Transcript Cardiovascular Emergencies I updated 2013

Assessment
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Primary survey/
resuscitation
Secondary survey
Factors For Consideration
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Unmodifiable
• Age
• Sex
• Heredity
• Race
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Modifiable
• B/P
• Obesity
• Dyslipidemia
• Smoking
• Sedentary life
style
• Stress
• Diabetes
Subjective data
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Chief complaint
History of present illness
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Onset: OPQRST
Pain: PQRST
Provocation
Quality
Region/radiation
Severity
Time
 Duration
 Development over time
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Periodicity (? Comes/goes)
Focused
Survey
Focused Survey
(Continued)
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Dyspnea
• SOB
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Dyspnea on
exertion
Positional dyspnea
• Paroxysmal
nocturnal dyspnea
• Orthopnea
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Cough
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Dry, “cardiac” cough
Hemoptysis
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Syncope
Palpitations
Fatigue Nausea and
Vomiting
Headache
Behavioral change
Activity limitations
Injury: mechanism and
time
Medical History
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Coronary Heart Disease
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Angina
Previous MI
Hypertension
CHF
Pulmonary Disease
Diabetes
Renal Disease
Previous Cardiac
Surgery
Congenital Anomalies
Allergies
Current/Past Medication Use
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Nitrates
Beta Blockers
Calcium
Channel
Blockers
Antihypertensives
Digitalis
Diuretics
Antidysrhythmics
Anticoagulants
Steroids
Specific
Pulmonary Drugs
Illicit Drugs
OVC Medications
Physical Exam
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General Survey
• LOC
• Respiratory status
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Rate, regularity, effort,
breath sounds
• Skin
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Color, temperature,
moisture, capillary refill
• Edema
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Dependent, extremities,
sacrum, pleural effusion,
ascitis, cardiac (pitting)
Physical Exam
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Cyanosis
• Central
• Peripheral
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Clubbing
B/P
Measurement
• Both arms
• Orthostatic
(supine, sitting,
standing)
0 = absent
1 = thready
2 = normal
3 = bounding
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Apical heart rate
• Regular, irregular,
regularly irregular,
irregular irregular
Peripheral pulses
Pupils
• Size, equality,
reactive
Physical Exam
Inspection
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Tracheal position
Neck veins
Thorax
• Configuration
 Deformities, anterior,
posterior, A-P diameter,
symmetrical movement
 Injuries, penetrating, blunt (ecchymosis,
contusions) evidence of scars, surgery
 Abnormal chest movement,
asymmetrical, paradoxical
Physical Exam (Inspection)
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Precordium
• Apical pulse
• Abnormal precordial
movements, heaves,
lifts, pulsations,
retractions
• Epigastrium,
pulsations
Physical Exam: Palpation
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Areas tender, or
crepitus
Epigastrium
Physical Exam: Auscultation
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Auscultatory sites
• Murmurs: systolic/diastolic
• Variations in rhythm
• Extra sounds
 Pericardial friction rub
 Venous hum
 Arterial bruits
• Clicks
Physical Exam:
Diagnostic Procedures
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ECG, 12 lead
• Rate, rhythm
• Presence of cardiac
dysrhythmias
• Evidence of myocardial
ischemia, injury
• Presence of
intraventricular
conduction defect
• Evidence of previous MI
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CBC
Serum electrolytes
Cardiac serum markers
• Troponin
• Basic metabolic profile
• Coagulation studies
• Digoxin level
• Serum creatinine, BUN
• T& C
• ABGs
• Routine urinalysis
Physical Exam:
Diagnostic
Procedures
Comparison of Diagnostic Markers
Marker
Time from
Obstruction
Appears
CK-MB
Specifi
c to
Cardiac
Specific
to AMI
Disappears
6 hours 36 hours
Yes
Yes
Myoglobin 2 hours 24 hours
No
No
Troponin I 2 hours 1 week
Yes
No
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Diagnostic
Procedures
Pulse oximetry
Radiography
• Chest x-ray
 Heart size and
location
 Presence of edema
 Pulmonary infiltrates
 Pleural effusions
 Air and fluid levels in
trauma patients
 Mediastinal width
 Bony structure
integrity
Cardiac catheterization
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Echocardiogram
Interventions
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Determine priorities
• Airway, vital signs, cardiac rhythm, ABGs, Pulse
oximetry,
• Control pain
• Relieve anxiety
• Education patient/other
• Prevent complications
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Establish care plan
