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Nur 3010 exams > CHF + CAD > Flashcards

CHF + CAD Flashcards

1
Q

iclicker: what labs do we draw for HF

A
  • BNP d/t stretch of ventricles from overload volume
  • TROP: r/t to cardiac cell death, or MI (heart attack)
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2
Q

what is heart failure (what, affects what system, results in s/sx (2)

A

clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of the ventricles to fill or eject blood
- sometimes called “CHF” d/t systemic & pulmonary congestion (FLUID backs up -> LUNGS)
- results in s/sx of 1) fluid overload, 2) inadequate tissue perfusion

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3
Q

what are the causes of CHF (5) medical

A
  • MAIN: coronary artery disease/ischemia/MI (atherosclerosis) (ineffective pumping)
  • valve disease: stenosis/regurgitation
  • structural heart disease: dilated, restrictive and hypertrophic cardiomyopathies
  • dysrhythmias: afib
  • congenital defects: peds
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4
Q

what are the risk factors for HF (7)

A
  • HTN
  • uncontrolled DM
  • illicit drug use
  • pregnancy
  • lung disease (R side HF)
  • sleep apnea (osa)
  • hyperthyroidism, severe anemia
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5
Q

specific causes of R sided HF (isolated)

A
  • left sided HF (fluid backs into R side, damages pump)
  • pulmonary HTN
  • lung disease (COPD, pulmonary fibrosis)
  • pulmonary embolism
  • OSA (obstructive sleep apnea)
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6
Q

2 types of HF

A

1) Heart failure with reduced ejection fraction (HFrEF): systolic failure
2) Heart failure with preserved ejection fraction (HFpEF): diastolic failure

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7
Q

describe heart failure with reduced ejection fraction (HFrEF): systolic failure (what, EF, leads to, danger)

A
  • inability of L ventricle to pump effectively
  • EF <40% (decreased CO) HALLMARK DIAGNOSTIC
  • decreased EF -> loss of perfusion along w/ congestion
  • if EF gets below 30% -> higher mortality s/d lethal arrhythmias (candidates for AICD - defib)
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8
Q

describe heart failure preserved ejection fraction (HFpEF): diastolic failure

A
  • L ventricle function >50% usually w/ high BP (relatively normal)
  • diastolic dysfunction
  • inability of L ventricle to RELAX d/t noncompliance
  • primary issue is: congestion

-TIP: blood -> peripheral tissues BUT still congestion

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9
Q

clinical manifestations of heart failure (where, consequences) general

A
  • where: Right and left
  • consequences: congestion, poor perfusion/low CO
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10
Q

clinical manifestations of R Heart Failure (6)

A
  • viscera/peripheral congestion
  • JVD (super distended, gorged)
  • dependent edema (abdomen, legs, all over)
  • hepatomegaly (edema in liver)
  • ascites (fluid in peritoneal cavity)
  • wt. gain (monitor, self weight QD)
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11
Q

clinical manifestations of L Heart failure (6)

A
  • pulmonary congestion, crackles
  • S3 or ventricular gallop
  • dyspnea on exertion (DOE)
  • Low O2 sat
  • dry, non-productive cough initially (MAIN)
  • oliguria (urine output <400mL/day) (sign of confusion)
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12
Q

Clinical manifestations (congestion sx.) (11)

A
  • Dyspnea
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Cough
  • Pulmonary crackles
  • Weight gain
  • Dependent edema
  • Abnormal bloating
  • Ascites
  • JVD
  • Fatigue
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13
Q

clinical manifestations of low CO/poor perfusion (9)

A
  • Decreased exercise tolerance
  • Muscle wasting/weakness
  • Anorexia
  • Weight loss
    -Lightheadedness or dizziness
  • Altered mental status
  • Resting tachycardia
  • Oliguria (low flow kidney -> decrease urine output)
  • Cool or vaso-constricted extremities
  • Pallor or cyanosis
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14
Q

what are the diagnostic tests used for HF (4)

