Presentation Chapter 27 Pulmonary Embolism and ARDS Case
Presentation Chapter 27 Pulmonary Embolism and ARDS Case
Presentation Chapter 27 Pulmonary Embolism and ARDS Case
Pulmonary embolism
(the most under-diagnosed cause of death)
Ross Klingsberg, MD
Clinical Vignette 1
A 62-year-old woman underwent
bilateral knee replacement and was
discharged without complications on
postoperative day two. Nine days after
surgery she develops severe respiratory
distress and dies suddenly in the
emergency department. Postmortem
examination of her pulmonary artery
reveals the pathology seen in the image:
A. Aspiration
B. Factor V
deficiency
C. Factor VIII
deficiency
D. Protein C
deficiency
E. Thrombocytope
nia
Clinical Vignette 2
A 68-year-old obese man presented to
the emergency department with
lightheadedness progressing to nearsyncope and progressive shortness of
breath of three days duration.
Learning objectives
Describe the clinical symptoms and sign of
patients presenting with pulmonary embolism
Define the pathophysiology of PE and the risk
stratification of patients diagnosed with
thromboembolism
Evaluate shock and right ventricular dysfunction
as a discriminator of outcome during or after PE
Provide a stepwise approach to the treatment of
patients diagnosed with acute PE
Important points to
remember
Pulmonary embolism (PE)
Venous Thrombo-Embolism (VTE)
Deep Vein thrombosis (DVT)
Pathophysiology
V/Q mismatch leads to hypoxemia
Occlusion of the vascular bed leads
to right ventricular failure
Important points
Diagnosis and therapy reduces
morbidity/mortality
Virchows triad: endothelial
injury/decreased venous
flow/hypercoagulable state
Greatest risk of embolization in the
first seven days after formation of a
DVT
Nonthrombotic pulmonary
emboli
Fat embolism
24-48 hour delay
Dyspnea, petechiae and mental confusion
Schistosomiasis
Septic emboli
Other emboli
Moderate
Prior VTE
Postpartum period
Malignancy
Estrogen therapy, oral contraceptives
Clinical presentation
Prevalence
Causes 10% of all in-hospital deaths
Biggest cause of maternal deaths associated
with live births
10.7% probability by age 80
Most fatal PE are unrecognized and undiagnosed
No previous
cardiopulmonary
disease (N=117)
(%)
Dyspnea
78
73
59
66
Cough
43
37
Leg Pain
27
26
Hemoptysis
16
13
Palpitations
13
10
Wheezing
14
Angina-like pain
Symptom
PIOPED 1990
Differential diagnosis
Pneumonia
Pneumothorax
Pleural effusion
Pulmonary edema
Asthma exacerbation
COPD exacerbation
Myocardial infarction
Congestive heart
failure
Acute pericarditis
Esophageal
dysmotility
Gastroesophageal
reflux disease
Pre-test probability of PE
(Wells criteria)
Clinical characteristic
Score
1.5
1.5
Hemoptysis
1.5
Clinical
signs and symptoms compatible with DVT
Low
Total Score
3
4
Moderate
4.5-6
High
>6
Wells PS et al 2000
D-dimer
Cross-linked fibrin derivative
>500 mcg/L: 98% sensitive; 39%
specific
If low D-dimer, RR<20, and pO2>80
mmHg PE is essentially ruled out
Low Wells score and negative DDimer: no further testing needed
If high clinical suspicion of VTE, Ddimer should not affect clinical
decisions
Cardiac biomarkers
Cardiac troponin T and troponin I
both elevated in acute PE
BNP may be elevated (e.g. 300-700)
in acute PE (caution: do not
misdiagnose CHF)
Chest radiograph
PIOPED: abnormal in 98 of 117 (84%)
Atelectasis and/or parenchymal abnormalities
(79 of 117 (68%)
Pleural effusion, infiltrates, elevation of
hemidiaphragm
Juxtapleural wedge-shaped opacity at
costophrenic angle (Hamptons hump)
Decreased vascularity (Westermarks sign)
Symptoms + no bronchospasm, no evidence of
anatomical cardiac shunt, and normal CXR
suggest PE
Electrocardiography
PIOPED: 44 of 89 patients (49%)
T-wave changes, ST-segment
abnormalities, left or right axis
deviation
S1Q3T3 pattern, RBBB, P-wave
pulmonale, right axis deviation
occurred in 26%
Limitations
IV contrast required
Reader expertise
required
Not portable
