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Advanced Med-Surg > Cardio2 > Flashcards

Cardio2 Flashcards

1
Q

Microbial infection of the endocardium. Staph or strep are the most common bacteria. Valves are the most often affected.

A

Infective endocarditis. Can be acute or chronic if they don’t respond well to the antibiotic. High rate of mortality.
Vegetative lesion from on endocardium. Large lesions may embolize.

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2
Q

S/s of endocarditis?

A

Fever/chills. Fatigue, anemia, anorexia w/ weight loss, murmur, HF, petechiae, splinter hemorrhages.

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3
Q

Both are associated with endocarditis.
Janeway lesions?
Osler’s nodes?

A

Janeway: Non-tender, macule on palms of hands and soles of feet.
Osler’s: Small, raised, tender, bluish areas on the fingers and toes. Look like little red hemorrhages.

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4
Q

Diagnostics for endocarditis?

A

Blood cultures, CXR, echocardiogram (TEE), cardiac catheterization

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5
Q

Treatment for endocarditis?

A

Rest, antimicrobial therapy, analgesics, aseptic technique, monitor for signs of HF. Surgical valve replacement: HF persistent, emboli. Prevent relapse.

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6
Q

Inflammation of the pericardium. May be chronic or acute. Causes?

A

Infective organism, MI (Dressler’s syndrome), autoimmune disorders, TB, radiation therapy, trauma, renal failure, malignancy of the heart and lung area. Post pericardiotomy syndrome after open-heart surgery.

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7
Q

S/s of pericarditis?

A

Pain similar to cardiac ischemia but aggravated by inspiration, relieved by tripod position. Dyspnea, fever, increased WBC, symptoms of HF when left untreated, atrial fib. Pericardial friction rub: the single most classic symptom that isn’t seen with an MI

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8
Q

Diagnostics for pericarditis?

Complications?

A

Echocardiogram, 12 lead EKG, cardiac enzymes, CXR

Pericardial effusion, cardiac tamponade

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9
Q

Interventions for pericarditis?

A

Underlying cause. Pain control: positioning, NSAIDS (24-48hrs turnaround), steroids, no morphine. Antibiotics, pericardiocentesis, radiation/chemo, pericardial window. Best rest, O2, education.

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10
Q

S/s of cardiac tamponade?

Treatment?

A

Decreased CO, JVD, muffled heart tones, low arterial BP, pulses paradoxus. Decreased PMI: decreased heart sounds/pulse pressure. Tachycardia.
Treatment is pericardiocentesis.

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11
Q

Systemic inflammatory disease that can involve the heart, kidneys, CNS, skin, and connective tissue.

A

Rheumatic fever.

Complication of group A beta-hemolytic strep URI.

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12
Q

Cardiac damage from rheumatic fever. Develops in 50% of rheumatic fever patients.

A

Rheumatic carditis. Thickened sac with effusion. Adult: mitral valve. Chronic inflammatory condition. Ask about childhood diseases.

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13
Q

S/s of rheumatic carditis?

A

Tachycardia, cardiomegaly, precordial pain. New or changed murmur. EKG changes, prolonged PRI. Pericardial friction rub. Symptoms of HF. Positive for strep infection.

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14
Q

Chronic disease of the heart muscle with ventricular dysfunction. High mortality. What are the four categories?

A

Cardiomyopathy.

Dilated is the most common. Hypertorphic. Restrictive. Dysrhythmogenic right ventricular.

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15
Q

This type of cardiomyopathy is more common in males. Dilation in one or both of the ventricles.

A

Dilated cardiomyopathy.

Results in decreased CO. S/s similar to HF.

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16
Q

Probable cause of SCD in athletes. 50% genetic.

Less common one, in which 1 or both ventricles are stiff.

A

Hypertrophic cardiomyopathy. LV is stiff and thick, it can’t relax.
Restrictive cardiomyopathy.

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17
Q

Treatment for cardiomyopathy?

A

Depends on the type, similar to HF. Diuretics, vasodilators, meds to increase contractility and mitigate compensatory responses. Monitor for rhythm disturbances. Surgical interventions like shaving away the muscle

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18
Q

Valve that separates the RA from the RV.

Separates the LA from the LV.

A

Tricuspid valve.

Mitral valve.

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19
Q

Valve that separates RV from pulmonary circulation.

Separates LV from the aorta.

A

Pulmonic valve.

Aortic valve.

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20
Q

S/s of mitral valve prolapse?

A

Asymptomatic. Atypical chest pain, palpitations, fatigue, dizziness, dyspnea, anxiety, late systolic murmur, mid-systolic click.