A
  • BNP
  • Chest XR
  • ECG
  • Echo
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15
Q

what does BNP cause

A
  • released from ventricles in response to wall stretch to stimulate vasodilation and diuresis
  • indicates: HEART FAILURE
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16
Q

most common HF

A

left sided HF

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17
Q

chest XR identify with HF

A
  • identifies B/L pulmonary infiltrates/engorged pulmonary vessels
  • may identify cardiomegaly (focal pneumonia?)
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18
Q

ECG identify with HF

A
  • sinus tachycardia
  • ventricular hypertrophy (cardiologist)
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19
Q

Echo identify with HF

A

GOLD STANDARD to track disease
- determines EF, diagnose structural issues (wall stiffness, valve regurgitation/stenosis)
- typically done q6-12 months to track disease progression in HF

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20
Q

what are the main medications we learned for HR management (8)

A
  • ACE inhibitors
  • ARBs
  • ARNI
  • vasodilators
  • beta blockers
  • diuretics
  • calcium channel blockers
  • digitalis
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21
Q

describe angiotensin-converting enzyme (ACE inhibitors) (function, causes, monitor, suffix)

A
  • first line medications for HF
  • function: drops BP
  • causes: vasodilation, diuresis, decreased afterload
  • monitor: hTN, HYPER-kalemia, altered renal function, DRY HACKING COUGH, ANGIOEDEMA (fatal, rare), teratogenic
  • pril suffix (ex: lisinopril)
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22
Q

describe angiotensin II receptor blockers (ARBs) (what, function, risk factors/ monitor, suffix)

A
  • alternative to ACE inhibitors
  • function: drops BP (similar to ACE), functions on different part of RAAS system)
  • risk factors/ monitor: HYPERkalemia, teratogenic
  • sartan suffix (Losartan)
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23
Q

describe vasodilators (function, prefix, meds? (5))

A
  • function: drops BP, lowers after load
  • nitroglycerin included (nitro-prefix)
  • hydralazine, nitroprusside, nitroglyceride, isosorbide digitate (rare), minoxidil (rare)
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24
Q

describe beta blockers (selective/nonselective) (function, efficiency, precaution in?, suffix, selective vs no selective, acute situation?, masks —?, inhibits, causes 3)

A
  • prescribed in addition to ACE inhibitors
  • function: drops HR (mainly) & BP
  • may be several wks. before effects seen; use with caution in patients with asthma
  • lol suffix (metoprolol)
  • selective: affects only the heart
  • non selective: affects heart & lungs
  • NOT ideal in ACUTE situations (it slows heart, reduces contractility - more common in Dcd in hospital)
  • may mask: hypoglycemia d/t diff. s/sx
  • inhibit sympathetic system of heart
  • causes: fatigue, malaise, erectile dysfunction
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25
Q

describe diuretics (3 types) (function, monitor)

A
  • function: drops BP, decreases fluid volume
  • monitor: Serum electrolytes (may decrease!)
    1) loop diuretic/k wasting
    2) K+ sparing diuretics/aldosterone antagonists
    3) thiazide diuretics
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26
Q

describe loop diuretic/k wasting (function, ex., teach)

A
  • drops serum K+
  • ex: lasix/furosemide, bumex/bumetanide
  • teach: avoid licorice root (drops k+)
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27
Q

describe K+ sparing diuretics/aldosterine antagonists (aka, function, ex, teach)

A
  • aka: aldosterone receptor antagonist (ARAs)
  • block action of aldosterone (Na/H2O retention)
  • ex: spironolactone
  • teach: avoid K+ rich foods - melons, salt sub., leafy veggies
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28
Q

describe thiazide diuretics (best for?, effectiveness, use for, function, ex, side effects)

A
  • first line antihypertensives for African Americans
  • less effective than diuretics, causes vasodilation effect
  • use for patients with HTN + mild retention
  • ex: hydrochlorothiazide
  • side effects: hyperkalemia, impaired kidney function
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29
Q

describe calcium channel blockers (function, ex: HR affect, ex: no HR affect)

