Week 1 - Cardiovascular Flashcards

Question

Nursing Care - Chronic Stable Angina: Drug Therapy ▪ Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) ▪ _________ and reduced blood volume ▪ Prevent or reverse ventricular remodeling ▪ β-Adrenergic blockers ▪ Decrease myocardial __________, HR, SVR, and BP ▪ Side effects: bradycardia, hypotension, wheezing, GI effects; weight gain, depression, fatigue, sexual dysfx ▪ Contraindicated: severe bradycardia, acute decompensated HF ▪ Cautious use: asthma, diabetes

Answer 1

▪ Angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) ▪ Vasodilation and reduced blood volume ▪ Prevent or reverse ventricular remodeling ▪ β-Adrenergic blockers ▪ Decrease myocardial contractility, HR, SVR, and BP ▪ Side effects: bradycardia, hypotension, wheezing, GI effects; weight gain, depression, fatigue, sexual dysfx ▪ Contraindicated: severe bradycardia, acute decompensated HF ▪ Cautious use: asthma, diabetes

Answer 2

▪ Calcium channel blockers (CCBs) ▪ Systemic vasodilation with reduced SVR, reduced myocardial contractility, coronary vasodilation, reduced HR ▪ Side effects: fatigue, headache, dizziness, flushing, hypotension, peripheral edema ▪ Enhance action of digoxin ▪ Lipid-lowering drugs ▪ Sodium Current Inhibitor ▪ Used when inadequate response to other antianginal drugs ▪ Side effects: dizziness, nausea, constipation, HA

Answer 3

▪ 12-lead ECG ▪ Lab studies: cardiac biomarkers, lipid profile, CRP ▪ Chest x-ray ▪ Echocardiogram ▪ Exercise stress test ▪ Electron beam computed tomography ▪ Coronary computed tomography anigography

Answer 4

catheterization

Answer 5

▪ Stent placement procedure & post procedure drugs ▪ Used to prevent platelet aggregation & stent thrombosis ▪ During PCI: unfractionated heparin or low-molecular weight heparin, a direct thrombin inhibitor and/or GP lIb/IIIa inhibitor ▪ After PCI: dual antiplatelet therapy (DAPT) ▪ Aspirin and clopidogrel

Answer 6

Nursing management: Cardiac catheterization and percutaneous coronary intervention (PCI) Assess: ▪ Allergy (contrast dye) ▪ Baseline assessment: VS, pulse ox, heart and breath sounds, neurovascular ▪ Laboratory studies ▪ Administer drugs ▪ Patient education: procedure and postprocedure

Answer 7

Nursing management: Cardiac catheterization and percutaneous coronary intervention (PCI) See: Box Postprocedure (RN): ▪ Compare assessments to preprocedure ▪ Assess catheter insertion site for hematoma, bleeding, bruit every15 minutes for first hour, then agency policy ▪ ECG for dysrhythmia; chest pain or other pain ▪ IV infusion of antianginals ▪ Monitor for complications ▪ Education: discharge care and drugs; signs and symptoms to report to HCP

Answer 8

graft [last resort or if issues with LMCA]

Answer 9

right and left coronary arteries

Answer 10

Minimally invasiv

Answer 11

24 to 48 hours

Answer 12

▪ CPB ▪ Systemic inflammation ▪ Bleeding and anemia ▪ Fluid and electrolyte imbalances ▪ Infection ▪ Hypothermia ▪ Dysrhythmias, especially atrial fibrillation ▪ Wound care ▪ Chest wound ▪ Harvest site

Answer 13

▪ Pain management ▪ Prevent VTE ▪ Early ambulation ▪ SCD ▪ Respiratory complications ▪ Splinting ▪ Incentive spirometry ▪ Postoperative cognitive dysfunction (POCD)

Answer 14

▪ Presentation of chest pain ▪ ST elevations on 12-lead ECG are most likely STEMI ▪ Compare to previous ECG ▪ ST elevation = potentially reversible myocardial injury ▪ UA or NSTEMI—may or may not have ST segment depression and/or T wave inversion ▪ If not, evaluate serum cardiac biomarkers

Answer 15

▪ Total coronary occlusion: cellular response to O2 and glucose deprivation ▪ Heart muscle hypoxic within 10 seconds ▪ Anaerobic metabolism, increased lactic acid ▪ Heart cells viable 20 minutes; damage irreversible if no collateral circulation ▪ If reperfused, aerobic metabolism and contractility restored and cellular repair begins

Answer 16

Chest pain: ▪ New onset; occurs at rest; or with increasing frequency, duration, or less effort than chronic stable angina pattern ▪ May be first clinical sign of CAD ▪ Pain lasting > 10 minutes ▪ Unpredictable; needs immediate treatment ▪ ECG may show ST depression and/or T wave inversion = ischemic changes

Answer 17

stoppage of blood flow

Answer 18

▪ STEMI ▪ Emergency; artery must be opened within 90 minutes with either PCI or thrombolytic ▪ NSTEMI ▪ PCI within 12 to 72 hours ▪ STEMI or NSTEMI ▪ Echocardiogram—hypokinesis or akinesis of infarcted areas ▪ Degree of LV dysfunction depends on area of heart and size of infarction