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21
Q

Increased LA pressure causes the LA to dilate, leading to a fixed left-sided CO and increased pressure in the pulmonary vascular bed.

A

Mitral stenosis.
Leads to pulmonary congestion and increased pressure in the RV, leading to RHF.
Risk for atrial fib due to the dilated LA.

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22
Q

S/s of mitral stenosis?

A

Fatigue, weakness, anemia, enlarged LA on CXR, diastolic murmur (can hear an opening snap), symptoms of right and left HF, atrial fib, decreased life expectancy

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23
Q

Diagnostic tests for mitral stenosis?

A

Clinical symptoms, echocardiogram and EKG, CXR, cardiac catheter

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24
Q

Most common significant cardiac dysrhythmia. Increases risk for stroke, HF, and all-cause mortality.

A

Atrial fibrillation.

Prevention of thromboembolism (anticoagulation reduces risk of stroke). Rhythm and rate control.

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25
Q

Interventions for mitral stenosis?

A

Digoxin, diuretics, beta blockers, calcium channel blockers, low Na diet, attempt conversion of a fib, surgery

26
Q

Causes of mitral regurgitation? S/s?

A

Aging, infective endocarditis, papillary muscle dysfunction (MI), rheumatic fever.
S/s: fatigue, weakness, right and left HF.

27
Q

Diagnostic tests for MR?

A

S3 and systolic murmur. CXR showing left atrial hypertrophy. EKG, echocardiogram, cardiac catheterization

28
Q

Earlier s/s of aortic stenosis?

A

Angina: oxygen demands increase supply.
Syncope: decrease oxygen
Dyspnea: pulmonary congestion

29
Q

Later s/s of aortic stenosis?

A

Fatigue, weakness, orthopnea, dyspnea, peripheral edema, JVD, ascites

30
Q

Interventions for aortic stenosis?

A

Oxygen, digoxin, beta blockers, diuretics, nitrates, low Na diet, balloon valvuloplasty, valve replacement

31
Q

S/s of aortic regurgitation?

A

May take many years to develop. Exertional dyspnea. PND. Nocturnal angina with diaphoresis.

32
Q

The volume of blood ejected from the LV into the aorta every minute.
The percent of blood in the LV ejected with each beat

A

Cardiac output, 4-6 L/min

Ejection fraction, 55-65/70%

33
Q

Caused by arteriosclerosis in the coronary arteries.

A

Coronary artery disease/heart disease.
Plaque can decrease blood flow to the heart muscle, causing angina. Plaque can rupture and block an artery, leading to ischemia or infarction.

34
Q

Hardening of arterial walls.

A

Arteriosclerosis. Walls of arteries becoming thick and stiff. Often results from the aging.

35
Q

Pathophysiology of CAD?

A

Accumulation of lipid and fibrous tissue within the coronary artery results in narrowing and possible occlusion of that artery.

36
Q

Med that decreases LDL and triglycerides by decreased synthesis of cholesterol in the liver.

A

Statins.
Side: Myalgia, GI symptoms.
Adverse: rhabdomyolysis. Contraindicated in liver disease and pregnancy.

37
Q

Nursing considerations for statins?

A

Monitor liver function tests before starting therapy, at 3-6 months and periodically. Most of these drugs recommend taking in the evening. Grapefruit can potentate these drugs. Pt should notify provider of any muscle weakness or aching.

38
Q

Ischemic event that is limited in duration and does not cause permanent damage. Interventions are aimed at decreased myocardial oxygen demands or increased oxygen supply.

A

Stable angina.

Meds include nitroglycerin, beta blockers, and Ca channel blockers.

39
Q

Etiology and clinical manifestations of stable angina pectoris?

A

Myocardial oxygen demands exceeds supply. Pattern familiar to pt.
Chest pain with exertion. Frequency, duration, and intensity of symptoms stable over time. Mild activity limitations. Relieved with rest or meds.

40
Q

This med causes vasodilation of vascular system in both coronary and peripheral arteries. Improves blood flow to the myocardium and decreases myocardial oxygen demand.

A 
Nitroglycerin (nitrate). Several different routes of admin.
isosorbide dinitrate (Isordil)
isosorbide mononitrate (Imdur).
41
Q

Patient teaching for nitrates?

A

Keep tabs in original dark bottle in a cool place. Replace q6months. Keep with them at all times.
When pain occurs, stop actives and sit/lie down. 1 tab sl q5minutes up to 3 times or until pain relieved. Call 911 if doesn’t work.
Take Tylenol for H/A. Don’t use ED meds.

42
Q

These meds are usually cardioselective for ACS and angina. Blocks SNS stimulation. Decreases HR, contractility, size of the infarct, reinfarction, mortality.

