Transcript EKG - UnionED

Cardiovascular
Emergencies –
Part II
Acute Aortic Dissection
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Uncommon but
lethal!
Tear in the intimal
layer of the aorta
that results in a
false lumen that is
usually
anterograde in
nature.
Usual locations:
ascending aorta superior to aortic valve
descending aorta at the ligamentum arteriosm
Acute Aortic Dissection
The most common
and most lethal
acute aortic
dissection, which
accounts for 2/3 of
all dissections,
occurs where?
Acute Aortic Dissection
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Most common in men
between the ages of 60
& 70
Factors:
• hypertension
• hereditary defects of
connective tissue
(Marfan’s)
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pregnancy
blunt trauma
iatrogenic factors
(intra-arterial
catheterization)
Acute Aortic Dissection
SUBJECTIVE DATA
 History
 Pain – sudden, sharp, tearing,
excruciating, medications may not
relieve, substernal (ascending),
back/flank (descending)
 Syncope
 Altered LOC
 Paraplegia
Acute Aortic Dissection
OBJECTIVE DATA
 Physical Exam
- variable BPs on right vs left
- decreased peripheral pulses/
peripheral cyanosis
- murmur
- pallor, oliguria, altered LOC,
- BP: hyper with distal dissection,
hypo with proximal
- extreme pain
Acute Aortic Dissection
OBJECTIVE DATA
 Diagnostics
- CBC (Hct tends to fall, WBC
12,000-20,000)
T&C,BUN/Creatinine
- EKG:
Normal in 1/3, LV
hypertrophy if hx of HTN,
signs of MI if proximal
dissection
-
Acute Aortic Dissection
CXR:
-widened aortic silhouette
-widened mediastinum,
-left-sided pleural effusion
Acute Aortic Dissection

Diagnostics cont.
- CT Scan
Acute Aortic Dissection
INTERVENTIONS

ABC

Pain relief

Large bore IVs
• – minimum of two sites
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
Monitoring
Medications:
1) to lower arterial BP:
nitroprusside, labetalol
Acute Aortic Dissection
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Medications cont:
2) To decrease contraction force:
beta blockers preferred, may give
calcium channel blockers if beta blockers
contraindicated
3) To relieve pain: Morphine
Position of comfort
IVF in hypotensive setting
Foley
Acute Aortic Dissection
Anticipate:
ED thoracotomy, immediate need
for OR, arterial & central venous
cannulation
 Therapeutics:
Explain all procedures to
patient/family, maintain calm,
allow family at bedside if possible
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Acute Pericarditis
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Result of inflammation of the
pericardium that may extend to
adjacent structures and may
produce exudate.
Factors:
- infections: idiopathic, viral,
bacterial, fungal
- connective tissue disease
(lupus, rheumatoid)
- renal disease
- neoplastic disorders
- tissue injury
Acute Pericarditis
Acute pericarditis is more
common in which gender and
which age group?
Acute Pericarditis
SUBJECTIVE DATA
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Chest Pain – deep inspiration,
recumbent, movement,
severe, sharp or dull ache,
retrosternal or epigastric
radiating to back/neck/ side,
sudden, persistent
General malaise, fever, chills, weight
loss
Dyspnea, cough
Acute Pericarditis
SUBJECTIVE DATA cont.
 Medical History may
include:
• TB, congenital anomalies,
immune disorders, MI,
neoplastic disease, drug
use, uremia, cardiac
surgery, cardiac trauma,
infections
Acute Pericarditis
OBJECTIVE DATA
 Physical Exam
- pericardial friction rub (hallmark) –
heard best
at the left lower sternum during
end expiration
with patient leaning forward
- tachycardia, fever, tachypnea
Acute Pericarditis
Diagnostics
- EKG: FOUR STAGES (best seen in inferior
leads)
1) ST elevation (early) with upright T waves,
2) T wave flattens and ST returns to baseline
3) T wave inversion
4) T wave returns to normal (weeks to
months)
- Lab: CBC, BUN/Cr, Electrolytes, cultures, UA
- CXR: helpful to detect pericardial effusion or
potential etiology
- Echocardiogram: most accurate in detecting!!
Acute Pericarditis
INTERVENTIONS
 Supplemental O2, cardiac
monitoring
 Position of comfort
 Anti-inflammatory medications
 Pericardiocentesis if necessary
 Labs as ordered
 Antibiotics as ordered
Acute Pericarditis
INTERVENTIONS cont
 Monitor/reassess
 Therapeutics:
• maintain calm
• explain all procedures
• allow family at bedside
if possible
• reassurance
Infective Endocarditis
Infection of the endocardium and heart valves
 SBE
• subacute bacterial endocarditis usually
occurs in patients with congenital or
acquired valvular disease; patients are less
toxic
 ABE
• acute bacterial endocariditis usually affects
normal heart valves and has a greatly
accelerated pace of development; patients
are extremely toxic with metastatic
infections.
