Exam III Flashcards
MI: pathophysiology
- atherosclerotic plaque rupture: breaks loose, lodges in coronary artery
- embolus travels
- occluded blood flow
- myocardial oxygen demand > supply
MI: pain assessment
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?
MI: assessment
- anxiety/confusion
- tachypnea: r/t pain
- palpitations
- hypo/hypertension
- diaphoresis
MI: diagnostics
- EKG
- cardiac markers: CK-MB, myoglobin, Troponin, LDH
- cardiac cath
EKG leads: II,III,AVF
Infarction site: inferior
vessel: RCA, LCX
EKG leads: I, V5, V6, AVL
infarction site: lateral
vessel: LCX, diag.
EKG leads: V1, V2, V3, V4
infarction site: anterior/septal
vessel: LAD
myoglobin
- 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
creatinine phospho kinase (CPK)
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)
CK-MB
- more sensitive (true +) & specific (true -) than myoglobin
- more definitive of cardiac damage than myoglobin or CPK
- rises later than myoglobin
Troponin I & T
best indicator, gold standard. Troponin I: - more specific than CK-MB or Troponin T Troponin T: - more sensitive than I - less specific than I
MI intervetions
- initial: MONA, medications
- thrombolytics
- PCI
- CABG
thrombolytic therapy
- “clot busters”
- absolute and relative contraindications
- nursing role: monitor for bleeding, changes in mental status, ECG changes.
thrombolytic therapy: absolute contraindications
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
thrombolytic therapy: relative contraindications
- 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)
PCI
- if thrombolytics contraindicated
- cardiogenic shock within 36 hours
- angioplasty/stenting
Emergency CABG
- high risk: bleeding problems
- thrombolytics & PCI fail
- cardiogenic shock
- not every CABG is an open thoracotomy
MONA
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.
MI: initial medications
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
MI: nursing care
- 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.
HF: patho
- 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.
HF: diagnostics
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.
HF: interventions
- ACE/ARB
- Beta blockers
- diuretics
- digoxin
- vasodilators
- Nesiritide
ACE inhibitors/ARBS
- 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.
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
diuretics
- reduce volume overload
- IV has fast effect
- foley cath PRN
- electrolyte disturbances: ACE inhibitors increase K, loop diuretics decrease K, hypomagnesemia–> arrythmias.
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.
Hydralazine
- direct vasodilation
- reduced afterload: heart not working as hard.
- concurrent beta blocker to avoid rebound tachycardia/increased O2 demand.
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
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
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
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.
cardiogenic shock: assessment
- tachycardia
- cold clammy skin (shunting blood to vital organs)
- confusion, restlessness
- narrowing pulse pressure
- rapid, shallow respiration
cardiogenic shock: treatment
- dopamine
- dobutamine
- milrinone
- epinephrine
- norepinephrine
- phenylepherin
Dopamine
- titrate to maintain MAP>60mmHg
- positing intotrope (2-8mcg/kg/min) Beta 1
- vasopressor (8-20mch/kg/min) alpha
- possible dysrhythmias
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
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)
Norepinepherine
- potent vasoconstrictor
- non selective adrenergic agonist
- chronotrop
- +inotrope
- microvascular hypoperfusion (capillaries shutting off)
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)
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
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
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)
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.
ARDS: labs & diagnostics
- acute onset
- PCWP <200
- whited out xray
ARDS: phase II
- increasing pulmonary edema
- intubation usually required at this point
ARDS: phase III
- days 2-10
- progressive hypoxemia
- 50-80% mortality rate
- get on vent
- adjust PEEP & Vt for maximum oxygenation.
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
ARDS: medications
- steroids for inflammation (get blood sugar)
- nitric oxide: vasodilator, good for pulmonary vasculature
- surfactant replacement
- antibiotics (get cultures first)
ARDS: mechanical ventilation
- low tidal volumes (4-6mL/kg PBW)
- PEEP (5-20 cm H2O)
- sedation
- paralytics
- proning: having patient prone.
ARDS vs. ACI
ARDS:
- PaO2/FiO2 ratio <200
ALI:
- PaP2/FiO2 ratio between 200-300
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
Virchow’s triad
- hypercoagulable state (hypovolemia, increased viscosity)
- stasis
- endothelial injury (smoking, trauma)
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
PE: diagnostic assessment
- ABG, pulse ox (low)
- EKG
- Radiology: never diagnostic
- other: pulmonary angiography (gold standard), V/Q scan, spiral CT
PE: nursing diagnoses
- hypoxemia
- decreased cardiac output: blocking= less blood return, leading to decreased preload.
- anxiety
- risk for injury
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
PE: surgical interventions
- embolectomy
- inferior vena cava interruption (IVC filter); inserted thru leg, deployed in abdomen. need to wear a medic alert bracelet.
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
PE: complications
- hypoxia
- bleeding
- shock
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)
