CC Chapter 12

defibs

ICD placed for prevention of lethal dysrhythmias, at risk of sudden cardiac death CANNOT GO IN MRI

aortic dissection

911 tear in intimal layer of the vessel creating false lumen where blood flows sudden severe chest pain is <C type A: most concerning bc involves ascending aorta type B: in descending thoracic and abdominal aorta, pain between scapulae. normally in younger with marfan. control bp, decrease contraction with bb , emergency surgery

The patient presents to the emergency department with severe substernal chest discomfort. Cardiac enzymes are elevated and his ECG shows ST-segment depression in V2 and V3. This patient is most likely experiencing: A) non-Q-wave myocardial infarction (MI). B) pulmonary embolism. C) Q-wave myocardial infarction (MI). D) right ventricular infarction.

A The non-Q-wave MI usually results from a partially occluded coronary vessel, and it is associated with ST-segment depression in two or more leads along with elevated cardiac enzymes.

An adult patient suffered an anterior wall myocardial infarction (MI) 4 days ago. Today the patient is experiencing dyspnea and sitting straight up in bed. The nurse's assessment includes bibasilar crackles, an S3 heart sound with a heart rate of 125 beats/min. What condition are these signs and symptoms consistent with? A) Heart failure B) Papillary muscle rupture C) Pericarditis D) Pulmonary embolism

A These are classic signs of fluid overload and heart failure. Presence of a heart murmur, not the S3, might alert the nurse to a papillary muscle rupture. The patient with pericarditis may have chest pain and a pericardial friction rub.

The patient presents to the emergency department after having crushing chest pain for the past 5 hours. The ECG and laboratory work confirm suspicions of an acute myocardial infarction (AMI). Which findings would be the most conclusive that the patient is having an AMI? (Select all that apply.) A) ECG changes with ST-elevation B) Elevated CK-MB isoenzymes C) Elevated serum troponin levels D) Elevated urinary myoglobin level

ABC ST-segment elevation and elevated cardiac enzymes are seen in Q-wave MI. Serum myoglobin may assist in diagnosis of AMI.

Which statements related to the management of unstable angina are true? (Select all that apply.) A) Aspirin is given at the onset of each chest pain episode. B) Calcium channel blockers help to reduce symptoms. C) Early revascularization (e.g., angioplasty) may be helpful. D) It is best treated with rest and nitroglycerin.

ABC Unstable angina can be treated by conservative management or early intervention with percutaneous intervention or surgical revascularization. Conservative intervention for the patient experiencing angina includes the administration of nitrates, beta-adrenergic blocking agents, and/or calcium channel blocking agents. Angioplasty, stenting, and bypass surgery are approaches to revascularization. Rest and nitroglycerin are treatments for stable angina.

Angiotensin-converting enzymes inhibitors (ACE inhibitors) should be started within 24 hours of acute myocardial infarction (AMI) to reduce the incidence of: A) hibernating myocardium. B) myocardial remodeling. C) myocardial stunning. D) tachycardia.

B Myocardial remodeling is a process mediated by angiotensin II, aldosterone, catecholamine, adenosine, and inflammatory cytokines, which causes myocyte hypertrophy and loss of contractile function in the areas of the heart distant from the site of infarctions. ACE inhibitors should be ordered.

The patient, who is being treated for hypercholesterolemia, complains of hot flashes and a metallic taste in the mouth. These are common side effects of: A) bile acid resins. B) clopidogrel. C) nicotinic acid. D) statins.

C Common side effects of nicotinic acid include metallic taste in mouth, flushing, and increased feelings of warmth.

A 67-year-old female is admitted to the emergency department complaining of mid-back pain and shortness of breath for the preceding 2 hours. She also complains of nausea and states that she vomited twice before coming to the hospital. She denies any chest discomfort or arm pain. The presenting symptoms suggest that this patient may be: A) exhibiting flu symptoms. B) having an anxiety attack. C) having a myocardial infarction (MI). D) suffering from osteoporosis.

C Women are more likely to have atypical signs and symptoms of acute myocardial infarction (AMI), such as shortness of breath, nausea and vomiting, and back or jaw pain.