Answer 19

▪ Evolution of MI—hours to a few days ▪ Subendocardium—ischemic first ▪ Entire thickness of heart muscle necrotic in 4-6 hours; Partial occlusion by thrombus—up to 12 hours ▪ MI described by location—anterior, inferior, lateral, septal or posterior wall ▪ Location of MI and ECG changes correlate with involved coronary artery (Table 37-13) ▪ Severity of MI influenced by collateral circulation ▪ Women often undertreated; worse outcomes

Answer 20

Pain ▪ Severe chest pain not relieved by rest, position change, or nitrate administration ▪ Heaviness, pressure, tightness, burning, constriction, or crushing ▪ Common locations: substernal or epigastric ▪ May radiate to neck, lower jaw, arms, back ▪ Often occurs in early morning; greater than 20 min. ▪ Atypical in women and older adult ▪ No pain if cardiac neuropathy (diabetes)

Answer 21

Sympathetic nervous system stimulation ▪ Release of catecholamines ▪ Diaphoresis ▪ Increased HR and BP ▪ Vasoconstriction of peripheral blood vessels ▪ Skin: ashen, clammy, and/or cool to touch

Answer 22

Cardiovascular ▪ Initially, increased HR and BP, then reduced BP (secondary to decrease in CO) ▪ Decreased renal perfusion leads to decreased urine output ▪ Crackles (LV dysfunction) ▪ Jugular venous distention, hepatic engorgement, peripheral edema (RV dysfunction) ▪ Abnormal heart sounds ▪ S3 or S4 ▪ New murmur: holosystolic

Answer 23

severe pain

Answer 24

cardiac output

Answer 25

▪ Inflammatory process: within 24 hours, leukocytes infiltrate the area of cell death; enzymes released ▪ Proteolytic enzymes of neutrophils and macrophages begin to remove necrotic tissue by fourth day resulting in thin wall ▪ Catecholamine-mediated lipolysis and glycogenolysis resulting in increased glucose ▪ Necrotic zone identifiable by ECG changes ▪ Collagen matrix laid down—scar tissue

Answer 26

blood pumped per minute

Answer 27

▪ 10 to 14 days after MI, scar tissue is still weak ▪ Heart muscle vulnerable to stress ▪ Monitor patient carefully as activity level increases ▪ By 6 weeks after MI, scar tissue has replaced necrotic tissue ▪ Area is said to be healed, but less compliant ▪ Ventricular remodeling ▪ Normal myocardium will hypertrophy and dilate in an attempt to compensate for infarcted muscle

Answer 28

▪ Dysrhythmias ▪ Most common complication ▪ Present in 80% to 90% of MI patients ▪ Can be caused by ischemia, electrolyte imbalances, or SNS stimulation ▪ VT and VF are most common cause of death in prehospitalization period

Answer 29

▪ Left-sided HF ▪ Mild dyspnea, restlessness, agitation, or slight tachycardia; pulmonary congestion on x-ray, S3 sounds, crackles, paroxysmal nocturnal dyspnea, and orthopnea ▪ Right-sided HF ▪ Jugular venous distention, hepatic congestion, lower extremity edema

Answer 30

▪ Cardiogenic shock—decreased O2 and nutrients related to: ▪ Severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, right ventricular infarction ▪ Requires aggressive management to: ▪ Increased O2 delivery, decreased O2 demand, and prevent complications ▪ Associated with a high death rate

Answer 31

▪ Papillary muscle dysfunction or rupture ▪ Causes acute and massive mitral valve regurgitation; new systolic murmur ▪ Aggravates an already compromised LV results in decreased CO resulting in rapid clinical deterioration ▪ Left Ventricular Aneurysm ▪ Myocardial wall is thin; bulges out during contraction; may rupture and hide thrombi ▪ Leads to HF, dysrhythmias, and angina

Answer 32

▪ Ventricular septal wall rupture and left ventricular free wall rupture ▪ New, loud systolic murmur ▪ HF and cardiogenic shock ▪ Emergency repair ▪ Rare condition associated with high death rate

Answer 33

▪ Pericarditis ▪ Inflammation of visceral &/or parietal pericardium ▪ Mild to severe chest pain ▪ Increases with inspiration, coughing, movement of upper body ▪ Relieved by sitting in forward position ▪ Pericardial friction rub, fever, decreased BP, ECG changes ▪ Treat with high dose aspirin

Answer 34

▪ Detailed health history ▪ 12-lead ECG ▪ Compare new ECG to previous ECG ▪ Changes in QRS complex, ST segment, and T wave ▪ Distinguish between STEMI and NSTEMI/UA ▪ Serial ECGs reflect evolution of MI

Answer 35

Acute Coronary Syndrome Diagnostic Studies Serum cardiac biomarkers ▪ Proteins released after MI (Table 31-6) ▪ Cardiac-specific troponin T (cTNT) ▪ Cardiac-specific troponin I (cTNI) --- Increased 4 to 6 hours after onset of MI --- Peak at 10 to 24 hours --- Return to baseline over 10 to 14 days ▪ Biomarkers negative for UA; positive for NSTEMI ▪ Cardiac-specific troponins are better indicators of MI than CK-MB or myoglobin

Answer 36

ST elevation MI

Answer 37

Severity when did it start radiation?

