Download Challenging ICU Cases

Challenging ICU Cases
Mazen Kherallah, MD, FCCP
Consultant Intensivist
Case #1
• 40 year old woman with PMH of major
depressive disorder with some psychotic
features and hyperthyroidism for which she
received ablation 2 years ago
• Admitted to ICU with confusion, agitation, and
fever. She has been having nausea, vomiting
and diarrhea for the past 24 hours prior to
admission
• No headache, no visual disturbances
Case #1
• Medications include paroxetine, haloperidole
and levothyroxine. Trazodone had been
added to her regimen for insomnia 2 days
prior, and her haloperidole dose was
increased.
• PE: T 39, B/P 180/95 mm Hg, pulse 120/min
and RR 22/min.
• Diaphoretic, mydriasis, no lid lag.
• Confused, agitated and has tremor, no focal
signs, no nuchal rigidity and her reflexes are
3+. She has 4 beats of myoclonus. There is
no muscular rigidity
• Labs are normal except CK of 900 U/L.
Case #1
a)
b)
c)
d)
e)
Neuroleptic malignant syndrome
Thyroid storm
Meningitis
Serotonin syndrome
Cocaine overdose
Serotonin Syndrome
• Mainly seen when multiple serotonin
modifying agents are used in combination
includiong SSRIs, TCAs, lethium, and
monoamine oxidase inhibitors
• Abrupt onset within 24 hours after initiating a
new medication regimen or changing the
dose, or in case of overdose
Serotonin Syndrome
• Autonomic dysfunction (hyperthermia,
tachycardia, tachypnea, hypertension,
diaphoresis,shivering)
• Neuromuscular abnormalities: trmors,
myoclonus, rigidity, hyperreflexia, trismus,
ataxia, seizure and coma
• Nausea, vomiting amnd diarrhea
• Mydriasis
Serotonin Syndrome Tx
•
•
•
•
•
•
•
•
•
Discontinuation of medication
Hydration
Cooling measures
Benzodiazepines
Anticonvulsants
Antihypertensives
Mechanical ventilation
Sedation
Direct or indirect serotonin antagonist such as
cyproheptadine
Case #2
• A 64 year old woman is admitted to the
hospital with pyelonephritis.
• She is moved to ICU with heart rate 150,
blood pressure 90/60, respiration of 20/min
and temperature of 39 degree
• Thyroid function tests were obtained
Case #2
Lab Test
Thyroxine (T4)
•Total
•Free
Patient Value
3.8 mcg/dL
1.2 ng/dL
Normal Value
5-12 mch/dL
0.8-2.84 ng/dL
Triiodothyronine (T3) 60 ng/dL
90-200 ng/L
Triiodothyronine,
reverse (rT3)
80 ng/dL
13-50 ng/dL
Thyroid stimulating
hormone (TSH)
4 mcg/mL
2-11 mcg/mL
Case #2
• In addition to antibiotics and supportive care,
what is the best treatment for this thyroid
disorder?
–
–
–
–
–
Intravenous triiodothyroxine
Intravenous thyroxine
Intravenous hydrocortisone
Intravenous triiodothyroxine and hydrocortisone
No other treatment
Euthyroid Sick Syndrome
• Sepsis, burns, malignancy, MI, severe injuries, major
surgical procedures and trauma
• Decreased T3
• Normal or low T4 and FT4
• Normal or low TSH
• Increased rT3
• Adaptive response to conserve energy, decreased
extrathyroid conversion of T4 to T3
• Total serum T4 may be reduced due to reduced
serum thyroid hormone-binding proteins
• With increasing severity of illness, free T4 levels may
also be reduced attributed to reduced hypothalamic
and pituitary functions
Case #3
• 68 year old woman enters the ICU with
hypotension and decreased urine output. She
has a 20-year-history of hypertension treated
with HCTZ and verapamil. Quit smoking 2
years ago after 40 years.
• She has morning productive cough and
intermittent wheezing treated with albuterol
inhalor as needed
Case #3
• 2 days ago she entered an outside hospital
with severe chest pain and evidence of acute
antero-apical MI, she was given t-PA , heparin
and aspirin.
• Her chest pain continued for two hours post
thrombolytic therapy and her troponin I rose
to 32, CK was 1,850 with82% creatine
kinase-myocardial band
Case #3
• 12 hours ago, blood pressure decreased from
150/80 to 80/60 and her urine output slowed
to less than 10 mL/h. She was transferred to
your hospital.
