Angina & MI Flashcards
CAD
- Coronary Artery Dz
- Accumulation of atherosclerotic plaque in the coronary arteries
-could lead to development of collateral circulation, angina, acute coronary syndrome, MI, dysrhythmias, HF, or death
MI
- caused by declining artery circumference or lack of blood supply
- increased demand for oxygen or decreased supply of oxygen
- usually occurs when a coronary artery is greater than 75% occluded (or stenosed)
- cardiac cells can sustain about 20 min of no O2 before necrosis
Collateral Circulation
- tiny vessels connecting the large coronary arteries
- often develops in the presence of atherosclerosis to allow for continued blood flow
- Alternative route for blood to flow from the aorta to the cardiac muscle tissue
Angina
- symptom not a dz (CP)
- chest pain resulting from reduced coronary blood flow
- imbalance between myocardial blood supply and demand
- 3 types of angina
Factors of Angina
- Physical exertion
- temp extremes
- anxiety/anger
- consumption of a heavy meal
- smoking
- sexual activity
- drugs
- dysrhythmias
Stable Angina
-predictable pattern of increased work of the heart resulting in chest pain and relieved by rest or nitrates
S/S:
- pain
- SOB
- N/V
- palpitations and weakness
Prinzmental Angina
- coronary artery vasospasm
- occurs unpredictably (not associated with physical activity)
- most often ocurrs at night while at rest
- unknown cause, though presumed to be caused by hyperactive sympathetic response, altered calcium flow, and reduced prostaglandins that promote vasodiation
Unstable Angina
- unpredictable pain without contributing factors
- at rest or during activity
- departing from the usual pattern
- may last more than 20 minutes
- marked by increasing frequency, severity, and duration of chest pain symptoms
Patient History
P: precipitating events
Q: quality of the pain
R: radiation of the pain
S: severity of the pain
T: timing when it began, with what activity?
Meds?
Risk factors? fam hx, stressors
ACS
Acute Coronary Syndrome
When the blood flow is significantly reduced but not fully occluded causing myocardial injury
Factors for ACS
-Rupture of atherosclerotic plaque resulting in a thrombus
formation
- Coronary artery vasospasm
- Increasingly occlusive atherosclerotic plaque
- Inflammation of coronary artery
- Diastolic and systolic dysfunction (heart failure)
Plaque rupture in ACS
- hemodynamic changes cause plaque to rupture….
- platelet aggregation….
- clot formation…..
- cell ischemia and injury….
- lactic acid production causes chest pain
Acute MI
- When blood flow to a portion of the cardiac muscle is completely blocked
- complete occlusion results in prolonged ischemia which kills cardiac cells permanently
- irreversible cell damage leads to poor cardiac functioning
AMI: Electrical changes
T wave will invert or the ST segment of the ECG tracing will become elevated
AMI: ST segment elevation
- greater than 0.04 seconds after J point
- greater than 1 mm in 2 or more contiguous chest leads
contiguous
limb leads that “look” at the same area of the heart or are numerically consecutive chest leads
Stages of Myocardial Insult
- Ischemia
- Injury
- Infarct
Ischemia stage
- lack of oxygenation
- ST depression or T wave inversion
- permanent damage avoidable
Injury stage
- prolonged ischemia
- may have ST elevation
- permanent damage avoidable
Infarct stage
- permanent death of myocardial tissue
- may have ST elevation and/or Q wave
STEMI
- ST segment elevation present
- May or may not have elevation in cardiac enzymes initially
Non-STEMI
- no ST segment elevation (possibly ST depression or T wave inversion)
- Diagnosed by elevated cardiac enzymes
CK (CPK) Enzyme
Normal level: 5-35 mcg/mL
- cardiac and skeletal muscle, brain
- Appears in serum 3-6 hrs
CK-MB
0%-6% of heart
- cardiac muscle
- 4-8hrs in serum
Troponin
less than 0.5 mcg/L
- cardiac muscle
- 2-4hrs in serum
Call for help when..
