CHF + CAD Flashcards
iclicker: what labs do we draw for HF
- BNP d/t stretch of ventricles from overload volume
- TROP: r/t to cardiac cell death, or MI (heart attack)
what is heart failure (what, affects what system, results in s/sx (2)
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
what are the causes of CHF (5) medical
- 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
what are the risk factors for HF (7)
- HTN
- uncontrolled DM
- illicit drug use
- pregnancy
- lung disease (R side HF)
- sleep apnea (osa)
- hyperthyroidism, severe anemia
specific causes of R sided HF (isolated)
- left sided HF (fluid backs into R side, damages pump)
- pulmonary HTN
- lung disease (COPD, pulmonary fibrosis)
- pulmonary embolism
- OSA (obstructive sleep apnea)
2 types of HF
1) Heart failure with reduced ejection fraction (HFrEF): systolic failure
2) Heart failure with preserved ejection fraction (HFpEF): diastolic failure
describe heart failure with reduced ejection fraction (HFrEF): systolic failure (what, EF, leads to, danger)
- 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)
describe heart failure preserved ejection fraction (HFpEF): diastolic failure
- 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
clinical manifestations of heart failure (where, consequences) general
- where: Right and left
- consequences: congestion, poor perfusion/low CO
clinical manifestations of R Heart Failure (6)
- 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)
clinical manifestations of L Heart failure (6)
- 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)
Clinical manifestations (congestion sx.) (11)
- Dyspnea
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Cough
- Pulmonary crackles
- Weight gain
- Dependent edema
- Abnormal bloating
- Ascites
- JVD
- Fatigue
clinical manifestations of low CO/poor perfusion (9)
- 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
what are the diagnostic tests used for HF (4)
- BNP
- Chest XR
- ECG
- Echo
what does BNP cause
- released from ventricles in response to wall stretch to stimulate vasodilation and diuresis
- indicates: HEART FAILURE
most common HF
left sided HF
chest XR identify with HF
- identifies B/L pulmonary infiltrates/engorged pulmonary vessels
- may identify cardiomegaly (focal pneumonia?)
ECG identify with HF
- sinus tachycardia
- ventricular hypertrophy (cardiologist)
Echo identify with HF
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
what are the main medications we learned for HR management (8)
- ACE inhibitors
- ARBs
- ARNI
- vasodilators
- beta blockers
- diuretics
- calcium channel blockers
- digitalis
describe angiotensin-converting enzyme (ACE inhibitors) (function, causes, monitor, suffix)
- 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)
describe angiotensin II receptor blockers (ARBs) (what, function, risk factors/ monitor, suffix)
- 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)
describe vasodilators (function, prefix, meds? (5))
- function: drops BP, lowers after load
- nitroglycerin included (nitro-prefix)
- hydralazine, nitroprusside, nitroglyceride, isosorbide digitate (rare), minoxidil (rare)
describe beta blockers (selective/nonselective) (function, efficiency, precaution in?, suffix, selective vs no selective, acute situation?, masks —?, inhibits, causes 3)
- 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
describe diuretics (3 types) (function, monitor)
- 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
describe loop diuretic/k wasting (function, ex., teach)
- drops serum K+
- ex: lasix/furosemide, bumex/bumetanide
- teach: avoid licorice root (drops k+)
describe K+ sparing diuretics/aldosterine antagonists (aka, function, ex, teach)
- aka: aldosterone receptor antagonist (ARAs)
- block action of aldosterone (Na/H2O retention)
- ex: spironolactone
- teach: avoid K+ rich foods - melons, salt sub., leafy veggies
describe thiazide diuretics (best for?, effectiveness, use for, function, ex, side effects)
- 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
describe calcium channel blockers (function, ex: HR affect, ex: no HR affect)
- 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
describe digitalis (causes, monitor, toxicity, ex)
- 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)
what should always be done for HF medical management
- check BP, renal function prior to drug administration
what should be done for meds that drop BP (3)
- beware of orthostatic changes
- slow position changes
- usually hold for less than systolic <100
what should be done for meds that drop HR
- hold for less than 60
how to treat hypokalemia (4)
- 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)
Non-pharmacological therapy for HF (6)
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)
what are some gerontologic considerations for HF (3)
- 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)
assessment for HF (focused, health hx, PE)
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
interventions of activity intolerance (8)
- 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
patient education for HF (9)
- 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)
complications/collaborative problems HF (5)
- hTN, poor perfusion, cariogenic shock (don’t meet O2 demands)
- pericardial effusion, cardiac tamponade
- pulmonary edema: increased fluid -> can’t breathe
- dysrhythmias
- thromboembolism
describe cardiogenic shock (hTN, poor perfusion) (what, causes, manifestation) (think: 2 bed 1)
- 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
cardiogenic shock management (4)
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
describe pericardial effusions
accumulation of fluid in pericardial sac (prevents cardiac relaxation)
describe cardiac tamponade
restriction of heart function bc of pericardial effusion, resulting in decreased venous return and decreased CO
what are the clinical manifestations of pericardial effusion/cardiac tamponade (5)
- 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
cardinal signs of cardiac tamponade (4) (Tip: Drowned)
- 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
pericardial effusion/cardiac tamponade mangement (surgical interventions) (2)
- 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)
describe pulmonary edema (what, s/sx, tx.)
