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med surg 2 > Angina and Myocardial Infarction > Flashcards

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
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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
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3
Q

CAUSES OF ISCHEMIA

A
  • atherosclerosis is most common cause
  • pt is put on blood thinners
  • BP decreases over time
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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
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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
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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)
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7
Q

ANGINAL PATTERNS

A

EKG, cardia enzymes, O2, vitals used to rule out pain from other causes other than the heart

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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
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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
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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
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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
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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
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13
Q

PLAQUE RUPTURE IN ACS

A
  1. hemodynamic changes cause plaque to rupture (BP changes)
  2. platelet aggregation
  3. clot formation
  4. cell ischemia and injury
  5. lactic acid production causes chest pain
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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)
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15
Q

AMI ELECTRICAL CHANGES

A
  • the t-wave will invert or the ST segment of the ECG tracing will become elevated
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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
  1. CK (CPK)- normal level : 5-35mcg/ml
    - appears in 3-6hrs
  2. 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
  1. 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

med surg 2 (17 decks)

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