Morbid obesity may
prevent
Relative
contraindications
Renal insufficiency
Contrast allergy
Echocardiography
May suggest PE
Clot may be directly observed
Treatment
Acute PE
Unfractionated heparin
Low-molecular weight heparin
Thrombolytics
Inferior vena cava filters
Chronic PE
Warfarin
Surgical/IR thrombectomy (usually for
chronic)
Unfractionated heparin
(UFH)
80 units/kg followed by 18
units/kg/hr
Significant bleeding in 7-30%
Warfarin may be started in first 1-2
days at 5-7.5 mg (10 mg in obese
patients) and overlap for 2 days with
INR at goal (2-3)
Reverse with 1mg protamine sulfate
per 100 units UFH
Long term use may cause
Heparin-induced thrombocytopenia
(HIT)
3.5% incidence with UFH
0.6% incidence with LMWH
50% reduction in platelets after 5
days or absolute reduction of
100,000 per mm
If present, then treat with argatroban or
hirudin
Thrombolytics
Streptokinase
Urokinase
Recombinant tissue plasminogen activator
(rt-PA)
Usually used in PE with shock
Evidence for use with large PE without shock
2% risk of intracranial hemorrhage
Mechanical thrombectomy sometimes
performed
Surgical thrombectomy
Usually for chronic PE
May be considered for acute PE when
anticoagulation is problematic
Being replaced by interventional
radiology mechanical thrombectomy
Only performed a specialized centers
Case studies
A 59-year-old man undergoes total knee
replacement for severe degenerative joint
disease. Two days after surgery, he
develops acute onset shortness of breath
and right-sided pleuritic chest pain. He is
now in moderate respiratory distress with
a respiratory f = 28 breaths/min, HR =
120 beats/min (sinus rhythm), and
systemic BP = 110/70 mm Hg. His S ao2 =
90% by pulse oximetry on room air
Suspicion of
PE
Stable ICU
probability patients Low
clinical probability
Follow the same
algorithm but STOP after
a negative spiral CT or
low-prob V/Q
Start
anticoagulation if
no contraindications
Spiral CT
or V/Q
scan
Positive CT or
high prob V/Q
Negative
CT or low
prob V/Q
Inadequate CT
or nondiagnostic V/Q
Treat for
PE
U/S of
legs and
upper
body if
CVC
U/S of
legs and
upper
body if
CVC
Treat for
PE
Stop
anticoagulation
Treat for
PE
Pulmonar
y
angiogra
m
Treat for
PE
Stop
anticoagulat
ion
Suspicion of PE
Unstable ICU
patients
Start anticoagulation if no
contraindications
+
Continue anticoagulation
Echocardiogram
RV dilation, dysfunction,
or clot
Consider
thromboly
sis
Normal RV
+
Continue
anticoagulation
Stop anticoagulation
Chapter 28
Key concepts
ARDS vs ALI
Cardiogenic vs non-cardiac
pulmonary edema
Lung protective strategy
PEEP
Alveolar recruitment
Learning objectives
Students will be able to:
Correctly diagnose ARDS using the consensus
definition of the syndrome and differentiate it from
volume overload and cardiogenic pulmonary edema
Define, list, and explain the pathophysiological
events during the acute proliferative and the
fibrosing-alveolitis stages of ARDS
Define and explain the physiologic rationale of PEEP
and the hazards of using positive pressure ventilation
Perform a basic interpretation of an arterial blood gas
Explain the effect of increased intrathoracic pressure
on left ventricular filling (preload) and blood pressure
Relevant terms
ARDS acute (adult) respiratory distress syndrome (aka,
shock lung, non-cardiogenic pulmonary edema)
ABG arterial blood gas
pCO2 partial pressure of carbon dioxide in blood
pO2 partial pressure of oxygen in blood
Ppeak peak airway pressure (on ventilator)
Pplat plateau airway pressure (on ventilator)
V/Q ventilation (inspired air)/perfusion (blood)
PEEP positive end expiratory pressure
VILI ventilator-induced lung injury
SpO2 - oxygen saturation of hemoglobin by pulse
oximetry
Case presentation
A 35-year-old previously healthy
woman is brought to the ER with a
close-range gunshot wound to the
abdomen. Thirty minutes after
arriving, her blood pressure is 40/0,
pulse 140/ minute, and respirations
are 30/minute.