Emergency equipment
Initiate appropriate interventions
Document data
Monitor responses and adjust
Pediatrics
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Growth & Development
• R/T congenital heart disease
(heart defects)
• Acquired heart disease (rheumatic
fever)
• Endocrine (diabetes)
• Other
 Drug ingestions, ex: tricyclics,
digoxin
 Trauma (falls, MVCs)
 Suffocation (plastic bags,
drowning, accidental hanging)
Pediatric
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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
Geriatric
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Presence of chronic
diseases
Altered drug metabolism
Multiple 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
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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”
Pearls
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“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
Angina
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Stable
• Symptom of
ischemia
• “pain or
discomfort”
• Poorly localized
• Flow/Demand
imbalance
• May be chronic,
acute, or
unstable
Angina (continued)
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Unstable angina
• New symptoms of
angina
• Increasing symptoms
that occur at rest or
with on exertion
• Usually due to platelet
aggregation
• Leads to atypical
chest pain
Angina (Continued)
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Unstable angina
diagnosis
• Angina 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
Angina cont’d
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Variant Angina
• May or may not be due to
atherotic changes
• Thought to be due to coronary
spasm
• Prinzmetal’s angina
• May occur at the same time,
daily
• Usually not associated with
exertion or stress
• Occurs at younger ages
• ST elevation seen during pain,
then disappears
Angina: Curveballs
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GERDs
Biliary Colic
Chest Wall Pain
Pericarditis
PE
Aortic Dissection
Dysrhythmias
Diagnostic Procedures: ECG
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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
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Diagnostic Procedures
(Continued)
CBC
Cardiac serum
markers…no
elevation should
occur unless cell
damage
Chest X-ray (
CHF,
cardiomegaly)
Interventions
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Continuous
monitoring
O2
IV, Draw labs
12 Lead ECG
Rest
Decrease anxiety
SL NTG, B/P 100 mm
HG followed by a drip
• Assess for H/A
• Reflex tachycardia
• Cautious with
elderly
Interventions (continued)
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Beta blockers
• If 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
Interventions (continued)
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Administer antiplatelet
agents
• ASA (4-5 baby aspirin)
• Administer ASAP
• Decreases platelet
activation and thrombus
formation
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TEACH/EDUCATION
Acute Myocardial Infarction
Myocardial
Infarction
(MI)Coronary
Occlusion
Heart
Attack
MI: Data
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Physical exam
General appearance: Anxious, restless,
clenched fist against chest (Levine sign) Look
of doom
Heart rate: may be ok, tachycardia (most
common), bradycardia (inferior and RV),
Regular or irregular PVCs common
Data (continued)
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Arterial BP
• Majority of patients with
uncomplicated MI are
normotensive
• May be elevated due to SNS
stimulation
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Pain and anxiety
• Decreased as a result of impaired
cardiac function or due to drug
administration (nitrates, M.S.)
Data (continued)
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Respiratory rate:
Initially elevated.
Should return to
normal after pain
relief
• Patients with CHF,
respiratory rate
correlates with
severity of condition
Data (continued)
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Peripheral: How bad is the patient’s condition?
• Pallor, cyanosis, diaphoreses, mottled, cool,
peripheral pulses variable
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Temperature: Often increases 4-8 hours post MI
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Heart Sounds: muffled. murmurs may be transient
or permanent
Diagnosis
Continuous cardiac monitoring
 12 lead ECG
 Determine Location of infarct
(next slide)
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Anterior Septal
ST
Leads 1, AVR,
V1 through V4
Lateral Apical
ST
Leads 1, AVL
V5 and V6
Posterior
Recipical Changes
V1,V2
No Q waves, Tall R’s
St
II,III,AVF
Upright t wave
ST
Leads II, III, AVF
Inferior
Serum Markers
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Myoglobin
• Elevated 1-4 hours after onset of
MI, peaks 6-7 hours, normal in
about 1 day
• Lacks specificity, found in skeletal
muscle
Serum Markers
(continued)
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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.
