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Pathophysiology > Ch. 8 (cardiovascular system) > Flashcards

Ch. 8 (cardiovascular system) Flashcards

1
Q

Layers of the heart

A

Pericardium: double-walled sac surrounding the heart
Epicardium (outer): CT, coronary arteries
Myocardium (middle): thick muscle
Endocardium (inner): smooth endothelium lining chambers

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2
Q

Right side of heart

A

RA, RV
pulmonary pump
circulates blood into pulmonary arteries and lungs

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3
Q

Left side of heart

A

LA, LV
systemic pump
circulates blood into aorta, organs, tissues

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4
Q

Atrioventricular valves

A

Tricuspid and Bicuspid (mitral) valves

flap-like, between atria and ventricles, prevents black-flow to atria when ventricles contract

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5
Q

Semilunar valves

A

pulmonary and aortic valve

cup-shaped, surround orifices of aorta and pulmonary artery, free margins of valves face upward, prevent back-flow into ventricles during diastole

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6
Q

pulmonary valve

A

directs blood flow from RV to pulmonary trunk

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7
Q

aortic valve

A

directs blood flow from LV to aorta

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8
Q

Describe the blood flow through the heart including valves that are encountered.

A 
Pulmonary circulation
Oxygen-poor blood enters Right Atrium --> 
Tricuspid valve -->
Pulmonary arteries --> 
Lungs 
Systemic circulation  
Oxygenated blood in lungs --> 
Pulmonary veins --> 
Left Atrium --> 
Mitral valve --> 
Aorta -->
Rest of body
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9
Q

What is the purpose of the coronary circulation?

A

main blood supply of the heart

  • Aorta branches to right and left coronary arteries carry arterial blood to the heart when relaxed
  • Blood passes through capillary beds of myocardium
  • Venous blood collected by cardiac veins
  • Cardiac veins join together and form the coronary sinus that empties blood into the RA
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10
Q

Right coronary artery (RCA)

A

Supplies posterior wall and posterior part of interventricular septum

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11
Q

Left anterior descending artery (LAD)

A

Supplies anterior wall, anterior part of interventricular septum

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12
Q

Left circumflex artery (LCA)

A

supplies lateral walls

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13
Q

LCA branches

A

LAD and LCA

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14
Q

Does adult cardiac muscle proliferate to replace damaged or destroyed muscle fibers?

A

NO

Most areas of cell death are repaired with non-contractile scar tissue

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15
Q

In what order does current flow through the cardiac conduction system?

A

ORDER:

  1. Sinoatrial node (SA node)
  2. Atrioventricular node (AV node)
  3. Bundle of His (AV bundle)
  4. Right and left bundle branches
  5. Purkinje fibers
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16
Q

How does the cardiac conduction system work?

A
  • A group of specialized muscle cells that initiate electrical impulses
  • Impulses are initiated in the SA (sinoatrial node) in RA near opening of the superior vena cava
  • Ability of cardiac muscle to depolarize and contract is intrinsic; does not depend on the nervous system
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17
Q

systole

A

contraction

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18
Q

diastole

A

relaxation
atria fill
all valves closed

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19
Q

atrial systole

A

increased atrial pressure causes atrial contraction, forcing blood into ventricles

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20
Q

atrial diastole / ventricular systole

A
  • AV valves close as pressure rises in ventricles
  • Atria relax
  • SL valves open when intraventricular pressures exceed pressure in aorta and pulmonary artery
  • Blood from LV enter pulmonary trunk
  • Blood from RV enters Aorta
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21
Q

ventricular diastole

A
  • Semilunar (SL) valves closed
  • Venous blood returning to atria, flows into ventricles through open atrioventricular (AV) valves
  • Additional blood pumped into ventricles during atrial systole
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22
Q

different types of blood vessels

A

Large elastic arteries: conduct the blood to various locations throughout the body.

Arterioles: smaller vessels with muscular walls that regulate flow from the large arteries into the capillaries.

Capillaries: thin endothelium-lined channels that deliver nutrients to cells and remove waste products.

Veins: return blood to the heart under low pressure and usually travel with the arteries.

