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NURS 312 > Cardiovascular > Flashcards

Cardiovascular Flashcards

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1
Q

Cardiac output (CO)

A

Stroke volume (SV) x Heart rate (HR)
Normal CO: 4 to 6 L/minute in adults

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2
Q

Stroke volume

A

The amount of blood pumped out of the left ventricle into the aorta in one minute.
Normal blood volume in adult body: 5 to 6 L

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3
Q

How do you increase cardiac output?

A

Increase stroke volume or increase heart rate - or both!

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4
Q

Preload

A

Pre-contraction workload (mm Hg). The volume of blood that fills ventricles (right side). Determined by venous return and the stretch of cardiac muscle fiber.

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5
Q

Afterload

A

Post-contraction workload (mm Hg). The pressure required to move blood into the aorta.
Systemic arterial pressure: Left side of the heart
Pulmonary arterial pressure: Right side of the heart

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6
Q

Frank Starling Law

A

“Volume of blood ejected by the ventricle depends on the volume present in the ventricle at the end of diastole”
SV and CO correlate directly with end-diastolic volume. As the heart fills up with more blood during diastole, it contracts harder and pumps out more blood during systole.

Matches output of right and left ventricles. Increased diastolic filling –> increase EDP –> increased myocardial fiber stretching –> increased CO

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7
Q

According to the Frank Starling Law, cardiac contractility is dependent on

A

Preload (volume)

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8
Q

Atherosclerosis etiology, risk factors, and causes

A

Etiology: Hardening of arteries due to fibrofatty lesions in the intimal lining; hypercholesterolemia
Risk factors: Family history of heart disease, gender/sex, old age, smoking, sedentary lifestyle
Causes: Peripheral artery disease, coronary artery disease, ischemic stroke

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9
Q

Clinical manifestations of atherosclerosis

A

Mild (asymptomatic): Hypertension
Severe (depends on vessel involved): Chest pain, dysrhythmias, neurological deficits, oliguria, protein cholesterol (HDL good, LDL bad), increased BUN/creatinine

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10
Q

Atherosclerosis plan, interventions, and evaluation

A

Plan: Correct underlying causes
Interventions: Smoking cessation, weight control, healthy diet (decreased fat intake), HMG-CoA reductase (decreased serum cholesterol), antiplatelet agents, surgical grafts/stents
Evaluation: Serum cholesterol levels within normal limits

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11
Q

Acute arterial occlusion etiology

A

Thrombus attached to vessel wall obstructs blood flow and pulses are absent below the occlusion. Freely moving emboli may be dislodged from the atrium and travel to smaller vessels causing atrial flutter and atrial fibrillation.

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12
Q

Acute arterial occlusion clinical manifestations

A

Extremities show the 7 Ps: Pistol shot, pallor, polar (cold), pulselessness, pain, paresthesia, paralysis. Cyanosis/mottling.

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13
Q

Acute arterial occlusion diagnosis and plan

A

Diagnosis: Medical history and assessment, radiography
Plan: Restore blood flow

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14
Q

Acute arterial occlusion sources

A

Freely moving emboli that travel to small vessels; cardiac valve surface emboli come from prosthetic cardiac valves (bacteria vegetation), fat emboli come from fractured bones/ortho surgery (look for petechiae), air emboli caused by lungs and IV lines, amniotic fluid emboli from childbirth.

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15
Q

Acute arterial occlusion interventions and evaluation

A

Interventions: Thrombolytic therapy, anticoagulant therapy (heparin), protect involved extremities from further injuries, embolectomy, amputation
Evaluation: Palpable distal pulses

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16
Q

Peripheral artery disease etiology and risk factors

A

Etiology: Atherosclerosis; symptoms of occluded arteries is subtle (femoral and popliteal arteries)
Risk factors: Older age, hypertension, cigarette smoking, diabetes mellitus

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17
Q

Peripheral artery disease clinical manifestations

A

Asymptomatic in less than 50% of occlusion. Weak pulses or loss of pulses below occlusion (pallor/polar), intermittent claudication (pain with walking), numbness, muscular atrophy, skin thin and shiny, brittle toenails, skin color pallor with elevation but red in dependent position, hair absent, lesions with gangrene, ulcers in toe tips, heels and lateral ankle, <5-15 sec capillary refill.