Interventions
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ABCs
Oxygen
IV or topical NTG, as B/P tolerated (B/P
100 or greater
IV with normal saline, KVO
Analgesia: M/S
ASA
12 Lead ECG
Blood samples for analysis
Interventions (continued)
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If appropriate consider PTCA
Follow ACLS Guidelines
Prepare for Thrombolytic
Therapy as appropriate
Administer aspirin, nitrates,
heparin, plavix, Integrillin,
Lopressor, Morphine,
antiarrhythmics
Interventions (continued)
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Observe patient:
• Bleeding,
reperfusions
dysrhythmias
• Vital signs,
ventricular ectopy,
and other
dysrhythmias
• Heart and lung
sounds
• LOC
Interventions (continued)
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Portable chest film
ACLS measures
Prepare for cath lab
Educate and explain
Allow visit from
significant other
Heart Failure & Cardiogenic
Pulmonary Edema
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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
Diagnostics
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Lab:
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H& H
Lytes
BUN, Creatinine
Liver function studies
Cardiac enzymes (if
AMI)
• BNP
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B-type natriuretic
peptide
Radiologic:
• often normal
• pulmonary vasculature,
edema, fluid
• Cardiac silhouette may
show cardiac
enlargement,
hypertrophy, dilation
• Enlarged RA and RV
• Pleural effusion
• Valve calcifications
Diagnostics cont’d
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ECG: nonspecific changes, electrolyte or
drug induced dysrhythmias
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Echo: chamber size,wall thickness,
thrombus formation, valvular function,
pericardial disease
Interventions
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ABCD
Provide
supplemental O2
IV Normal Saline
ABGs and other labs
Provide rest
ECG continuous
Monitor
hemodynamics
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Administer
Morphine
Administer
vasodilator
• Decreases
afterload, arterial
dilations. Also preload
Vasodilators (continued)
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NTG, Isosorbide
• Increases
venous pooling
• NTG preferred
in pulmonary
edema, CAD
since improves
coronary artery
perfusion
• Venous dilation
Vasodilators (continued)
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Diuretics:
• Decrease preload
• Foley catheter,
possible
• I&O
• Monitor serum K+
Vasodilators (continued)
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ACE Inhibitors:
• Captopril, Enalapril
• Block formation of
Angiotensin II,
yields vasodilation
• Reduce mortality,
by improving
cardiac function
• Avoid overdiuresis
• Cleared by kidney
Hypertensive Emergencies
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Life-threatening elevation of B/P necessitating
reduction to prevent end-organ damage and potential
death
Essential hypertension
• unknown cause
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Secondary hypertension
• elevated pressure whose cause is known (renal vascular
disease)
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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
Precipitating Factors
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Untreated/uncontrolled essential or secondary
hypertension
Poor patient compliance with antihypertensive
medications
Renal dysfunction
Eclampsia of pregnancy (not tolerated well)
Adrenergic crises
AMI,
Cerebral dysfunction
Pituitary tumors
Assessment
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History
Severe H/A
Epistaxis
Family hx hypertension
MAO inhibitors
CAD, Renal Disease
Diabetes, obesity, smoker,
hyperlidemia, stress
Exam
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Diastolic pressure exceeding diastolic or
120mmHG
Retinopathy with exudates, Retinal hemorrhages
Papilloedema (diastolic pressure > 140)
H/A, confusion, restless stupor, somnolence
Epistaxis
Tachycardia
Chest discomfort
N&V
Rales
Oliguria, azotemia
Diagnostics
Lab:
• ABG:
 metabolic acidosis
• CBC HCT
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in renal failure,
polycythemia in renal
• Electrolytes:
 Hypocalcemia
 Hyponatremia
 aldosteronism causes
hypokalemia ( half of
patients)
• Glucose: elevated in
Cushing’s Syndrome,
diabetes
• BUN and creatinine
elevated in renal
disease
• Uric acid: hyperuricemia in renal
failure
• U/A: proteinuria,
possible renal
dysfunction
Radiologic Findings
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Chest film: cardiomegaly may be seen
ECG: LV hypertrophy may be seen
CT scan: Diffuse brain edema with hypertensive
crises
ECHO: diastolic function impaired.
Interventions
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ABCD, O2, IV @ KVO rate
ACLS protocols
Administer medications
NTP:
• Most common and most effective
• 0.5-10mcg/kg/min
• Titrate with B/P
• Watch for cyanide toxicity
• Drug is light sensitive
Interventions (continued)
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NTG:
• Drug of choice for unstable angina and
ischemia, LV failure, adrenergic crises
• Provides immediate response
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Sympathetic Blocking Agent (Labetalol)
• Alpha and beta blocker
• Onset and cessation of action slower than
NTP and NTG
• Contraindicated in patients with heart
failure, greater than 1st degree block,
bradycardia, and reactive airway disease
Interventions (continued)
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ACE Inhibitors
• Used in presence of LV failure
• Captopril: 6.25-50 mg orally every 30-45
minutes
• Enalapril: 1.25-5 mg IV every 6 hours
• Onset of action for both 10-15 minutes
Interventions (continued)
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Calcium Channel Blockers
• Nifidipine: 10 mg PO or sublingual (10-20 mg
orally every 30-45 minutes of sublingually every
15 minutes)
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Beta Blocker: Metoprolol, Esmolol
• Blocks effects of increased adrenergic tone
• Metoprolol 5 mg IV every 5 minutes up to 15 mg
total
Interventions (continued)
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Administer diuretics
Closely monitor patient’s response
Continuous arterial monitoring
Watch medication side effects
Observe for signs of ischemia
I&O
Monitor for dysrhythmias
Monitor for ↑ ICP
Possible ICP monitoring
Sudden chest pain may suggest aortic dissection
Reassure patient/family Calm environment
Questions????????