A
  • drops BP, sometimes HR (depending on drug)
  • function: blocks influx of calcium, decreases vascular resistance (vasodilation)
  • ex: (HR affect) nifedipine, verapamil, cardizem
  • ex: (no HR affect) Norvasc
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30
Q

describe digitalis (causes, monitor, toxicity, ex)

A
  • decreases HR; no affect on BP
  • causes: improved contractility
  • monitor: digitalis toxicity esp. if patient is HYPOkalemic (monitor K+)
  • toxicity: vision changes (color changes, fuzziness, difficulty reading - retina issues), nausea/vomiting (notify provider if occurs)
  • ex: digoxin (inotrope)
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31
Q

what should always be done for HF medical management

A
  • check BP, renal function prior to drug administration
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32
Q

what should be done for meds that drop BP (3)

A
  • beware of orthostatic changes
  • slow position changes
  • usually hold for less than systolic <100
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33
Q

what should be done for meds that drop HR

A
  • hold for less than 60
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34
Q

how to treat hypokalemia (4)

A
  • PO (easier), taste/size of pills/NPO status can limit efficacy
  • replace IV slowly: 10 mEq in 50cc/hour
  • large bore is preferred! -> K+ is painful to veins
  • KEY: slowing rate, piggy back with NS, ICE over IV may help (1 hour)
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35
Q

Non-pharmacological therapy for HF (6)

A

nutrition:
- limit Na <2mg
- limit fluids <2L
- no fried foods
- no canned foods
- no processed foods -> high relationship to type II DM
- no OTC meds -> contains sodium -> cold & flu, acetaminophen, antacids, NSAIDs)

  • risk for falling: S/D orthostatics
  • elevate legs about level of the heart (dependent edema)
  • daily weight ( >3Ibs/ day, >5 Ibs/week) (call DOC, can be treated outpatient, catch before pul. congestion)
  • sexual activity, only safe if they can climb 2 flights of stairs w/o SOB
  • stocking/TED hose: decrease venous pooling (@home)
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36
Q

what are some gerontologic considerations for HF (3)

A
  • atypical s/sx: fatigue, weakness, somnolence (always exhausted)
  • decreased renal function can make older patients RESISTANT to DIURETICS and MORE SENSITIVE to changes in volume (may alter dose when Cr >1.3)
  • administration of diuretics to older men (BPH) requires nursing surveillance for bladder distention caused by urethral obstruction from an enlarged prostate gland (tx: bladder scan -> call provider -> straight Cath -> urology)
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37
Q

assessment for HF (focused, health hx, PE)

A

focused (quantifiable information)
- effectiveness of therapy (diuretics= I/O, wt. gain?)
- patient’s self management (when take meds? what they eat?)
- s/sx if increased HF
- emotional or psychosocial response (doesn’t improve w/ time)
health history
Physical exam
- mental status; decreased perfusion
- lung sounds: crackles, wheezes
- heart sound: S3
- fluid status, signs of fluid overload
- daily weight, I/O (>3Ibs/day, >5Ibs/week)
- assess responses to medications

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38
Q

interventions of activity intolerance (8)

A
  • BR for acute exacerbations
  • encourage regular physical activity (30-45min QD)
  • exercise training
  • pacing of activities
  • wait 2 hours after eating for physical activity
  • avoid activities in extreme hot, cold, or humid weather
  • modify activities to conserve energy
  • positioning: elevation of HOB to facilitate breathing and resting, support of arms <45 semi-fowlers
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39
Q

patient education for HF (9)

A
  • medications
  • limit use of OTC meds (contain sodium)
  • diet: low sodium diet, fluid restriction (nothing pre-packaged, processed)
  • monitoring for signs of excess fluid, hTN, sx. of disease exacerbation, including daily weight
  • exercise and activity program
  • stress mangement
  • prevention of infection: pulmonary infections (I/S exercise)
  • know how and when to contact health care provider
  • include family in education (engage in education process to maximize benefits)
40
Q

complications/collaborative problems HF (5)

