Exam III Flashcards

1
Q

MI: pathophysiology

A
  • atherosclerotic plaque rupture: breaks loose, lodges in coronary artery
  • embolus travels
  • occluded blood flow
  • myocardial oxygen demand > supply
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2
Q

MI: pain assessment

A

P: precipitating factors/palliative measures
Q: quality: what does it feel like?
R: region (can you point to it with one finger?)/radiation
S: severity
T: timing: how long does it last, when did it start?

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3
Q

MI: assessment

A
  • anxiety/confusion
  • tachypnea: r/t pain
  • palpitations
  • hypo/hypertension
  • diaphoresis
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4
Q

MI: diagnostics

A
  • EKG
  • cardiac markers: CK-MB, myoglobin, Troponin, LDH
  • cardiac cath
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5
Q

EKG leads: II,III,AVF

A

Infarction site: inferior

vessel: RCA, LCX

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6
Q

EKG leads: I, V5, V6, AVL

A

infarction site: lateral

vessel: LCX, diag.

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7
Q

EKG leads: V1, V2, V3, V4

A

infarction site: anterior/septal

vessel: LAD

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8
Q

myoglobin

A
  • first lab that changes
  • iron binding protein in striated muscle
  • released with muscle damage
  • not specific to myocardial muscle
  • released early if myocardium damaged
  • amount of myoglobin correlates to infarct size
  • other causes of elevated myoglobin: exercise, seizures (tonic-clonic), muscle trauma, rhabdomyolysis
  • normal around 100
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9
Q

creatinine phospho kinase (CPK)

A

enzyme found in heart, skeletal muscles
divided into 3 isoenzymes
- CK-MM: skeletal muscles (major muscles)
- CK-BB: brain, bowel, bladder
- CK-MB: cardiac muscle (myocardial boo boo)

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10
Q

CK-MB

A
  • more sensitive (true +) & specific (true -) than myoglobin
  • more definitive of cardiac damage than myoglobin or CPK
  • rises later than myoglobin
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11
Q

Troponin I & T

A
best indicator, gold standard. 
Troponin I:
- more specific than CK-MB or Troponin T
Troponin T:
- more sensitive than I
- less specific than I
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12
Q

MI intervetions

A
  • initial: MONA, medications
  • thrombolytics
  • PCI
  • CABG
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13
Q

thrombolytic therapy

A
  • “clot busters”
  • absolute and relative contraindications
  • nursing role: monitor for bleeding, changes in mental status, ECG changes.
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14
Q

thrombolytic therapy: absolute contraindications

A

cost vs. benefit analysis

  • active internal bleeding
  • history of hemorrhagic CVA (when?)
  • known intracranial/intraspinal surgery or trauma
  • known clotting disorders (Von Willebrands, hemophilia)
  • severe, uncontrolled HTN
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15
Q

thrombolytic therapy: relative contraindications

A
  • recent major surgery (head to hips)
  • recent GI/GU bleeding
  • recent trauma
  • cerebrovascular disease (TIA, stroke)
  • pregnancy
  • advanced age
  • endocarditis/pericarditis (concurrent -itis around the heart)
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16
Q

PCI

A
  • if thrombolytics contraindicated
  • cardiogenic shock within 36 hours
  • angioplasty/stenting
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17
Q

Emergency CABG

A
  • high risk: bleeding problems
  • thrombolytics & PCI fail
  • cardiogenic shock
  • not every CABG is an open thoracotomy
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18
Q

MONA

A
morphine
- decreased myocardial oxygen consumption
- venous dilation
- decreased anxiety
oxygen
- increased oxygen supply for myocardium
- first thing we can do
nitroglycerin
- SL initially; IV gtt (10mcg/min then titrate)
- coronary artery dilation. headache.
- need constant BPs
aspirin
- antithrombotic effect (interferes w/platelet aggregation)
 - full size; can chew up.
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19
Q

MI: initial medications

A
Metoprolol
- 5mg IV q5m x 3
- decreased afterload (decreased O2 demand)
- negative chronotrope
- beta 1 selective
Heparin
- 60 unit/kg bolus (max 5000u)
- 12u/kg/hr (max 1000u)
- heparin protocol
- can run in same line as nitro on its own pump
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20
Q

MI: nursing care

A
  • pain control: morphine and O2
  • ECG monitoring
  • medication administration: give meds on time!
  • vitals during anginal/arrhythmic periods
  • cardiac rehabilitation/education: ambulation;diet;exercise. If pain comes back, put back in bed, notify HCP. possible reocclusion.
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21
Q