Answer 38

Cardiac catheterization ▪ Within 90 minutes for patients with a STEMI or receive thrombolytic therapy within 30 minutes (if no PCI available) ▪ Within 12 to 72 hours for patients with UA or NSTEMI ▪ May have PCI, medical therapy, or referral for CABG depending on findings

Answer 39

▪ 12-lead ECG ▪ Upright position ▪ Oxygen—keep O2 sat > 93% ▪ IV access ▪ Nitroglycerin (SL) and ASA (chewable) ▪ Morphine ▪ Statin

Answer 40

▪ ECG shows ST elevation leading to cardiac cath lab for PCI or thrombolytic therapy ▪ ECG shows ST depression or T-wave inversion leading to critical care or telemetry unit ▪ Dysrhythmias—treat as per agency ▪ Monitor serum biomarkers

Answer 41

▪ UA and NSTEMI ▪ Heparin ▪ Glycoprotein IIb/IIIa inhibitors before or during PCI ▪ STEMI ▪ Glycoprotein IIb/IIIa inhibitors during PCI

Answer 42

Admit to ICU/telemetry unit ▪ Monitor VS and pulse oximetry ▪ Continuous ECG ▪ Serial 12-lead ECGs ▪ Serial cardiac biomarkers ▪ Bed rest/ limit activity for 12 to 24 hours; increase gradually

Answer 43

▪ Heparin—UA and NSTEMI ▪ DAPT—NSTEMI and UA with stent ▪ Aspirin—UA ▪ Cardiac Catheterization—UA and NSTEMI ▪ Medical management, PCI, or CABG ▪ Reperfusion therapy—STEMI ▪ Emergent PCI ▪ Thrombolytic therapy

Answer 44

▪ Emergent PCI is first treatment with confirmed STEMI ▪ Goal: open blocked artery within 90 minutes of arrival to facility with cardiac catheterization lab; BSM or DES ▪ If severe LV dysfunction—IABP and/or inotropes ▪ Emergent CABG

Answer 45

▪ Advantages of PCI versus CABG ▪ Faster reperfusion ▪ Local anesthesia ▪ Ambulatory sooner ▪ Length of stay shorter (reduced costs) ▪ Faster return to work ▪ Complications of PCI ▪ Dissection or rupture of artery ▪ Abrupt artery closure ▪ Acute stent thrombosis ▪ Failure to cross blockage ▪ Extended infarct

Answer 46

Acute Care: Thrombolytic Therapy ▪ Thrombolytic—IV administration of selected medication to open blocked arteries by lysis ofthrombus/clot; concern for bleeding with other sites ▪ Inclusion criteria: ▪ Chest pain less than 12 hours and 12 lead shows STEMI ▪ No absolute contraindications

Answer 47

Procedure ▪ Prior to administration: ▪ Obtain baseline labs ▪ 2 to 3 lines for IV therapy ▪ Complete any invasive procedures ▪ Administer IV bolus or infusion ▪ Monitor heart rhythm, VS, and pulse ox ▪ Assess heart, lungs, and neuro status

Answer 48

▪ Reperfusion occurs ▪ ST segment returns to baseline ▪ No chest pain ▪ Early, rapid rise of serum biomarkers; peak within 12 hours ▪ Reperfusion dysrhythmias—less reliable ▪ Major concern—reocclusion ▪ IV heparin ▪ Monitor for chest pain and ECG changes ▪ Major complication—bleeding

Answer 49

Suspected ACS ▪ Antiplatelet therapy, IV NTG, atorvastatin NSTEMI or UA ▪ Anticoagulation and glycoprotein IIb or IIIa MI ▪ DAPT, Aspirin, B-blockers, calcium channel blockers, ACE inhibitors, and/or nitrates

Answer 50

▪ IV nitroglycerin (NTG) ▪ Morphine ▪ β-Adrenergic blockers ▪ ACE inhibitors and ARBs ▪ Antidysrhythmic drugs ▪ Lipid-lowering drugs ▪ Aldosterone antagonists ▪ Stool softeners

Answer 51

Progress to low salt, low saturated- fat and low cholesterol

Answer 52

Subjective

Answer 53

Subjective data: Functional health patterns ▪ Health-perception–health management family history ▪ Nutritional–metabolic- Indigestion/heartburn; nausea/vomiting ▪ Elimination- Urinary urgency or frequency; Straining at stool ▪ Activity–exercise- Palpitations, dyspnea, dizziness, weakness ▪ Cognitive–perceptual- Chest pain ▪ Coping–stress tolerance- Stress, depression, anger, anxiety