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18
Q

Peripheral artery disease diagnosis and plan

A

Diagnosis: Medical history and assessment, doppler, ultrasound, contrast resonance imaging (MRI)
Plan: Correct underlying issues

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19
Q

Peripheral artery disease interventions and evaluation

A

Interventions: Smoking cessation, protect affected tissue, ambulation, statins (decreases cholesterol), antiplatelet agents, vascular surgery, amputation
Evaluation: Palpable distal pulses, prosthetic placement

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20
Q

Venous thrombosis etiology and risk factors

A

Etiology: Presence of thrombus and intravascular inflammatory response
Risk factors: Inherited factor V deficiency, immobilization (increased DVT), orthopedic surgeries (joint replacement), oral contraceptives, increased blood viscosity (thickening) from airplane travel, prolonged sitting, and dehydration

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21
Q

Venous thrombosis clinical manifestations

A

Asymptomatic (partial occlusion), pulses present/weak, fever, malaise, lower extremities have pain/tenderness/swelling/dependent purplish color, flaky/thick/hardened skin (brown and blotchy), venous stasis ulcers in medial ankle or lower leg, >2 sec capillary refill, edema present, hair present/absent

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22
Q

Venous thrombosis diagnosis and plan

A

Diagnosis: Venography, ultrasonography, increased plasma D-dimer (>250 ng/mL), increased WBC, increased erythrocyte sedimentation rate
Plan: Prevent Virchow’s Triad (venous blood stasis, hypercoagulation, vessel wall injury)

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23
Q

Venous thrombosis interventions and evaluation

A

Interventions: Prevention; early ambulation post-surgery, avoid hip and knee flexion positions, HOB <30 degrees, apply heat to relieve venous spasms (NO MASSAGE), sequential compression devices for bedrest clients (prevention only-not for DVT), properly fitted anti-embolus stockings, anticoagulant therapy (heparin, warfarin, lovenox)
Evaluation: Pain free

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24
Q

During the initial admission assessment, the nurse documented abnormal lower extremity findings. Which finding reflects venous thrombosis?

