q

Endocardium

A

inner wall of the heart. forms the heart valves.

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5
Q

Atriventicular valves

A

atria from ventricles. Right side tricuspid, left bicuspid.

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6
Q

Semilunar valves

A

aortic and pulmonary valves

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7
Q

How does cardiac muscle differ from skeletal muscle?

A

multinucleated, involuntary, has intercalated discs, autonomic, doesn’t store calcium, no nerves in cardiac muscle (there is more here, double check)

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8
Q

SA node

A

initiates impulses “pacemaker” of the heart. Wall of R atrium. Initiates sinus rhythm (70bpm) - can be altered by ANS and hormones like epinephrine

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9
Q

AV node

A

floor of R atrium, slight delay in conduction to allow for filling,

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10
Q

AV bundle

A

impulse from AV node continues to left and right bundle branches

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11
Q

Purkinje fibers

A

terminal network of fibers, simultaneous contraction of two ventricles.

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12
Q

ECG:
P wave
QRS wave
T wave

A

Contraction of atria
Depolarization of ventricles (masks atrial repolarization)
Repolarization of ventricles

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13
Q

Where is the cardiac control center?

A

Medulla oblongata, controls rate and force of contraction.

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14
Q

Baroreceptors

A

detect changes in BP, located in aorta and internal carotid.

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15
Q

Sympathetic stimulation of the heart

A

Cardiac accelerator - increases HR & contractility, beta-1 adrenergic receptors (important for some drugs like beta blockers)

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16
Q

Parasympathetic stimulation of the heart

A

CN X - vagus

decreases HR

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17
Q

Factors that increase HR

A 
increased thyroid hormone or epinephrine
elevated body temperature/increased environmental temperature
exertion/exercise
smoking
stress response
pregnancy
pain
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18
Q

What are the two major arteries?

A

Right & Left coronary arteries, part of systemic circulation, branch of aorta distal to aortic valve.

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19
Q

Left coronary artery divides into

A

Left anterior descending (interventricular) - supplies anterior wall of of ventricles, anterior septum, and bundle branches
Left circumflex - supplies L atrium, lateral/posterior walls of L ventricle

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20
Q

Obstruction of the L coronary artery leads to..

A

disturbances in the pumping capability of L ventricle, leads to CHF.

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21
Q

R coronary artery divides into

A

right marginal
posterior interventricular artery
Supplies R side of heart and inferior portion of L ventricle and posterior interventricular septum. SA & AV node.

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22
Q

Obstruction of R coronary artery

A

disturbances of AV node, dysrhythmias.

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23
Q

When in blood flow in the myocardium greatest?/reduced?

A

greatest - diastole

reduced - systole

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24
Q

How does most of the blood return into the heart

A

via coronary sinus emptying into R atrium.

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25
Q

Cardiac cycle

A

Atria relaxed (fills with blood) –> AV valves open –> blood flow into ventricles –> atria contract remaining blood forced into ventricles –> atria relax –> ventricles contract –> AV valves close/semilunar valves open –> blood into aorta and pulmonary artery –> ventricles relax

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26
Q

“Lub” “dub”

A

closure of AV valves (beginning of systole), closure of semilunar valves respectively (w/ ventricular diastole)

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27
Q

Murmurs

A

Caused by incompetent valves

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28
Q

Pulse deficit

A

Difference in rate between apical and radial pulses

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29
Q

Cardiac output

A

Blood ejected by a ventricle in 1 minute

CO = SV x HR

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30
Q

Stroke volume

A

Volume of blood pumped out of 1 ventricle in 1 contraction.

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31
Q

Cardiac reserve

A

ability of the heart to increase output in response to increased demand

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32
Q

Preload

A

Amount of blood delivered to heart by venous return. Mechanical state of the heart at teh end of diastole with the ventricles at their max volume

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33
Q

Afterload

A

Force required to eject blood from ventricles
(Determined by peripheral resistance in arteries).
Increased by high diastolic pressure resulting from excessive vasoconstriction.

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34
Q

Normal blood pressure

A

120/70 mmHg @ rest

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35
Q

Systolic pressure

A

Exerted when blood is ejected from ventricles (high)

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36
Q

Diastolic pressure

A

Sustained pressure when ventricles relax (lower)

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37
Q

What is BP altered by?

A

Cardiac output, blood volume/viscosity, venous return, rate and force of heart contractions, elasticity of arteries, and peripheral resistance to blood flow.