A
  • hTN, poor perfusion, cariogenic shock (don’t meet O2 demands)
  • pericardial effusion, cardiac tamponade
  • pulmonary edema: increased fluid -> can’t breathe
  • dysrhythmias
  • thromboembolism
41
Q

describe cardiogenic shock (hTN, poor perfusion) (what, causes, manifestation) (think: 2 bed 1)

A
  • what: life-threatening loss of CO with high mortality rate
  • causes: inadequate tissue perfusion, initiation of shock syndrome
  • clinical manifestations: sx. HF, shock state, hypoxia, anaerobic metabolism -> lactic acid production

decreased BP -> pulmonary congestion -> increase lactic acid

42
Q

cardiogenic shock management (4)

A

1) correct underlying problem

2) reducing preload and afterload to decrease cardiac workload:
-meds (decrease contractility): diuretics, inotropes, vasopressors (constrict heart)
-invasive ventricular offloading/circulatory assist: external devices on patient, echmo, heart/lung bypass machine
-GOAL: improve blood flow

3) improve oxygenation, restore tissue perfusion

4) monitor hemodynamic parameters, monitor fluid status, and adjust medications and therapies based on assessment data

43
Q

describe pericardial effusions

A

accumulation of fluid in pericardial sac (prevents cardiac relaxation)

44
Q

describe cardiac tamponade

A

restriction of heart function bc of pericardial effusion, resulting in decreased venous return and decreased CO

45
Q

what are the clinical manifestations of pericardial effusion/cardiac tamponade (5)

A
  • ill defined chest pain or fullness
  • pulses paradoxes (pulse change w/ each breath)
  • engorged neck veins (vex triade)
  • labile/low BP (make sure diastolic doesn’t dip too low)
  • SOB
46
Q

cardinal signs of cardiac tamponade (4) (Tip: Drowned)

A
  • falling systolic BP
  • narrowing pulse pressure
  • rising venous pressure
  • distant heart sounds (muffled, chemo patients)

D= distended jugular veins
R= respiratory tract and lungs clear
O= o2 sat low
W= weak rapid pulses
N= no pulse
E= ecg/qrs complex short and even
D= decreased CO

47
Q

pericardial effusion/cardiac tamponade mangement (surgical interventions) (2)

A
  • pericardiocentesis: puncture to pericardial sac to aspirate pericardial fluid
  • pericardiotomy: under gen. anesthesia, portion of pericardium is excised to permit exudative pericardial fluid to drain into lymphatic system (divert fluid)
48
Q

describe pulmonary edema (what, s/sx, tx.)

A

what: result of LEFT sided HF (fluid backing up into lungs)

s/sx: acute, rapid, sudden onset
- crackles, pink frothy sputum, tachycardia

tx.: get fluid off
- Diuresis (lasix)
- Oxygen + positive pressure if needed (intubate sometimes)
- HOB 45 degrees
- STOP ALL FLUIDS

49
Q

describe thromboembolism (what, PE, s/sx PE, s/sx DVT, tx)

A

what: reduced mobility and circulation increase the risk for thromboembolism in patient with cardiac disorders, including those with HF

pulmonary embolism: blood clot from legs moves to obstruct pulmonary vessels

s/sx PE: dyspnea, pleuritic chest pain, tachypnea, cough

s/sx DVT: swelling, pain, redness, warmth (unilateral)

tx: anticoagulant therapy (unfractionated heparin, low molecular weight heparin (DOAC), fondaparinux (arixtral), rivaroxaban (xarelto)

50
Q

sudden cardiac death or cardiac arrest (mgmt, abcd)

A
  • emergency management: cardiopulmonary resuscitation
  • A: airway
  • B: breathing
  • C: circulation
  • D: defibrillation for VT and VF (no defibrillator in Asystole)
51
Q

end of life considerations (3)

A
  • HF is CHRONIC and often progressive condition (need to consider issues r/t end of life, palliative or hospice care should be considered)
  • transplant is an option for YOUNGER patients (usually with familial heart conditions) where disease is isolated to the heart
  • life long immunosuppression
52
Q

summary of HF (what, etiology, clinical manifestations, diagnostics, meds, patient education, major complications)