Answer 54

▪ Impaired cardiac function ▪ Pain ▪ Anxiety ▪ Activity intolerance

Answer 55

▪ Pain ▪ NTG, morphine, O2 ▪ Monitoring ▪ ECG: v-fib, PVCs, VT, ST segment ▪ Physical assessment, VS, I & O, O2 ▪ Rest and comfort ▪ Bed rest, gradual increase in activity; promote relaxation; rehabilitation

Answer 56

▪ Anxiety ▪ Explore fears and concerns; provide education ▪ Emotional and behavioral reactions ▪ Psychosocial responses Support systems ▪ Patient teaching ▪ Assess literacy and learning needs; consider timing

Answer 57

▪ Cardiac rehabilitation to restore optimal function: ▪ Physiological ▪ Psychological ▪ Mental ▪ Spiritual ▪ Economic ▪ Vocational ▪ Outpatient or home-based

Answer 58

Nitro sublingual q 5 mins [MAX = 3 doses]

Answer 59

Resumption of sexual activity ▪ Sexual counseling important ▪ Include when discuss other physical activity ▪ Erectile dysfunction drugs contraindicated with nitrates ▪ Prophylactic nitrates before sexual activity ▪ When to avoid sex ▪ Typically 7 to 10 days post MI or when patient can climb two flights of stairs or walk briskly

Answer 60

▪ Maintain stable signs of adequate CO ▪ Have relief of pain and/or shortness of breath ▪ reduced anxiety and increased sense of self-control ▪ Achieve realistic program of activity ▪ Describe the disease process, measures to reduce risk factors, and rehabilitation activities necessary to manage the therapeutic regimen

Answer 61

▪ Abrupt, unexpected death from cardiac causes; occurs within 1 hour of symptom onset; ~350,000 annually (reduced due to ICDs) ▪ Acute ventricular dysrhythmia (e.g., VT, VF) causes disruption in cardiac function, resulting in loss of CO and cerebral blood flow ▪ Most commonly caused by: ▪ CAD ▪ Structural heart disease ▪ Conduction disturbances

Answer 62

▪ Symptoms within one hour: angina, palpitations, dizziness, or lightheadedness ▪ SCD occurs with: ▪ Prior (old) MI—most common ▪ Acute MI ▪ If survive, increased risk of another event due to electrical instability from scarred muscle; referred for ICD after 40 days medical therapy

Answer 63

▪ Diagnostic workup: rule out or confirm MI ▪ Serial cardiac biomarkers ▪ Serial ECGs ▪ Cardiac catheterization ▪ PCI or CABG, if indicated ▪ Electrophysiology Study (EPS) ▪ Outpatient monitor; Mobile Cardiac Outpatient Telemetry (MCOT); implanted monitor

Answer 64

defibrillator

Answer 65

Psychosocial adaptation ▪“Brush with death” ▪“Time bomb” mentality ▪ Anxiety, anger, depression ▪ Additional issues ▪ Driving restrictions ▪ Role reversal ▪ Change in occupation ▪ Provide emotional support

Answer 66

Disease of the endocardium, innermost layer of the heart, and the heart valves IE is associated with a poor prognosis and a decreased life expectancy Increase in the number of cases of IE largely related to an increase in IV drug use

Answer 67

troponin CK-MB Myoglobin

Answer 68

left side- more pulmonary/respiration right side- more circulatory/cardiac- edema/vein distention

Answer 69

By cause -IV drug use (IVDA IE), fungal IE By site of involvement -Prosthetic valve endocarditis (PVE) Subacute form affects those with preexisting valve disease Acute form affects those with healthy valves

Answer 70

Bacterial most common - Staphylococcus aureus (about 50%) -Streptococcus viridans - Coagulase Negative Staphylococci Colonizers of the oropharynx - HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)

Answer 71

-History of IE -IV drug use -Prosthetic valve -Health care–associated infection from use of an intravascular device - Methicillin-resistant S. aureus (MRSA) -Renal dialysis

Answer 72

Bacteremia Adhesion Vegetation

Answer 73

Fibrin, leukocytes, platelets, and microbes Stick to the valve or endocardium Parts break off and enter circulation (embolization) Left-sided vegetation can move to brain, kidneys, spleen, and extremities Right-sided vegetation can move to lungs (PE)

Answer 74

Fever Chills Weakness Malaise Fatigue Anorexia

Answer 75

Arthralgias Myalgias Back pain Abdominal discomfort Weight loss Headache Clubbing of fingers

Answer 76

Splinter hemorrhages in nail beds Petechiae Osler’s nodes on fingertips or toes Janeway’s lesions on fingertips, palms, soles of feet, and toes Roth’s spots

Answer 77

New or worsening systolic murmur in most pts Heart failure Manifestations secondary to septic embolism -Central nervous system -Extremities -Spleen -Kidneys

Answer 78

Health history Laboratory tests Blood cultures CBC with differential ESR, C-reactive protein (CRP) Echocardiography Duke criteria

Answer 79

Prophylactic antibiotic treatment for select patients having Certain dental procedures Respiratory tract incisions Tonsillectomy and adenoidectomy Surgical procedures involving infected skin, skin structures, or musculoskeletal tissue