Infective Endocarditis
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Infective agents (most
common):
- ABE: staphylococcus aureus
- SBE: streptcoccus viridans
Risk factors:
- Valvular disease, congenital
heart defects, rheumatic heart
disease, prosthetic heart valves,
IV drug abusers, LT vascular
access catheters
Infective Endocarditis

General pathophysiology:
• platelets and fibrin deposit on abnormal
endothelium
• organisms adhere and colonization begins
• microorganisms or fragments shed into
blood
• infarction or infection can occur at any distal
site
• infection of cardiac tissue can lead to
progressive heart failure, conduction
disturbances, and dysrhythmias.
Infective Endocarditis
Which age population
is infective
endocariditis rarely
seen in?
Infective Endocarditis
SUBJECTIVE DATA
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Fever: SBE – low grade, ABE – 102
degrees F
Anorexia, weight loss, night sweats
Arthralgia, myalgia, fatigue, malaise
Dyspnea, cough, pleuritic chest pain,
hemoptysis
HA, signs of stroke, confusion
Abdominal and back pain
Infective Endocarditis
Subjective Data
Suspect if history of:
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Cardiac surgery
Congenital or
aquired heart valve
disease
IV drug use
Rheumatic heart
disease
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Cardiac pacemaker
Recent GI or GU
disorder with valve
disease
Prosthetic valves
with recent dental
procedures without
prophylactic ATX
Infective Endocarditis
OBJECTIVE DATA
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Fever – may be absent in elderly, chronic
renal
Murmur
“Janeway lesions” - petechial lesions on
hands, feet; “Roth’s Spots” on ophthalmic
exam; splinter hemorrhages on nails;
“Osler’s nodes” – painful lesions of
fingertips; petechiae
Splenomegaly, hematuria, proteinuria,
clubbing with LT SBE, neurological
changes
Infective Endocarditis
DIAGNOSTICS
 Blood cultures – most important in
decision making process!
 CBC (anemia common with SBE), BUN/Cr,
Electrolytes, Glucose, Sed rate (elevated
in both types), UA
 EKG – conduction abnormalities may be
present with septal abscess
 Echocardiogram – can view vegetation
and amount of dysfunction
 Head CT
Infective Endocarditis
INTERVENTIONS
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ABC/monitoring/reassessments
IV and NS at TKO
Labs as ordered – especially MULTIPLE
blood cultures!
Medications: Anti-pyretics, antibiotics
Therapeutics – family at bedside, calm,
etc.
Acute Arterial Occlusion
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Caused by acute disruption of
blood flow from an embolism
(most common), thrombosis,
or trauma.
Majority of emboli lodge in
femoral artery.
Leads to ischemia in
areas/tissues supplies by the
affected artery
Immediate recognition and
treatment required to maintain
limb or organ viability.
Acute Arterial Occlusion
Approximately 80% of emboli
originate in the __________.
Acute Arterial Occlusion
SUBJECTIVE DATA
 Pain
• with movement or rest, burning, throbbing,
radiates distal to occlusion, excruciating,
relentless
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Coldness, numbness
Paralysis
Past Medical HX:
• MI, Rheumatic heart disease, a-fib, cardiac
surgery, LV aneurysm, chronic CHF, extremity
trauma, recent placement of intra-atrial
catheters.
Acute Arterial Occlusion
OBJECTIVE DATA
 Pallor, cyanosis, mottled, coldness
 Pulseless (distally), paresthesia,
paralysis
 Tenderness on palpation, muscle
rigor with prolonged ischemia
 Petechiae
Acute Arterial Occlusion
DIAGNOSTICS
 PT, PTT, CBC
 EKG
Acute Arterial Occlusion
INTERVENTIONS
 Elevate HOB (allow for
increased
flow to ischemic extremity
 Anticoagulants as ordered
Acute Arterial Occlusion
INTERVENTIONS cont
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Monitor and reassess (especially the 5 Ps)
Position of comfort
Warm environment (DO NOT apply heat to
area!)
Maintain extremity at level position (DO
NOT elevate)
Explain procedures and allow family as
able
Venous Thrombosis
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An occlusion of a vein by a blood
clot, commonly of the lower
extremities, often involves
inflammation.
