Angina and Myocardial Infarction Flashcards
1
Q
CORONARY ARTERY DISEASE
A
- accumulation of atherosclerotic plague in the coronary arteries
- could lead to development of collateral circulation, angina, acute coronary syndrome, myocardial infarction (MI) , disrythmias, heart failure, or death
2
Q
MYOCARDIAL ISCHEMIA
A
- 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 20min of no oxygen before necrosis
3
Q
CAUSES OF ISCHEMIA
A
- atherosclerosis is most common cause
- pt is put on blood thinners
- BP decreases over time
4
Q
COLLATERAL CIRCULATION
A
- tiny vessels connecting the large coronary arteries
- often developes in the presence of atherosclerosis to allow for continued blood flow
- an alternative route for blood to flow from the aorta to the cardiac muscle tissue
5
Q
ANGINA
A
- not a disease it is a symptom
- CHEST PAIN resulting from reduced coronary blood flow
- imbalance between myocardial blood and oxygen supply and demand
- 3 types of angina: stable, unstable, prinzmental
6
Q
PERCIPITATING FACTORS OF ANGINA
A
- physical exertion
- temperature extremities
- anxiety/ anger
- consumption of a heavy meal
- smoking
- sexual activity
- drugs ( stimulants)
- dysrhythmias
- emotions ( sns stimulation)
7
Q
ANGINAL PATTERNS
A
EKG, cardia enzymes, O2, vitals used to rule out pain from other causes other than the heart
8
Q
TYPES OF ANGINA: STABLE
A
- predictable pattern of increased work of the heart resulting in chest pain and relived by rest or nitrates
symptoms:
- pain
- shortness of breath
- nausea and vomiting
- palpitations and weakness
9
Q
TYPES OF ANGINA: PRIZMENTAL
A
- coronary artery vasospasm
- occurs unpredictably(not associated with physical activity)
- most often occurs at night while at rest
- unknown cause, through presumed to be caused by:
1. hyperactive sympathetic response
2. altered calcium flow
3. reduced prostaglandins that promote vasodilation
10
Q
TYPES OF ANGINA: UNSTABLE
A
- 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
11
Q
PATIENT HISTORY
A
P- precipitating events Q- quality of the pain R- radiation of pain S- severity of the pain T- timing when it began, with what activity?
- do they take medication?
- risk factors: family history, stressors
12
Q
ACUTE CORONARY SYNDROME (ACS)
A
- when the blood flow is significantly reduced but not fully occluded causing myocardial injury
PRECIPITATING FACTORS:
- rupture of atherosclerotic plaque resulting in a thrombus formation
- coronary artery vasospasm
- inflammation of coronary artery
- diastolic and systolic dysfunction (heart failure)
- increasingly occlusive atherosclerotic plaque
13
Q
PLAQUE RUPTURE IN ACS
A
- hemodynamic changes cause plaque to rupture (BP changes)
- platelet aggregation
- clot formation
- cell ischemia and injury
- lactic acid production causes chest pain
14
Q
ACUTE MYOCARDIAL INFARCTION
A
- 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 ( dysrhythmias, death, shock , heart failure)
15
Q
AMI ELECTRICAL CHANGES
A
- the t-wave will invert or the ST segment of the ECG tracing will become elevated
16
Q
AMI: ST SEGMENT ELEVATION
A
- > 0.4 sec after J point
- > 1mm in 2 or more continuous chest leads
- continguous means limb leads that look at the same area of the heart failure, cardiogenic shock, and death
17
Q
STAGES OF MYOCARDIAL INSULT
A
- Ischemia
- injury
- infarct
18
Q
ISCHEMIA
A
- lack of oxygenation
- ST depression or T wave inversion
- Permanent damage avoidable
19
Q
INJURY
A
- prolonged ischemia