Answer 80

Accurate identification of organism Blood cultures IV antibiotics (long-term) Repeat blood cultures Valve replacement if needed Antipyretics Fluids Rest

Answer 81

Subjective data Health history Valvular, congenital, or syphilitic heart disease Previous endocarditis Staph or strep infection Drugs—Immunosuppressive therapy Recent surgeries and procedures Subjective data: Functional health patterns IVDA Alcohol use Weight changes Chills Hematuria Exercise intolerance, weakness, fatigue Cough, DOE, orthopnea, palpitations Night sweats Pain, headache, joint, or muscle tenderness

Answer 82

cardiac output

Answer 83

Patient teaching need to avoid people with infections Avoidance of stress and fatigue Plan rest periods Good oral hygiene Schedule regular dental visits Prophylactic antibiotics Drug rehabilitation

Answer 84

IE Ambulatory care Antibiotic therapy for 4 to 6 weeks Assess home setting Monitor laboratory data, including blood cultures Assess IV lines Coping strategies Adequate rest Moderate activity Compression stockings ROM exercises Deep breath and cough every 2 hours

Answer 85

temperature

Answer 86

Maintain adequate tissue and organ perfusion Maintain normal body temperature Report an increase in physical and emotional comfort

Answer 87

open or close properly

Answer 88

-Valve opening is smaller -Forward blood flow is impeded -Pressure differences on the two sides of the valve reflect degree of stenosis

Answer 89

Incomplete closure of valve leaflets Results in backward flow of blood

Answer 90

rheumatic heart disease

Answer 91

Results in decreased blood flow from left atrium to left ventricle Increased left atrial pressure and volume Increased pulmonary vasculature pressure Risk for atrial fibrillation

Answer 92

Normal valve function depends on intact: Mitral leaflets Mitral annulus Chordae tendineae Papillary muscles

Answer 93

Exertional dyspnea Loud S1 Diastolic murmur Fatigue Palpitations Hoarseness, hemoptysis Atrial fibrillation with risk for stroke

Answer 94

Incomplete valve closure Backward flow of blood Acute MR -Pulmonary edema -Untreated- cardiogenic shock Chronic MR -Left atrial enlargement, ventricular dilation, eventual ventricular hypertrophy, decreased CO

Answer 95

Mitral Valve Regurgitation Acute clinical manifestations Thready peripheral pulses Cool, clammy extremities Chronic clinical manifestations Asymptomatic for years Weakness, fatigue, palpitations, dyspnea Progress to orthopnea, paroxysmal nocturnal dyspnea Peripheral edema Audible S3, murmur

Answer 96

Confirmed with echocardiography - M-mode or 2-D Clinical manifestations Most patients asymptomatic for life Only 10% with symptoms Murmur d/t regurgitation Severe MR uncommon

Answer 97

Dysrhythmias can cause palpitations, light-headedness, and syncope Infective endocarditis Chest pain unresponsive to nitrates Treat symptoms with β-blockers Valve surgery for MR

Answer 98

Patient teaching important Antibiotic prophylaxis if MR present Take drugs as prescribed Healthy diet; avoid caffeine Avoid OTC stimulants Exercise When to call HCP or EMS

Answer 99

Congenital aortic stenosis (AS) generally found in childhood, adolescence, or young adulthood In adults, can be degenerative or caused by rheumatic fever

Answer 100

-Obstruction of blood flow from left ventricle to aorta -Left ventricular hypertrophy and increased myocardial oxygen consumption -Decreased CO leads to decreased tissue perfusion, pulmonary hypertension, and HF >Poor prognosis if left untreated

Answer 101

Angina Syncope Exertional dyspnea

Answer 102

Normal to soft S1 Decreased or absent S2 Systolic murmur with radiation to the carotids Prominent S4

Answer 103

Poor prognosis if symptomatic and not corrected Use nitroglycerin cautiously --Reduces preload and BP --Can worsen chest pain

Answer 104

Systolic murmur

Answer 105

Acute AR IE, trauma, or aortic dissection Life-threatening emergency Chronic AR Rheumatic heart disease, congenital bicuspid aortic valve, syphilis, connective tissue problem, or post-surgical cause

Answer 106

Backward blood flow from ascending aorta into left ventricle With chronic AR, left ventricular dilation and hypertrophy Decrease in myocardial contractility Pulmonary hypertension and right ventricular failure

Answer 107

Severe dyspnea Chest pain Hypotension Cardiogenic shock Life-threatening emergency

Answer 108

May be asymptomatic for years Exertional dyspnea, orthopnea, paroxysmal dyspnea Angina Water-hammer pulse if severe Soft or absent S1 S3 or S4 Murmur

Answer 109

Usually caused by rheumatic fever Clinical manifestations- -Fluttering discomfort in neck -Fatigue -Right upper quadrant pain

Answer 110

Often symptomatic Crescendo-decrescendo murmur Potential causes -Pulmonary hypertension -Surgical repair of tetralogy of Fallot (TOF) -Congenital valve disease Can cause RV dilation.