A

what: weakened myocardium results in loss of perfusion, ventricular remodeling

etiology: anything that weakens heart OR prevents blood moving forward

clinical manifestations:
- congestion (peripheral edema, pulmonary edema)
- low CO (altered mental status, fatigue)
- L sided (pulmonary congestion)
- right sided (peripheral edema)

diagnostics: BNP, CXR, ECG, Echo

meds: Ace/Arbs, vasodilators, beta blockres, diuretics, Ca channel blockers, contractility agents (digoxin, digitalis)

patient education: wt. gain, dietary/nutrition, med administration

major complications: hTN, poor perfusion, cariogenic shock, pericardial effusion, cardiac tamponade, pulmonary edema, dysrhythmias, thromboembolism, cardiac arrest

53
Q

atherosclerosis: pathophysiology

A
  • accumulation of LIPID deposits and FIBROUS tissue within arterial intima
  • heart has MORE O2 DEMAND per tissue mass than any other organ
  • in CORONARY ds. = reduces blood flow to myocardium
  • with CHRONIC ds. = collateral circulation develops into circumvent diseased area
  • obstruction of blood flow can be:
    1) chronic (gradual narrowing that causes decreased function with increases in demand - stable angina, demand ischemia)
    2) acute (plaque rupture resulting in immediate occlusion of vessels, resulting in myocardial infarcts)
  • results in TISSUE DEATH
54
Q

4 categories of acute coronary syndrome/ ischemic heart disease

A

1) stable angina (okay @ rest, exertion = sx.)
2) unstable angina (pain @ rest, with nitroglycerin)
3) NSTEMI (NON-ST elevation myocardial infarction) (blood flow obstruction, muscle withers + dies)
4) STEMI (ST elevation MI) (same as NSTEMI, but occurs earlier -> can readily intervene to save myocardium from dying)

55
Q

types of coronary artery disease (3)

A

1) RCA - right coronary artery
2) LAD - left anterior descending
3) circumflex (all around)

56
Q

risk factors of coronary artery disease (modifiable) (9)

A
  • hyperlipidemia (statin)
  • tobacco use (smoke, chew, vape)
  • HTN
  • DM
  • Metabolic syndrome
  • obesity
  • physical inactivity
  • chronic inflammatory conditions (RA, lupus)
  • chronic kidney disease
57
Q

risk factors of coronary artery disease (un-modifiable) (7)

A
  • family hx. CAD (vasoconstriction)
  • increasing age (30-50 years)
  • gender (male develop CAD earlier, women die more) (N/V/fatigue)
  • race: CAD (African/american, hispanics)
  • premature menopause (before 40), hx. preeclampsia)
  • primary hypercholesterolemia (genetically elevated LDL)
  • environmental still plays a role
58
Q

risk factors of metabolic syndrome (5)

A
  • enlarged waist circumference: 35.4 male, 31.4 female
  • high triglycerides >175
  • low HDL (<40 men, <50 women)
  • HTN: 130/80
  • elevated fasting glucose >100
59
Q

what is an inflammatory marker for RA, lupus

A

hs-CRP (high sensitivity C-reactive protein)

60
Q

prevention of CAD (7)

A
  • control cholesterol
  • dietary measures
  • physical activity (30 min elevated HR/day)
  • medications
  • cessation of tobacco use
  • manage HTN
  • control diabetes
61
Q

what meds are used for cholesterol (5)

A

5 different categories of lipid lowering agent:
1) coenzyme A (HMG-CoA): -statins (atorvastatin)
2) fibric acids (or fibrates): (fenofibrate)
3) bile acid sequestrates: -resins (cholestyramine)
4) cholesterol absorption inhibitors: (ezetimibe)
5) proprotein convertase subtilisin-kexin type 9 (PCSK9) agents: (alirocumab)

62
Q

clinical manifestations of Coronary artery disease/ Coronary atherosclerosis (4)