- CP unrelieved with rest
- new onset CP
- increasing SOB
- prolonged period of pain
- unable to identify cause
- do not try to drive
- do not wait
Caring for patients with chest pain
- EKG priority
- Quick hx and description of symptoms
- VS
- IV access with blood draw (enzymes)
- meds
- closely monitor patient’s VS and reports of chest pain
MONA
M: Morphine
O: Oxygen
N: Nitroglycerin
A: ASA
Morphine
- relieves pain….reduces metabolic demand…allows for more oxygen to be available to cardiac cells
- vasodilates…increases coronary perfusion and decreases afterload
- closely monitor pt’s blood pressure
Oxygen
- increases amount of oxygen available to patient’s cardiac muscle
- start with 2 L/min, increase as necessary
- no need for O2 if SpO2 is 94% or greater
Nitroglycerin (Short acting)
- first line therapy
- dilates peripheral blood vessels, coronary arteries/collateral vessels
- SL nitro (pill or spray)
- 1 q5 mins x3
Nitroglycerin (Long acting)
- Isordil (isosorbide dinitrate) or Imdur (isosorbide mononitrate)
- ointment
ASA
- must be administered before or upon arrival
- ok if given and documented by EMS
- Either dose is acceptable: 162mg or 325mg
- if patient can not take ASA by mouth, get order for rectal
- contraindications must be documented by the MD, ARNP, or PA
- OK if pt takes at home and you document “took asa prior to arrival”
- decreases platelet aggregation
Manifestations in the acute phase
- chest pain
- dyspnea, SOB
- Diaphoresis, pale, cool skin
- N/V
- reports weakness
- JVD
- murmurs, abnormal heart sounds
- crackles in lung bases
- sense of impending doom
JC core measures for AMI
- ASA on arrival and prescribed at discharge
- ACEI or ARB or LVSD
- smoking cessation advice/counseling
- BB prescribed at discharge
- Fibrinolytic therapy within 30 mins of arrival
- PCI within 90 mins (door to balloon)
- Statin prescribed at discharge
Fibrinolytics
- used when interventional procedures are not available
- need to know when the chest pain began within a 12 hr widow
- ideal delivery within 30 mins of arrival
- Monitor S/S of bleeding
- be prepared for reperfusion dysrhythmias
Fibrinolytic most common
Reteplase (recombinant plasminogen activator)
Fibrinolytic method of action
works by accelerating the formation of plasmin from plasminogen, allowing rapid lysis of clots
Fibrinolyric Absolute contraindications
Absolute
Any prior Intra-cranial hemorrhage
Cerebral vascular lesions
Intra cranial neoplasms
Ischemic stroke within 3 months
Suspected Aortic dissection
Active bleeding (excluding menses)
Head or facial trauma within 3 months
Intracranial surgery within 2 months
Uncontrolled hypertension
Fibrinolyric Relative contraindications
History of chronic/severe poorly controlled hypertension
HTN on presentation (SBP >180 or DBP >110)
History of prior ischemic stroke
Dementia
Traumatic or prolonged CPR
Major surgery within 3 weeks
Recent internal bleeding (2-4 wks)
Non-compressable vascular punctures
Pregnancy
Active peptic ulcer
Currently taking oral anticoagulant therapy
PCI
Percutaneous Coronary Intervention
- catheter is fed through the groin
- dye is shot through the catheter to locate occlusion
- occlusion is repaired via catheter, no scapel needed
- patient is recovered in the ICU and closely monitored for at least 24 hrs
- Pt is on blood thinners for at least 1 year post PCI
Complications that may develop post-MI
Dysrhythmias
Heart Failure
Cardiogenic shock
Structural defects
Pericarditis
Healing
- within 24 hrs dead tissues is being removed by macrophages
- 10days to 3 weeks scar tissue is being laid down
- 6 weeks for stability
Angina and Acute Coronary Syndrome Summary
Patients can have intermittent ischemia from atherosclerosis called angina
When the diseased vessel becomes totally occluded it results in a myocardial infarction (cell death).
Patients with chest pain should be treated rapidly…TIME IS MUSCLE!
Treatment options are determined based on the type of MI, the patient’s vital signs during event, and the resources available at each facility.
Patients who have experienced a MI should receive thorough education about managing their diagnosis as well as frequent follow up post-discharge.