A patient is complaining of midsternal chest discomfort radiating down the right arm. The discomfort has been present for about 5 minutes. The patient is also asthmatic and allergic to calcium channel blockers. The medication of choice for this patient at this time is: A) isoptin. B) metoprolol. C) nifedipine. D) nitroglycerin sublingual.

D

The most sensitive cardiac enzyme to assess myocardial necrosis is: A) CK. B) CK-MB. C) potassium. D) troponin I.

D Troponin I has a greater specificity than other tests in the diagnosis of acute myocardial infarction (AMI) at 7 to 14 hours after the onset of chest pain.

CAD dx

EKG: find rhythms, pericarditis, pulmonary diseases, lv hypertrophy, mi, injury Cxray: find cardiomegaly, cardiac positioning, fluid infiltrating pulmonary space, structural changes holter: find dysrhythmias. do normal activities ETT: if oxygen demand exceeds supply, ischemia. BB held before test echo: assess valvular function, congenital defect, measure size, cardiac disease, eval ventricular function, dx myocardial tumors, measure CO. ejection fraction is blood ejected from lv during systole 55-60% TEE:visualize prosthetic valves, mitral valve, aortic dissection, endocarditis, congenital, cardiac masses, embolic phenomena MRI: tissues, structures and blood flow. DO NOT DO WITH PACE MAKER, D FIB< COCHLEAR, BRAIN CLIP cardiac cath and angio: to measure pressure in chambers, CO, and blood gas, confirm lesions in coronary arteries, assess lv function. R sided- ra, rv, pulmonary artery and measures pressures. l sided- coronary arteries to note lesions and bypass grafts to eval angina spasms in infart and do percutaneous angio or stent

AMI: dx

based on symptoms of 12 lead and enzymes ecg: st elevation in two or more contiguous leads lab: elevated serum enzymes- ck, ckMB, trops, myoglobin

AMI: patho

caused by imbalance between myocardial oxygen supply and demand because of decreased coronary artery profusion. secondary to atheroscleoris. reduced blood flow causes oxygen deprivation to myocardial cells and then cellular death

variant angina

d/t coronary artery spasms at rest. marked ST elevation during spasm

factos that influence oxygen demand and supply

demand: increased hr (exercise, tachy, fever, pain...), increased preload (volume overload), increased after load (htn, aortic stenosis, vasopressor), increased contractility (exercise, meds, anxiety) reduced: coronary artery disease, coronary spasms, anemia, hypoxemia

management after cardiac surgery

pulmonary artery cath, arterial cath, peripheral iv lines, pleural chest tubes, mediastinal tubes, indwelling urinary cath

lab dx

electrolytes: sodium, pot, calc, and mag can cause dysrhythmias enzymes: injured cells release enzymes CK: increase within 2-6hr after myocardial muscle damage, peak 18-36hr, normal 3-6day CK-MB: normal is 0-6% or 0.3-4.9. elevated after AMI, cardiac surgery, trauma. within 4-8hr, peak 18-24hr, normal 3day trop I and trop T: normally undetectable. within 1hr. normal trop I is <0.5, normal trop II is <0.1 myoglobin: within 30-60min, normal in women are 58, normal in men are 72. test only used with other tests

HF: s/s

exertional dyspnea, paroxysmal nocturnal dyspnea, orthopnea, fatgability, loss of appetite, abdominal bloating, nv, organ system dysfunction especially renal

care after cath and angio

extremity immobile, mark hematoma, bed rest, hob <30, peripheral pulses, fluid intake, io, adverse reaction, pains

angina

from myocardial ischemia from imbalance between oxygen supply and demand

AMI: interventions

goals: establish reperfusion, reduce infarct size, prevent and treat, emotional support pain: morphine sulfate. observe for hypotension and respiratory depression. then nitro to reduce pain. increases coronary perfusion. give until chest pain absent O2: main o2 above 90% antidysrhytmics: common prevent platelet aggregation: aspirin immediately if suspected. add thienopyridine (clopidogrel, prasugel, or ticagrelor) or gp IIb inhibitor thrombolytic: pt must be symptomatic for less than 6hr, pain for 20 min unrelieved by nitro, 12 lead with st elevation in two or more ECG. give w/i 30-60min. (nursing care: identify rapidly, screen contraindications, 3 iv lines, ecg)