HF: patho

A
  • heart muscles’s inability to maintain CO to meet metabolic needs
  • activation of RAAS; increased catecholamines
  • systolic vs. diastolic: systolic means not enough squeeze, diasolic means heart can no longer expand easily.
  • left sided vs. right sided
  • high output vs. low output (think sepsis)
  • pulmonary edema d/t increased pulmonary capillary pressure–> poor gas exchange. fluid backs up into alveoli.
  • increased SVR: causing heart to work harder.
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22
Q

HF: diagnostics

A
echocardiogram
- blood flow
- valve function
- wall motion
ejection fraction: normal is 55-75%
- LVEDV-LVESV/LVEDV x 100
BNP: less than 100 is normal
- HF pt b/t 100-400. trying to counteract RAAS by getting rid of Na & H2O.
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23
Q

HF: interventions

A
  • ACE/ARB
  • Beta blockers
  • diuretics
  • digoxin
  • vasodilators
  • Nesiritide
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24
Q

ACE inhibitors/ARBS

A
  • end in -pril
  • decreased afterload
  • monitor for hyperkalemia (peaked, tall T waves)
  • caution in renal patients with potassium problems
  • no pregnant patients
  • ARBS: share a parking space with potassium. watch levels.
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25
beta blockers
- end in -olol - low dose initially - negative intotrope & chronotrope (less effective squeeze, decreased HR) - monitor BP/pulse HOLD PARAMETERS: - SBP < 100 - DBP < 50 - Pulse < 60 beta 1 selective Carvedilol: non selective, but prevents remodeling
26
diuretics
- reduce volume overload - IV has fast effect - foley cath PRN - electrolyte disturbances: ACE inhibitors increase K, loop diuretics decrease K, hypomagnesemia--> arrythmias.
27
Digoxin
CHECK K LEVELS - loading dose IV: total of 1mg over 24 hours - positive inotrope; negative dromo and chrono - potassium interaction: compete for same binding site. If pt is hypokalemic, more spaces for Dig to bind. Can OD pt with dig within therapeutic level. - dig level: 0.8-2.0 ng/ml - dig toxicity: halos, very bradycardic.
28
Hydralazine
- direct vasodilation - reduced afterload: heart not working as hard. - concurrent beta blocker to avoid rebound tachycardia/increased O2 demand.
29
Nesiritide
- synthetic BNP - IV bolus followed by gtt - vasodilation--> increased CO - natriuresis/diuresis (decreased afterload) - hypotension major side effect - discontinue in cases of cardiogenic shock - causes renal damage in some people
30
HF: nursing care
- HOB - supplemental oxygen - frequent assessments, esp with interventions - ECG monitoring (changes, new rhythms) - monitor lab values (electros, renal fx) - monitor for edema - cluster care/maximize rest periods - bed rest; DVT precautions; ROM exercises - education - baseline labs
31
cardiogenic shock: patho
- true pump failure - hypotension and cardiac function unable to meet metabolic needs of peripheral tissue - elevated LV filling pressure (wedge) - 15% of all MI patients - infarction > 40% LV mass= 85% mortality
32
cardiogenic shock: values
- cardiac index: decreased. - SvO2: decreased - SVR: increased - RAP: increased (holding onto fluid- maintain bp) - RVP: increased - PAP: increased - PCWP: increased mixed venous gases drawn off distal port- most deoxygenated blood.
33
cardiogenic shock: assessment
- tachycardia - cold clammy skin (shunting blood to vital organs) - confusion, restlessness - narrowing pulse pressure - rapid, shallow respiration
34
cardiogenic shock: treatment
- dopamine - dobutamine - milrinone - epinephrine - norepinephrine - phenylepherin
35
Dopamine
- titrate to maintain MAP>60mmHg - positing intotrope (2-8mcg/kg/min) Beta 1 - vasopressor (8-20mch/kg/min) alpha - possible dysrhythmias
36
Dobutamine
- beta 1 adrenergic agonist - positive intotrope - increased coronary artery perfusion - increased CO - minimal alpha-1 and beta-2 effects - decreased SVR - tachycardia major side effect - possible dysrhythmias
37
Milrinone
- posphodiesterase inhibitor - positive inotrope - little chronotropic activity (doesn't speed it up) - peripheral vasodilator - dysrhythmogenic - correct hypokalemia prior to infusion (cometes w/K like Dig)
38
Norepinepherine
- potent vasoconstrictor - non selective adrenergic agonist - + chronotrop - +inotrope - microvascular hypoperfusion (capillaries shutting off)
39
Phenylepherine
- alpha adrenergic agonist - potent vasoconstrictor @ arteriolar level - increases venous return to heart (better squeeze) - immediate onset IV requires careful titration - ventricular dysrhythmias if overdosed - possible reflex bradycardia (titrate very slowly)