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38
Q

Pulse pressure

A

Difference between systolic and diastolic

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39
Q

Hormones affecting BP

A

ADH - increase BP
Aldosterone - increase BV increase BP
Renin-angiotensin-aldosterone - vasoconstriction/increase BP

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40
Q

SNS & epinephrine at beta-1 adrenergic receptors do what?

A

Increase both rate and force of contraction.

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41
Q

SNS, epinephrine and norepinephrine increase what?

A

vasoconstriction by stimulating alpha 1 receptors in the arterioles of skin and viscera (increases venous return)

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42
Q

General treatment measures for cardiac disorders

A

Dietary modification, regular exercise program, cessation of smoking, drug therapy

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43
Q

Arteriosclerosis

A

General term for all types of arterial changes , loss of elasticity, lumen gradually narrows, cause of increased BP

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44
Q

Atherosclerosis

A

Differentiated by the presence of atheromas that form in large arteries.

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45
Q

Atheroma

A

plaques consisting of lipids, cells, fibrin, and cell debris, often with attached thrombi. Presence of turbulent blood floe (esp at bifurcations) encourage development.
Primary sites: abdominal aorta, femoral and iliac arteries.

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46
Q

Low density lipoproteins

A

LDL - transports cholesterol from liver to cells “bad” lipoprotein (high lipid content), major contributor to atheroma formation.

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47
Q

High density lipoproteins

A

HDL - transports cholesterol away from the peripheral cells to the liver “good” low lipid content. Catabolism and excretion in the liver.

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48
Q

Process for atherosclerosis

A

Begins with endothelial injury of artery, inflammation in area, elevated c-reactive protein, WBC and lipids accumulate in the intima & media, smooth muscle cells proliferate, plaque forms/inflammation persists, platelets adhere to rough damaged surface, lipids/fibrous tissue continue to build up, arterial flow becomes turbulent, cycle continues until there is total occlusion.

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49
Q

Non-modifiable risk factors for atherosclerosis

A

Age (> 40), gender (men), genetic/familial

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50
Q

Modifiable risk factors for atherosclerosis

A 
Obesity/diets high in cholesterol/animal fat. 
Sedentary
Smoking
DM
Poorly controlled hypertension
Oral contraceptives + smoking
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51
Q

Angina Pectoris

A

Deficit of oxygen to the heart muscle. Chest pain can occur in different patterns: classic/exertional, variant (vasospasm at rest), unstable (prolonged pain at rest). Generally no permanent damage to myocardium unless episodes are frequent, prolonged and severe.

52
Q

S/S Angina Pectoris

A

Recurrent, intermittent brief episodes of substernal chest pain
Triggered by physical or emotional stress
Pallor, diaphoresis, nausea

53
Q

Emergency Tx of angina pectoris

A 
Rest/stop activity
Pt seated in upright position
Sublingual nitroglycerin
check pulse/respiration
administer O2
if Hx 2nd dose NTG if pain > 5 min
if 1st time emergency medical aid after 1 min w/o pain relief
54
Q

Myocardial Infarction

A

Occurs when coronary artery is totally obstructed. Atherosclerosis is the most common cause. Size and location of the infarct determine damage

55
Q

Warning Signs of MI

A

Feeling of sudden pressure, heaviness, burning in chest (esp with increased activity)
Sudden SOB, weakness, fatigue
Nausea, Indigestion
Anxiety/Fear
Pain may occur & IF present usually substernal, crushing/radiating (L arm, shoulder, jaw, or neck)

56
Q

Complications of MI

A

Sudden death, cocaine usage, cardiogenic shock, CHF

57
Q

Cardiac Dysrhythmias/Arrhythmias

A

Deviations from normal cardiac rate or rhythm.

Caused by damage to hearts conduction system or systemic changes.

58
Q

Sinus node abnormalities

A

Bradycardia (

59
Q

What is the most common dysrhythmia?

A

Atrial conduction

60
Q

Premature atrial contractions or beats

A

extra contractions (ectopic beats), arise from focus of irritable atrial muscle cells outside the conduction pathway, sometimes people feel palpitations.

61
Q

Atrial flutter

A

Atrial HR of 160 to 350 BPM, AV node delays conduction - ventricular rate slower

62
Q

Atrial fibrillation

A

Rate over 350 bpm. Causes pooling of blood in the atria. Thromubs formation is a risk.

63
Q

Are atrial arrhythmias always symptomatic?

A

No, not always because ventricular filling isn’t totally dependent on atrial contraction. SO unless it spreads to ventricular conduction pathways it may be asymptomatic.