A

Flaky skin, deep calf tenderness, and dependent purple color

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25
Systolic BP
Peak pressure produced; ventricles contract. S1 "lub" (mitral and tricuspid valves close)
26
Diastolic BP
Arterial pressure; ventricles are relaxed and filling. S2 "dub" (aortic and pulmonic valves close); coronary arteries fill and oxygenate the myocardium
27
Pulse pressure
Force generated during systole creates pulse pressure. Systole - Diastole = Pulse Pressure
28
Narrow pulse pressure
Hypovolemic shock (uncompensated BP drop); decreased stroke volume, increased heart rate
29
Wide pulse pressure
Increased intracranial pressure (head trauma), Cushing's Triad (increased BP, bradycardia, irregular breathing), narrowed arterial lumens from increased systemic vascular resistance
30
Primary hypertension etiology and risk factors
Etiology: Idiopathic (insidious onset) Risk factors: Age, race (prevalent in African Americans), heredity, smoking, excess ETOH, heavy salt diet, type 2 diabetes, dyslipidemia, cocaine
31
Secondary hypertension etiology
Adrenal cortical disorder (retention of water and salt), renal disease (atherosclerosis of the proximal renal artery/fibromuscular dysplasia), type 2 diabetes, oral contraceptives
32
Hypertension clinical manifestations
Headache, malaise, fatigue, angina, vision changes. Emergency: Headache, restlessness, SOB, motor and sensory deficits, convulsions, seizures, death
33
Hypertension diagnosis and plan
Diagnosis: 2-3 BP readings x 3 appointments of both arms, 24 hour blood pressure monitoring test to confirm Plan: Reduce BP
34
Hypertension interventions and evaluation
Interventions: Active lifestyle, healthy diet, smoking cessation, diuretics, vasodilator. Avoid a rapid decrease in BP which can cause subdural hematoma, hypoperfusion, and ischemia. Evaluation: BP <120/80
35
Describe the layers of the pericardium (outside to inside)
Fibrous layer, potential space, parietal layer, visceral layer
36
Describe the layers of the myocardium (outside to inside)
Epicardium (surface of heart muscle), myocardium (middle cardiac muscle layer), endocardium (inner endothelial layer and cardiac valves)
37
Pericarditis clinical manifestations and diagnosis
Clinical manifestations: Fever, dyspnea, sharp chest pain with deep inspiration relieved by sitting up and leaning forward. Diagnosis: Patient history and assessment, hallmark sign is pericardial friction rub heard during auscultation of anterior thorax (sounds like squeaky leather), 12-lead EKG shows increased ST concaved elevation and depressed PR intervals, radiography, serum lab tests (increased WBC, CRP, ESR)
38
Pericarditis plan, interventions, and evaluation
Plan: 30% relapse in clients with autoimmune disorders; continue colchicine therapy prophylaxis Interventions: NSAIDs, colchicine if NSAID response is slow, antibiotics, corticosteroids if colchicine response is slow, pericardiocentesis, pericardiectomy Evaluation: Infection free
39
Cardiac tamponade (pericardial effusion)
Medical emergency; prevents stretching and filling of all four heart chambers, increasing venous pressures. Identified by Beck's Triad: Distant muffled heart sounds, JVD, decreased BP
40
Cardiac tamponade interventions
Pericardiocentesis, pericardiectomy (thoracotomy)
41
Pericardial effusion
Fluid enters pericardial space and compresses the heart. Leads to chronic inflammation where pericardium becomes thick, fibrous, loses elasticity. Decrease in cardiac output leads to heart failure.
42
Endocarditis clinical manifestations
Fever >38 C, petechiae, Olser nodes, jane way lesion, splinter hemorrhages, heart murmurs
43
Endocarditis diagnosis
Medical history and assessment (screening intravenous drug use), serum cultures (streptococcus aureus), echocardiogram to visualize pathogen vegetation
44
Endocarditis plan, interventions, evaluation
Plan: Infection control, substance abuse counseling Interventions: Antibiotics (IV x4 weeks), prosthetic cardiac valve, heart transplant Evaluation: Infection free
45
Normally coronary artery perfusion occurs...
during diastole (ventricle relaxation); if diastole duration is shortened there is less myocardium perfusion which increases the risk for ischemic heart muscle
46
Penumbra
Ischemic band of minimally perfused cells; area surrounding core of dead or dying cells. Survival is dependent on time-get adequate blood circulation, remove toxic substances, decrease degree of edema. NECROTIC TISSUE IS IRREVERSIBLE!
47
Coronary artery disease risk factors
Age, gender, men >45 years old/women after menopause, family history of heart disease, smoking, obesity, sedentary lifestyle, diabetes mellitus, hypertension
48
Coronary artery disease clinical manifestations
Substernal chest pain/pressure that radiates, pain that radiates into the neck/jaw/shoulders/back and arms, epigastric discomfort, dyspnea, dizziness, anxiety ("impending doom"), diaphoresis
49
Coronary artery disease diagnosis
- 12-lead EKG shows ischemic myocardium affecting repolarization, inverting the T-wave and STEMI (transmural), ST depression (sub endocardium) - Medical history and assessment - Serum biomarkers (troponin I&T, creatine kinase muscle brain) - Cardiac catheterization, coronary arteriography, insert stents - Exercise stress test - Echocardiography, computed tomography
50
Coronary artery disease plan
Notify EMS/provider, initiate BLS if required, start a 12-lead EKG before administering nitroglycerine (vasodilates coronary artery) or analgesics (don't want to mask chest pain)
51
Coronary artery disease interventions and evaluation