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23
Q

systolic BP

A

pressure during ventricle contraction (highest BP)

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24
Q

diastolic BP

A

pressure during ventricular relaxation (lowest BP)

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25
Q

ECG and uses

A

measures electrical activity of heart; used as a diagnostic tool; detects disturbances in rate, rhythm, conduction, muscle injury, extent of muscle damage

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26
Q

P wave

A

atrial depolarization by SA node

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27
Q

PQ segment

A

delay at AV node when atrial depolarization is complete

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28
Q

QRS complex

A

ventricle depolarization and atrial repolarization

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29
Q

ST segment

A

ventricle depolarization is complete

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30
Q

T wave

A

ventricular repolarization

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31
Q

depolarization

A

contraction, systole

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32
Q

repolarization

A

relaxation, diastole

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33
Q

Arrhythmia

A

any deviation from the normal heartbeat, i.e., the normal sinus rhythm

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34
Q

signs / symptoms of arrhythmias

A
  • Palpitations
  • Tachycardia
  • Bradycardia
  • Skipped heartbeats
  • Syncope
  • Fatigue
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35
Q

Etiology of arrhythmias

A
  • Results when there is interference within the conduction system of the heart
  • Ischemia and drugs cause many arrhythmias
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36
Q

normal sinus rhythm

A
  • ECG that is within normal limits with a heart rate between 60-100 bpm
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37
Q

sinus bradycardia

A

A regular rhythm with a heart rate of <60 bpm

This may be normal in an athlete

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38
Q

sinus tachycardia

A

A regular rhythm with a heart rate of >100 bpm

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39
Q

atrial fibrillation (A-fib)

A
  • Multiple areas of atrial depolarization
  • extremely rapid, incomplete atrial contractions of 400-500 bpm
  • Only some of these impulses reach the ventricles
  • Causes ventricles to beat irregularly at 140-160 bpm
  • Atria quiver
  • seen in older people and those with CVD, COPD, hyperthyroidism
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40
Q

A-fib ECG

A

small, irregular, and uncoordinated P waves that cannot be distinguished; ventricular contraction also occurs at irregular intervals

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41
Q

A-fib treatment

A
  • Slow down heart rate
  • electrical cardioversion or pharmacologic therapy
  • Anticoagulation
  • Left atrial appendage occlusion device (Watchman device)
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42
Q

Premature Ventricular Contractions (PVCs) and causes

A

one of the most common and least harmful arryhthmias

causes:
- Lack of Sleep
- Caffeine
- Nicotine
- Alcohol
- Anxiety/Stress

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43
Q

Premature Ventricular Contractions (PVCs) ECG

A
  • Characterized by a beat that comes early in the cycle, has no P wave, a wide QRS complex, and a different T wave
  • The PVC is followed by a pause before the occurrence of the next normal cycle
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44
Q

Ventricular tachycardia (V-tach)

A
  • Seen in patients with cardiac disease

- life threatening and can rapidly deteriorate into ventricular fibrillation and cardiac arrest

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45
Q

Ventricular tachycardia (V-tach) ECG

A
  • Characterized by 3 or more PVCs that occur at a rate of 150-250 bpm
  • There are no P waves and the QRS complexes are distorted
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46
Q

Ventricular Fibrillation (V-fib) and ECG

A
  • One of the more serious arrhythmias
  • Rapid and uncoordinated ventricular beat
  • Heart cells are contracting spontaneously and the heart just quivers
  • It is totally ineffective for pumping blood and will quickly lead to death if not corrected
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47
Q

Cardiac arrest, symptoms, etiology, and treatment

A

Sudden, unexpected cessation of cardiac activity

Symptoms: patient is unresponsive, with no respiratory effort and no palpable pulse

Etiology: results from anoxia or interruption of the electrical stimuli to the heart

Treatment:

  • CPR must be initiated within 4-6 minutes
  • Defibrillation
  • Epinephrine or dobutamine to stimulate the heart
  • Antiarrhythmic drugs (lidocaine, amiodarone)
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48
Q

treatments for arrhythmias

A

Depends on the cause:

  • Anti-arrhythmic drugs
  • Anticoagulants
  • oxygen
  • Cardioversion (defibrillation)
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49
Q

who invented the defibrillator

A

Dr. Bernard Lown, MD

nobel prize in 1985

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50
Q

What are the 2 types of valvular malfunction?