64
Q

AV node abnormalities

A

Heart blocks - conduction excessively delayed or stopped at AV node or bundle of His

65
Q

First degree heart block

A

Conduction delay between atrial and ventricular contractions (PR interval)

66
Q

Second degree heart block

A

Every second to third atrial beat dropped at AV node (partial-longer delays lead periodically to a missed ventricular contraction)

67
Q

Third degree heart block

A

No transmission from atria to ventricles.

Ventricles contract spontaneously @ slow rate totally independent of atrial contraction

68
Q

Bundle-branch block

A

interference with conduction in one of the bundle branches. Does not alter CO but does appear on ECG as wide QRS wave.

69
Q

V-tach

A

likely to reduce CO as reduced diastole occurs

70
Q

V-fib

A

muscle fibers contract independently and rapidly, cardiac standstill occurs if not treated immediately.

71
Q

PVC

A

additional beats from ventricular muscles or ectopic pacemaker, may lead to v-fib

72
Q

Cardiac arrest or Standstill (asystole)

A

Cessation of all heart activity, loss of consciousness, respiration ceases.

73
Q

Reasons for cardiac arrest

A

Excessive vagal nerve stimulation, potassium imbalance, cardiogenic shock, drug toxicity, insufficient oxygen, respiratory arrest, blow to heart

74
Q

Congestive Heart Failure

A

heart unable to pump out sufficient blood to meet metabolic demands of the body. Usually one side of the heart fails first, then the other.

75
Q

L ventricle affected first with ___

A

w/ MI in L ventricle, or essential HTN

76
Q

R ventricle affected first with ___

A

pulmonary valve stenosis or pulmonary disease

77
Q

Compensations for CHF initially

A

reduced blood flow to systemic circulation
SNS response
Chambers of heart dilate and cardiac muscle hypertrophies.

78
Q

What happens when the heart cannot maintain pumping capability?

A

CO or SV decreases so less blood to organs/tissues, decreased cell function, fatigue & lethargy, mild acidosis develops
Backup and congestion develop as coronary demands for O2 and glucose are not met

79
Q

Forward effects of CHF

A

decreased blood supply to the tissues, general hypoxia, fatigue and weakness, dyspnea and SOB.

80
Q

Compensation mechanisms of CHF

A

tachycardia, cutaneous and visceral vasoconstriction, daytime oliguria

81
Q

Backup effects of L sided CHF

A

pulmonary congestion, dyspnea and orthopnea (fluid accumulates in lungs while laying down), cough, paroxysmal nocturnal dyspnea, infections like pneumonia

82
Q

Signs of R sided CHF/systemic back up

A

dependent edema in feet/legs/buttocks. Increased pressure in jugular veins leads to distention, hepatomegaly, splenomegaly, ascites (fluid in peritoneal cavity, marked abdominal distention)

83
Q

Acute right sided failure (CHF)

A

flushed face, distended neck veins, HA, visual disturbances

84
Q

Congenital heart defects

A

valvular defects, septal defects, shunts or abnormalities in position or shape of large vessels.

85
Q

Cardiac anomalies

A

Structural defects in the heart that develop during the first 8 weeks of embryonic life

86
Q

How are congenital heart defects detected?

A

Detected by the presence of heart murmurs

If untreated, child may develop heart failure.

87
Q

S/S large defects

A

Pallor
Tachycardia
Occurs with very rapid sleeping pulse and frequent pulse deficit
Dyspnea on exertion
Squatting position—toddlers and older children
Appears to modify blood flow, more comfortable
Clubbed fingers
Intolerance for exercise and exposure to cold weather
Delayed growth and development

88
Q

L –> R shunt

A

blood recycled to R side of heart & lungs. Increased volume in pulmonary circulation, decreased CO

89
Q

R –> L shunt

A

deoxygenated blood from R enters the L. Often cyanotic.

90
Q

What is the most common congenital heart condition?

A

Ventricular septal defect

91
Q

Ventricular septal defect

A

Opening in IV spetum, usually L to R shunt. Usually acyanotic

92
Q

Valvular defects

A

usually affect aortic and pulmonary valves.

93
Q

How are Valvular defects classified?

