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Cardiovascular Emergencies Part 1. Assessment. Primary survey/ resuscitation Secondary survey. Factors For Consideration. Unmodifiable Age Sex Heredity Race. Modifiable B/P Obesity Dyslipidemia Smoking Sedentary life style Stress Diabetes. Focused Survey. Subjective data - PowerPoint PPT Presentation
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Primary survey/ resuscitationSecondary survey
UnmodifiableAgeSexHeredityRace
ModifiableB/PObesityDyslipidemiaSmokingSedentary life
styleStressDiabetes
Subjective dataChief complaintHistory of present illness
Onset: OPQRST Pain: PQRST Provocation Quality Region/radiation Severity Time
DurationDevelopment over timePeriodicity (? Comes/goes)
DyspneaSOB
Dyspnea on exertionPositional dyspnea
Paroxysmal nocturnal dyspnea
OrthopneaCough
Dry, “cardiac” coughHemoptysis
SyncopePalpitationsFatigue Nausea and
VomitingHeadacheBehavioral changeActivity limitationsInjury: mechanism and time
Coronary Heart Disease AnginaPrevious MIHypertensionCHF
Pulmonary DiseaseDiabetesRenal DiseasePrevious Cardiac
SurgeryCongenital AnomaliesAllergies
NitratesBeta BlockersCalcium Channel
BlockersAnti- hypertensivesDigitalisDiuretics
Antidysrhythmics
Anticoagulants
Steroids
Specific Pulmonary Drugs
Illicit Drugs
OVC Medications
General SurveyLOCRespiratory status
Rate, regularity, effort, breath sounds
SkinColor, temperature, moisture,
capillary refillEdema
Dependent, extremities, sacrum, pleural effusion, ascitis, cardiac (pitting)
CyanosisCentralPeripheral
ClubbingB/P MeasurementBoth armsOrthostatic
(supine, sitting, standing)
0 = absent
1 = thready
2 = normal
3 = bounding
Apical heart rateRegular, irregular,
regularly irregular, irregular irregular
Peripheral pulsesPupils
Size, equality, reactive
Tracheal positionNeck veinsThorax
ConfigurationDeformities, anterior, posterior, A-P diameter,
symmetrical movementInjuries, penetrating, blunt (ecchymosis,
contusions) evidence of scars, surgeryAbnormal chest movement, asymmetrical,
paradoxical
PrecordiumApical pulseAbnormal precordial
movements, heaves, lifts, pulsations, retractions
Epigastrium, pulsations
Areas tender, or Areas tender, or crepituscrepitus
EpigastriumEpigastrium
Auscultatory sitesMurmurs: systolic/diastolicVariations in rhythm
Extra soundsPericardial friction rubVenous humArterial bruits
Clicks
ECG, 12 leadRate, rhythmPresence of cardiac
dysrhythmiasEvidence of myocardial
ischemia, injuryPresence of intraventricular
conduction defectEvidence of previous MI
CBCSerum electrolytesCardiac serum markers
TroponinBasic metabolic profileCoagulation studiesDigoxin levelSerum creatinine, BUNT& C ABGsRoutine urinalysis
MarkerMarkerTime fromTime from
ObstructionObstruction
SpecifSpecific to ic to
CardiaCardiacc
Specific Specific to AMIto AMI
AppearAppearss
DisappeaDisappearsrs
CK-MBCK-MB 6 6 hourshours
36 36 hourshours
YesYes YesYes
MyoglobiMyoglobinn
2 2 hourshours
24 24 hourshours
NoNo NoNo
Troponin Troponin II
2 2 hourshours
1 week1 week YesYes NoNo
Pulse oximetryRadiography
Chest x-rayHeart size and
locationPresence of edemaPulmonary infiltratesPleural effusionsAir and fluid levels in
trauma patientsMediastinal widthBony structure
integrityCardiac catheterization
Echocardiogram
Determine prioritiesAirway, vital signs, cardiac rhythm, ABGs, Pulse oximetry, Control painRelieve anxietyEducation patient/otherPrevent complications
Establish care plan Emergency equipmentInitiate appropriate interventionsDocument dataMonitor responses and adjust
Growth & DevelopmentR/T congenital heart disease (heart
defects)Acquired heart disease (rheumatic
fever)Endocrine (diabetes)Other
Drug ingestions, ex: tricyclics, digoxinTrauma (falls, MVCs)Suffocation (plastic bags, drowning,
accidental hanging)
Pearls:Cardiac arrest usually d/t
progressive deterioration in respiratory and heart function
CHF, cardiogenic shock, dysrhythmias are unusual. If occur congenital.