A
  • myocardial ischemia (ischemia to heart muscles)
  • angina pectoris (chest pain s/d schema)
  • myocardial infarction/acute coronary syndrome (death)
  • sudden cardiac death
63
Q

s/sx CAD (9)

A

classic signs:
- acute chest pain may radiate down left arm or up neck jaw (elephant sitting on chest) (relieved or unrelieved by rest, sudden, Cushing, acute)
- epigastric/abdominal pain
- SOB/dyspnea
- sweating (diaphoresis)
- N/V
- anxiety, fatigue, weakness
- syncope (fainting)
- dysthymia’s (ECH changes_
- troponin

64
Q

gero CAD considerations (4)

A
  • diminished pain that occurs with aging may affect presentation of symptoms
  • GERO may NOT have chest pain “silent CAD”
  • teach older adults to recognize “chest pain” sx. (i.e weakness)
  • pharmacologic stress testing: cardiac catheterization

tip: meds should be used different

65
Q

diabetes CAD considerations

A

may not have chest pain

66
Q

describe female CF

A

may not have typical chest pain

67
Q

diagnosis of stable angina, unstable angina, STEMI, NSTEMI (main, STEMI, NSTEMI)

A

main:
- ECG changes (ST elevation in injury -> no tissue death yet, ST depression with ischemia (w/ affects), development of Q wave

STEMI: full obstruction of coronary artery, tissues will die)

NSTEMI: trickle of blood still flowing, do not affect d/t repolarization
- troponin elevation: >0.4ng/L, cardiac issues
- CK-MB and myoglobin may also be elevated (not routinely checked though -> not specific to cardiac)

68
Q

describe stable angina/demand ischemia (what, trop, types of tests)

A

1) what: paroxysmal pain caused by narrow (but not fully blocked) coronary arteries (demand O2, but can supply)
- pain/SS Increases when demand Increases
- pain/SS goes away when demand Decreases OR supply of O2 increases (nitroglycerin -> O2 -> heart)

2) mild elevated in troponin may be seen (not above 0.4ng/mL threshold though)
- nitroglycerin, education, EKG/trop normal, follow up cardiology

3) confirmed diagnosis: cardiologist
- STRESS test: ECG monitored w/ stress. ST depression may be seen when O2 demands isn’t met
- if ST changes occur = STOP TEST (indicates issues with coronary artery)
- NUCLEAR stress test: radioactive isotope injected and imaged to highlight coronary blood flow (if impaired physical)
- NPO 4 hour, pre test

69
Q

stable angina/demand ischemia treatment (5)

A

1) improves O2 supply, reduce O2 demand

2) meds:
- Nitroglycerin (selective vasodilation in heart, 1 SL tab OR 1 spry Q5 x3 - call 911 if sx not relieved)
- AVOID nitrates -> Sildenafil
- erectile dysfunction meds)
- Beta blockers & Ca channel blockers
- Ace/Arbs
- Anti platelet meds
- Statins

3) oxygen (NC 2-6L)
4) reduce and control RFs
5) repercussion therapy may be done at some point but for most part, pharmaceuticals

70
Q

myocardial infarction/acute coronary syndrome (ST elevation, what, severity, ECG, trop, other labs?)

A
  • ST elevation: cut off for treatable MI
  • plaque rupture resulting in immediate occlusion of vessels, when fully occluded results in ST elevation
  • overall blood flow (or lack thereof) determines severity of insult: blockage to main artery, worse than distal artery
  • ECG changes: ST elevation in affected leads, develop Q wave
  • troponin elevation much HIGHER than stable angina (d/t full blockage)
  • CK-MB and myoglobin may also be elevated
71
Q

STEMI vs nstemi vs unstable angina (STEMI) (what, s/sx, trop, ECG, tx.)

