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NUR 213 > Unit 2: Acute Coronary Syndrome > Flashcards

Unit 2: Acute Coronary Syndrome Flashcards

1
Q

how do you find cardiac output? and what does the tell you ?

A

stroke volume x heart rate; the amount of blood pumped out the left ventricle in each minute.

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2
Q

what are non modifiable risk factors for ACS?

A

family hx, age, gender, ethnicity . African Americans are at a greater risk and men are more prone to get it at an earlier age.

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3
Q

what are modifiable risk factors for ACS?

A

type II diabetes, hypertension, hyperlipidemia, sedentary lifestyle, high fat diet, smoking, obesity, cocaine use, excessive use of ETOH, stress

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4
Q
  • pain, usually intermittent or short term. lasts longer than stable angina
  • can produce EKG changes, no ST segment elevation
  • usually does not elevate cardiac enzymes
  • no long term damage to the myocardium
  • can be a precursor to or warning of a future MI
  • differs from stable b/c it comes frequently and is poorly relieved by rest or nitro.
  • (ex): temporary loss of circulation to finger
A

unstable angina

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5
Q
  • didn’t treat angina properly/ignored and the next step is a ___-____.
  • pain usually lasts longer than 20 minutes
  • may produce EKG changes, but not elevation of the ST segment
  • elevates cardiac enymes
  • indicates partial blockage not a total occlusion
  • risk for potential long term damage to myocardium
  • requires treatment, usually non invasive
A

Non STEMI

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6
Q
  • pain usually lasting longer than 20 minutes
  • produces elevation of the ST segment on EKG
  • elevates cardiac enzymes
  • indicates complete blockage
  • requires immediate and invasive treatment
  • most serious of ACS
  • all of the tissue where occlusion is will die.
A

STEMI

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7
Q

amount ventricles stretch at the end of diastole

A

preload

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8
Q

pressure ventricles work against to open semilunar valves

A

afterload

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9
Q

amount of blood ejected by left ventricle during each contraction

A

stroke volume

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10
Q

percent of blood ejected from the heart during systole (50-70%)

A

ejection fraction

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11
Q
  • Chest pain
  • no EKG changes
  • no ST segment elevation
  • no cardiac enzymes
A

unstable angina

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12
Q
  • Chest Pain
  • no ST elevation on the EKG
  • positive for cardiac enzymes
  • partial blockage
A

Non STEMI

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13
Q
  • chest pain (sometimes the worst)
  • positive ST elevation on the EKG
  • positive cardiac enzymes
  • must be treated immediately
  • COMPLETE blockage
A

STEMI

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14
Q

plaque in coronary artery becomes unstable/inflamed. plaque ruptures. rough area of collagen in artery is exposed and platelets adhere. platelets release chemical that attracts more platelets. thrombus forms in artery. artery is occluded.

A

Myocardial Infarction (MI)

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15
Q

cardiac muscle death begins as soon as there is ischemia. TIME IS MUSCLE.

  • w/o function of the muscle wall (myocardium) the heart itself begins to fail. no effective electrical conduction or pump.
  • as soon as there is a thrombus in the vessel feeding this muscle, O2 perfusion to this muscle stops. It is dying, all the way through. mechanical action will eventually cease.
A

necrosis

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16
Q

ST depression is indicative of ?

A

previous MI damage

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17
Q
  • gather a hx
  • physical assessment
    pain: rate, describe, where, onset, radiate, precipitating (sudden), does anything make it better?
    associated symptom
    appearance: pale, weak, clammy, tired, fatigued = decreased CO
    auscultation: lungs and heart
    VS
    perfusion: cap refill distal pulses
    oxygenation: pulse ox
A

assessment of cardiac client

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18
Q
  • chest/back pain. radiates to the left arm and jaw.
  • shortness of breath
  • cool, clammy, diaphoretic
  • “heartburn”, nausea, and/or vomiting
  • dizziness, fatigue, sense of doom
A

What it look like

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19
Q

what does C-reactive protein measure ?

A

inflammation

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20
Q

what does BNP measure?

A

the stretch of the heart. if greater than 300 the patient is in heart failure.

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21
Q

what does a D-Dimer indicate?

A

pulmonary embolism

22
Q

women show symptoms differently.

  • back pain more common then men
  • showcase GI problem more
  • description is just intense pain
A

differences in women and men

23
Q

what is the first thing done to a patient that comes in with chest pain. must be done within 10 minutes or less.

A

EKG

24
Q

evidence based practice that doing things in a certain time frame leads to a more favorable outcome.

A

poor measures

25
Q

if the EKG doesn’t show elevation this doesn’t mean that a MI is completely ruled out. Just means that there isn’t a complete occlusion. The next step is to check cardiac enzymes

A

ST segment elevation in more than 2 segments one must consider a MI

26
Q
  • first to be elevated, as early as 1 hour after onset
  • peaks 4 to 12 hours
  • not specific to myocardial damage
A

myoglobin

27
Q
  • elevated 4 to 9 hours after onset of symptoms

- most concentrated in myocardium, can be a false positive in trauma

A

creatine kinase - myocardial bound (CK-MB) isoenyme

28
Q

highest mortality rate of all type of MI

  • this is due to how much responsibility of the left side has in regards to perfusing the body.
  • vessel that has greatest impact on the heart.
A

left anterior descending (LAD)

29
Q
  • levels increase around 6 hours after onset, peak in 12 to 24 hours. the higher the level the greater the damage.
  • this is measure every four hours
  • Troponin I: an stay elevated for 7 to 10 days
  • trends upwards until an intervention is done and even after intervention it simply start to trend down b/c of the damage to the heart.
  • Troponin T: can stay elevated for 7 to 14 days
A

Troponin

30
Q

how many patients will suffer from right ventricular failure?