Answer 111

Almost always congenital Causes right ventricular hypertension and hypertrophy Clinical manifestations Syncope Dyspnea Angina Often asymptomatic until adulthood

Answer 112

History and physical assessment Real-time 3-D echocardiography TEE Doppler color flow Chest x-ray ECG Heart catheterization

Answer 113

-Dependent on valve involved and disease severity -Prevent exacerbations of HF, pulmonary edema, thromboembolism, and recurrent RF and IE -Prophylactic antibiotic therapy to prevent recurrent RF and IE

Answer 114

Drugs to treat/control HF Vasodilators (e.g., nitrates, ACE inhibitors) Positive inotropes (e.g., digoxin) Diuretics β-blockers Low sodium diet For atrial dysrhythmias -Calcium channel blockers, β-blockers -Anti-dysrhythmic drugs -Anticoagulation therapy for A-fib

Answer 115

Valve repair -Preferred surgical procedure -Lower operative mortality rate than replacement -May not restore total valve function Valve replacement

Answer 116

Commissurotomy (valvulotomy) Closed Open (more common) Valvuloplasty Open Minimally invasive Annuloplasty

Answer 117

Mechanical (artificial) More durable, last longer Risk of thromboembolism Require long-term anticoagulation Biologic (tissue) Bovine, porcine, and human More natural blood flow No anticoagulation required Less durable

Answer 118

Subjective data Medical history IVDA, fatigue Palpitations, weakness, activity intolerance, dizziness, fainting DOE, cough, hemoptysis, orthopnea, PND Angina or atypical chest pain Objective data Fever Diaphoresis, flushing, cyanosis, clubbing, peripheral edema Crackles, wheezes, hoarseness S3 and S4 Dysrhythmias Increase or decrease in pulse pressure Hypotension Water-hammer or thready peripheral pulses Hepatomegaly, ascites Weight gain

Answer 119

Impaired cardiac function Fatigue Fluid imbalance

Answer 120

Normal heart function Improved activity tolerance Understanding of the disease process and health maintenance measures

Answer 121

Early treatment of streptococcal infections Prophylactic antibiotics for patients with history Teach patient symptoms to report

Answer 122

Individualize rest and exercise Limit activities that cause fatigue and dyspnea Discourage tobacco use Ongoing cardiac assessments to monitor drug effectiveness Monitor INR for patient on anticoagulants

Answer 123

Drug actions and side effects Importance of prophylactic antibiotic therapy Information related to anticoagulation therapy When to seek medical care

Answer 124

Notify HCP for --- Signs of infection, HF, or bleeding Monitor INR level if on Warfarin INR 0.8-1.0 Planned invasive or dental work Medical-alert device or bracelet

Answer 125

Maintain adequate tissue and organ perfusion Achieve fluid balance Achieve optimal level of activity Describe disease process and measures to prevent complications

Answer 126

Morphine Oxygen Nitroglycerin Aspirin

Answer 127

under 1 [0.8-1]

Answer 128

stable angina - shorter, responds to NTG unstable angina - longer duration & does not respond to NTG

Answer 129

atypical or asymptomatic

Answer 130

provocation quality Radiation/region Severity Timing

Answer 131

PCI within 90 mins thrombolytic therapy within 30 mins

Answer 132

platelet aggregation

Answer 133

Metoprolol tartrate is short-acting and is usually taken at least twice a day. Metoprolol succinate ER (extended-release) is longer-acting and normally taken once a day. Both medications are FDA approved for treating HTN and chest pain (angina).

Answer 134

White males, then black genetics/ family history older HTN, diabetes, obesity, smoking, sedentary

Answer 135

Atherosclerosis begins with the formation of fatty streaks, where lipids collect in the arterial walls, forming yellow streaks. [no symptoms] Over time, fibrous plaques develop as cholesterol and lipids accumulate, thickening the arterial wall and narrowing the blood flow. This partial blockage can lead to stable angina, where chest pain occurs during activity and resolves with rest. If the plaque becomes unstable, it may rupture, triggering clot formation (thrombus). A partial blockage from a clot can cause unstable angina, where chest pain is unpredictable and happens even at rest. A complete blockage of the artery results in myocardial infarction (MI), where blood flow stops entirely, causing permanent heart muscle damage.

Answer 136

STEMI: ST-segment elevation Full-thickness myocardial damage Urgent treatment (PCI or thrombolysis) NSTEMI: No ST-segment elevation ST-segment depression or T-wave inversion Partial-thickness myocardial damage Medical therapy and possible PCI

Answer 137

Atrial fibrillation (AFib) Ventricular arrhythmias Bradycardia Supraventricular tachycardia (SVT) Heart block ?