Immature conduction system and autonomic innervation may contribute to dysrhythmias
Presence of chronic diseases
Altered drug metabolismMultiple physiological
differences and changes in lab values must be considered when assessing the older patient
Psychological and social changes: patient may have different goals for their treatment, discuss with patient
Geriatric patients can adapt to disease so well that symptoms are not obvious
Arteriosclerotic changes in aorta and peripheral pulses may pose a difficulty in palpating
Rhythm abnormalities are so common that they may be “normal”
“Go slow, stay low” with medications
Concurrent use of other medications cause problems, Easy to use meds are
helpful (transdermals)
One time or two time doses daily
Evaluate medications on a frequent basis
StableSymptom of
ischemia“pain or discomfort”Poorly localized Flow/Demand
imbalanceMay be chronic,
acute, or unstable
Unstable anginaNew symptoms of anginaIncreasing symptoms that
occur at rest or with on exertion
Usually due to platelet aggregation
Leads to atypical chest pain
9
Unstable angina diagnosisAngina is at rest, as well as
minimal exertion (usually 20 minutes or longer)
Angina of new onset (several weeks), starting with physical exertion, and markedly limits activity
Previously diagnosed stable angina
Normal ECG
Abnormal ECG Same Patient, Inverted T Waves
Variant AnginaMay or may not be due to
atherotic changesThought to be due to coronary
spasmPrinzmetal’s anginaMay occur at the same time,
dailyUsually not associated with
exertion or stressOccurs at younger agesST elevation seen during pain,
then disappears
GERDsBiliary ColicChest Wall PainPericarditisPEAortic DissectionDysrhythmias
ST depression may accompany pain with stable angina
Transient ST-segment deviations (depression or elevation), and T wave inversion occur commonly with unstable angina
Variant angina: ST elevation occurs with pain, subsides when pain does
May see LV hypertrophy, old MI, nonspecific ST and T-wave abnormalities and AV defects
CBCCardiac serum
markers…no elevation should occur unless cell damage
Chest X-ray ( CHF, cardiomegaly)
Continuous monitoring
O2IV, Draw labs12 Lead ECGRestDecrease anxietySL NTG, B/P 100 mm
HG followed by a dripAssess for H/AReflex tachycardiaCautious with elderly
Beta blockersIf clinical situation
deteriorates after B Blocker, consider coronary artery spasm
Assess for signs of heart failure
Adverse effects of blockers are considered more common and severe in geriatric
Administer antiplatelet agentsASA (4-5 baby aspirin) Administer ASAPDecreases platelet activation
and thrombus formationTEACH/EDUCATION
Physical examGeneral appearance: Anxious, restless, clenched fist
against chest (Levine sign) Look of doomHeart rate: may be ok, tachycardia (most common),
bradycardia (inferior and RV), Regular or irregular PVCs common
Arterial BPMajority of patients with uncomplicated MI are normotensive
May be elevated due to SNS stimulationPain and anxiety
Decreased as a result of impaired cardiac function or due to drug administration (nitrates, M.S.)
Respiratory rate: Initially elevated. Should return to normal after pain reliefPatients with CHF,
respiratory rate correlates with severity of condition
Peripheral: How bad is the patient’s condition?Pallor, cyanosis, diaphoreses, mottled, cool, peripheral
pulses variable
Temperature: Often increases 4-8 hours post MI
Heart Sounds: muffled. murmurs may be transient or permanent
DiagnosisDiagnosisContinuous cardiac monitoring12 lead ECGDetermine Location of infarct(next slide)
Anterior SeptalAnterior Septal ST Leads 1, AVR,ST Leads 1, AVR,
V1 through V4V1 through V4
Lateral ApicalLateral Apical ST Leads 1, AVLST Leads 1, AVL
V5 and V6V5 and V6
PosteriorPosterior Recipical Changes Recipical Changes V1,V2V1,V2
No Q waves, Tall R’sNo Q waves, Tall R’s
St II,III,AVFSt II,III,AVF
Upright t waveUpright t wave
InferiorInferior ST ST
Leads II, III, AVFLeads II, III, AVF
Right VentricularRight Ventricular ST VST VRR 4 – VR 6 4 – VR 6
MyoglobinElevated 1-4 hours after onset of
MI, peaks 6-7 hours, normal in about 1 day
Lacks specificity, found in skeletal muscle
Troponins:Most recent marker, most
sensitive and specific for cardiac damage
Elevated 3-12 hours after MI, Peaks in 24 hours, with TnI , returns to normal in 5-12 days
TnT may be elevated in patients with renal failure, which is not the case with TnI; therefore TnI is utilized.
