Angina & Myocardial Infarction Flashcards
CAD
- Accumulation of atherosclerotic plaque in the coronary arteries
- could lead to development of collateral circulation, angina, acute coronary syndrome, myocardial infarction, dysrhythmias, heart failure, or death
Myocardial ischemia
- 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 >75% occluded (or stenosed)
- cardiac cells can sustain about 20 mins of no O2 before necrosis
- most common cause is atherosclerosis
Collateral circulation
- tiny vessels connecting the large coronary arteries
- often develops in the presence of atherosclerosis to allow for continued blood flow
- an alternative route blood to flow from the aorta to the cardiac muscle tissue
- reroute blocked artery by minor vessels
Angina
-chest pain resulting from reduced coronary blood flow
-imbalance between myocardial blood (and O2) supply and demand
-3 types of angina
S/S: chest pain & tightness, indigestion
Precipitating factors of angina
- physical exertion
- temperature extremes
- anxiety/anger
- consumption of a heavy meal
- smoking
- sexual activity
- drugs (stimulants)
- dysrhythmias
Stable angina
- predictable pattern of increased work of the heart resulting in chest pain and relieved by rest or nitrates
- symptoms: pain, SOB, nausea and vomiting, palpitations and weakness
Prinzmental angina
- coronary artery vasospasm
- occurs unpredictably (not associated w/ physical activity)
- most often occurs at night while at rest
- unknown causes, though presumed to be caused by : -hyperactive sympathetic respsonse
- Altered calcium flow
- reduced prostaglandins that promote vasodilation
Unstable angina
- unpredictable pain without contributing factors
- at rest or during activity
- departing from usual pattern
- May last more than 20 minutes
- marked by increasing frequency, severity, and duration of chest pain symptoms
- patho: atherosclerosis
Patient history
- PQRST
- P:precipitating events
- Q:quality of pain
- R:radiation of pain
- S:severity of pain
- T:timing-when is began, with what activity?
- do they take medications?
- risk factors : family history, stressors
Acute coronary syndrome (ACS)
-when blood flow is significantly reduced but not fully occluded causing myocardial injury
-precipitating factors: -coronary artery vasospasm
-rupture of atherosclerotic plaque resulting in a thrombus formation
-increasingly occlusive atherosclerotic plaque
-inflammation of coronary artery
-diastolic and systolic dysfunction (HF)
Some symptoms: SOB, dizzy, light headed, sweating, nausea, not feeling right
Plaque rupture in ACS
1) hemodynamic changes cause plaque to rupture
2) platelet aggregation
3) clot formation
4) cell ischemia and injury
5) lactic acid production causes chest pain
Acute myocardial infarction
- 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 (ie: arrhythmias, HF, cardiogenic shock, death)
AMI: electrical changes
The T-wave will invert or the ST segment of ECG tracing will become elevated
AMI: ST segment elevation
- > 0.04 secs after J point
- > 1 mm (1 small box) in 2 or more contiguous chest leads
- contiguous means limb leads that “look” at the same area of the heart or are numerically consecutive chest leads
Stages of myocardial insult
1) ischemia
2) injury
3) infarct
Ischemia stage of myocardial insult
- lack of oxygenation
- ST depression or T wave inversion
- permanent damage avoidable
Injury stage of myocardial insult
- prolonged ischemia
- may have ST elevation
- permanent damage avoidable
Infarct stage of myocardial insult
- permanent death of myocardial tissue
- may have ST elevation and/or Q wave
STEMI vs. Non-STEMI
STEMI: ST segment elevation present
- may or may not have elevation of cardiac enzymes initially
- complete occlusion
Non-STEMI: no ST segment elevation(possible ST depression or T wave inversion)
- diagnosed by elevated cardiac enzymes
- partial occlusion
Diagnostic tests for ACS
- 12 lead EKG
- cardiac enzymes
- CXR (portable)
- echocardiogram
- trans-esophageal Echo (TEE)
- exercise stress test
- nuclear cardiology
- cardiac cath
Call for help!