Answer 138

Nursing Diagnoses for Valve Disorders: Decreased Cardiac Output Activity Intolerance Risk for Ineffective Tissue Perfusion Excess Fluid Volume Ineffective Breathing Pattern Risk for Infection Nursing Diagnoses for Acute Coronary Syndrome (ACS): Acute Pain Decreased Cardiac Output Ineffective Tissue Perfusion Anxiety Activity Intolerance Risk for Ineffective Coping Risk for Fluid Imbalance

Answer 139

blood pumped by the heart per minute

Answer 140

cardiac output

Answer 141

stretching

Answer 142

resistance

Answer 143

The number of times the heart beats per minute. A higher heart rate directly increases CO as more blood is pumped out per unit time, assuming stroke volume remains constant

Answer 144

The force of ventricular contraction, determined by the intrinsic strength of the cardiac muscle. Increased contractility leads to increased stroke volume and therefore, increased CO, as the heart pumps more blood with each beat.

Answer 145

* Direct relationship: Increased preload, heart rate, and contractility generally lead to increased CO. * Inverse relationship: Increased afterload typically leads to decreased CO. * Clinical application: By monitoring CO and CI, healthcare providers can assess the overall cardiac function and identify potential issues related to preload, afterload, heart rate, or contractility

Answer 146

Fluids increase preload diuretics decrease preload, dopamine CA channel blockers improve contractility

Answer 147

lying supine

Answer 148

* Over hydration increases venous return * Heart failure or pulmonary artery stenosis limiting venous outflow * Positive pressure breathing due to straining.

Answer 149

Hypovolaemic

Answer 150

* Pneumothorax * Bloodstream infections * Thrombosis

Answer 151

* Misplacement – placing the catheter usually requires the patient adopting a Trendelenburg or at least supine position. This may be difficult in pregnancy as it may cause aortocaval compression. * Air embolus – lines attached to a CVC must be kept air free * Haemorrhage and formation of a haematoma.

Answer 152

blood pumped by the heart

Answer 153

OUT of the LV during systolic contraction

Answer 154

* Valvular regurgitation - backward flow of blood * Valvular incompetence or insufficiency - incomplete closure of the leaflets

Answer 155

Cause: Rheumatic disease, aging, endocarditis, collagen vascular disease, papillary muscle dysfunction Management: vasodilators, diuretics, nitrates, anticoagulants, IABP

Answer 156

ACUTE Symptoms: Pulmonary edema, shock, thready pulses, cool and clammy extremities CHRONIC Symptoms: Asymptomatic or vague, weakness, general malaise, dyspnea, orthopnea, peripheral edema, S3 heart sound, loud holosystolic murmur at apex (heard during systole)

Answer 157

Cause: smaller valve area, resulting in increased LA and Pulm pressure (usually due to rheumatic heart disease) Symptoms: dyspnea, A Fib/Palpitations, chest pain, diastolic murmur, high risk for emboli Management: Restrict Na+ intake, diuretics, nitrates, beta-blockers, digitalis, calcium antagonist, anticoagulants, surgery

Answer 158

Cause: rheumatic fever, systemic hypertension, Marfan syndrome, syphilis, rheumatoid arthritis, aging, or discrete subaortic stenosis. Symptoms: Chest pain, Dyspnea/DOE, orthopnea, paroxysmal nocturnal dyspnea Management: inotropic agents, ACE Inhibitors, diuretics,nitrates

Answer 159

Cause: Calcification of the leaflets of the valve (valve doesn't open properly) Symptoms: Angina pectoris, Syncope, Dyspnea/DOE, S4 heart sound, Systolic crescendodecrescendo murmur, S/S for LV systolic failure Management: Use nitroglycerin with caution, low Na diet, antiHTN, anti- arrhythmetics, digitalis, diuretics, ACE Inhibitors, surgery

Answer 160

dysrhythmias

Answer 161

Mechanical * Pro: longer lasting, more durable, good for younger patients * Con: higher risk of blood clots, lifelong anticoagulant therapy, hemorrhage or stroke risk, hear clicking, valve failure Biological * Pro: low clot risk, no anticoagulant therapy needed, better for elderly * Con: can calcify just like original tissue, replacement needed every 7-10 years, risk for endocarditis

Answer 162

d) Have you had dental work done recently? Dental procedures place this patient at risk for IE. The other options are not risk factors.

Answer 163

b) Patient who has just returned to the unit after balloon valvuloplasty * This patient needs to be assessed for post procedure complications, like bleeding and hypotension. While the other patients also need to be assessed, their findings are consistent with their diagnoses and do not require urgent attention.

Answer 164

*Left anterior descending * Anterior LV, Lateral LV, Anterior 2/3 of septum *Left circumflex * LA, Posterior LV, SA node 45%, AV node 10%

Answer 165

non-mod * Age * Gender (sex from genetic chromosomes) * Ethnicity * Genetic predisposition * Family history mod * Elevated serum lipids * HTN * Smoking * Inactivity * Obesity

Answer 166

* DM * Stress * Metabolic syndrome * Substanceabuse * Elevated homocysteine levels

Answer 167

Angina types Stable: Chest pain is intermittent and predictable Variant/Prinzmetal: Coronary artery spasm Unstable: acute and unpredictable **Stable can turn into unstable**

Answer 168

Stable angina: Chest pain is intermittent and predictable * Occurs with activity and stops when activity is stopped. * Controlled with meds

Answer 169

* Occurs at rest * Treated with calcium channel blockers

Answer 170

* Squeezing, constricting pain * Risk for MI

Answer 171

* NSTEMI = non-ST elevation MI * Transient thrombosis or incomplete coronary artery occlusion * STEMI = ST elevation MI * Extensive and complete coronary artery occlusion * Q-Wave MI: pathologic Q-wave seen after a complete infarction * Can indicate a prior MI

Answer 172

Elevation of the patient's LDL level This is the only MODIFIABLE risk factor listed

Answer 173

The patient states the pain resolves with one sublingual nitroglycerin tablet Chronic stable angina is typically relieved by rest or nitroglycerin.