atherosclerosis

inflammation from endothelial injury to fatty streak, plaque, and lesion. due to fat lazy smokers with diabetes. injury -> inflamed endothelial -> released cytokines -> macrophages adhere to endo -> release enzymes and toxic oxygen -> oxidative stress-> oxidize ldls -> further injury -> macrophages engulf ldl -> foam cells -> fatty streak -> plaque -> release of angiotensin 2 and fibroblast -> stimulate smooth muscle proliferation -> collagen cap

pericarditis

inflammation of pericardium, the fluid squeezes heart=tamponade. epicardium can thicken precordial pain radiating to shoulder, neck, back, arm. intensified during breathing, movement, coughing, swallowing. friction rub, dyspnea, weak, fatigue, temp elevation, increased wbc and sed rate, anxiety pericardial friction rub is dx ecg can help confirm: concave ST elevation and PR deviations, flat T treat: analgesics or anti-inflammatory (colchicine and ibuprofen), antibiotics if bacterial tampon treatment: pericardiocentesis

unstable angina

more severe, may occur at rest, more frequent nitrate therapy. ST depression, T way inversions, or normal

CAD

narrowing or occlusion of coronary arteries

angina: meds

nitrates, bb, ccb, and ranozaline and/or angioplasty, stenting, bypass

AMI

non ST segment elevation myocardial infarction (NSTEMI) or STEMI

angina: s/s

pain in jaw, l shoulder, l arm diaphoresis, pressure, burning, squeezing, 1-5 min, clenched fist.

HF: complications

pulmonary edema: vascular system full and engorged= increasing volume and pressure of blood in pulmonary vessels, increased pressure inc capillaries, leaking fluid into lung tissue spaces. edema reduces lung tissue space= dyspnea, cyanosis, anxiety, pallor, blood tinged frothy sputum, rr acidosis med- iv diuretics, ultrafiltration, or hemodialysis. furosemide is MC loop diuretic. IV nitro for reduction in preload and afterload cardiogenic shock: most acute form of pump failure. after severe mi, dysrhythmias, decompensated hf, pulmonary embolus, tamponade, ruptured aaa

parasympathetic nervous system

releases acetylcholine through stimulation of vagus nerve and slows conduction

intracoronary stent

tubes implanted at site of stenosis to widen arterial lumen by squeezing athrolsclerotic plaque against walls. anticoagulation before, during, and after assess peripheral pulses, skin color, temp gp IIb inhibitor after stent must take antiplatelet like aspirin and clopidogrel, prasugrel, or ticagrel. aspirin forever.

heart murmur

turbulence of blood flow through the valves 1-6

stable angina

with exertion and is relieved by rest

complications of cardiac surgery

dysrhythmias (a fib, a flutter, v tach, v fib), mi, shock, pericarditis, pericardial effusion, cardiac tamponade

AMI: complications

dysrhythmias, hf, rupture of portion of heart, thromboembolism, pericarditis, infarct, cardiogenic shock

CAD management

risk factor management: low fat, low cholesterol, exercise, weight loss, smoking cessation, control diabetes and htn. if ldl not regular after 6 month then meds meds: statins, bile acid resin, nictonic acid

HF: interventions treat s/s, prevent, treat cause

1. improve pump function, fluid removal, and perfusion: first line med ACE inhibitors, angiotensin blockers, diuretics. when volume status stable add bb. ace and bb is hallmark 2. add digoxin, spironolactone, eplerenone, hydralazine, nitrate 3. nesirtide admin for dyspnea at rest 4.reduce cardiac workload and o2 consumption 5. aortic balloon pump and LVAD 6. biventricular pacing for cardiac resynchronization improves exercise tolerance 7. schedule rest periods 8. optimize gas exchange 9. semi fowlers 10. iv diuretics (furosemide and bumetanide is preferred) 11. anticoagulation 12. control sodium and fluid retention. no more than 2l a day and 2g sodium 13. daily weights

The initial drug recommended at the onset of acute myocardial infarction (AMI) to reduce platelet aggregation is: A) aspirin. B) lidocaine. C) nitroglycerin. D) oxygen.