• PE: ill looking, pulse 120/min, B/P 85/60, RR
22/min, T 38,2. She is apprehensive and her
skin is cool. JVD 15 cm H2O, B/L wheezes
with crackles, quiet pericardium, no murmurs,
rubs or gallops
Case #3
Hemodynamic
measurment
Patient variable
Oxygen saturation
Arterial blood pressure
82/55/60 mm Hg (S/D/M) 92%
Right atrium
18 mm Hg
45%
Right ventricle
40/20 mm Hg
44%
Pulmonary artery
42/18/24 (S/D/M)
Pulmonary artery
occlusion pressure
19 mm Hg
Cardiac output
2.2 L/min
Cardiac index
1.2 L/min/m2
Case #3
• A transthoracic echocardiogram is technically
difficult due to chronic lung disease
• While preparing to perform a
transesophageal echocardiogram, the
patient’s systolic blood pressure decreases to
50 mm Hg.
Case #3
• Which of the following diagnoses is most
probable?
–
–
–
–
–
Ruptured mitral papillary muscle
Ventricular septal defect
Cardiac rupture with pericardial tamponade
Right ventricular infarction
Pulmonary embolism
Case #3
• Low cardiac output
• Equalization of diastolic right heart pressures
and PCWP (all elevated with 5 mm Hg of
each other)
• Pericardial tamponade most likely secondary
to cardiac rupture
Case #3
• Ruptured mitral papillary muscle
– Loud murmur and thrill, severe left heart failure with prominent V waves on
PA occlusion tracing
• Ventricular septal defect
– An oxygen step-up of more than 5% when advancing the catheter from RA to
PA
• Cardiac rupture with pericardial tamponade
– Low cardiac output
– Equalization of diastolic right heart pressures and PCWP (all elevated with 5
mm Hg of each other)
• Right ventricular infarction
– Equalization of diastolic right heart pressures but not PCWP (usually low)
– In the setting of inferior myocardial infarction
• Pulmonary embolism
• Elevated right hear pressures but normal PA occlusion pressure
Case #4
• A 47-year-old man with a past medical history significant for chronic
obstructive pulmonary disease, asthma, and major depression.
• Patient presented with worsening shortness of breath for the past few
hours without fever or chest pain
• Despite a continuous albuterol nebulized solution and steropid therapy,
he remained tachycardic and tachypneic with an oxygen saturation that
had decreased to 87% on room air. There was minimal air movement
upon examination with no wheezes or dullness to percussion.
• His arterial blood gas at this time demonstrated a pH of 7.42; pCO2 of
46; and a SaO2 of 96% with a FiO2 of 40% delivered by facemask.
• His respiratory distress remained refractory to all standard therapy
including continuous nebulized bronchodilators, intravenous magnesium
sulfate, subcutaneous epinephrine, and intravenous solumedrol. He was
emergently sedated, paralyzed, intubated, and admitted to the intensive
care unit for further evaluation and treatment.
Case #4
• The patient remained difficult to ventilate with very high
peak airway pressures (greater than 80 cmH2O).
• Several ventilatory changes were attempted without
change in the patient's condition.
• He continued to receive nebulized bronchodilators. An
additional two grams of intravenous magnesium sulfate
were administered along with subcutaneous terbutaline,
epinephrine, and intravenous theophylline - all produced
no noticeable effects on the patient's condition.
• In an attempt to improve laminar flow (and decrease airway
resistance), the patient was changed to a HeliOx mixture
without improvement. At this point, the patients pH was
7.04; pCO2 was 91; and SaO2 was 86% on 100% FiO2.
Case #4
• The patient was given a bolus of 25 mg of intravenous ketamine and
started on a ketamine infusion at 15 mg/hr.
• Within minutes of administration, his airway resistance decreased
rapidly such that peak airway pressures fell to 36 cmH2O
• the patient was then placed on assist control with rapid improvement
in ventilation (pH increased to 7.19 within 30 minutes).
• The ketamine infusion was continued for 72 hours and then gradually
weaned while maintaining adequate sedation with midazolam.
• Ketamine was discontinued after 80 hours without occurrence of
emergence phenomena or significant dysphoria.
• The patient was extubated successfully on hospital day five and
discharged to home on hospital day 9
Vitals, PCO2 and Oxygenation over
time
Change of pH over time
Case #5
71 year old male with past history of:
– Ascending aortic aneurysm, s/p repair and aortic
valve replacement in 2001, currently on
anticoagulation with coumadine.