A

Stenosis or valvular imcompetence

94
Q

Stenosis

A

Narrowing of the valve restricts forward flow of blood

95
Q

Valvular incompetence

A

failure of valve to close completely, blood regurgitates

96
Q

Mitral valve prolapse

A

common. Abnormally enlarged and floppy valve leaflets - balloon backward with pressure. permits regurgitation of blood

97
Q

Tetralogy of Fallot

A

most common cyanotic defect. shunt bypasses pulmonary circulation.
Includes: pulmonary valve stenosis, VSD, dextroposition of the aorta (to the right over VSD), right ventricular hypertrophy

98
Q

Pathophys of ToF

A

pulm valve stenosis restricts outflow from R venticle, R ventricle hypertrophy/high pressure in R vent, R–>L shunting through VSD, flow of O2 blood into systemic circ thru aorta

99
Q

End result of ToF

A

Pulm circ gets small amnt unoxy blood from R vent, Systemic circ recieves larger amnt blood consisted of mixed oxygenation.

100
Q

Rheumatic fever

A

Acute systemic inflammatory condition. May result from abnormal immune reaction can occur a few weeks after untreated infection. involves hear joint/skin. ages 5-15.

101
Q

Acute stage Rheumatic fever

A

percarditis, myocarditis, endocarditis/incompetent heart valves (mitral usually)

102
Q

Other sites of inflammation with acute Rheumatic fever

A

large joints (legs), skin, nontender subcutaneous nodes, basal nuclei in brain (Involuntary jerky movement of the face, arms, legs)

103
Q

S/S Rheumatic fever

A

Low-grade fever, leukocytosis, malaise, anorexia, fatigue, tachycardia

104
Q

Infective endocarditis (subacute)

A

defective heart valves invaded by organisms of low virulence (Streptococcus viridans - normal flora in the mouth)

105
Q

Infective endocarditis (acute)

A

normal heart valves attacked by highly virulent organisms (Staphylococcus aureus) which tend to cause severe tissue damage and may be difficult to treat.

106
Q

Factors that predispose to infection by endocarditis

A

presence of abnormal tissue in heart, bacteremia, reduced host defenses

107
Q

S/S acute endocarditis

A

sudden, marked onset (spiking fever, chills, drowsiness)

108
Q

S/S Subacute endocarditis

A

insidious onset, increasing fatigue, anorexia, cough and dyspnea, intermittent low grade fever or fatigue, anorexia, splenomegaly, oslers nodes, CHF

109
Q

Pericarditis

A

Usually secondary to another condition. Classified by type of exudate associated with the inflammation.

110
Q

Acute pericarditis

A

may involve simple inflammation of the pericardium, may be secondary to open heart Sx, MI, Rheumatic fever, SLE, cancer, renal failure, trauma, viral infection.
Effusion may develop, large volume of fluid accumulates in pericardial sac, leads to distended neck veins, faint heart sounds, pulsus paradoxus.

111
Q

Chronic pericarditis

A

Results in formation of adhesions between the pericardial membranes, limiting movement of the heart, reduced CO, causes fatigue, weakness, abdominal discomfort,

112
Q

Hypertension

A

High BP, common. 3 major classifications

113
Q

3 major classifications of hypertension

A

Primary (essential), Secondary, Malignant or resistanct

114
Q

Primary (essential) hypertension

A

Idiopathic. BP consistently above 140/90. increase in arteriolar vasoconstriction. Increase in peripheral resistance, increases afterload substantially.
Decreased blood flow to the kidneys (increased renin, angiotensin, and aldosterone which further promote vasoconstriction, damage to arterial walls

115
Q

Secondary hypertension

A

Results from renal or endocrine disease benign tumor of adrenal gland (pheochromocytoma)

116
Q

Malignant or resistant

A

uncontrollable, severe, and rapidly progressive form with many complications, diastolic pressure is extremely high.

117
Q

Areas most frequently damaged by hypertension

A

Kidneys, heart, brain, retina

118
Q

How is essential hypertension treated?

A

In steps:

lifestyle changes, reduction of sodium intake, weight reduction, reduction of stress, drugs

119
Q

Shock (hypotension)

A

results from decreased circulating blood volume –> decreased tissue perfusion, general hypoxia

120
Q

Hypovolemic shock

A

loss of circulating blood volume

121
Q

Cardiogenic shock

A

inability of heart to maintain cardiac output to circulation

122
Q

Obstructive shock

A

subcategory of cardiogenic shock, interference with blood flow through the heart.

123
Q

Distributive, vasogenic, neurogenic, septic, or anaphylactic shock

A

changes in peripheral resistance leading to pooling of blood in the periphery.

124
Q

Early manifestations of shock

A

thirst and agitation. followed by anxiety, tachycardia, pallor, light headedness, syncope, sweating, oliguria.

125
Q

Compensation mechanism for shock

A

SNS and adrenal medulla stimulated, Renin secretion, ADH and glucocorticoids increased. Acidosis increases respiration.

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