Download 2012 CCU Competency

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Obstructive shock implies there is an obstruction
to blood flow.
This means treatment requires alleviation of the
obstruction.
Therefore, this type of shock needs to be clearly
and early identified so the correct treatment
can be applied.
If an arrest occurs in the patient with obstructive
shock, CPR and associated ACLS strategies will
not be effective because there is an
obstruction to flow.
Additionally, the mechanical complications of
ventricular septal rupture and papillary muscle
rupture represent surgical emergencies and
thus must be immediately identified.
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Tension Pneumothorax

Cardiac Tamponade

Aortic Dissection

Pulmonary Embolus
This module will focus on
patient risk factors and
nursing assessment and
recognition.
Who is at risk?
 Blunt trauma
 Positive pressure mechanical
ventilation
 PEEP
 Underlying pulmonary disease
 Clamped or clotted water seal
drainage system (chest tube)
 Airtight dressing on open
pneumothorax
Accumulation of air into the pleural space without a means of
escape causes complete lung collapse and potential
mediastinal shift. Emergency decompression or a chest tube is
required.
Chest pain
Dyspnea, cough
Tachycardia
Asymmetrical chest excursion
Diminished to absent breath sounds on
affected side
› Dramatic increases in peak inspiratory
pressures on a mechanical ventilator
Early
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If mediastinal shift:
› Tracheal shift away from affected side
Late
› JVD
› Hypotension
Note: Tension pneumothorax
can be diagnosed with
bedside assessment.
When a patient becomes hypotensive after
being put on positive pressure mechanical
ventilation – always consider tension
pneumothorax as a possible cause.
 Other possible causes of hypotension after
positive pressure mechanical ventilation
include:
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› Volume depletion
› Development of auto PEEP (patient needs a
longer expiratory time)
Who is at risk:
Post CABG
Post myocardial infarction – free wall
rupture
o Post ablation / post pacemaker
o Malignancy / S/P radiation therapy
o Infection resulting in pericarditis
o Anyone with known pericardial effusion
o Trauma
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Clinical syndrome
caused by
accumulation of fluid
in the pericardial
space.
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Results in reduction in
ventricular filling and
ultimately
hemodynamic
compromise.
› The right ventricle
cannot relax and fill.
Tamponade must be identified
because it requires treatment with
pericardiocentesis or surgical
pericardial window.
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Patient feeling of impending doom
Pulses alternans or electrical alternans
Beck’s Triad
 Hypotension, Distended neck veins, Muffled
heart sounds
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Pulses paradoxus
Equalization of filling pressures if a PA
catheter is present (RAP, PAD, PAOP
within 5mm of each other)
An echocardiogram will provide a
definitive diagnosis.
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To measure the pulsus paradoxus, patients are
often placed in a semirecumbent position;
respirations should be normal. The blood pressure
cuff is inflated to at least 20 mm Hg above the
systolic pressure and slowly deflated until the first
Korotkoff sounds are heard only during expiration.
At this pressure reading, if the cuff is not further
deflated and a pulsus paradoxus is present, the first
Korotkoff sound is not audible during inspiration. As
the cuff is further deflated, the point at which the
first Korotkoff sound is audible during both
inspiration and expiration is recorded. If the
difference between the first and second
measurement is greater than 12 mm Hg, an
abnormal pulsus paradoxus is present.
(Yarlagadda, Chakri, 2005 Cardiac Tamponade. Retrieved 3-22-06 from
www.emedicine.com)
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Who is at risk?
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Hypertension is present in most patients
with dissections
Congenital disorders affecting
connective tissue such as Marfan
Syndrome or Ehlers-Danlos syndrome;
also presence of bicuspid aortic valve
After procedures where aorta or the
aortic branches have been
Note: A retrograde
cannulated.
aortic dissection can
also cause a
myocardial infarction.
A Tear in the Intima of
the Aorta – Allows Blood
in the False Channel
Blood in the False Channel
can Obstruct Flow in the
True Lumen
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Chest or back pain often described as
ripping or tearing.
Variation in upper extremity blood
pressure > 20 mmHg.
Pulse deficit.
Focal neurological change.
New murmur of aortic regurgitation.
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Timing: Begins early in
diastole
Location: 3rd intercostal
space LSB
Radiation: Toward apex
Configuration:
Decrescendo
Pitch: High
Quality: Blowing
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What are the Risk Factors?
Stasis of blood
Prolonged immobilization after surgical procedures
Venous obstruction
Heart failure
Shock / Hypovolemia
Varicose veins
Obesity
Hypercoagulability
Polycythemia vera
Sickle cell disease
Malignancy
Recent trauma
Injury to the vascular endothelium
Central venous and arterial catheters
Phlebitis
Significance of PE
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Death within 1 month of diagnosis:
› 12% of PE cases
PE cause of death in 10% of hospitalized
patients
 PE from DVT is leading cause of
preventable hospital mortality
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› 20% of untreated proximal DVT will result in PE
› 10-20% of these PE will be fatal
› Anticoagulation decreases mortality 5 to 10
fold
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Massive PE results in an
obstruction to blood flow.
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Large to massive
when 50% of
pulmonary artery bed
is occluded
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Medium-sized
emboli
› Dyspnea
› Substernal chest
› Impending doom
› Hypoxemia
› Syncope
› Sign and symptoms of right
heart strain or right-ventricular
failure
› Signs of right-ventricular strain
on ECG.
› Sudden shock.
› Pulseless electrical activity.
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discomfort/pleuritic
chest pain
Many non-specific
signs
Tachypnea
Tachycarida
Rales
Accentuated 2nd
heart sound
Respiratory alkalosis
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Transient ECG
changes
T wave inversion (or
other ECG signs of
ischemia, injury,
infarction) in both
inferior and
anteroseptal leads
Elevated ST
segments aVR and
V1-V2
Signs of Right Heart Strain
• ST or atrial tachycardia (or
fib / flutter)
• Prominent S waves in I and
aVL
• Deep S wave in Lead I
(S1); and Q wave/inverted
T in Lead III (Q3/T3)
• RAD or incomplete or
complete RBBB
• Widespread S waves
• Prominent P waves in
inferior leads
(right atrial strain)
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Note the T wave inversion in the limb
leads and precordial leads. Also - big P
waves in II, III, and aVF.
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 Incidence
› 10% MI deaths
 Definition
› Myocardial leakage from free wall – hemipericardium –
Tamponade
› Perceived sudden; often slow tear
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Associated Factors : Delayed presentation to the
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Septal involvement = VSD
Posterior wall = Risk for papillary muscle
hospital
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Free wall rupture.
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Post-infarction regional pericarditis
precedes rupture (94% of the time)
T Wave Patterns in Post-infarction
Regional Pericarditis
Persistently positive T
waves 48 hours after an MI
ST segment
reelevation
Premature reversal of T
wave inversion to
positive
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If myocardial rupture involves the free
wall it will result in cardiac tamponade.
› We have already reviewed the signs and
symptoms of cardiac tamponade.
The next two slides show a patient with anterior
wall MI . In the second slide – note that the T
waves in lead V3 have failed to invert 48 hours
after admission. The patient developed cardiac
tamponade and went to OR for a cardiac
window.
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Timing: Continuous
Location: 3-4 LSB
Radiation: Widely
throughout the
precordium
Configuration:
Plateau
Pitch: High
Quality: Harsh
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Timing: Holosystolic
Location: Mitral
area
Radiation: To the
left axilla
Configuration:
Plateau
Pitch: High
Quality: Blowing,
harsh or musical
Acute papillary muscle
rupture will identified by a
new murmur of mitral
regurgitation and by the
presence of new onset
pulmonary edema.
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There are many
reasons for
hypotension.
However, when
hypotension is not
easily corrected by
interventions such as
volume
administration, it is
important to rule out
obstructive shock.
Remember:
Obstructive shock
requires interventions
beyond BCLS and
ACLS and thus must
be identified early.
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Tamponade
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Tension Pneumothorax

