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Critical Care > Exam III > Flashcards

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
Q

beta blockers

A
  • 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
Q

diuretics

A
  • reduce volume overload
  • IV has fast effect
  • foley cath PRN
  • electrolyte disturbances: ACE inhibitors increase K, loop diuretics decrease K, hypomagnesemia–> arrythmias.
27
Q

Digoxin

A

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
Q

Hydralazine

A
  • direct vasodilation
  • reduced afterload: heart not working as hard.
  • concurrent beta blocker to avoid rebound tachycardia/increased O2 demand.
29
Q

Nesiritide

A
  • 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
Q

HF: nursing care

A
  • 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
Q

cardiogenic shock: patho

A
  • 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
Q

cardiogenic shock: values

A
  • 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
Q

cardiogenic shock: assessment

A
  • tachycardia
  • cold clammy skin (shunting blood to vital organs)
  • confusion, restlessness
  • narrowing pulse pressure
  • rapid, shallow respiration
34
Q

cardiogenic shock: treatment

A
  • dopamine
  • dobutamine
  • milrinone
  • epinephrine
  • norepinephrine
  • phenylepherin
35
Q

Dopamine

A
  • titrate to maintain MAP>60mmHg
  • positing intotrope (2-8mcg/kg/min) Beta 1
  • vasopressor (8-20mch/kg/min) alpha
  • possible dysrhythmias
36
Q

Dobutamine

A
  • 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
Q

Milrinone

A
  • 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
Q

Norepinepherine

A
  • potent vasoconstrictor
  • non selective adrenergic agonist
    • chronotrop
  • +inotrope
  • microvascular hypoperfusion (capillaries shutting off)
39
Q

Phenylepherine

A
  • 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
Q

cardiogenic shock: nursing care

A
  • 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
Q

ARDS: patho

A
  • 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
Q

ARDS: cause

A

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
Q

ARDS: s/s

A
  • 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
Q

ARDS: labs & diagnostics

A
  • acute onset
  • PCWP <200
  • whited out xray
45
Q

ARDS: phase II

A
  • increasing pulmonary edema

- intubation usually required at this point

46
Q

ARDS: phase III

A
  • days 2-10
  • progressive hypoxemia
  • 50-80% mortality rate
  • get on vent
  • adjust PEEP & Vt for maximum oxygenation.
47
Q

ARDS: phase IV

A
  • fibrotic phase
  • if survived, permanent damage to lung tissue (younger people can recover better)
  • avoid complications: VAP, malnutrition from NGT
  • weaning from vent
48
Q

ARDS: medications

A
  • steroids for inflammation (get blood sugar)
  • nitric oxide: vasodilator, good for pulmonary vasculature
  • surfactant replacement
  • antibiotics (get cultures first)
49
Q

ARDS: mechanical ventilation

A
  • low tidal volumes (4-6mL/kg PBW)
  • PEEP (5-20 cm H2O)
  • sedation
  • paralytics
  • proning: having patient prone.
50
Q

ARDS vs. ACI

A

ARDS:
- PaO2/FiO2 ratio <200
ALI:
- PaP2/FiO2 ratio between 200-300

51
Q

PE: patho

A
  • 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
Q

Virchow’s triad

A
  • hypercoagulable state (hypovolemia, increased viscosity)
  • stasis
  • endothelial injury (smoking, trauma)
53
Q

PE: assessment

A 
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
Q

PE: diagnostic assessment

A
  • ABG, pulse ox (low)
  • EKG
  • Radiology: never diagnostic
  • other: pulmonary angiography (gold standard), V/Q scan, spiral CT
55
Q

PE: nursing diagnoses

A
  • hypoxemia
  • decreased cardiac output: blocking= less blood return, leading to decreased preload.
  • anxiety
  • risk for injury
56
Q

PE: medical interventions

A

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
Q

PE: surgical interventions

A
  • embolectomy
  • inferior vena cava interruption (IVC filter); inserted thru leg, deployed in abdomen. need to wear a medic alert bracelet.
58
Q

PE: nursing interventions

A

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
Q

PE: complications

A
  • hypoxia
  • bleeding
  • shock
60
Q

PE: discharge teaching

A
  • 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)

Critical Care (3 decks)

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