A
  1. stenosis

2. insufficiency (incompetence, regurgitation)

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51
Q

Stenosis and common causes

A
  • Hardening of cusps of valves that prevents complete opening of valves
  • Impedes blood flow into next chamber
  • Causes the heart to have to work harder to pump blood forward

Common causes:

  • Rheumatic heart disease
  • Infective endocarditis
  • Congenital malformations
  • Calcification of the valve cusps
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52
Q

Insufficiency (incompetence, regurgitation)

A
  • Failure of valves to close completely
    (Allows blood to be forced back into the previous chamber as the heart contracts)

-This exerts added pressure on that chamber and overloads the heart
(Ultimately the ventricle will dilate and fail)

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53
Q

Rheumatic fever

A

an immunologic reaction that develops weeks after initial streptococcal infection (NOT a bacterial infection)

  • Commonly encountered in children
  • Complication of group A beta hemolytic streptococcal infection (sore throat and scarlet fever)
  • Anti-streptococcal antibodies against strep antigens cross react with similar antigens in tissues
  • Antigen-antibody reaction injures connective tissue and causes fever
54
Q

Rheumatic fever signs and symptoms

A
  • Fever
  • Inflammation of connective tissue throughout the body, especially heart and joints
  • Acute arthritis (multiple joints)
  • Inflammation of heart
55
Q

Rheumatic fever clinical outcomes

A
  • Death from severe inflammation and acute heart failure
  • Healing with scarring of tissues (heart valves)
  • Can recur if another streptococcal infection reactivates hypersensitivity and tissue damage
56
Q

Rheumatic fever treament

A

After the development of rheumatic fever:
o Antibiotics
o Anti-inflammatory agents (NSAIDs and steroids)
o Antipyretics (fever reducers)

57
Q

Rheumatic heart disease / cause

A

complication of rheumatic fever; primarily affects mitral and aortic valves

  • In acute disease, valves become red, thickened, and swollen
  • Inflammatory damage produces scarring causing stenosis or incompetence
58
Q

Rheumatic heart disease prevention

A
  • Treat beta strep infection promptly
  • Prophylactic penicillin to prevent strep infections, reduce risk of recurrent rheumatic fever and further heart valve damage
59
Q

mitral stenosis, etiology, treatment

A
  • Most common of all valve diseases
  • Impairs the passage of blood from the left atrium to the left ventricle

Etiology: rheumatic heart disease

Treatment:

  • Diuretics
  • Anticoagulants
  • Surgical intervention includes commissurotomy, balloon valvuloplasty, valve replacement
60
Q

two types of non-rheumatic aortic stenosis

A

Type 1: Aortic stenosis secondary to bicuspid aortic valve

Type 2: Calcific aortic stenosis

61
Q

Type 1: Aortic stenosis secondary to bicuspid aortic valve

A
  • Aortic valve has 2 cusps than usual 3 cusps
  • Functions satisfactorily for a time, then becomes thickened, calcified, and rigid from increased strain on valve, leads to heart failure
  • Occurs in 2% of population (RARE)
62
Q

Type 2: Calcific aortic stenosis

A

Common valvular heart disease:

  • Normal 3 cusps
  • Leaflets undergo connective tissue degenerative changes → fibrotic, calcified, rigid → restricts valve mobility, stenosis
  • Recent studies: also occurs with deposits of lipids and macrophages as in coronary atherosclerosis
63
Q

clinical outcomes, of non-rheumatic aortic stenosis

A

Clinical outcomes:

  • increased strain
  • left ventricular hypertrophy
  • heart failure
64
Q

prevention and treatment of non-rheumatic aortic stenosis

A

Prevention: Control risk factors (high cholesterol, diabetes, hypertension, smoking)

Treatment:
• Digitalis can be used as an inotropic agent
• Anticoagulants
• Balloon valvuloplasty and valve replacement

65
Q

Mitral valve prolapse

A
  • Fairly common
  • One or more of the cusps of the mitral valve protrudes back into the left atrium during ventricular contraction
  • Prolapsing leaflets may not fit together tightly → blood leaks back into LA; mitral regurgitation
  • Usually a benign, asymptomatic condition and does not require treatment
66
Q

Etiology of mitral valve prolapse

A
  • Abnormally long or short chordae tendineae may not allow the valve to close properly
  • Malfunctioning papillary muscles
67
Q

Infective endocarditis and what it can cause

A
  • Bacterial endocarditis is most common
  • Vegetations: build up of large, easily fragmented infective masses

Can cause:

  • Erosion of valve leaflets
  • Seeding of the blood with infective agent
  • Embolization
68
Q

Subacute infective endocarditis and symptoms

A

Caused by organisms of low virulence

Affects abnormal or damaged (mitral, aortic valves)

Platelets and fibrin may deposit on abnormal or damaged valves; then serve as sites for bacteria to implant or for thrombi to form followed by emboli and tissue infarction