40
cardiogenic shock: nursing care
- titration of IV medications: best effect with minimal side effects - hemodynamic monitoring: want wedge to come down - ECG monitoring - urine output (at least 0.5mL/kg/hour): hallmark sign of shock! - VS q1hour - trouble shoot ventilator, PA cath - lab draw and interpretation - education of family
41
ARDS: patho
- damage to alveolar capillary membrane - protein rich fluid leaks into/around alveoli; pulls fluid in. - surfactant production reduced - alveoli collapse due to edema - V/Q shunt (ventilation:perfusion) increases inflammatory not infectious process
42
ARDS: cause
massive inflammatory response - trauma (surgery) - sepsis (systemic inflammation/infection - pulmonary embolism: in bloodstream, not airway - blood products: reaction. - tumors (especially when broken apart and starting to metastasize)
43
ARDS: s/s
- refractory hypoxemia: poor gas exchange - increased work of breathing - tachypnea and tachycardia - hypotension from inflammation - mental status changes - normal breath sounds: airways are ok, no crackles/protein fluid.
44
ARDS: labs & diagnostics
- acute onset - PCWP <200 - whited out xray
45
ARDS: phase II
- increasing pulmonary edema | - intubation usually required at this point
46
ARDS: phase III
- days 2-10 - progressive hypoxemia - 50-80% mortality rate - get on vent - adjust PEEP & Vt for maximum oxygenation.
47
ARDS: phase IV
- fibrotic phase - if survived, permanent damage to lung tissue (younger people can recover better) - avoid complications: VAP, malnutrition from NGT - weaning from vent
48
ARDS: medications
- steroids for inflammation (get blood sugar) - nitric oxide: vasodilator, good for pulmonary vasculature - surfactant replacement - antibiotics (get cultures first)
49
ARDS: mechanical ventilation
- low tidal volumes (4-6mL/kg PBW) - PEEP (5-20 cm H2O) - sedation - paralytics - proning: having patient prone.
50
ARDS vs. ACI
ARDS: - PaO2/FiO2 ratio <200 ALI: - PaP2/FiO2 ratio between 200-300
51
PE: patho
- particulate matter enters the systemic venous circulation and lodges in the pulmonary vessels - emboli obstruct the pulmonary circulation and cause systemic and pulmonary hypoxia, or death - most common acute pulmonary disease - most from DVT (hazard of immobility) - risk factors for DVT: Virchow's triad, immobilization, hypercoagulability, surgery, obesity, advancing age, hx thromboembolism
52
Virchow's triad
- hypercoagulable state (hypovolemia, increased viscosity) - stasis - endothelial injury (smoking, trauma)
53
PE: assessment
``` Respiratory - dyspnea (sudden onset), pleuritic chest pain, apprehension - cough, hemoptysis, crackles Cardiovascular - tachypnea, tachycardia, fever - S3 or S4, PFR (pleural friction rub) Misc. - diaphoresis, petechiae ```
54
PE: diagnostic assessment
- ABG, pulse ox (low) - EKG - Radiology: never diagnostic - other: pulmonary angiography (gold standard), V/Q scan, spiral CT
55
PE: nursing diagnoses
- hypoxemia - decreased cardiac output: blocking= less blood return, leading to decreased preload. - anxiety - risk for injury
56
PE: medical interventions
oxygen therapy - NC, face mask, mechanical ventilation shock decreased CO - IV fluids to keep a blood pressure - positive inotropic agents (dobutamine) to increase myocardial output if it's low anticoagulation-thrombolytic therapy - heparin: monitor aPTT - warfarin: monitor INR - alteplase - streptokinase: PTT/INR before administration cardiac, pulmonary artery and CVP monitoring
57
PE: surgical interventions
- embolectomy - inferior vena cava interruption (IVC filter); inserted thru leg, deployed in abdomen. need to wear a medic alert bracelet.
58
PE: nursing interventions
evaluate chest pain auscultate lug sounds (will probably be clear) monitor: - respiratory pattern; respiratory failure - determinants of tissue oxygen delivery (temp, color of skin) - lab values: increased WBC count due to inflammation. - client for bleeding (use an electric razor, look at IV sites) notify HO or NP of changes treat anxiety - speak calmly and clearly - explain - acknowledge protect from bleeding document response to treatment
59
PE: complications
- hypoxia - bleeding - shock
60
PE: discharge teaching
- bleeding precautions - continue medication (don't stop abruptly, don't run out of it) - Notify MD: injury, excessive menstrual bleeding, blood in BM or urine, bruises or petechiae (bruises that won't heal) - DVT prevention: clothing, avoid prolonged sitting, standing, or positions with bent knees, stockings (TED)