– Hypertension managed with lopressor and
triamterene/hydrochlorthiazide.
– Hypercholesterolemia on zocor.
– Peptic ulcer disease on protonix.
– S/P craniotomy in 1980 for intracranial
hemorrhage post snow mobile accident
Case #5
• Presented to the hospital with left sided nonanginal chest pain associated with fever but
no nausea, vomiting, shortness of breath or
dizziness.
Contained rupture of the descending thoracic aneurysm
Case #5
• CT scan of the chest and abdomen revealed
expansion of the descending thoracic
aneurysm with what appeared to be a
contained rupture that measures 12.6 cm in
transverse dimension. There is a dissection
flap with true and false lumens extending
down to the level of the celiac axis. There is
small bilateral pleural effusion.
false and true lumens of the descending aortic aneurysm with dissection
the splenic artery coming off from the false lumen of the dissection
the celiac artery coming off from the true lumen
OR Findings
• Patient was taking to the operating room
where a 22 mm hemashield graft was placed
and the aneurysm was repaired. Gram stain
of the surgical specimen of the aneurysm
revealed comma-shaped organism.
.
Cultures were positive for campylobacter fetus subspecies fetus
Further History
• Upon further questioning of the patient, he
stated that he slaughtered a dead buffalo and
dissected him few weeks, and he has not
been feeling well since that time.
Biologic and Clinical Characteristics of Campylobacter jejuni
and Campylobacter fetus subsp. fetus
Feature
Campylobacter jejuni
Campylobacter fetus
subsp. fetus
Major reservoir
Avian species, food animal
Cattle and sheep
Affected hosts
Normal hosts, all ages: often in
clusters of cases
Opportunistic agent in
debilitated hosts, clustering
rare, healthy hosts may be
affected
Usual source of infection
Feces
Blood stream
Diarrheal Illness
Common
Uncommon
Clinical manifestation
Acute gastroenteritis, colitis
Systemic illness with
bacteremia, meningitis,
vascular infections, abscesses
and gastroenteritis
Outcome of infection
Usually self-limited
May be fatal in debilitated
hosts
Antibiotic Susceptibility
Erythromycin
Gentamicin
Case #6
• A 24 year old woman with status asthmaticus
has been sedated and placed on mechanical
ventilation in the volume control mode for
respiratory support (VT 6 mL/kg, rate 20,
PEEP 0 cm H2O and FIO2 0.40)
• ABG’s show PO2 78 mm Hg, PCO2 38 mm
Hg, and pH 7.46.
• CXR shows clear lung fields and flattened
diaphragm
Flow/Time Curve
Flow
(L/m)
Flow does not
return to zero
Time (sec)
Case #6
a) Increase the tidal volume
b) Increase the inspiratory time
c) Change to pressure assist control ventilation
with the same tidal volume and ventilatory
timing
d) Decrease the respiratory rate
e) Add positive end-expiratory pressure
0
Gradient
-5
0
-5
0
Gradient
-5 +10
Auto PEEP
Increased Work of
-15
Breath
Administration of External PEEP
PEEP
10
Gradient
5
Auto PEEP
+10
-5
Case #7
• A chronically ill 65 year old patient in the ICU has fever to 39.0 as well
as hypotension (70/40 mm Hg) and tachycardia (120/,im).
• Physical examination is remarkable for toxic-appearing man who is
orotracheally intubated and sedated.
• He has a triple lumen central venous catheter at the right subclavian
vein site that was inserted 10 days ago for TPN
• The skin is mildly erythematous around the catheter site, but not
tender and no drainage from the insertion site is noted
• Serum creatinine 140 mmol/L), WBC 14,500, 90% Neutrophils with
toxic granulation
• Blood cultures obtained 3 days ago are growing Candida Krusei.
• There is no clinical or radiographic evidence of pneumonia, sinusitis or
other source of infection.
The most appropriate treatment
regimen?
a) Remove central venous catheter, replace at a
new site and begin amphotericine B
b) Exchange central venous catheter over a
guidewire and begin amphotericine B
c) Maintain central venous catheter at current
site, begin amphotericine B
d) Remove central venous catheter, replace at a
new site and begin fluconazole
e) Maintain central venous catheter at current
site, begin fluconazole through the catheter
Case #8
• A 29-year-old woman (gravida 3, para 2 at 35 weeks of
gestation) presents to the obstetrics department with
complaints of right quadrant pain, nausea, vomiting,
fatigue, malaise, and anorexia for the past 2 days
• She also reports dark urine for the past 24 hours.