A
  • what: typically 100% blockage - clot blocking entire coronary artery
  • s/sx: myocardial ischemia: chest pain, N/V, etc.
  • elevated troponin
  • ECG: ST elevation
  • tx: emergent PCI, thrombolytics
72
Q

stemi vs NSTEMI vs unstable angina (NSTEMI) (what, s/sx, trop, ECG, tx)

A
  • what: 99.9% blockage - blood trickles past obstruction
  • s/sx: myocardial ischemia
  • elevated troponin
  • ECG: NO st elevation
  • tx: medical management: statin, aspirin
73
Q

stemi vs istemi vs UNSTABLE ANGINA (what, s/sx, trop, ECG, tx)

A
  • what: not enough ischemia to cause permanent tissue damage
  • s/sx: of myocardial ischemia: pain is constant, doesn’t go away with rest/nitro
  • normal troponin
  • ECG: NO st elevation
  • tx: medical mangement
74
Q

ACS initial treatment (unstable angina, stemi, nstemi) (7)

A
  • oxygen: SOB, SpO2 <90%
  • aspirin: 325 mg, prevents plaque from becoming larger, risk for GIB
  • nitroglycerin: NEED TO KNOW WHERE, drop BP
  • morphine: can be used for pain, no affect of 30 day survival (no chest pain = no narcotic)
  • heparin IV bolus followed by drip: prevents clots (normal range: 46-70 -> x3 therapeutic) (antidote: protamine sulfate)
  • beta blockers IV (sometimes)
  • at this point: ECG + troponin will determine next course of action
75
Q

STEMI tx (2)

A

emergent PCI (sooner = better, door to balloon: goal 90 minutes)

thrombolytics (tPa, streptokinase):
- if PCI center <2.5hrs (not as effective as PCI)
- only indicated for 12 hours post onset of chest pain
- contraindications: major bleeding risks, recent strokes, trauma, uncontrolled HTN, recent surgery
- signs its working: resolution chest pain, ST elevation gone

TIP: if bled before, no candidate for thrombolytics

76
Q

what is PCI (what, teaching)

A

percutaneous intervention
- arterial access via FEMORAL or RADIAL artery
- catheter advanced retrograde (against flow of blood) intro aortic arch
- coronary arteries illuminated with iodinated contrast (allergy precaution) and fluoroscopy
- atheroma lesions then -> balloon, stented
- catheter/sheath removed -> hemostasis obtained from accessed artery

teaching:
- pt. lay flat 2-6 hours
- observe s/sx blood loss -> direct manual pressure q30 min
- monitor pedal pulses -> arterial clot
- monitory kidney function >1.3 Cr.
- AVOID METFORMIN w/ diabetic patient
- NO BLOOD THINNERS FOR 6 HOURS POST CATH)

77
Q

describe collateral circulation

A
  • prolonged blockage (gap in artery)
  • NSTEMI (blood leaking through)
78
Q

describe CAD

A
  • widow maker (letft main kills you)
79
Q

stent

A

shadow present, metal gauge instead via catheter, mains latency of sclerotic artery

80
Q

percutaneous coronary intervention (most common, what, meds?)

A
  • drug elating stents are most common
  • metal is coated with medication that slowly releases over a period of 6+ months to PREVENT INFARCT
  • patients who received stents: should be on PAI like clopidogrel for at least 6 months (plavix)
81
Q

NSTEMI tx (3)

A
  • NO PCI, NO THROMBOLYTICS
  • medical therapy: nitroglycerin, aspirin, heparin, beta blockers to reduce sympathetic burden, may undergo Cath but meds are best (elective cardiac Cath)
  • risk reduction therapy: manage HTN (ACE), smoking cessation, etc.
82
Q

ACS post care (assess, teach, meds, other)

A
  • assess site monitoring if underwent PCI (IV fluid to flush iodinated contrast, no heavy lining no soaking wound, showers OK)
  • teaching: smoking cessation, stress reduction, nutrition
  • medications: same as anti-HTN, anti-lipid drugs as with CHF & stable Angina -> home BP monitor, aspirin + PAI (plavix, brilinta)
  • cardiac rehab: gym membership, exercise with nurse, established pattern, insurance pays
83
Q

coronary artery bypass grafts (CABG) (what, indications, type if sx., mechanism)

