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CV487 > Class 2 CV > Flashcards

Class 2 CV Flashcards

1
Q

HF pathophysiology

A

Impaired pumping ability of the ventricle

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2
Q

-Hypotension or the presence of pulsus paradoxus is a blank and suggests what

A

A decrease in systolic blood pressure of > 10 mmHg with inspiration; suggests tamponade

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3
Q

Etiology of HF

A

-MI
-Cardiomyopathy
-Ischemia
-Congenital defects
-Cor pulmonale
-Hepatic dysfunction

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4
Q

Cor pulmonale

A

Right sided problem

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5
Q

Hepatic dysfunction

A

Right sided problem

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6
Q

HF is a blank problem whereas angina and MI’s are blank problems

A

HF is an inside problem, angina & MI’s are outside problems

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7
Q

Types of HF

A

Left sided & right sided

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8
Q

Left sided HF definition & common cause

A

Dysfunction of the left ventricle’s ability to pump
-Commonly caused by anterior MI

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9
Q

Right sided HF

A

-Dysfunction of the right ventricle
-Decreased blood being pumped to lungs

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10
Q

Left sided HF pathophysiology

A

-Impaired contractility
-Less contractility, leads to increase in Preload and afterload to compensate and provide an adequate CO that will perfuse the body
-Leads to sustained action of the RAAS and the SNS

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11
Q

Left sided HF characteristics (systolic vs diastolic)

A

-Systolic HF (contractility)
-Diastolic HF (preload)

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12
Q

Left sided HF manifestations

A

-Pulmonary vascular congestion
-SOB, orthopnea, coughing, fatigue, decreased urine output, and edema

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13
Q

Left sided HF assessment (neurological)

A

-LOC, lethargic, dizziness

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14
Q

Left sided HF assessment (CV)

A

-Heaves, pulsus alternans, tachycardia, possible S3 & S4

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15
Q

Left sided HF assessment (respiratory)

A

-Crackles, pulmonary edema, coughing, nocturnal dyspnea

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16
Q

Left sided HF assessment (renal)

A

-Urine output (usually low), 24 hr fluid balance, nocturia

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17
Q

Right sided HF pathophysiology

A

-Inability of the right ventricle into the pulmonary circulation

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18
Q

Right sided HF etiology

A

-Diffuse hypoxic pulmonary diseases such as CorPulmonale, MI
-Increased PVR inhibits RV pump causing it to dilate and fail, pulmonic valve dysfunction, left sided HF

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19
Q

Right sided HF manifestation

A

-Hepatomegaly, heaves, murmurs, weight gain, tachycardia, ascites, anasarca, right-sided pleural effusion

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20
Q

Right sided HF assessment (neurological)

A

LOC, lethargic, dizzy

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21
Q

Right sided HF assessment (CV)

A

RV heaves, JVD, RUQ pain (hepatomegaly), tachycardia, S3 or S4, slow cap refill

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22
Q

Right sided HF assessment (respiratory)

A

Crackles, pulmonary edema, tachypnea

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23
Q

Right sided HF assessment (GI)

A

Anorexia, nausea, bloating, ascites

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24
Q

Right sided HF assessment (renal)

A

Low urine output, 24 hour fluid balance

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25
Q

Labs to draw for HF

A

-Na+
-K+
-Kidney function (left sided), low urine output (increased K+)
-Troponin
-BNP (only relates to HF; stretching of ventricles)
-CRP (inflammatory markers)

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26
Q

Labs to draw for HF

A

-Na+
-K+
-Kidney function (left sided), low urine output (increased K+)
-Troponin
-BNP (only relates to HF; stretching of ventricles)
-CRP (inflammatory markers)

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27
Q

Ejection fraction

A

-HF with preserve ejection fraction (HFpEF): >50%
-HF with a mid-range ejection fraction (HFmEF): 41-49%
-HF with a reduced ejection fraction (HFrEF): <=40%

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28
Q

Pericardial disorders

A

-Pericardial disease is a localized manifestation of another disorder
-Can result in: Acute pericarditis, pericardial effusion, or constrictive pericarditis (develops over time)

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29
Q

Acute pericarditis etiology

A

-Idiopathic cause or viral infection

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30
Q

Common causes of acute pericarditis

A

-HIV
-MI
-Trauma
-Neoplasm
-Surgery
-Uremia
-Bacterial infection (especially Tuberculosis)
-Connective tissue disease such as systemic lupus erythematosus (SLE)
-Rheumatoid arthritis (RA)
-Radiation therapy