• On PE: B/P 110/70, HR 100/min, RR 24/min, and afebrile.
• Abdominal exam is notable for a gravid uterus with normal
fetal heart tones. There is mild tenderness in RUQ, there is
trace pedal edema and normal neurological examination.
Case #8
• WBC 8,000 with normal differentiation
• Hg 13 g/dL, hematocrit 34%, platelet count
100,000 and normal coagulation studies
• ALT 150, AST 125, and total bilirubin 48 mg/L)
• Urinalysis shows trace bilirubin without protein
• Right upper quadrant ultrasound is normal
without dilation of the gallbladder or bile duct.
The liver is normal in size. No stones are
visualized
Case #8
• Over the next 24 hours the patient becomes increasingly
confused and lethargic and is transferred to the ICU.
• Vital signs remain stable but neurologic examination now
reveals confusion and disorientation.
• There is scleral icterus.
• AST 1500, ALT 1000, LDH 270 total bilirubin 77 and
crreatinine 115. Hematocrit 35%, platelets 90,000,
cogulation parameters reveal INR of 3.1 and a PT of 27
seconds
• Peripheral blood smear is normal
DDX
a)
b)
c)
d)
e)
HELLP Syndrome
Acute fatty liver of pregnancy
Thrombotic thrombocytopenic purpura
Pre-eclampsia
Cholestasis of pregnancy
DDX
a) HELLP Syndrome:
a)
Red blood cell fragments, schistocytes, mild elevation of LFT and low platelets,
jaundice is uncommon and hypoglycemia and coagulopathy are unusual
b) Acute fatty liver of pregnancy:
a)
Nausea, vomiting, RUQ pain, jaundice and elevated LFT. No hemolysis, and
peripheral blood smear is normal
c) Thrombotic thrombocytopenic purpura:
a)
Associated with hemolysis, fever, thrombocytopenia, neurological and renal
abnormalities. Coagulopathy and transaminitis are rare
d) Pre-eclampsia:
a)
Associated with hypertension, edema and proteinuria
e) Cholestasis of pregnancy:
a)
Benign condition of the second trimester that is associated with mild
elevation of toatal bilirubi with nause, vomiting, abdominal pain or
constitutional symptoms
Case #9
• 60 year old man with history of ethanol abuse was
admitted to the hospital with severe acute pancreatitis.
• On the second hospital day he developed progressive
hypotension and respiratory failure and was transferred to
the ICU.
• He was endotracheally intubated and mechanical
ventilation was initiated.
• To control his agitation and minimize peak inspiratory
pressures, he was sedated with lorazepam using bolus and
infusion dosing and paralyzed using cis-atracurium.
• As a result of marked agitation, possibly associated with
ethanol withdrawal, escalating doses of sedation were
required.
Case #9
• Other medication included norepinephrine
infusion to maintain MAP of 60 mm Hg,
intravenous pantoprazole and
piperacillin/tazobactam.
• On the 6th hospital day, WBC 21,000, Hg 106,
Na 135, K 5, Cl 99, total CO2 15, BUN 12.5,
creatinine 70 and glucose 18
• Plasma lactic acid was 4.7 mmol/L, serum
osmolality 327 mOsm/kg H2O
• pH 7.26, PCO2 35 and PO2 126, [H+]= 55
Case #9
a)
b)
c)
d)
e)
Sepsis
Propylene glycol intoxication
Isopropyl alcohol intoxication
Ethylene glycol intoxication
Hypoventilation
Acid Base Disturbance Approach
•
•
•
•
•
•
•
•
•
•
•
[H+]=24 X PCO2/HCO3: 55= 24 X 35/15
pH= 7.26: Acidosis
Predicted PCO2 (Respiratory compensation): PCO2= 1.5 X[HCO3]+8
2: therefore PCO2 should have been 1.5X15+8= 30.5 2: combined
respiratory and metabolic
AG= Na-(Cl+HCO3)= 135-(99+15)= 21
∆ AG= 21-12= 9
∆ HCO3= 24-15= 9
∆ HCO3 = ∆ AG
Added anions= 9 mmol/L= 4.5 Lactic acid + 4.5 ??