Etiology – “Virchow’s Triad”
- integrity of veins, stasis of blood flow, &
hypercoagulability states
Factors: age > 40, cardiac disease,
malignancy, hx of hypercoag., and use of
estrogens and BCPs
Venous
Thrombosis
The major
complication
associated with
venous
thrombosis is
emboli.
?
Venous Thrombosis
SUBJECTIVE DATA
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Pain – aching, localized at point of occlusion,
constant, worse with walking
Swelling, deep muscle tenderness, fever
Medical Hx
Recent surgery or anesthesia, recent
traumatic event, postpartum, prolonged
bedrest, heart failure, malignancy, obesity,
BCPs, recent MI, thrombotic disease,
hematological disorders
Venous Thrombosis
OBJECTIVE DATA
 Erythema, swelling, indurations,
warmth
 Deep muscle tenderness
 Asymmetry between extremities
 Fever
 Positive Homan’s sign
Venous Thrombosis
DIAGNOSTICS
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CBC, Sed rate, PT/PTT
Doppler US flow study
Venous Thrombosis
INTERVENTIONS
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Position of comfort, elevate effected
extremity, bed rest
Analgesia, anticoagulants, and
thrombolytics as ordered
Warm, moist compresses to area
Elastic stockings or ACE wraps as ordered
I&O, reassessments
PVD
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Major cause is arteriosclerosis, or
hardening of the large and
medium-sized arteries.
Symptoms related to the decrease
in blood flow to the specific areas;
Worsen as disease worsens.
Factors: Heredity, male sex,
increasing age, cigarette smoking,
HTN, & hyperlipidemia.
Other types: Raynaud’s Disease &
Buerger’s Disease
PVD
RAYNAUD’S
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Episodic intense vasospasms of
the digits in response to cold or
stress.
Affects women more than men.
Vasospasm produces ischemia,
which produces pallor followed by
cyanosis, coldness, and
numbness of the affected digit.
As spasm resolves, there is an
intense rubor and throbbing pain
prior to digit returning to normal.
PVD
BUERGER’S DISEASE
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Inflammatory disorder characterized by
thrombous formation in usually medium
sized arteries of the lower leg and foot.
Men affected more than women.
Results in ischemia, pain, intermittent
claudication, decreased or absent pulses,
and changes in skin color.
Skin becomes thin and shiny, hair growth
retarded, nails thicken, and
gangrene/ulcerations may develop.
PVD
SUBJECTIVE DATA
 Pain – cold environment, stress,
exercise, relieved by removal of
agonist, severe, throbbing
 Numbness, tingling
OBJECTIVE DATA
 Cold to touch, decreased/absent
pulses, pallor, cyanosis, rubor
 Thin, shiny skin; thickened nails;
ulcerations/ necrosis
PVD
DIAGNOSTICS
 CBC
 Doppler studies
PVD
INTERVENTIONS
 Stop precipitating factors
 Vasodilators (calcium channel
blockers or adrenergic blockers) and
analgesics as ordered
 Reassess 5 P’s
 Position of comfort, DO NOT elevate
affected extremity
 Warm environment
 General therapeutics
Myocardial Contusion
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Usually a result of blunt trauma
Injuries may range from petechiae to fullthickness contusions to rupture of the heart
Lesions caused are similar to that of acute MI
from occlusions; major difference is amount of
hemorrhage!
RARELY FATAL!
At risk for sudden dysrhythmias
Myocardial Contusion
SUBJECTIVE DATA
 Recent blunt trauma to chest, chest pain
similar to MI but does not respond to
vasodilatory drugs
 Pain with inspiration usually secondary to
fractured sternum
 Medical HX – angina, previous MI, HTN,
CHF, ETOH or drug use, previous CV
surgery
Myocardial Contusion
OBJECTIVE DATA
 Exam may be normal without signs
of trauma or may be associated with
severe trauma
 Contusion to chest wall, tachycardia,
tachypnea, hypo- or hypertension
 Signs of LV failure
• crackles
Myocardial Contusion
DIAGNOSTICS
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EKG: Premature atrial or ventricular
contractions, A-Fib, SA block, nodal
rhythm, AV block, nonspecific ST & T wave
abnormalities, BBB (usually right), and
infarct pattern.
Cardiac serum markers
Echocardiography
CXR
Myocardial Contusion
INTERVENTIONS
 ABC
 Supplemental O2, monitoring
 Large bore IV (minimum of 2) & IVF
as needed
 Medicate with antidysrhymics and
analgesics as ordered/needed
 Position of comfort
 General therapeutics
Cardiac Tamponade
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Fluid accumulation in the pericardial sac,
which elevates intracardiac pressure,
progressive decrease in diastolic pressure,
and ultimately decrease in stroke volume
and cardiac output. Prognosis dependent on
etiology & timelines of intervention.