- may have ST elevation
- Permanent damage avoidable
20
Q
INFARCT
A
- permanent death of myocardial tissue
- may have ST elevation and / or Q wave
21
Q
STEMI
A
- ST segment elevation present
- may or may not have elevation in cardiac enzymes initially
22
Q
NON- STEMI
A
- no ST segment elevation ( possibly ST depression or T-wave inversion
- diagnosed by elevated cardiac enzymes
23
Q
DIAGNOSTIC TESTS FOR ACUTE CORONARY SYNDROME
A
- 12 lead ekg
- cardiac enzymes
- chest x-ray
- echocardiogram
- trans-esophageal echo (TEE)
- exercise stress test
- nuclear cardiology
- cardiac catheterization
24
Q
CARDIAC ENZYMES
A
- CK (CPK)- normal level : 5-35mcg/ml
- appears in 3-6hrs - CK-MB- normal level : 0-6% of heart
- appears in 4-8hrs
3.Troponin-normal level:
25
Q
CALL FOR HELP
A
- chest pain unrelieved with rest
- new onset chest pain
- increasing shortness of breath
- prolonged period of pain
- unable to identify the cause
- do not try to drive
- do not wait
26
Q
CARING FOR PATIENTS WITH CHEST PAIN
A
- EKG priority
- quick history and description of symptoms
- vital signs
- IV access with blood draw (cardiac enzymes)
- medications
- closely monitor patients vital signs and reports of chest pain
27
Q
TIME IS MUSCLE!!!!!!
A
- when a patient is having chest pain you go fast
- all chest pain is a MI until proven otherwise
- work with your team don’t try to tackle all the tasks alone
28
Q
RULE OUT MI
A
-MONA greets every patient with chest pain
- morphine(pain, vasodilator, decreases BP)
- Oxygen
- nitroglycerin
- aspirin
29
Q
MORPHINE
A
- 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
30
Q
OXYGEN
A
- increases amount of oxygen available to patients cardiac muscle
- start with 2L/ min increase as necessary
- No need for oxygen if SPO2 is 94% or greater
31
Q
NITROGLYCERIN
A
- short acting nitrates
- first line therapy
- dilates peripheral blood vessels, coronary arteries/collateral vessels
-SL nitro
1 every 5min x 3
32
Q
Aspirin
A
-DECREASS PLATLET SGGREGATION
- MUST BE TAKEN BEFORE OR UPON ARRIVAL
- IF T CANT TAKE BY MOUTH , ODER A RECTALLY GIVEN
-ok if EMS gives and documents it is given
either dose is acceptable : 162mg or 325mg
- contraindications must be documented by the MD (ex. allergy, or active bleeding present)
33
Q
WHAT YOU MAY SEE IN THE ACUTE PHASE
A
- chest pain
- dyspnea, SOB
- diaphoresis, pale,cool skin
- nausea and vomiting
- reports of weakness
- JVD
- murmurs, abnormal, heart sounds,
- crackles in lung bases
- sense of impeding doom
34
Q
INFERIOR WALL EKG LEAD
A
- use caution when giving nitroglycerin to patients with an 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
35
Q
FIBRINOLYTICS(TPA)
A
- used when interventional procedures are not available
- need to know when chest pain began within a 12 hour window
- ideal delivery within 30min of arrival
- monitor S&S of bleeding
- be prepared for reperfusion dysrhythmias
36
Q
PCI -PERCUTANEOUS CORONARY INTERVENTION
A
- catherter is fed through the groin
- dye is shot through the catheter to locate occlusion
- occlusion is repaired via catherter…no scapel needed
- patient is recovered in the ICU and closely monitored for at least 24hrs
- pt is on blood thinners for at least 1 year post PCI
37
Q
COMPLICATIONS MAY DEVELOPE POST MI
A
- dysrhythmias
- heart failure
- cardiogenic shock
- structural defects
- pericarditis
38
Q
HEALING
A
-within 24hrs dead tissues is being removed by macropahges
- 10 days to 3 weeks scar tissue is being laid down
- 6 weeks for stability