Interventions: Chest pain protocol (morphine, oxygen, nitroglycerine, aspirin), beta adrenergic blocker (decreases myocardial oxygen demand), stable angina, coronary artery bypass graft Evaluation: Normal sinus rhythm & pain free
52
CAD first treatment goal
Cardiac catheterization lab within 60-90 minutes after chest pain with STEMI; percutaneous coronary intervention (balloon angioplasty, coronary artery stents)
53
CAD second treatment goal
Fibrinolytic therapy has best results within 30 minutes after chest pain with STEMI; benefits achieved up to 12 hours, risk of intracranial hemorrhage
54
Cardiomyopathy etiology
Condition that weakens and hypertrophy (enlarges) cardiac muscles. Genetic (60%): Autosomal dominant, hypertrophic Mixed: Dilated, restrictive Acquired: Myocarditis
55
Cardiomyopathy clinical manifestations
Variable may progress to end stage heart failure; syncope, systolic/diastolic murmurs, dysrhythmias, angina, pulmonary & peripheral edema, JVD
56
Cardiomyopathies with decreased cardiac output:
Cardiomyopathy dilated, cardiomyopathy restrictive
57
Cardiomyopathy hypertrophic diagnosis, plan, interventions, evaluation
Most common cause of sudden cardiac death (SCD) in young athletes. Diagnosis: Echocardiography shows decreased left ventricular chamber size, EKG shows atrial fibrillation/LV hypertrophy, CO remains adequate Plan: Monitor with echocardiogram starting at 12 y/o Interventions: Implantable cardioverter defibrillators, beta blockers, calcium channel blockers, heart transplant Evaluation: Adequate cardiac output
58
Cardiomyopathy dilated diagnosis, plan, interventions, evaluation
MOST COMMON cause of HF Diagnosis: Echocardiography shows ventricular enlargement & wall thinning & impaired systolic function. Histologically there is interstitial fibrosis. Ejection fractions is <25%, decreased CO Plan: Relieve symptoms Interventions: Diuretics, beta blockers, anticoagulants, heart transplant Evaluation: Adequate CO
59
Cardiomyopathy restrictive diagnosis, plan, interventions, evaluation
Least common cardiomyopathy. Diagnosis: Echocardiogram shows restricted ventricle filling, rigid ventricle walls, and decreased CO Plan: Relieve symptoms Interventions: Heart transplant Evaluation: Adequate cardiac output
60
Cardiomyopathy acquired diagnosis, plan, interventions, evaluation
Inflammation of myocardium Diagnosis: Positive pathogen cultures, echocardiogram shows LV failure and dilated cardiomyopathy, biopsy, decreased CO Plan: Relieve symptoms Interventions: Supportive care Evaluation: Adequate cardiac output
61
Stenosis
Cardiac valve incomplete OPENING; forward blood flow is impeded. Chamber does not completely empty before valve closes, therefore there is increased pressure in the over filled chamber. Result is hypertrophy and decreased CO
62
Regurgitation
Cardiac valves incomplete CLOSING; backwards blood flow into chamber. Increased workload on cardiac muscles results in hypertrophy and dilation of heart chambers
63
P wave
SA node; atrium depolarization
64
PQ interval
Depolarization; AV node, bundle branches, Purkinje fibers
65
QRS complex
Ventricle depolarization; atrium repolarization
66
ST segment
Line from S wave that curves upward to meet T wave Change in ST = Cardiac perfusion issue
67
T wave
Ventricular repolarization
68
U wave
Not always present; drug toxicity, hypokalemia
69
Cor pulmonale (right-sided HF)
Fatigue, increase in peripheral venous pressure, ascites, enlarged liver and spleen, may be secondary to chronic pulmonary problems, JVD, anorexia & complaints of GI distress, weight gain, dependent edema
70
Left-sided cardiac failure
Paroxysmal nocturnal dyspnea, elevated pulmonary capillary refill wedge pressure, pulmonary congestion (cough, crackles, wheezes, blood-tinged sputum, tachypnea), restlessness, confusion, orthopnea, tachycardia, exertional dyspnea, fatigue, cyanosis
71
Shock
"Shock not only stops the machine, but it wrecks the machinery" Inadequate tissue & organ perfusion at the cellular level
72
Shock: Initial stage
Body switches from aerobic to anaerobic metabolism. Elevated lactic acid levels, subtle changes in clinical signs.
73
Shock: Compensatory stage
Sympathetic nervous system stimulated increased catecholamine release and increased cardiac contractility. Neurohormonal response: vasoconstriction and blood shunted to vital organs. Aldosterone released (decreased urine output <30 mL/hr), increased HR, increased glucose levels.
74
Shock: Progressive stage
Electrolyte imbalance, metabolic acidosis, respiratory acidosis, peripheral oedema, irregular tachyarrhythmias, hypotension, pallor, cool and clammy skin, altered level of consciousness
75
Shock: Refractory stage
Irreversible cellular and organ damage, impending death
76
Hypovolemic shock
15% or more fluid volume, whole blood and plasma, extracellular fluid; excessive dehydration, internal hemorrhage, third space losses; extracellular fluid shifts from vascular compartment to interstitial space
77
Cardiogenic shock
Heart fails to pump blood sufficiently. Acute myocardial infarction (most common), myocardial contusion, mitral valve regurgitation, arrhythmias, cardiomyopathy
78
Obstructive shock
Mechanical obstruction of blood flow through central circulation. Dissecting aortic aneurysm, traumatic vena cava rupture, cardiac tamponade, pulmonary embolism (most common), pneumothorax (blunt/penetrating trauma), atrial myxoma (tumor), ruptured hemi-diaphragm
79
Distributive shock
Loss of peripheral blood vessel tone, enlargement of peripheral vascular compartment, displacement of vascular blood volume (shunt) away from heart and central circulation. Neurogenic: Bradycardia, hypotension Anaphylactic: Wheezing, hypotension Sepsis: Warm flushed skin, hypotension

NURS 312 (5 decks)

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