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31
Q

Acute pericarditis manifestations

A

-Low fever (< 38°C)
-Tachycardia, aBreathing (lying down is worse)
-Chest pain radiating to back
-Dysphagia, weakness and malaise

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32
Q

Acute pericarditis assessment (neuro)

A

LOC, numbness & tingling, fever, anxiety

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33
Q

Acute pericarditis assessment (CV)

A

-Friction rub, chest pain (progressive & sharp), pleuritic CP, decrease in CO, PR segment depression, ST segment elevation without Q waves

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34
Q

Acute pericarditis assessment (respiratory)

A

-Dyspnea d/t rapid & shallow breaths, tachycardia to compensate

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35
Q

Acute pericarditis labs

A

-Troponin
-WBC
-C reactive protein

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36
Q

Pericardial effusion lab tests

A

-Troponin
-WBC
-C reactive protein
-Platelets
-BUNs
-Na+
-Clotting factors

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37
Q

Cardiac tamponade lab tests

A

-Troponin
-WBC
-C reactive protein
-Platelets
-BUNs
-Na+
-Clotting factors
-Blood cultures

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38
Q

Pathophysiology of pericardial effusion

A

-Accumulation of fluid in the pericardial cavity that can occur in all forms of pericarditis
-If the effusion develops gradually the pericardium is able to stretch and accommodate large quantities without compressing the heart
-If the fluid accumulates rapidly (50 to 100ml), it can cause cardiac compression (tamponade)

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39
Q

Pericardial effusion manifestations (AP)

A

-Distant or muffled heart sounds
-Poorly palpable apical pulse
-Dyspnea on exertion
-Dull chest pain
-Pulsus paradoxus may indicate cardiac tamponade

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40
Q

Pericardial effusion assessment (neuro)

A

LOC, numbness & tingling, fever, anxiety

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41
Q

Pericardial effusion assessment (CV)

A

aHeart sounds, pulse deficits

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42
Q

Pericardial effusion assessment (respiratory) & what to monitor for

A

-SOB, cyanosis, aPerfusion, aSpO2
-Monitor for acute and significant changes with neurological, CV, and respiratory as it can lead to cardiac tamponade

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43
Q

Beck’s triad

A

-Used to diagnose cardiac tamponade
-Hypotension, JVD, and muffled heart sounds

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44
Q

Cardiac tamponade + breathing

A

Pain in the chest causes patient to breath quick & shallow

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45
Q

Cardiac tamponade pathophysiology, what may occur?

A

-Acute fluid accumulation in the pericardial space
-Can lead to the pressure exerted by the pericardial fluid equal to diastolic pressure within the heart chambers leading to impaired right atrial filling during diastole
-Decreased right atrial filling leads to decreased ventricular filling, decreased SV&CO….Life threatening circulatory collapse may occur

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46
Q

Cardiac tamponade manifestations

A

-Dyspnea, tachycardia, JVD, cardiomegaly, and pulsus paradoxus

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47
Q

Cardiac tamponade assessment (neuro)

A

-LOC, numbness & tingling, fever, anxiety

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48
Q

Cardiac tamponade assessment (CV)

A

-aHeart sounds, pulse deficits, JVD, peripheral edema, pulsus paradoxus

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49
Q

Cardiac tamponade assessment (respiratory)

A

aBreathing, SOB, cyanosis, aPerfusion

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50
Q

Cardiac tamponade assessment (GI)

A

Hepatomegaly

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51
Q

Infective endocarditis definition & cause

A

Inflammation of the endocardium due to bacteria such as streptococcus, staphylococcus, or enterococci

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52
Q

Risk factors contributing to infective endocarditis

A

-Valve disease, prosthetic heart valves, pacemakers, long-term indwelling catheters
-Congenital lesions ie. Septal defect
-Previous diagnosis of endocarditis
-IV drug use

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53
Q

Infective endocarditis manifestations

A

-Murmur, conjunctiva, petechial lesions (low platelets), splinter hemorrhages
-Weight loss, night sweats, back pain, HF
-Osler lesions (painful erythematous nodules on the pads of the fingers and toes); Janeway lesions (non-painful hemorrhagic lesions on the palms and soles)

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54
Q

Infective endocarditis assessment (Neuro)

A

LOC, dizziness, fever, numbness/tingling, aMotor power, signs of CVA (facial droop, weakness, aVision)

55
Q

Infective endocarditis assessment (CV)

A

Cyanotic, LV/RV heaves, JVD, RUQ pain (hepatomegaly), tachycardia, S3 and S4, slow cap refill