Pulmonary Embolus
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Risk factors (trauma, post OHS / procedure, large MI – late presentation)
Beck’s triad
Pulses Paradoxus
Pulses / Electrical Alternans
Risk factors (Conversion to PPV, existing chest tube, trauma)
Lung sounds
Hypotension
JVD
Mediastinal shift (very late sign)
Risk factors (Virchow’s triad)
Tachypnea (most common sign)
Respiratory Alkalosis
ECG signs
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Right axis deviation
RBBB
Tall P waves inferior leads
T wave inversion (limb and precordial leads)
Prominent S waves 1 and aVL
 Deep S wave in Lead I (S1); and Q wave/inverted T in Lead III (Q3/T3)
› ST / New atrial arrhythmia
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 Acute Aortic Dissection
› Risk factors (HTN most common)
› Tearing or ripping description of CP or back pain
› Diastolic murmur of Aortic regurgitation
› Bilateral arm BP variation
› Pulse deficit
› Focal neurological deficit
› Co-existing Inferior MI
 Mechanical Complications of MI
› Warning signs – regional pericarditis (failure of T wave to
invert within 48 hours, premature reversal of T wave
inversion, Re-elevation of ST segments)
› Papillary Muscle Rupture
 Holosystolic murmur
 Acute pulmonary edema
› VSD
 Continuous murmur
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Please reflect on a
patient you have
cared for with one of
the emergency
situations discussed in
this module. Describe
any assessment findings
you observed in this
patient and your
response to these signs
and symptoms.

Please identify one new
concept you learned
during this module.
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Please identify one
change in clinical
practice you will make
based on what you
have learned in this
module.
Thank You.
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Please add to your portfolio a clinical
example where your patient assessment
resulted in change in patient care or
outcomes. Note: This does not need to be in
a patient with obstructive shock.