Case (continued)
She quickly receives 1.5 liters of
colloid and 2 liters of normal saline.
Her blood pressure rises to 80/40
mmHg. During five hours of surgery,
the spleen is removed, her stomach,
diaphragm and liver are repaired,
and she receives a total of 21 units
(250 ml each) of blood and 700 mL of
IV fluids.
Case (continued)
Later in the day, her breathing becomes
more difficult and labored. She is breathing
rapid shallow breaths at 40 per minute. An
arterial blood gas at that time shows
pH of 7.4/pCO2, 30 mmHg/pO2,42 mmHg
breathing ambient air.
Physical Examination
Gen: well-oriented, but ill-appearing
Chest: anterior and posterior
crackles, without rubs, and no
dullness to percussion
Heart: no displacement of PMI, no
gallops, rubs, or murmurs, normal
JVD
Abd: post-surgical
Ext: diffusely decreased deep-tendon
reflexes
Blood pressure
120/60
She continues to have rapid shallow labored
breathing. What is the next best step?
Intubate and initiate mechanical ventilation
Course (continued)
She is intubated and mechanical
ventilation is initiated
Tidal volume, 600 ml
Rate, 20 breaths per minute
FIO2, 1.0 (100% oxygen)
Peak airway pressure is recorded at 48 cm
H2O (normal is <30)
ABG
pH 7.35/pCO2 40 mmHg/pO2 65 mmHg
Findings
Echocardiogram: normal right and left
ventricular function
Tidal volume (Vt) decreased to 350 mL
based upon her predicted body weight
of 59 kg.
ABG
pH 7.3, pCO2 65, and pO2 53 mmHg
Hospital Course
In spite of this therapy, forty-eight
hours later, the pO2 had again fallen
to 48 mmHg while breathing 100%
O2 (FiO2 1.0). Because of this, the
positive end-expiratory pressure
(PEEP) was increased to 12 cm H2O.
Questions
Why didnt 100% oxygen raise her arterial pO 2 more?
Right to left shunting of blood through flooded alveoli
350/16 = 21.9
Plateau
Question
What does PEEP do?
PEEP reopens alveoli that are collapsed
but still can be recruited with positive
airway pressure
PEEP keeps the collapsing alveoli from
continuous opening and closing with each
respiratory cycle
PEEP keeps the respiratory cycle on the
most favorable portion of the
volume/pressure curve (see graph of
volume/pressure relationship)
Compliance = vol/
pressure =
=Tidal volume/(Pplat- PEEP)
Normal = 80-100 ml/cm
H 2O
Hazard of
positive
pressure
mechanical
ventilation
MV x 8 weeks,
Ppeak 50-70
mmHg
FiO2 80-100%
Follow-up questions
What caused the damage to her lungs
after her initial surgery?
Likely shock, multiple transfusions and
probable sepsis
Damage to the lungs can be direct (i.e.
pneumonia, aspiration of gastric content) or
indirect (i.e. sepsis, severe
trauma/shock/multiple transfusions)
Follow-up questions
What physiologic changes caused her to
hyperventilate after surgery?
Hypoxemia
Sepsis
Can cause lactic acidosis (when severe) and
hyperventilation (even to the point of
overcompensation and induction of respiratory
alkalosis)
Follow-up questions
Can shunt be overcome with increased FiO2?
No, shunt cannot be overcome by increased oxygen administration
because there is no alveolar ventilation
Follow-up questions
Does hydrostatic pressure play a role in
worsening of the alveolar filling process in
ARDS? Oncotic pressure?
Yes, hydrostatic pressure can play an
important role, especially if there are
damaged, leaky capillaries
Oncotic pressure also plays a role, especially
when coexisting health problems exist like
malnutrition, nephrotic syndrome, and/or liver
cirrhosis which will all lower the serum
albumin
The end
Coming next:
Chapter 28, Pathophysiology and Diseases
of the Pleural Space,
Chapter 29, Principles and Goals of
Mechanical Ventilation