56
Q

Infective endocarditis assessment (respiratory)

A

Crackles, pulmonary edema, tachypneic

57
Q

Infective endocarditis (GI)

A

Anorexia, nausea, bloating, ascites

58
Q

Infective endocarditis assessment (renal)

A

Urine output, 24 hour fluid balance

59
Q

Infective endocarditis assessment (skin)

A

Petechiae, nodules

60
Q

Infective endocarditis labs to monitor

A

Hemoglobin, platelet, WBCs, clotting factors, BNP, Na+, K+

61
Q

Deep vein thrombosis pathophysiology

A

Thrombus to thromboembolism, Virchow’s triad

62
Q

Virchow’s triad

A

-Venous stasis
-Venous endothelial damage
-Hypercoagulable states

63
Q

DVT manifestations

A

-Thrombus may cause pain & redness
-Positive sign of DVT is pain during plantar flexion
-Thrombus can cause edema

64
Q

If left untreated, DVT

A

-Can break off into an embolism leading to PE
-Can lead to scarring & vein damage

65
Q

Pertinent labs for DVT

A

Platelets, WBC, clotting, electrolytes, kidney function and specialty labs

66
Q

DVT assessment

A

Palpate peripheral pulses

67
Q

Arterial diseases

A

-Aneurysm
-Spontaneous coronary artery dissection

68
Q

Aneurysm etiology

A

-75% occur in the abdominal aorta
-Atherosclerosis is the most common cause
-HTN can cause outpouching of a vessel wall or cardiac chamber
-Collagen-vascular disorders (Marfan’s syndrome), sphylis, and other infections

69
Q

The greater the pressure prior to the aneurysm

A

The worse the outcome

70
Q

True aneurysms

A

Involve all 3 layers of the arterial wall and is a extravascular hematoma that communicates with the intravascular space

71
Q

Aortic aneurysm manifestations

A

-Usually asymptomatic
-If located in the ascending aorta and the aortic arch, patients report hoarseness
-Dysphagia, dysrhythmias, dyspnea, distended neck veins
-Edema of the head and arms
-HF, bruits, ischemia
-Mobilization of clots

72
Q

Aortic aneurysm manifestations cont’d

A

-Pain upon rupture, abdominal or back pain
-Glucose syndrome: Pain in toes, feet are modeled but pulses still present
-AAA identified by a pulsatile mass in the periumbilical area slightly to the left of the midline

73
Q

Aortic aneurysm assessment (neuro)

A

Pain in the back or peripheries, inspect the abdominal area

74
Q

Aortic aneurysm assessment (CV)

A

Bruits, rule out other causes for dysphagia, pulses, color, capillary refill

75
Q

Aortic aneurysm assessment (GI)

A

Pain upon palpation

76
Q

Aortic aneurysm assessment (renal)

A

Monitor for renal failure

77
Q

Further complications of aortic aneurysms

A

-Dissection- Occurs when there is a tear in the intima and blood enters the wall of the artery…SURGICAL EMERGENCY! (dissection worse than aneurysm)
-Thrombus formation d/t possible pooling of blood at the aneurysm site

78
Q

A type dissection of aorta

A

-Develops in the ascending part of the aorta as it branches off the heart
-Worse than B type

79
Q

B type dissection of aorta

A

-Involves a tear in the descending part of the aorta and may extend into the abdomen

80
Q

Spontaneuos coronary artery dissection etiology and S&S

A

-S&S of AMI & cardiogenic shock
-Unknown etiology, possibly r/t fibromuscular disease

81
Q

Spontaneous coronary artery dissection

A

-Rare, mostly in females
-Triggered by the disruption of the intimal layer, a clot develops in the false lumen eventually occluding the true lumen

82
Q

Arterial thrombi threats to circulation

A

-Thrombus occludes the artery leading to tissue ischemia
-Thrombus dislodgement resulting in a thrombo-embolus occluding blood flow into a distal vascular bed

83
Q

Arterial thrombi lab values

A

All lab values are important

84
Q

Pediatric cardiovascular dysfunction

A

-Congenital heart disease (cyonatic and acyanotic)
-Acquired heart disease (Kawasaki disease & rheumatic fever)

85
Q

Acyanotic shunting of blood

A

Left to right

86
Q

Acyanotic cyanosis

A

Not usual (unless CHF)

87
Q

Acyanotic surgery

A

Usually done in one stage

88
Q

Acyanotic prognosis

A

Very good/excellent

89
Q

Acyanotic types

A

-Ventricular septal defect (VSD)
-Coarctation of the aorta (CoA)