Mild symptoms of infection

69
Q

Prophylactic antibiotics are given prior to dental or surgical procedures to prevent

A

Subacute and actute infective endocarditis

70
Q

Acute infective endocarditis, symptoms, at risk groups

A
  • Caused by highly pathogenic organisms, commonly staphylococci
  • Affects normal heart valves
  • Severe symptoms of infection and valve destruction
  • at risk groups: intravenous drug
71
Q

treatment and prevention for acute infective endocarditis

A
  • IV anti-infective therapy
  • Antipyretics
  • Anticoagulants
  • surgical repair or replacement of valves

prevention: prophylactic antibiotics given prior to dental or surgical procedures

72
Q

hypertension and how it develops

A

Elevated blood hydrostatic pressure in the systemic arterial system

Excessive vascoconstrition of small arterioles resulting in:
o Increased peripheral resistance –> increased diastolic blood pressure
o Results in an increased force of ventricular contraction –> Compensatory increase in systolic pressure

73
Q

BP categories:

  • normal
  • elevated
  • hypertension stage 1
  • hypertension stage 2
A

normal: <120/<80 max
elevated: 120-129/<80
stage 1: 130-139/80-89
stage 2: >140/90

74
Q

hypertension treatment goal and symptoms

A

<130/80 for most people, depending on:

  • Calculated 10-year risk for heart disease and stroke
  • Other medical conditions of patient

usually asymptomatic

75
Q

risk factors of hypertension

A
  • Genetics
  • Race
  • Increased age
  • Smoking
  • Obesity
  • Stress
  • Sedentary lifestyle
76
Q

Primary/essential Hypertension (HTN)

A

90-95% of cases
IDIOPATHIC CAUSE

  • Thought to be due to some defect in the blood pressure control mechanism
  • Has an insidious onset, with few if any symptoms until permanent damage has occurred
77
Q

Secondary Hypertension and examples of causes

A

some other specific disorder is identified as the cause of elevated BP

Kidneys: chronic kidney disease

excessive hormone levels: pituitary or adrenal tumor, hyperthyroidism

78
Q

Consequences of systemic hypertension (cardiac, vascular, renal)

A

Cardiac effects: increased peripheral resistance → higher workload → heart enlarges → heart failure

Vascular effects: increased pressure → premature wearing out of vessels; accelerates atherosclerosis; injury to arterioles → weakened areas may rupture and hemorrhage
( linked to strokes and heart attacks)

Renal effects: narrowed renal arterioles → decreased blood supply to kidneys → injury and degenerative changes in glomeruli and tubules → renal failure

79
Q

treatment of hypertension

A
  1. reduce unfavorable factors
  2. drugs therapies:
    - diuretics
    - beta blockers
    - ACE inhibitors
    - Angiotensin receptor blockers (ARBs)
    - calcium channel blockers
    - vasodilators
80
Q

diuretics

A

enhance fluid loss and reduce circulating blood volume

81
Q

beta blockers

A

block sympathetic nervous system input to heart, slow heartbeat and force of contraction –> reduce cardiac output

82
Q

ACE inhibitors

A

inhibits the formation of angiotensin II

  • Reduces systemic vasoconstriction
  • Reduces aldosterone secretion
83
Q

Angiotensin receptor blockers (ARBs)

A

accomplish the same results as ACE inhibitors by blocking the receptors that angiotensin II work at

84
Q

calcium channel blockers

A

restrict the available calcium present in the smooth muscles of arterioles

  • Produces vasodilation
  • Also slows the heart rate
  • Reduces cardiac output
85
Q

vasodilators

A

directly dilate vessels

86
Q

What is myocarditis, what usually causes it, and what is the typical course of the disease?

A

Active inflammation of heart muscle associated with injury and necrosis of individual muscle fibers

  • Usually viral cause
  • Abrupt onset may lead to acute heart failure
  • Usually complete recovery
87
Q

primary cardiomyopathy

A

A non-inflammatory disease of the cardiac muscle resulting in enlargement of myocardium and ventricular dysfunction that occurs in the absence of other cardiac conditions

88
Q

Secondary cardiomyopathy

A

caused by a known medical condition (such as hypertension, valve disease, congenital heart disease, or coronary artery disease)

89
Q

Dilated cardiomyopathy

A
  • Diffuse degeneration of myocardial fibers leading to decreased contractile effort
  • Heart becomes enlarged and dilated, impairing ventricular action and leading to chronic heart failure
90
Q

etiology, symptoms, and treatment for dilated cardiomyopathy

A

Etiology: chronic alcoholism, an autoimmune process, or viral infections
(often idiopathic)