Calculated osmolality= 2Na+Glucose+BUN=2(135)+18+12.5= 301
Osmolar gap= 26
Metabolic acidosis with high anion gap due to lactic acidosis high
osmolality acid in addition to mild respiratory acidosis
Case #9
• Sepsis
– High AG metabolic acidosis but no increased osmolar gap
• Propylene glycol intoxication
– Osmolar gap with high AG metabolic acidosis
• Isopropyl alcohol intoxication:
– Elevation of osmolar gap but not associated with AG
metabolic acidosis
• Ethylene glycol intoxication
– Unlikely to develop during the course of hospitalization
• Hypoventilation
– PCO2 of 35 would not in isolation be associated with
acidemia
Propylene Glycol Intoxication
• Colorless, odorless fluid that is used as a solvent for
many intravenous medications (such as lorazepam,
diazepam, etomidate, phenytoin, digoxin, esmolol,
nitroglycerin, and timethoprim-sulfamethoxazole)
• Toxicity is seen with infusion duration of >96 hours
• Half of the propylene glycol is excreted in the kidney
and the rest is metabolized in the liver by alcohol
dehydrogenase to lactaldehyde, methylglycoxal
• Manifestation as acid base disturbance, depression,
seizure, cardiac arrhythmias, respiratory arrest
hemolysis and acute renal failure
Case #10
•
•
•
•
52 y/o with ARDS on ventilator
IBW = 80Kg
40% shunt fraction
VCV - R:16 FiO2: 32 TV: 0.48L PEEP: 10
cm H2O
• Recruitment maneuver improves sats from
88%  98%
Case #10
•
What do you do now?
a)
b)
c)
d)
e)
Repeat recruitment at intervals
Increase PEEP
Increase I:E ratio
Increase TV
Increase rate
ARDS
Recruitment Maneuvers
• Application of high airway pressure (35-40cmH2O) for
approximately 40 seconds.
• Employed to open atelectatic alveolar units that occur with
ARDS and particularly with any disconnection from ventilator
ARDS
Recruitment Maneuvers
• If successful, PaO2 will increase by 20% or
more.
• Must use PEEP after procedure to keep
recruited alveoli open.
• Post maneuver PEEP level needed is
uncertain
ARDS
Recruitment Maneuvers
• No data to support utility of repeated maneuvers
• Increasing I:E may be helpful in this scenario but
there are no data to support this strategy
• Increasing TV will lead to alveolar over distension
and VILI
• Increased RR will also cause more lung injury
Case #11
• Which COPD patient will most likely benefit from noninvasive
positive-pressure ventilation (NPPV)?
Breath sounds
RR
pH
PCO2
PO2
FiO2
No wheeze
20
7.38
40
50
0.3
Decreased air movement
20
7.28
60
60
0.4
End-expiratory wheeze
18
7.38
42
65
0.3
Irregular respirations
8
7.18
70
50
0.5
(infiltrate on CXR)
Noninvasive Positive Pressure
Ventilation in Acute Respiratory Failure
• Full face or nasal mask
• Usually use pressure support but any mode may be
used
• Benefits
–
–
–
–
Reduced WOB
Increased TV
Improved gas exchange and diaphragm function
Avoids risks and complications from ETT
• RR nosocomial pneumonia = 0.15
Noninvasive Positive Pressure
Ventilation
Indications
• Strong Evidence
– Acute exacerbation COPD
• Pronounced benefit – RR of death 0.41
• Patients with severe respiratory failure should get a trial
• 30% failure rate overall
– Cardiogenic pulmonary edema
– Compromised host with pneumonia
Noninvasive Positive Pressure
Ventilation
Indications
• Less Evidence
–
–
–
–
Asthma
CF
Prevent extubation failure
Post op respiratory failure
• Weak Evidence
– ARDS, UAO, trauma
– pneumonia
Noninvasive Positive Pressure
Ventilation
Contraindications
•
•
•
•
•
•
•
•
•
Cardiac arrest
Respiratory arrest
Severe encephalopathy (GCS <10)
Severe UGI bleed
Hemodynamic instability
Facial injury, surgery, deformity
Upper airway obstruction
Inability to protect airway or clear secretions
Lack of cooperation!
Noninvasive Positive Pressure
Ventilation
Complications
•
•
•
•
•
Gas leak
Skin necrosis
Increased dead space
Gastric distension
claustrophobia
Case #11
• Which COPD patient will most likely benefit from noninvasive
positive-pressure ventilation (NPPV)?