A
  • MAJOR SURGERY
  • indicated for patients with “heavy atherosclerotic” burden and diabetes (w/o multiple other comorbidiites)
  • traditional “open heart” procedure requiring cardiopulmonary bypass in OR (minimally invasive strategies are evolving)
  • artery/vein from elsewhere in the body is grafted into the coronary artery beyond the blockage (isolated-> remove or relocate)
  • prevention of re-infarct involves same medications as with PCI (anti-platelets -> aspirin, plavix)
84
Q

major complications with surgery (7)

A

1) vfib/vtach: occurs in up to 90% of post MI pt.
- tx: defibrillator

2) cariogenic shock: lack tissue perfusion

3) heart failure: new s3, rapid wt. gain, sudden edema

4) wall rupture -> pericardial tamponade (muscle will split open -> ventricles contract -> fill pericardian

5) mitral valve blowout/regurgitation -> flash pul. edema (blood goes wrong way)
6) new murmur, new onset AFIB
7) wall rupture and mitral regurgitation occurs 1-2 weeks post MI, results in DEATH if not sitting next to cardiothoracic OR

85
Q

nursing interventions for MI (4)

A

1) treat angina (TOP PRIORITY)
- pt. stop all activities and sit or rest in bed (semi)
- assess pt. while performing other necessary interventions (VS, resp. distress, pain, ECG)
- administer meds as ordered (NGT), reassess pain, administer NTG up to 3 doses
- administer O2 2L/min by nasal cannula

2) reduce anxiety
- calm manner
- stress reduction technique
- patient teaching
- addressing patient’s spiritual needs may assist in allaying anxieties
- address both patient and family needs

3) prevent pain
4) educate patients about self care

86
Q

what is the first intervention for MI (3)

A

1) assessment: onset, resolution chest pain + all characteristics
2) first 12 lead ECG (first)
3) vitals (first)

87
Q

post MI teaching (9)

A
  • diet: Low Na + Low fluid (2g, 2L)
  • daily wts.
  • pulse monitoring
  • reduce stress
  • medication teaching: carry NTG at all times (nitro)
  • reduce cholesterols, red meat, processed foods (include more FIBER)
  • exercise: 30 min/5 days/week (avoid exercising during extreme weather conditions, avoid workout supplements)
  • smoking cessation
  • CHF teaching applies to post MI patients
88
Q

summary: myocardial ischemia

A
  • lipid/inflammatory plaque formation that can be chronic or acute
89
Q

summary: 4 varieties of MI

A
  • Stable angina: relieved by REST
  • unstable angina: unrelieved by rest but enough blood gets through so damage is limited. No cardiac markers
  • NSTEMI: no ST elevation, elevated drops - medical therapy
  • STEMI: ST elevation, elevated drops -> Cath lad or thrombolytics
90
Q

summary: causes MI (6)

A

atherosclerosis, HTN, smoking, genetics, men>women, age

91
Q

s/sx of MI

A
  • sudden, acute, rapid onset
  • chest pain, jam/arm/neck pain
  • fatigue, pallor, syncope, N/V
92
Q

diagnostics for MI

A
  • Trop, ECG, stress test, cardiac Cath
93
Q

meds for acute MI (NOAH)

A
  • oxygen
  • aspirin 325mg
  • nitroglycerin
  • morphine can be used for pain (old school method), no effect of 30 day survival
  • heparin IV bolus followed by drip
94
Q

meds for maintenance MI (4)

A
  • statins
  • ASA (sometimes a PAI like plavix(clopidogrel))
  • ACE’s, ARB’s
  • Beta blockers (metoprolol)
95
Q

alternative meds (case by case) (3)

A
  • vasodilators (hydralaine, isordbid dinitrite)
  • diuretics: reduce congestion (loop, K+ sparing thiazide)
  • Ca channel blockers
96
Q

major complications for MI (5)

A
  • VFib/Vtach
  • cardiogenic shock
  • HF
  • tamponade/wall rupture
  • mitral valve regurgitation

Nur 3010 exams (13 decks)

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