Symptoms: CHF

Treatment:

  • Control of the CHF
  • Cardiac glycosides
  • Diuretics
  • Anticoagulants
  • Vasodilators
91
Q

Hypertrophic cardiomyopathy

A
  • Disorganized muscle fibers
  • The left ventricular wall and interventricular septum hypertrophies / thickens
  • impedes flow into aorta
  • Thick septum blocks outflow from left ventricle
92
Q

etiology, symptoms, and treatment of Hypertrophic cardiomyopathy

A

Etiology: idiopathic, hereditary dominant transmission

Symptoms: as with CHF

Treatment (to reduce workload):

  • Beta blockers
  • Calcium channel blockers
  • Surgical resection of septum
93
Q

Fetal circulation: how blood flows through the foramen ovale and ductus arteriosus.

A

The shunt that bypasses the lungs is called the foramen ovale. This shunt moves blood from the right atrium of the heart to the left atrium. (right to left)

The ductus arteriosus moves blood from the aorta to pulmonary artery

94
Q

Why do congenital heart diseases usually occur, what are some causes, and how are they prevented?

A

Usually due to persistence of normal fetal blood channels or faulty embryologic development

ex) German measles, Down syndrome

causes: drugs, genetic factors
(over 90% are idiopathic)

Prevention: protect developing fetus from intra-uterine injury

95
Q

Left-to-right shunt

A

Blood is diverted from systemic circulation to the lungs

Causes pulmonary hypertension and damage lungs

96
Q

Right-to-left shunt

A

Blood is diverted from pulmonary circulation to systemic circulation

Blood is poorly oxygenated
Results in cyanosis, polycythemia, clubbing of fingers and toes

(immediately obvious after birth)

97
Q

What are the 4 main causes of congenital heart disease?

A
  1. Fetal bypass channels fail to close normally
  2. Atrial, ventricular, or combined septal defects
  3. Abnormalities obstructing flow
  4. Abnormal formation of the aorta and pulmonary artery of abnormal connection of vessels
98
Q

abnormalities obstructing flow examples (3)

A
  • Pulmonary stenosis
  • Aortic stenosis
  • Coarctation of the aorta
99
Q

Abnormal formation of the aorta and pulmonary artery or abnormal connection of vessels examples (2)

A
  • Tetralogy of Fallot

- Transposition of great vessels

100
Q

Fetal bypass channels fail to close normally examples (2)

A
  • Patent ductus arteriosus (PDA)

- Patent foramen ovale (PFO)

101
Q

Patent ductus arteriosus (PDA), type of shunting caused, symptoms, treatment, result of unrepaired)

A
  • The ductus arteriosus does not close after birth
  • Blood is shunted from aorta to pulmonary artery
  • Often asymptomatic
  • causes right-sided heart failure
  • PDAs may be surgically repaired w/suture
102
Q

Atrial Septal Defect (ASD), type of shunting caused, symptoms, treatment, result of unrepaired

A
  • Abnormal opening between the right and left atria
  • Blood is shunted from the left-to-right side (because left side is stronger)
  • Often goes undetected (asymptomatic) in childhood
  • Catheter closures with amplatzer
  • If unrepaired, will cause right-sided heart failure
103
Q

Ventricular septal defect (VSD), type of shunting caused, symptoms, treatment, result of unrepaired

A
  • Abnormal opening between the right and left ventricles
    [more problematic]
  • Blood is shunted from the left-to-right in large volumes
  • most common congenital defect of infancy

Symptoms:

  • Pulmonary congestion
  • Dyspnea
  • Fatigue
  • Susceptibility to pulmonary infections

Treatment:
- Closed surgically with a patch

If unrepaired: will cause right-sided CHF

104
Q

Coarctation of the Aorta

A
  • Narrowing of the aortic lumen causes a partial obstruction of the flow of blood
  • Occurs primarily in males
  • Large pressure gradient across narrowing
105
Q

symptoms and treatment of Coarctation of the Aorta

A

Symptoms:

  • Hypertension in the head and upper limbs
  • Hypotension in the abdomen and lower limbs
  • Left ventricular hypertrophy

Treatment:
- Repaired by surgically removing the defective area and reconstructing the aorta

If untreated, will cause left-sided CHF

106
Q

Tetralogy of Fallot, type of shunting caused, symptoms, treatment, result of unrepaired

A

Is a combination of four defects:

  1. Ventricular septal defect
  2. Pulmonary stenosis
  3. Displacement of the aorta
  4. Right ventricular hypertrophy
  • causes right-to-left shunting
  • Blood is diverted through the VSD to the systemic circulation and bypasses the lungs
  • Leads to cyanosis
  • Corrected surgically
107
Q

Transposition of the Great Vessels

A

The aorta and pulmonary arteries are reversed

  • aorta connected to RV
  • pulmonary valve connected to LV

Results in 2 closed-loop circulatory systems

Treatment: Prostaglandins are administered to keep the ductus arteriosus and the foramen ovale from closing

Blood flow is redirected by surgical correction

108
Q

Aneurysm

A

weakening of portion of arterial wall

and resulting local dilation or ballooning out

109
Q

Etiology of aneurysms

A
  • most common = build up of atherosclerotic plaque

- Congenital (usually the ones in the head)

110
Q

consequences of aneurysms (5)

A
  • Thrombosis
  • Thromboemboli
  • Pressure on adjacent structures (nerves, brain)
  • *Rupture
  • *Dissection
111
Q

symptoms of aneurysms

A

Depend on location and size

Often asymptomatic

112
Q

Abdominal aortic aneurysms

A

most common aneurysm

  • abdominal or back pain and a pulsating mass in the abdomen
  • May rupture leading to massive and fatal hemorrhage
  • Hard to detect clinically
  • high fatality
113
Q

Dissecting aneurysm of aorta and symptoms

A
  • Degenerative changes (tear) causes middle layer to lose cohesiveness and separate
  • Pressure forces blood through a tear and causes separation of the layers

Symptoms: severe chest and back pain

114
Q

How are aneurysms treated?

A
  • Depends on size, location, likelihood of rupture, surgical candidacy
  • surgical repair
    (May be done by replacing the damaged area with a synthetic graft, by endovascular stenting, or coiling)
  • If the aneurysm is small or the patient is not a good surgical candidate, watchful waiting is employed (regular ultrasounds)
115
Q

Thrombophlebitis

A

inflammation of a vein caused by or associated with the formation of a blood clot,

in the superficial leg veins

causes an interference with blood flow and resulting edema

116
Q

etiology of Thrombophlebitis

A
  • Disruptions in blood flow
  • Hypercoagulable state
  • Injury or infection to the venous wall
    (same as Virchod’s triad)
117
Q

symptoms and treatment of Thrombophlebitis

A

Symptoms;

  • Pain, swelling, and warmth in the affected
  • Involved area is tender to palpation
  • cord like

Treatment:

  • RICE /supportive care (if uncomplicated)
  • Antibiotic treatment (if sign of infection)
  • Anticoagulation (if risk of getting to deep circulation)
  • Heparin
118
Q

Varicose veins and etiology and at risk people

A
  • Dilated, tortuous, and knotted veins
  • Usually occur in superficial veins of the legs

Etiology: elevated venous pressure; dilation leads to failing of the valves (incompetent) and worsening of the problem

at risk: standing on feet a lot, obese, pregnant women

119
Q

symptoms and treatment of varicose veins

A

Symptoms:

  • fatigue in legs
  • dull ache
  • leg cramps at night
  • swollen ankles
  • thickening of veins
  • hurt to touch

Treatment:
- rest, elevate legs
- compression stockings
For superficial ones: injection of sclerosing agent
For big ones: vein stripping and ablation (newer)
- surgery (advanced)

120
Q

what comes first, rheumatic fever or rheumatic heart disease?

A

rheumatic fever

121
Q

joint arthritis, heart inflammation, systemic CT inflammation are symptoms of rheumatic fever of rheumatic heart disease?

A

rheumatic fever

122
Q

atherosclerosis often leads to the development of

A

aneurysm

123
Q

orthopnea

A

difficulty breathing when laying down

124
Q

symptoms of right side heart failure

A

peripheral edema and hepatosplenomegaly

125
Q

what is digitalis

A

cardiac glycoside

126
Q

angina is caused by

A

coronary heart disease

127
Q

most common symptom of hypertension

A

asymptomatic

128
Q

why is digitalis used to treat CHF?

A

increase contraction

raise stroke volume and cardiac output

129
Q

foramen ovale

A

The shunt/hole that bypasses the lungs

This shunt moves blood from the right atrium to the left atrium.

130
Q

Ductus arteriosus

A

Moves blood from aorta to the pulmonary artery

Pathophysiology (3 decks)

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