- CP unrelieved with rest
- new onset CP
- increasing SOB
- prolonged period of pain
- unable to identify the cause
- do not drive
- do not wait
Caring for pts. With chest pain
- EKG priority
- quick history and descriptions of symptoms
- vital signs
- IV access with blood draw (cardiac enzymes)
- medications
- closely monitor pts. Vitals and reports of chest pain
When a pt is having chest pain…
You go fast!
- all chest pain is MI until proven otherwise
- work with your team, don’t try to tackle all the tasks alone.. Your pt will suffer
Rule out MI
- MONA= every pt with chest pain
- M- morphine
- O - oxygen
- N- nitroglycerin
- A- aspirin
Morphine
- relieves pain-> reduces metabolic demand -> allows for more oxygen to be available to cardiac cells
- vasodilates (increases coronary perfusion and decreases after load)
- closely monitor pts BP (too much =drop in BP)
Oxygen
- increases amount of oxygen available to pts cardiac muscle
- starts with 2L /min and increases as necessary
- no need for O2 if SPO2 is 94% or greater
Nitroglycerin
-short acting nitrates: first line therapy
- dilates peripheral blood vessels, coronary arteries/ collateral vessels
- SL nitroglycerin (pill or spray) 1 every 5mins
X 3
- Long acting nitrates: nitroglycerin ointment
- Isordil (isosorbide dinitrate) or Imdur (isosorbide mononitrate)
Aspirin
- must be administered before or upon arrival
- OK if given and documented by EMS before arrival, or if pt says they took it at home and you document “pt tookprior to arrival”
- either dose is acceptable: 162mg or 325mg
- if pt cannot take it by mouth, must get order to take rectally
- contraindications must be documented by the MD, ARNP, PA (ie: allergy or active bleeding present)
- decreases platelet aggregation
What may be seen in acute phase
- chest pain
- dyspnea, SOB
- diaphoresis, pale, cool skin
- N&V
- reports of weakness
- JVD
- murmurs, abnormal heart sounds
- crackles in lung bases
- sense of impending doom
Incidence of CAD
- American heart association estimates that 1.2 million people will have a heart attack each year
- 1/4 will die prior to getting to the ER
- leading cause of death
inferior wall
- use caution when giving nitroglycerin to pts with inferior wall MI
- inferior infarcts are usually from RCA occlusion resulting in right ventricular failure
- typically will see hypotension and bradycardia with inferior wall MI
joint commission core measures for AMI
- aspirin on arrival and prescribed at discharge
- ACEI or ARB for LVSD
- smoking cessation advice/counseling
- beta-blocker prescribed at discharge
- fibrinolytic therapy within 30 mins of arrival or
- PCI (“door-to-balloon”) within 90 mins
- statin prescribed at discharge
fibrinolytics
- used when interventional procedures are not available
- need to know when the chest pain began within a 12 hr window
- ideal delivery within 30mins of arrival
- monitor S/S of bleeding
- be prepared for reperfusion dysrhythmias
fibrinolytic therapy
- most common: reteplase (recombinant plasminogen activator)
- method of action: works by accelerating the formatin of plasmin from plasminogen, allowing rapid lysis of clots
fibrinolytic 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
fibrinolytic contraindications: RELATIVE
- 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 groin
- dye is shot through the catheter to locate occlusion
- occlusion is repaired via catheter.. no scalpel needed
- pt is recovered in the ICU and closely monitored for at least 24 hrs
- pt is on blood thinners for at least 1 yr post PCI
complications that may develop post MI
- dysrhythmias
- heart failure
- cardiogenic shock
- structural defects
- pericarditis
healing
- within 24 hrs tissues are being removed by macrophages
- 10 days to 3 weeks scar tissue is being laid down
- 6 weeks stability
angina and ACS summary
- pts can have intermittent ischemia from atherosclerosis called angina
- when the diseased vessel becomes totally occluded it results in a myocardial infarction (cell death)
- pts with chest pain should be treated rapidly
- treatment options are determined based on the type of MI, pts vitals during event, & resources available at facility
- pts who have experienced an MI should receive thorough education about managing their diagnoses as well as frequent follow up post- discharge