Breath sounds
RR
pH
PCO2
PO2
FiO2
No wheeze
20
7.38
40
50
0.3
Decreased air movement
20
7.28
60
60
0.4
End-expiratory wheeze
18
7.38
42
65
0.3
Irregular respirations
8
7.18
70
50
0.5
(infiltrate on CXR)
Case #12
• 64 year old with severe sepsis (not septic shock)
• Infection
– Acute onset fever, chills, cough
– RML and RLL infiltrates
• SIRS Criteria
– Tachycardia, tachypnea, leukocytosis with shift
• Organ dysfunction
– Renal, pulmonary
• Hypotension
– Improving with fluid boluses
Case #12
• In addition to continuing fluids and antibiotics,
which of the following will you recommend
now?
– Methylprednisolone in supraphysiologic doses
– Hydrocortisone in physiologic doses
– Hydrocortisone and fludrocortisone in physiologic
doses
– No corticosteroids
Corticosteroids in Sepsis
• **first measure the serum lactate
– Look for cryptic shock
• Physiologic doses
– Replacement
– Stress dose
• Pharmacologic doses
– Anti-inflammatory
Corticosteroids in Sepsis
Surviving Sepsis Campaign Recommendations
• Treat patients who still require vasopressors despite
fluid resuscitation with hydrocortisone 200-300mg/d
for 7 days.
or
Treat and do ACTH stimulation test
stop treatment if cortisol increase
> 9mcg/dL.
Do not use > 300mg/day
Corticosteroids in Sepsis
The Severe Sepsis Bundles: Surviving Sepsis
Campaign/Institute for Healthcare Improvement
Resuscitation Bundle
(To be accomplished as soon as possible and scored over first 6
hours):




Serum lactate measured.
Blood cultures obtained prior to antibiotics
administered.
From the time of presentation, broadspectrum antibiotics within 3 hours for ED
admissions and 1 hour for non-ED ICU
admissions.
For hypotension and/or lactate > 4 mmol/L:



Deliver an initial minimum of 20 mL/kg of
crystalloid (or colloid equivalent)
Apply vasopressors for hypotension not
responding to initial fluid resuscitation to
maintain MAP > 65 mmHg.
For persistent hypotension despite fluid
resuscitation (septic shock) and/or lactate >
4 mmol/L:


Achieve CVP > 8 mmHg.
Achieve ScvO2 of > 70%.
Management Bundle
(To be accomplished as soon as possible and
scored over first 24 hours):

Low-dose steroids administered
for septic shock in accordance
with a standardized ICU policy.

Drotrecogin alfa (activated)
administered in accordance with
a standardized ICU policy.

Glucose control maintained >
lower limit of normal, but < 150
mg/dL (8.3 mmol/L).

Inspiratory plateau pressures <
30 cmH2O for mechanically
ventilated patients.
http://www.ihi.org Accessed 3/23/05.
Corticosteroids in Sepsis
Case #13
• Immunosuppressed host with gram negative
pneumonia and hypoxemic respiratory failure.
• Hemodynamically stable
• moderate respiratory distress
– RR 32
– using accessory muscles
• ABG 7.37/40/50 on 50% FiO2
Case #13
• Which of the following should you order next?
–
–
–
–
NRB mask at 60% FiO2
Transtracheal oxygen
Noninvasive ventilation
Intubation and mechanical ventilation
Noninvasive Ventilation in
compromised host with
pneumonia
• Immunocompromised patients with respiratory
failure do poorly after endotracheal intubation.
Noninvasive Ventilation in immunosuppressed
patients with pulmonary infiltrates, fever and acute
respiratory failure.
Hilbert G, et al. N Engl J Med 2001; 15;344:481-7.
Case #14
• Compare outcome of thrombolytic therapy to heparin
in massive PE.
– Decreases PA clot burden at 7 days
– Decreases mortality in hemodynamically unstable patients
– Decreases need for escalation therapy (pressors, intubation,
secondary thrombolysis) in patients with RV dysfunction.
– Affords long term improvement in respiratory quality of life.
Thrombolysis in Massive
Pulmonary Embolism
No data to support reduced mortality in any subgroup
No data to suggest improved respiratory quality of life
Clot lysis is accelerated
Thrombolysis in Massive PE
Heparin plus Alteplase Compared with Heparin Alone in
Patients with Submassive Pulmonary Embolism
Konstantinides et al. NEJM; 347 (15): 1143, Table 2
October 10, 2002
Case #15
•
•
•
•
H/o Morbid obesity, presents with obtundation
Exam:
P2 increased, 2-3+ pedal edema
Lab: Hct 52% (50), ABG 7.25/80/45
CXR: Pulmonary HTN
Case #15
• Which of the following disorders is most likely
contributing to respiratory failure?