ABCsOxygenIV or topical NTG, as B/P tolerated (B/P
100 or greaterIV with normal saline, KVOAnalgesia: M/SASA12 Lead ECGBlood samples for analysis
If appropriate consider PTCAFollow ACLS GuidelinesPrepare for Thrombolytic Therapy as appropriate
Administer aspirin, nitrates, heparin, plavix, Integrillin, Lopressor, Morphine, antiarrhythmics
Observe patient:Bleeding, reperfusions
dysrhythmiasVital signs, ventricular
ectopy, and other dysrhythmias
Heart and lung soundsLOCI & OLevel of pain
Portable chest filmACLS measuresPrepare for cath labEducate and explainAllow visit from
significant other
Clinical syndrome, can occur from any heart disease
Pediatric..usually due to congenital heart defects
Inability to discharge contents
Inability to pump enough blood to meet metabolic needs
Radiologic: often normalpulmonary vasculature,
edema, fluidCardiac silhouette may
show cardiac enlargement, hypertrophy, dilation
Enlarged RA and RVPleural effusion Valve calcifications
Lab: H& HLytesBUN, Creatinine Liver function studiesCardiac enzymes (if AMI)BNP
B-type natriuretic peptide
ECG: nonspecific changes, electrolyte or drug induced dysrhythmias
Echo: chamber size,wall thickness, thrombus formation, valvular function, pericardial disease
ABCDProvide
supplemental O2IV Normal SalineABGs and other labsProvide restECG continuousMonitor
hemodynamics
Administer Morphine
Administer vasodilatorDecreases
afterload, arterial dilations. Also pre-load
NTG, IsosorbideIncreases
venous poolingNTG preferred in
pulmonary edema, CAD since improves coronary artery perfusion
Venous dilation
Diuretics:Decrease preloadFoley catheter,
possibleI&OMonitor serum K+
ACE Inhibitors:Captopril, EnalaprilBlock formation of
Angiotensin II, yields vasodilation
Reduce mortality, by improving cardiac function
Avoid overdiuresisCleared by kidney
Life-threatening elevation of B/P necessitating reduction to prevent end-organ damage and potential death
Essential hypertension unknown cause
Secondary hypertension elevated pressure whose cause is known (renal vascular
disease)Produces changes in arterioles (necrosis and
inflammation over time) causing decrease in bloodflow to end organs
Accelerated and/or malignant hypertension:Diastolic pressure higher than 140 mmHg
Untreated/uncontrolled essential or secondary hypertension
Poor patient compliance with antihypertensive medications
Renal dysfunctionEclampsia of pregnancy (not tolerated well)Adrenergic crisesAMI, Cerebral dysfunction Pituitary tumors
HistorySevere H/AEpistaxisFamily hx hypertensionMAO inhibitorsCAD, Renal DiseaseDiabetes, obesity, smoker, hyperlidemia, stress
Diastolic pressure exceeding diastolic or 120mmHG
Retinopathy with exudates, Retinal hemorrhagesPapilloedema (diastolic pressure > 140)H/A, confusion, restless stupor, somnolenceEpistaxisTachycardiaChest discomfortN&VRalesOliguria, azotemia
Lab: ABG:
metabolic acidosis CBC HCT
in renal failure, polycythemia in renal
Electrolytes: HypocalcemiaHyponatremiaaldosteronism causes
hypokalemia ( half of patients)
Glucose: elevated in Cushing’s Syndrome, diabetes
BUN and creatinine elevated in renal disease
Uric acid: hyper-uricemia in renal failure
U/A: proteinuria, possible renal dysfunction
Chest film: cardiomegaly may be seenECG: LV hypertrophy may be seenCT scan: Diffuse brain edema with hypertensive
crisesECHO: diastolic function impaired.
ABCD, O2, IV @ KVO rateACLS protocolsAdminister medicationsNTP:
Most common and most effective0.5-10mcg/kg/minTitrate with B/PWatch for cyanide toxicityDrug is light sensitive
NTG:Drug of choice for unstable angina and ischemia,
LV failure, adrenergic crisesProvides immediate response
Sympathetic Blocking Agent (Labetalol)Alpha and beta blockerOnset and cessation of action slower than NTP and
NTGContraindicated in patients with heart failure,
greater than 1st degree block, bradycardia, and reactive airway disease
ACE InhibitorsUsed in presence of LV failureCaptopril: 6.25-50 mg orally every 30-45 minutesEnalapril: 1.25-5 mg IV every 6 hoursOnset of action for both 10-15 minutes
Calcium Channel BlockersNifidipine: 10 mg PO or sublingual (10-20 mg orally every
30-45 minutes of sublingually every 15 minutes)Beta Blocker: Metoprolol, Esmolol
Blocks effects of increased adrenergic toneMetoprolol 5 mg IV every 5 minutes up to 15 mg total
Administer diureticsClosely monitor patient’s responseContinuous arterial monitoringWatch medication side effectsObserve for signs of ischemiaI&OMonitor for dysrhythmiasMonitor for ↑ ICPPossible ICP monitoringSudden chest pain may suggest aortic dissectionReassure patient/family Calm environment