A

AAA

atherosclerosis and degeneration of elastin and collagen are causes hereditary, males risks: fat lazy smokers with htn, and diabetes mostly asymptomatic, back of ab pain, avoid rupture larger than 6cm carrying great risk treat larger than 5.5 is surgery

AMI: assessment

chest pain, severe crushing, tight, squeeze, back, arms, neck, jaw, skin cool clammy pale diaphoretic, dusky or ashen (hyperthermia), dyspneic, tachypneic faint, NV, hypotension, bradycardia, tachy, heart block, anxious, restless. behavioral: denial, depression and impending doom women more likely to have atypical signs: fatigue, diaphoresis, indigestion, arm or shoulder pain, NV

aneurysm

diseased area of an artery causing dilation and thinning false: from a complete tear in arterial wall with blood leaks forming clot true: fusiform, saccular, and dissection ones, fusiform in aaa is MC

CAD patho

due to atheroscleoris. results in ischemia when vessel is reduced by 70%/

HF: manifestations

dyspnea, fatigue, exercise intolerance, fluid retention

HF

hearts inability to pump blood sufficiently to meet body metabolic demands. from any disorder that impairs the ability of ventricle to fill or eject CAD is primary cause

critical lab values

hypokalemia: <2.5 hyperkalemia: >6.6 hypocalcemia: <7 hypercalcemia >12 hypomagnesemia: <5 hypermagnesemia: >3

CABG

ischemic area of myocardium is revascularized by implantation of internal mammary artery or bypassing coronary occlusion with saph vein graft indications: chronic stable angina, l main coronary occlusion, triple vessel CAD, unstable angina, lv failure, lesions not amenable to PTCA, and PTCA failure with cardiopulmonary bypass. cardioplegia stops heart internal mammary revascularization has better long term patency and is preferred graft for lesions of the l anterior descending coronary artery chest and mediastinal tubes are places

endocarditis

microorganisms attach into endocardial surface like staph aureus s/s: fever, shaking, chills, night sweats, cough, weight loss, malaise, weak, fatigue, ha, msk complaints, murmurs, hf s/s janeway lesions (palms and soles), osler nodes (red purple on fingers and toes), roth spots (retinal hemorrhages) treat: antibiotics, valve replacement, prevention, antibiotic prophylaxis

HF: dx

physical exam edema perfusion status lung sounds cxray hemodynamic monitoring noninvasive imaging (echo is most useful test) arterial blood gas serum electrolyte (low sodium is a sign of advanced hf) cbc (anemia) normal bnp is less than 100. greater than 500 is mortality risk liver function studies (enlarged and tender, transaminase and bili elevated) ecg (l bundle blocks, pvc, pac)

minimally invasive coronary artery surgery

port access artery bypass or minimally invasive coronary artery bypass PACAB: heart is stopped, ports in chest MIDCAB: no bypass, only when one or two arteries will be bypassed

sympathetic nervous system

releases norepi causing arterial vasoconstriction and increased sinus node discharge, increase contraction, accelerated av conduction time

angina: percipitators

stress, temp extremes, big meal

HF: patho

systolic HF: from impaired pumping of ventricles diastolic hf: from impaired filling or relax of ventricles MC is l sided: ventricle cannot pump right, decreases CO= poor perfusion. causing congestion, fluid accumulates in lungs, increased lung pressure, gas exchange impaired, back flow in heart. co2 increase, rr increase, hr increase = overload renin angiotensin aldosterone and adrenergic nervous system turns on. angiotensin II is a vasoconstrictor promotes salt and water retention so blood volume increases adrenergic nervous system causes tachy, vasoconstriction, and increased contractility

Percutaneous transluminal coronary angio

to compress intracoronary plaque to increase blood flow to myocardium. treatment of choice for pt with uncompromised collateral flow, non-calcified lesions, and lesions not at vessels goal: open arteries

radiofrequency cath ablation

to treat dysrhythmias when meds, cardioversion dont work to permanently interrupt electrical conduction in region of dysrhythmogenic cardiac tissue indications: v tach, a fib, a flutter, av nodal reentry tach, symptomatic paroxysmal atrial fib starts with ep, cath with electrode, painless radiofreqeuncy, causes coagulation and necrosis without killing tissues, stops area from sending extra impulses

permanent pacemakers

treat conduction disturbances sinus node, av block, neurocardiogenic syncope, tachys through the venous system and into the RA and or RV