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