90
Q

Cyanotic shunting of blood

A

right to left

91
Q

Cyanotic cyanosis

A

Always “blue babies”

92
Q

Cyanotic surgery

A

Usually done in several stages

93
Q

Cyanotic prognosis

A

Guarded

94
Q

Cyanotic types

A

Tetralogy of Fallot
-Transposition of the great arteries (TGA)

95
Q

Cyanotic babies

A

Are more sick than acyanotic

96
Q

Hemodynamic classification of congenital heart disease (acyanotic)

A

-Increased pulmonary blood flow; ventricular septal defect
-Obstruction to blood flow from ventricles; coarctation of aorta

97
Q

Hemodynamic classification of congenital heart disease (cyanotic)

A

-Decreased pulmonary blood flow; tetralogy of Fallot
-Mixed blood flow; transposition of great arteries

98
Q

Congenital heart disease (acyanotic) pathophysiology

A

-Defects with increased pulmonary blood flow
-Obstructive defects

99
Q

Defects with increased pulmonary blood flow

A

-Intra-cardiac communication along the septum or an abnormal connection between the great arteries allows blood to flow from the high-pressure left side of the heart to the low-pressure right side of the heart
-ie. Ventricular septal defect; hole in the septum

100
Q

Ventricular septal defect (VSD)

A

-An opening between the two ventricles allowing for unoxygenated blood to mix with oxygenated blood
-More common for oxygenated blood to mix with a small amount of unoxygenated blood

101
Q

Common comorbidities with ventricular septal defect (VSD)

A

-Pulmonary stenosis
-Transposition of the great vessels
-Patent ductus arteriosus (PDA)
-Atrial defects and coarctation of the aorta

102
Q

Pathophysiology of ventricular septal defect (VSD)

A

-Blood flows from left to right side through the pulmonary artery
-High pressures in the left ventricle move to the right side because there is more resistance to pump against systemic arterial circulation
-More blood to the right ventricle; crackles in lungs, JVD, increased PVR
-Left to Right shunting and pulmonary resistance causes the muscle to hypertrophy

103
Q

Clinical manifestations of ventricular septal defect (VSD)

A

-HF
-Murmur
-Bacterial endocarditis
-Pulmonary obstructive disease

104
Q

Obstructive defects

A

-Blood exiting portion of the heart meets an area of anatomical narrowing (stenosis), causing obstruction to blood flow
-The location of narrowing is usually near the valve of the obstructive defect
-ie. Coarctation of aorta

105
Q

Coarctation of the aorta

A

-Localized narrowing near the insertion of the ductus arteriosus

106
Q

Pathophysiology of coarctation of the aorta

A

-Due to the narrowing, there is increased pressure proximal to the defect (upper extremities) and decreased pressure distal to it (lower extremities)

107
Q

Clinical manifestations of coartation of the aorta

A

-Blood pressure is higher in the upper extremities (bounding pulse) than the lower extremities (weak pulse; cool to touch)

108
Q

Congenital heart disease: Cyanotic definition

A

-Defects with decreased pulmonary blood flow
-Mixed blood flow

109
Q

Defects with decreased pulmonary blood flow

A

-Obstructed pulmonary blood flow and an anatomical defect (ASD or VSD) between the right and left side of the heart are present
-Right sided pressure exceeds left sided pressure, allowing desaturated blood to shunt right to left, causing desaturation in the left side of the heart and in the systemic circulation
-ie. Tetralogy of Fallot

110
Q

Tetralogy of Fallot

A

Ventricular septal defect (VSD)

111
Q

Pathophysiology of tetralogy of Fallot

A

-Flow of blood depends on the degree of pulmonic stenosis, the size of the ventricular septal defect and the pulmonary and systemic resistance to flow
-Pulmonic stenosis reduces the amount of oxygenated blood that returns to the left side of the heart
-Mixing of oxygenated and unoxygenated blood due to ventricular septal defect

112
Q

Tetralogy of Fallot septal defect manifestations

A

-Acute to mild cyanosis that progresses over the first year of life, systolic murmur
-Episodes of cyanosis and hypoxia called blue spells or tet spells
-Anoxic spells occur during crying or after feeding, apnea
-Patients are at risk for emboli, seizures, aLOC or sudden death following an anoxic spell
-Bradycardia (bad, babies have no reserve)

113
Q

Mixed congenital heart defects

A

-Fully saturated systemic blood flow mixes with the desaturated blood flow, causing desaturation of the systemic blood flow
-Pulmonary congestion occurs and cardiac output decreases
-ie. Transposition of the great arteries (TGA); anatomically incorrect allowing blood to mix