Cardiac Tamponade
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Causes:
- malignancies, pericarditis,
uremia, & trauma
Types:
- acute: patient is in extremis; may
be less than 100c
- chronic: patient not in extremis;
may be 1-2L
Cardiac Tamponade
Cardiac Tamponade
SUBJECTIVE DATA
 Penetrating or blunt injury,
recent repair of cardiac
lesions
 Dyspnea, anxious, chest
pain, fatigue, malaise
 Medical Hx:
Cardiac disease, infectious
or neoplastic disease, renal
failure
Cardiac Tamponade
SUBJECTIVE DATA
cont.
 Cold, moist skin;
cyanotic lips and
digits
 Decreased UO
 Decreased LOC, coma
 Hepatomegaly
Pericardial Tamponade
OBJECTIVE DATA
 Visual wound
 Tachypnea, rales,
Kussmal’s sign (rise in
venous pressure with
inspiration)
 JVD,tachycardia
Pericardial Tamponade
OBJECTIVE DATA
 Beck’s Triad:
•Venous pressure elevation
•Arterial pressure decline
•Muffled heart tones
Cardiac Tamponade
DIAGNOSTICS
 CXR
 Pericardiocentesis (Hct will be lower
in pericardial blood than venous
sample & generally pericardial blood
will not clot)
 Echocardiogram
 T&C, CBC
 EKG
Cardiac Tamponade
ANALYSIS
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Cardiac output
decreased related to
impaired cardiac
filling and contractility
and decreased
venous return
secondary to
increased
intrathoracic pressure
Cardiac Tamponade
INTERVENTIONS
 ABC
 Large bore IVs (minimum of 2),
IVF as needed
 Monitoring, reassessment
 Prepare: pericardiocentesis,
thoracotomy, internal cardiac
massage
 Foley & NG
 Prepare for immediate surgical
intervention
Traumatic Aortic Injury
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Result from blunt or penetrating trauma - MVCs
are the most common cause
90% result in complete rupture and sudden
death at “the scene”
Tearing may occur at points of attachment or
may be pinched between the spinal column and
manubrium.
Tears not involving the adventital layer (outer)
may result in patient survival.
Traumatic Aortic Injury
Traumatic Aortic Injury
SUBJECTIVE DATA
 Deceleration mechansim, blunt force
to chest or abdomen
 Pain: severe, unrelenting pain in
chest, midscapular, or back region
 Medical Hx: atherosclerotic heart
disease, prior thoracic injuries or
surgeries
Traumatic Aortic Injury
OBJECTIVE DATA
 Dyspnea, tachypnea
 Tachycardia, discrepancy between
BPs in right and left arms, harsh
systolic murmur, varying degrees
of shock, decreased quality of
femoral vs radial pulses
 Chest wall ecchymosis, paraplegia
Traumatic Aortic Injury
DIAGNOSTICS
 CXR: widened mediastinum,
obliteration of aortic knob,
tracheal deviation to the right,
presence of pleural cap, fx of
1st & 2nd ribs, depression of
left main stem bronchus,
deviation of esophagus to
right, shift of right main stem
bronchus up and to right
Traumatic Aortic Injury
DIAGNOSTICS cont
 CT scan
 EKG
 T&C
 CBC
Traumatic Aortic Injury
INTERVENTIONS
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ABC, monitoring, reassessment
Large bore IVs (minimum of 2), IVF as needed
Prepare for blood transfusion & autotransfusion as
needed
Foley & NG
Monitor arterial pH
Prepare for immediate surgical intervention
Administer antihypertensives & beta blockers as
ordered if surgical repair delayed
Arterial Trauma
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Result from blunt (MVC & crush injuries) or
penetrating (GSW & stab wounds) trauma
Vessels injuries include lacerations, hematomas,
and pseudoaneurysms
Neurological signs usual present due to close
proximity of nerves
Major consequence is ischemia distal to injury;
immediate surgery required is damage is severe
Arterial Trauma
SUBJECTIVE DATA
 Numbness, tingling, pain, paralysis
 Mechanism
 Medical Hx: diabetes, PVD
Arterial Trauma
OBJECTIVE DATA
 Hemorrhage from wound, varying stages
of shock related to volume of blood loss,
pulsatile or expanding hematoma
 Difference in BPs in different extremities,
prolonged cap refill, diminished or absent
distal pulses
 Pallor, paresthesia, coolness, paralysis
Arterial Trauma
DIAGNOSTIC
 Doppler study
Questions?????