s/sx of CAD/MI
ischemia vs. infarction
ischemia: insufficient oxygen supply to meet requirements of myocardium
infarction: necrosis or cell death that occurs when severe ischemia is prolonged and decreased perfusion causes irreversible damage to tissue
medications used to treat CAD
- statins: inhibit cholesterol synthesis, decrease LDL and increase HDL. Monitor for liver damage and myopathy
- niacin: lowers LDL and triglycerides, increases HDL. SE: flushing, pruritus, GI s.e, orthostatic hypotension
- antiplatelets: ASA, clopidogrel
*HTN & DM2 should be well managed*
modifiable risk factors
- physical activity (30min daily for 5 days)
- obesity (BMI of 30kg/m2)
- diabetes (A1c should be <7%)
- psychologic state, homocysteine, substance abuse
ways CAD is diagnosed & what the tests look for
- chest xray to look for cardiac enlargement, pulmonary congestion
- 12 lead ecg obtained to compare to previous tracing
- echocardiogram confirms CAD
- calcium score screening: locates calcium deposits in atherosclerotic plaque
- exercise stress test: to know the impact of the lesion on coronary blood flow
what is the most common complication of an MI
- dysrhythmias are present in 80% of MIs. They are the most common cause of death.
- can be caused by ischemia, electrolyte imbalances or SNS stimulation
- life threatening seen most often with anterior MI, heart failure or shock
what occurs during angina and define the s/sx between unstable and stable
- reversible ischemia when 75% of arteries are blocked. They become hypoxic within 10 seconds of occlusion and are viable for ~20minutes.
- chronic: transient lasting 5-15min, ST segment depression and/ or T-wave inversion
- unstable: easily provoked (can occur at rest), may last longer than chronic, rest/medicine do not help, can lead to heart attack
medications for ACS
- ASA to make platelets slippery
- nitrates: dilate peripheral blood vessels and coronary arteries/ collateral vessels (coronary perfusion)
- morphine: helps reduce pain, promote comfort, relax smooth muscle, decrease myocardial oxygen demand and reduces circulating catecholamines
- beta blockers: decrease heart rate, force of contraction, blood pressure, o2 myocardial demand
- ACEs, IV heparin to prevent reocclusion
- thrombolytic/ fibrinolytics: directly targets clot in coronary arteries, restores blood flow since fibrinolytics dissolves the clot
- calcium channel blockers: vasodilation and myocardial perfusion, not given for acute emergent situation
give examples of saturated fats and cholesterol to reduce and complex carbs to increase for prevention/ early treatment of CAD
- reduce saturated fats and cholesterol such as red meat, egg yolks and whole milk
- increase complex carbs such as whole grains, fruit and vegetables
- if triglyceride levels are elevated, reduce/ eliminate intake of simple sugars and alcohol
laboratory studies for CAD
- cardiac enzymes
- lipid profile
- C reactive protein
what are other complications of MIs
- heart failure: when the pumping power of the heart has diminished, can occur with signs of mild dyspnea, restlessness, agitation or tachycardia
- cardiogenic shock: when oxygen and nutrients supplied to tissues are inadequate due to LV failure
- acute pericarditis
CAD vs. ACS
CAD: blood vessel disorder which is progressive of plaque in the lining of coronary arteries
ACS: includes unstable angina and MI (NSTEMI/STEMI). When ischemia is prolonged and not immediately reversible. Deterioration of a once stable atherosclerotic plaque > ruptures > platelet aggregation > thrombus
*Medical Emergency*
if a patient lives in a rural area and a PCI is not available, what are other options? (non-surgical)
- thrombolytic therapy: stops infarction process by dissolving thrombus. Ideal to start within first hour, given IV.
- monitor closely for signs of bleeding
- assess for signs of reperfusion (return of ST segment to baseline)
management for ACS
- semi fowler's
- supplemental oxygen >90%
- ASA, nitroglycerin (SL), morphine
- 12 lead ecg (watch for changes in QRS, ST, and T wave to distinguish between NSTEMI/STEMI
- IV access, labs, cath lab
what is a PCI and when is it indicated?
- first line of treatment for patients with confirmed MI (ECG changes and positive cardiac markers). It visualizes and opens blockages.
- goal is 90min from door of ER to cath lab
- balloon angioplasty + drug eluting stents
nursing interventions for MI
- continuous cardiac monitoring
- heart/ lung sounds
- VS, I/O, rest, cardiac rehab
- anxiety reduction
define MI and its s/sx
- most serious ACS, result from irreversible sustained ischemia >20min, necrosis, hypoxia, ischemia starting in sub endocardium
- necrosis of entire myocardium takes 4-6 hours, losing contractile function
- s/sx: chest pain not relieved by rest/ nitrates. Heaviness, crushing tight pain. Substernal, retrosternal, epigastric (indigestion) that radiates to neck, jaw and arms
- atypical in women/ elderly, no pain if pt has cardiac neuropathy (DM)
modifiable risk factors for CAD
- elevated serum lipids (cholesterol >200, triglycerides >150, HDL, LDL)
- hypertension: the second major risk factor
- tobacco use
what do we monitor post cardiac cath?
- monitor recurrent angina
- frequent VS/ cardiac rhythm
- monitor site for bleeding/ hematoma
- neurovascular assessment (perfusion/pulses)
- bedrest per policy
- foley care
what occurs after CABG surgery?
- ICU for 24-36 hours
- pulmonary artery cath (measures CO)
- intraarterial line (measures BP cont.), pleural/mediastinal chest tubes (drainage)
- ET tube w/ mechanical vent, epicardial pacing wires (emergency pacing of the heart)
- urinary cath/ NG tube (monitor urine output/ gastric decompression)
when are surgical options recommended for MI?
- when patient has failed medical management, not a candidate for PCI, failed PCI with ongoing chest pain, hx of DM, long term benefits of CABG are superior to PCI
- CABG: uses arteries and veins for grafts, requires sternotomy and cardiopulmonary bypass.
-MIDCAB: alternative to CABG
assessment findings for MI
- initially increased HR and BP, then decreased BP 2ndary to decrease in CO
- crackles, JVD, N/V with severe pain, vasovagal reflex
- elevated temp in the first 24 hours (inflammatory process by cell death)
difference between STEMI/NSTEMI
- STEMI: coronary artery is completely blocked resulting in severe damage to the heart muscle. ST segment elevation
- NSTEMI: coronary artery is partially blocked
post op care after CABG
- assess for bleeding
- monitor hemodynamic status, pain, fluid status
- pulmonary hygiene, cognitive dysfunction
- restore temperature, monitor afib
what labs are increased during/after an MI
- troponin
- CK-MB
- myoglobin
* serum cardiac markers are important in the diagnosis of MI
what is SCD?
- unexpected death with sudden disruption in cardiac function, producing abrupt loss of CO and cerebral blood flow.
- most commonly caused by ventricular dysrhythmias
- no warning sugns
- prodromal symptoms associated with MI (chest pain, palpitations, dyspnea) death within 1 hour of onset of symptoms