114
Q

Mixed defects: Transposition of the great arteries (TGA)

A

-The pulmonary artery leaves the left ventricle and the aorta exits from the right ventricle, with no communication between the pulmonary and systemic circulation

115
Q

Pathophysiology of transposition of the great arteries (TGA)

A

-Septal defects or patent ductus arteriosus allows for mixing of saturated and desaturated blood in SVC or PVC
-Most common defect is the patent foramen ovale
-VSD increases risk of heart failure because it allows blood to flow from the left to right ventricle and produces high pulmonary blood flow under high pressure which increased PVR (right sided problems)

116
Q

Manifestation of transposition of the great arteries (TGA)

A

-Cyanotic newborns that have depressed function at birth
-Those with large septal defects or patent ductus arteriosus may be less cyanotic
-Cardiomegaly

117
Q

Assessment of congenital heart defects

A

-Cyanotic and acyanotic
-Familial history

118
Q

Child related factors of congenital heart disease

A

-Chromosomal abnormalities/syndromes and congenital defects in other body systems (e.g. Down Syndrome)
-Difficulty Feeding

119
Q

Nursing assessment of congenital heart defects

A

-Tachycardia (HR >160 beats/min), tachypnea (RR >60 breaths/min), audible murmurs, aBP
-Cyanosis, SOBOE
-Cyanotic heart defects: “Tet spells”, clubbing of fingers and toes, increased red blood cells
-Failure to grow at a normal rate, developmental delays

120
Q

Most common form of cardiac disease in children

A

Congenital heart disease

121
Q

Factors predisposing children to CHD

A

-Infection, drinking during pregnancy, maternal age, and maternal type 1 diabetes

122
Q

Major categories to investigate in the cardiac history r/t congenital heart defects

A

Poor weight gain & feeding habits, fatigue during feeding, exercise intolerance

123
Q

Common tests used to assess cardiac function

A

-Radiography, echocardiography
-ECG
-Cardiac catheterization

124
Q

Acquired heart disease

A

-Kawasaki disease
-Rheumatic fever
-Acquired heart disease is much more common in adults than in children
-Result of damage to heart by disease, virus, or bacteria

125
Q

Kawasaki disease

A

-Acute, febrile, multisystem disorder* believed to be autoimmune in nature
-Affects skin and mucous membranes of the respiratory tract, lymph nodes, and heart
-Unknown cause
-1-14 year olds; 75% of cases occur in children <5 years old
-Spontaneous recovery occurs within 3-4 weeks

126
Q

Assessment of Kawasaki disease (acute stage)

A

-High fever (38.9°-41°) >5 days
-Conjunctivitis
-Red throat
-Swollen hands and feet, rash, irritability

127
Q

Assessment of Kawasaki disease (subacute stage)

A

-Dry, red, cracked lips, “strawberry tongue”*
-Peeling of the palms & soles
-Joint pain
-Monitor for development of coronary artery aneurysms→ MI

128
Q

Lab tests for Kawasaki disease

A

Elevated platelet & WBC count

129
Q

Diagnostic criteria for Kawasaki disease

A

-Child must have a fever for >5 days along with 4 or 5 clinical criteria:
-Changes in extremities
-Bilateral conjunctivitis
-aOral mucous membranes (i.e. “strawberry tongue”)
-Rash
-Cervical lymphadenopathy

130
Q

Rheumatic fever

A

-Acute, systemic, inflammatory disease affecting multiple organs & systems (heart, joints, brain & skin)
-Age 5-15 years old
-Caused by untreated group A beta-hemolytic streptococcal pharyngitis

131
Q

Diagnostic evaluation of rheumatic disease (major manifestations)

A

-Jones criteria: Major manifestations
-Carditis
-Polyarthritis
-Erythema marginatum
-SC nodules
-Chorea

132
Q

Diagnostic evaluation of rheumatic disease (minor manifestations)

A

-Jones criteria:
-Joint pain (arthralgia), fever
-Erythrocyte sedimentation, anemia
-Positive C-reactive protein
-Supportive evidence: Positive throat culture for streptococcus

133
Q

Summary of acquired CV disease

A

-Most common are Kawasaki disease & rheumatic fever
-Acute rheumatic fever is a systemic inflammatory disease that can damage cardiac valves
-Kawasaki disease causes inflammation of small vessels & capillaries that can progress to the coronary arteries

CV487 (15 decks)

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