–
–
–
–
–
Bronchitis
Chronic PE
Diaphragm paralysis
Obesity hypoventilation
Myocardial ischemia
Obesity Hypoventilation
Syndrome
• Defined: Extreme obesity and alveolar
hypoventilation during wakefulness.
• Clinical features
–
–
–
–
Massively obese
Often concomitant OSA
Plethora, cyanosis
right heart failure
• P2
• Pedal edema
• Labs
– Hypercapnea while awake, elevated hematocrit
– CXR – high diaphragms, RV enlargement
Case #16
• Which patient will most likely benefit from
CPAP by face mask?
– Heroin OD with hypoxemia due to acute
pulmonary edema
– End stage cirrhosis with hypoxemia secondary to
hepatopulmonary syndrome
– Cardiogenic pulmonary edema
– Aspiration pneumonia with confusion
CPAP in CHF
• Indications for NIPPV
– Exacerbation COPD
– Hyoxemic respiratory failure in
immunocompromised host
– CHF
CPAP in CHF
advantages
• Decreases preload and afterload
• Decreases work of breathing
• Improves oxygenation
– Reduced catecholamines
• More rapid stabilization
CPAP in CHF
advantages over intubation
• Improved comfort
• Less sedation
• Easier transition to spontaneous breathing
– “on-off option”
• Fewer complications related to intubation
– VAP!!
Noninvasive Positive Pressure
Ventilation
•
•
•
•
•
•
•
•
•
Contraindications
Cardiac arrest
Respiratory arrest
Severe encephalopathy (GCS <10)
Severe UGI bleed
Hemodynamic instability
Facial injury, surgery, deformity
Upper airway obstruction
Inability to protect airway or clear secretions
Lack of cooperation!
Case #17
• Which patient with refractory hypotension is
most likely to respond to vasopressin?
–
–
–
–
–
Bilateral adrenal hemorrhage
SIADH
Prolonged severe sepsis
Calcium channel blocker toxicity
Acute RV myocardial infarction
Vasopressin in septic shock
Physiology
• Neurohormone
• Produced in posterior pituitary in response to
hypotension, hypovolemia, osmotic stress
– V1 receptor – constriction of vascular smooth muscle
– V2 receptor – water resorption in kidney
• Little role in blood pressure regulation under normal
conditions
Vasopressin in septic shock
Physiology
• Plasma concentrations increase in response to shock
• Important to maintaining BP in early shock (sepsis
and hemorrhagic)
• Plasma levels decrease over time due to depletion of
pituitary stores
Vasopressin in septic shock
Physiology
• Administration of exogenous vasopressin increases
raises BP by 20 – 50 mm Hg.
• Low dose vasopressin has been advocated by some
but definitive data supporting improved outcome are
lacking.
• May potentiate norepinephrine effects.
• Surviving Sepsis Campaign
– Grade E recommendation
– 0.04 units/min not titrated
When not to use Vasopressin
• Congestive heart failure
– Causes vasoconstriction and fluid retention
• Bilateral adrenal hemorrhage
– Use steroids
• SIADH
– It’s the offending agent
• Ca blocker toxicity
– No data
Case #18
• Patient with advanced idiopathic pulmonary fibrosis (IPF)
presents with acute respiratory failure. Patient is intubated.
Respiratory acidosis persists despite high minute ventilation. No
reversible cause is evident on exam or CXR.
• What do you do next?
–
–
–
–
–
Prone position
Increase tidal volume to PIP >35 cm H2O
Increase tidal volume to Plat P >35 cm H2O
Increase PEEP and Decrease FiO2 to < 75
Discuss end of life decisions with patient’s wife
IPF and Mechanical Ventilation
Outcomes
• IPF – progressive fibrosing inflammatory lung disease
• Mean survival 3-5 years after diagnosis
• Several studies now show extremely poor prognosis for ICU and
hospital survival when respiratory failure occurs
• Stern et al.
– 23 patients
– 1 patient had lung transplant
– No immediately reversible
causes identified.