A

1/3

31
Q
  • palpitations
  • doesn’t feel good
  • not well perfused
A

circumflex artery

32
Q

what is chostochondritis?

A

inflammation of the intercostal space

33
Q
  • inflammation of the heart muscle
  • caused by bacteria/virus
  • s/sx: similar to heart failure, may have fever, dysrhythmias
A

myocarditis

34
Q
  • inflammation of the pericardial sac
  • cause may be idiopathic, virus, post MI, and trauma
  • s/sx: SHARP chest pain, decreased CO, dysrhythmias, or palpitations, cough
A

pericarditis

35
Q
  • infection of endocardium
  • caused by bacteria/virus/fungus making its way to heart from elsewhere. (dental, IV drug use)
  • s/sx: flu like, fever, heart murmur, chest pain with breathing***
A

endocarditis

36
Q
  1. aspirin (core measure)
  2. nitroglycerin
  3. fibronlytic therapy if needed (core measure) this is to be given within 90 minutes
A

acute pharmacological interventions

37
Q

why is it a med error if you administer nitroglycerin without a patent IV access?

A

the patient could bottom out. its hard to get access on a patient with a HR less than 60. if patient does bottom out we should be able to give fluids immediately. check BP prior to administration.

38
Q

what does fibrinolytic therapy do?

A

breaks up clot

39
Q

what does nitroglycerin do?

A

increases blood flow through vasodilation

40
Q

how many mg of aspirin should be given in a cardiac event?

A

325 mg or 4 tablets 81 mg of children aspirin

41
Q
  • reperfusion, the sooner the better! CORE MEASURE: the goal is less than 90 minutes for a STEMI patient
  • clot removal, angioplasty, and or stent placement
  • post PCI: direct pressure to patient artery. monitor for bleeding, VS, (especially hypotension), cardiac dysrhythmias, hypokalemia
  • may have heparin drip pre and post procedure
  • discharged on a platelet inhibitor
A

cardiac catherization or percutaneous coronary intervention

42
Q
  • for significant stenosis, or stenosis in 3 or more vessels
  • poor ejection fraction
  • may be scheduled or emergent procedure
  • pre-op: cardiac monitor. indwelling catheter (maybe temp probe), teaching
  • teaching: what to expect, what the outcomes will be, what the patient will need to know to care for oneself after (pillow over chest)
  • echo must be done to prove the patient has a poor ejection fraction
  • should not have chest pain after this. if they do then it’s an emergency
  • toes should be warm and the body should be perfused.
A

coronary artery bypass graft (CABG)

43
Q
  • on vent for 3 to 6 hours (the less time the better)
  • maintain chest tubes
  • monitor pulmonary artery and arterial pressures, monitor VS and cardiac rhythm
  • maintain epicardial pacer (it will come out prior to d/c) this sticks out of the cheset wall.
A

interventions immediately post op to coronary artery bypass graft

44
Q
  • cough and deep breath very important
  • early ambulation is vital
  • continuous cardiac and electrolyte monitoring, more teaching on what life should be like after operation
  • cardiac rehab
  • CORE MEASURE: d/c on beta blocker
  • pain management (most at vein harvest site)
  • should not have chest pain
A

ongoing post op to coronary artery bypass graft

45
Q

blood gathering in the pericardial sac, can cause constriction because of the excess blood and causes poor cardiac output.

A

cardiac tamponade

46
Q
  • electrolyte imbalance
  • hypo/hypertension
  • dysrhythmias (#1 cause of death after surgery)
  • hypopthermia (temp probe)
  • bleeding
  • heart failure (b/c cardiac tissue is not working)
  • cardiac tamponade (red flag chest pain)
  • altered LOC
  • pain
A

complication of coronary artery bypass graft (CABG)

47
Q
  • may cause cardiac arrest and death.

- the first hour is crucial and the risk remains elevated for 72 hours

A

dysrhythmias

48
Q
  • paroxysmal nocturnal dyspnea
  • elevated pulmonary capillary wedge pressure
  • pulmonary congestion (cough, crackles, wheezes, blood tinged sputum, tachypnea)
  • restlessness
  • confusion
  • orthopnea
  • tachycardia
  • exertional dyspnea
  • fatigue
  • cyanosis
A

left sided heart failure

49
Q
  • fatigue
  • increased peripheral venous pressure
  • ascites (dependent edema in lower extremities)
  • enlarged liver and spleen
  • may be secondary to chronic pulmonary problems
  • distended jugular veins
  • anorexia, complaints of GI distress
  • weight gain
  • dependent edema
A

right sided heart failure

50
Q

left ventricular dysfunction leads to reduced ejection because the atria are not pushing blood out and the ventricles don’t contract which leads to pulmonary volume and pressure increase which leads to crackles and tachypnea, S3 which leads to wheezing and frothy sputum (pulmonary edema)

A

pg. 780

51
Q
  • occurs d/t necrosis of more than 40% of left ventricle.
  • s/sx: tachycardia, tachypnea, hypotension SBP <90 mmHg, urine output <0.5to1 mg/kg/hr, altered LOC/confusion or agitation, chest pain, decrease
  • peripheral pulses, cold/clammy skin
  • cautious management of vasodilators, diuretics, and positive inotropes to reduce preload, but maintain organ perfusion. It’s a very delicate balance.
A

cardiogenic chock

NUR 213 (20 decks)

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