A

Beta blockers.
metoprolol succinate (Toprol XL)
atenolol (Tenormin)
carvedilol (Coreg)

43
Q

Syndrome seen in patients with coronary atherosclerosis, emergent due to clot rupture. Varying degrees of coronary artery occlusion which may result in?

A

Acute coronary syndromes (ACS).

Unstable angina, MI, NSTEMI, STEMI

44
Q

Coronary artery occlusion stages in ACS?

A

Ischemia, injury, infarction.

Ischemia and injury may be reversible. Infarction is permanent.

45
Q

Causes of occlusion in ACS?

A

Coronary artery thrombosis, coronary artery spasm. Decreased coronary blood flow due to dysrhythmias, pulmonary embolism, hypotension, shock. Increased myocardial workload beaus of emotional stress, increased blood volume, or exertion.

46
Q

Chest pain or discomfort that occurs at rest or with exertion. Marked activity limitations.

A

Unstable angine.

Increase in pain, frequent, duration, or intensity. Lasts longer than 15 minutes and is poorly relieved.

47
Q

Death of myocardial tissue (necrosis) due to a blockage of one or more branches of the coronary arteries. Occurs over hours, not days.

A

Myocardial infarction (AMI/MI)
Ischemia can lead to tissue necrosis or cell death if blood flow is not restored
Check the PT/INR and PTT if the patient is going to the cath lab

48
Q

Clinical manifestations of MI? Diagnosis of MI?

A

Sudden, severe, crushing pressure mid or sub-sternal. May radiate into the back, jaw, the left arm, the right arm. Unrelieved by sl nitro or rest. Dyspnea, indigestion, n/v, diaphoresis, denial.
Patient history, EKG changes, elevated cardiac enzymes

49
Q

Includes unstable angina, MI, STEMI, NSTEMI.

A

Acute coronary syndrome (ACS)
STEMI: ST elevation MI. Necrosis (injury) and requires immediate treatment
NSTEMI: Non-ST elevation MI. ST changes or depression indicates myocardial ischemia

50
Q

What does injury show as on an EKG?

A

Produces ST segment elevation. Injury can be myocardial infarction or necrois

51
Q

Explain troponin labs (especially used for MI)?

A

Increases three hours after the onset of pain and peaks in 16-24 hours. Returns to normal in 14 days.
Norm: 0-0.05 ug/L

52
Q

Explain CK-MB labs (especially for MI)?

creatinine-kinase

A

Becomes increased in 4-6 hours after an MI and peaks in 24 hours. Returns to normal in 14 days.
Norm: 0-3 ng/mL

53
Q

ONMA for MI? Other emergency interventions?

A

Oxygen, nitrates, morphine, aspirin.
Monitoring of EKG and 12 lead. Labs, especially for enzymes and coagulation studies. Transport for emergent cardiac catheterization

54
Q

Interventions for MI?

A

Priorities are to improve coronary perfusion, coronary oxygenation, relieve chest pain. Monitor for dysrhythmia, decrease workload of the heart. Anticipate, prevent, and treat complications. Phase I cardiac rehab.

55
Q

Examples of meds for AMI/MI?

A

Oxygen, morphine, thrombolytic agents for emergencies. Nitrates, beta blockers, ACE inhibitors, anti platelets, cholesterol lowering agents.

56
Q

This medication increases arterial saturation. Helps to relieve the pain of MI.

A

Oxygen. Key to increasing myocardial oxygen supply. 2-4L/min via nasal cannula. Semi-fowler’s position.

57
Q

This type of med primarily works in the veins. Inhibits platelet aggregation and vasoconstriction.

A

Antiplatelet agents.
Aspirin 162-325mg daily. 325mg chewed immediately for suspected MI. Other antiplatelets added to aspirin to prevent occlusion of stents (clopidogrel, prasugrel, ticlopidine)

58
Q

Meds that decrease preload and after load. Given for 6 weeks post MI, or indefinitely for HF. Retains potassium.

A

Angiotensin converting enzyme inhibitors. Ends in -pril.

Avoid NSAIDs

59
Q

These meds are to be used if angioplasty is unavailable. Works by lysing the clot that is obstructing the coronary artery, restoring perfusion to the myocardium. Need to be given emergently within 6-12 hours after onset of STEMI. Screen for bleeding risks first.

A

Thrombolytic agents.
Pt must be monitored continuously for signs of bleeding. May cause repercussion dysrhythmias.
alteplase (tPA), rteplase, tenectaplase (TNK)

60
Q

Examples of complications of MI?

A

Extension of infarct, cariogenic shock, cardiac wall or septal rupture, HF (systolic), dysrhythmias

Advanced Med-Surg (11 decks)

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