Answer 174

D) Cardiac specific troponin Troponin levels increase for approx. 4-6 hours after MI and are highly specific indicators for MI. Myoglobin, though released, lacks specificity.

Answer 175

C) Heparin prevents the development of new clots in the coronary arteries * Heparin helps prevent the conversion of fibrinogen to fibrin and decreases coronary artery thrombosis due to blood thinning abilities. It does not dissolve already existing clots ("clotbusting")

Answer 176

C) What time did your chest pain begin? * Time is muscle! * Thrombolytic therapy should be started within 6 hours of the onset of the MI, and knowing when the pain began can help determine this

Answer 177

Aspirin bleeding

Answer 178

Used to prevent abnormal cardiac rhythms such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation Works by blocking sodium, potassium, and calcium channels in the heart muscles

Answer 179

a. Captopril would be added. It is an angiotensin-converting enzyme (ACE) inhibitor that vasodilates and decreases endothelial dysfunction and may prevent ventricular remodeling. Clopidogrel (Plavix) is an antiplatelet agent used as an alternative for a patient unable to use aspirin. Diltiazem (Cardizem), a calcium channel blocker, may be used to decrease vasospasm but is not known to prevent ventricular remodeling. Metoprolol (Lopressor) is a β-adrenergic blocker that inhibits sympathetic nervous stimulation of the heart

Answer 180

c. Decreasing level of consciousness (LOC) may reflect hypoxemia resulting from internal bleeding, which is always a risk with thrombolytic therapy. Oozing of blood is expected, as are reperfusion dysrhythmias. BP is low but not considered abnormal because the pulse is within normal range. Idioventricular dysrhythmias are common with reperfusion.

Answer 181

a. Morphine sulfate decreases anxiety and cardiac workload as a vasodilator and reduces preload and myocardial O2 onsumption, which relieves chest pain. Calcium channel blockers, amiodarone, and angiotensin-converting enzyme (ACE) inhibitors will not relieve chest pain related to an MI.

Answer 182

b. Docusate sodium (Colace) is a stool softener, which prevents straining and provoking dysrhythmias. It does not do any of the other options. Antidysrhythmics are used to control ventricular dysrhythmias; morphine sulfate is used to decrease anxiety and cardiac workload; and glycoprotein IIb/IIIa inhibitors and antiplatelets prevent the binding of fibrinogen to platelets.

Answer 183

b. It is recommended that patients with hypertension and after an MI be on β-adrenergic blockers indefinitely to decrease oxygen demand. They inhibit sympathetic nervous stimulation of the heart; reduce heart rate, contractility, and BP; and decrease afterload. Although calcium channel blockers decrease heart rate, contractility, and BP, they are not used unless the patient cannot tolerate β-adrenergic blockers. ACE inhibitors and angiotensin II receptor blockers (ARBs) are used for vasodilation.

Answer 184

b. Patients with mechanical valves have an increased risk for thromboembolism and require long-term anticoagulation to prevent systemic or pulmonary embolization. Nitrates are contraindicated for the patient with aortic stenosis because an adequate preload is necessary to open the stiffened aortic valve. Antidysrhythmics are used only if dysrhythmias occur and β-adrenergic blocking drugs may be used to control the heart rate if needed.

Answer 185

2 atrioventricular valves Mitral Tricuspid 2 semilunar valves Aortic Pulmonic

Answer 186

relaxes fills with blood

Answer 187

Fatty streaks form early but don’t cause symptoms. Fibrous plaques develop, partially blocking arteries and causing stable angina. Plaque rupture leads to clots, causing unstable angina (partial block) or MI (complete block).

Answer 188

atherosclerosis

Answer 189

asymptomatic

Answer 190

Dual anti platelet

Answer 191

Myoglobin, CK-MB

Answer 192

MONA: morphine, oxygen, nitroglycerin, aspirin (inhibits platelet aggregation)

Answer 193

reduce platelet aggregation

Answer 194

ST segment depression Myocardial ischemia ST segment elevation Myocardial infarction

Answer 195

cardizem [Calcium channel blocker]

Answer 196

Fluid is accumulating somewhere & something is not going right. Indicative of CABG failing so blood may be leaking out to other parts of the body. Report to DR right away. They will likely want to do pericardiocentesis to remove fluid.

Answer 197

anti coagulation

Answer 198

the patient

Answer 199

UA is longer

Answer 200

, call 911

Week 1 - Cardiovascular Flashcards

(278 cards)