– 96% ICU mortality
IPF and Mechanical Ventilation
Outcomes
• Other studies with similarly grim results
• Conclusions:
– Very low value of mechanical ventilation unless
• rapidly reversible cause of respiratory compromise can
be identified immediately (pneumothorax, medication
overdose)
• Lung transplant can be performed
Case #19
• Which patient is best candidate for prone positioning.
Diagnosis
PCO2
PO2
FiO2
PEEP
Bronchiectasis
50
50
0.5
0
Diffuse infiltrates
46
50
1.0
15
COPD exacerbation
70
60
0.5
5
Severe Lobar
pneumonia
40
50
0.75
5
Severe IPF
40
50
1.0
10
Prone positioning in ARDS
• Prone positioning of patients with ARDS improves
arterial oxygenation in patients with hypoxemia
refractory to high FiO2 and PEEP.
• Despite improved oxygenation, no studies have
shown improved outcomes.
• Use should be limited to ARDS patients with
hypoxemia refractory to high FiO2 and PEEP
• There are presently no data to support use in COPD,
Lobar pneumonia, ILD, bronchiectasis.
Prone positioning in ARDS
proposed mechanism
• CT imaging in ARDS shows heterogeneous
predominantly dependent consolidation
• In prone position, there is higher dependent
transpulmonary pressure (Ptp = Paw – Ppl) so there
is less compressive atelectasis and shunt.
Prone positioning in ARDS
proposed mechanism
• Increased FRC
• Blood flow is not dependent in prone position
(dorsal lung still gets most flow)
• Much derecruitment probably occurs while
patient is supine and breathing
spontaneously. Thus, derecruitment is
prevented.
Case #20
• Compared to standard, early goal directed
therapy (EGDT) includes which of the
following?
–
–
–
–
Keep lactate < 4 mEq/L
Keep central venous O2 sat (ScVO2) >70%
Keep HCT >40% if ScVO2 is <70%
Afterload reduction if ScVO2 is<70% after
transfusion.
Early Goal-directed therapy in the
treatment of severe sepsis and septic
shock
Rivers et al; NEJM 2001;345:1368
High-Risk Patients in ED
Rivers et al
2 Signs of SIRS
+
• Temp < 36o or >38oC
• Hr > 90 bpm
• RR > 20 bpm or PaCO2 <
32 mm Hg
• WBC > 12,000 or < 4,000
or > 10% immature bands
Sign of Global
Tissue Hypoxia
• SBP < 90 mm Hg
or
• Lactate > 4 mm/L
The PreSeptm Central Venous
Oximetry Catheter
EGDT reductions in
sepsis-related* mortality
NNT=7
Case #21
• Which of the following best describes the use
of permissive hypercapnia in this patient?
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–
–
–
Accentuates lung inflammation
Improves hypotension
May elevate PA pressure
A rise in PCO2 of 15-20 mm Hg over 10-15 min is
the therapeutic goal
Permissive Hypercapnic
Ventilation
• A strategy to decrease the risk of ventilator induced
lung injury (VILI) by the deliberate induction of
alveolar hypoventilation and acceptance of
hypercapnia.
• Prevents alveolar over distension (volutrauma)
• May reduce local inflammation
• No PRCTs documenting improved outcomes
Permissive Hypercapnic
Ventilation
physiology – stretch vs pressure
Capillary filtration coefficient vs inspiratory pressure
Impact of a body cast
Hernandez et al. J Appl Physiol 1989,66:2364
Permissive Hypercapnic
Ventilation
physiology - hemodynamic effects
• Increased
– HR
– Pulmonary artery pressures
• PCOP
– CVP
– RV work
– O2 delivery
– Cardiac output
Carvalho et al. Am J Respir and Crit Care Med 1997. Nov;156(5): 1458
Permissive Hypercapnic
Ventilation
•
•
•
•
contraindications
Elevated intracranial pressure
Seizure disorder
Arrhythmia, CAD, CHF (relative)
Pulmonary HTN
Case #22
• Patient with decompensated congestive heart failure
and respiratory distress. Typical therapies have been
initiated (O2, diuretic, nitrates, morphine). What’s
next?
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–
–
–
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Aminophylline
Diltiazem
CPAP by face mask
Intermittent positive pressure breathing (IPPB)
Intubation and ventilation
CPAP in Congestive Heart
Failure
• Beneficial effects
– Improves oxygenation
– Increased intrathoracic pressure
• Decreased venous return
– Reduced filling pressures
• Compresses heart
– Decreased wall tension
– Improved diastolic coronary perfusion
– Reduced myocardial O2 demand