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
describe thromboembolism (what, PE, s/sx PE, s/sx DVT, tx)
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)
sudden cardiac death or cardiac arrest (mgmt, abcd)
- emergency management: cardiopulmonary resuscitation
- A: airway
- B: breathing
- C: circulation
- D: defibrillation for VT and VF (no defibrillator in Asystole)
end of life considerations (3)
- 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
summary of HF (what, etiology, clinical manifestations, diagnostics, meds, patient education, major complications)
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
atherosclerosis: pathophysiology
- 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
4 categories of acute coronary syndrome/ ischemic heart disease
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)
types of coronary artery disease (3)
1) RCA - right coronary artery
2) LAD - left anterior descending
3) circumflex (all around)
risk factors of coronary artery disease (modifiable) (9)
- hyperlipidemia (statin)
- tobacco use (smoke, chew, vape)
- HTN
- DM
- Metabolic syndrome
- obesity
- physical inactivity
- chronic inflammatory conditions (RA, lupus)
- chronic kidney disease
risk factors of coronary artery disease (un-modifiable) (7)
- 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
risk factors of metabolic syndrome (5)
- 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
what is an inflammatory marker for RA, lupus
hs-CRP (high sensitivity C-reactive protein)
prevention of CAD (7)
- control cholesterol
- dietary measures
- physical activity (30 min elevated HR/day)
- medications
- cessation of tobacco use
- manage HTN
- control diabetes
what meds are used for cholesterol (5)
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)
clinical manifestations of Coronary artery disease/ Coronary atherosclerosis (4)
- myocardial ischemia (ischemia to heart muscles)
- angina pectoris (chest pain s/d schema)
- myocardial infarction/acute coronary syndrome (death)
- sudden cardiac death
s/sx CAD (9)
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
gero CAD considerations (4)
- 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
diabetes CAD considerations
may not have chest pain
describe female CF
may not have typical chest pain
diagnosis of stable angina, unstable angina, STEMI, NSTEMI (main, STEMI, NSTEMI)
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)
describe stable angina/demand ischemia (what, trop, types of tests)
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
stable angina/demand ischemia treatment (5)
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
myocardial infarction/acute coronary syndrome (ST elevation, what, severity, ECG, trop, other labs?)
- 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
STEMI vs nstemi vs unstable angina (STEMI) (what, s/sx, trop, ECG, tx.)
- 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
stemi vs NSTEMI vs unstable angina (NSTEMI) (what, s/sx, trop, ECG, tx)
- what: 99.9% blockage - blood trickles past obstruction
- s/sx: myocardial ischemia
- elevated troponin
- ECG: NO st elevation
- tx: medical management: statin, aspirin
stemi vs istemi vs UNSTABLE ANGINA (what, s/sx, trop, ECG, tx)
- 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
ACS initial treatment (unstable angina, stemi, nstemi) (7)
- 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
STEMI tx (2)
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
what is PCI (what, teaching)
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)
describe collateral circulation
- prolonged blockage (gap in artery)
- NSTEMI (blood leaking through)
describe CAD
- widow maker (letft main kills you)
stent
shadow present, metal gauge instead via catheter, mains latency of sclerotic artery
percutaneous coronary intervention (most common, what, meds?)
- 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)
NSTEMI tx (3)
- 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.
ACS post care (assess, teach, meds, other)
- 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
coronary artery bypass grafts (CABG) (what, indications, type if sx., mechanism)
- 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)
major complications with surgery (7)
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
nursing interventions for MI (4)
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
what is the first intervention for MI (3)
1) assessment: onset, resolution chest pain + all characteristics
2) first 12 lead ECG (first)
3) vitals (first)
post MI teaching (9)
- 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
summary: myocardial ischemia
- lipid/inflammatory plaque formation that can be chronic or acute
summary: 4 varieties of MI
- 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
summary: causes MI (6)
atherosclerosis, HTN, smoking, genetics, men>women, age
s/sx of MI
- sudden, acute, rapid onset
- chest pain, jam/arm/neck pain
- fatigue, pallor, syncope, N/V
diagnostics for MI
- Trop, ECG, stress test, cardiac Cath
meds for acute MI (NOAH)
- 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
meds for maintenance MI (4)
- statins
- ASA (sometimes a PAI like plavix(clopidogrel))
- ACE’s, ARB’s
- Beta blockers (metoprolol)
alternative meds (case by case) (3)
- vasodilators (hydralaine, isordbid dinitrite)
- diuretics: reduce congestion (loop, K+ sparing thiazide)
- Ca channel blockers
major complications for MI (5)
- VFib/Vtach
- cardiogenic shock
- HF
- tamponade/wall rupture
- mitral valve regurgitation
