afternoon delight - The University of Chicago Department of Medicine

AFTERNOON DELIGHT 

Pathophysiology Review 

August 11, 2010

Case 

A 54-year-old man is evaluated in the emergency department for a 1hour 

history of chest pain with mild dyspnea. The patient had been 

hospitalized 1 week ago for a colectomy for colon cancer. His medical 

history also includes hypertension and nephrotic syndrome secondary to 

membranous glomerulonephritis, and his medications are furosemide, 

ramipril, and pravastatin. 

On physical examination, the temperature is 37.5 °C (99.5 °F), the 

blood pressure is 110/60 mm Hg, the pulse rate is 120/min, the 

respiration rate is 24/min, and the BMI is 30. Oxygen saturation is 89% 

with the patient breathing ambient air and 97% on oxygen, 4 L/min. 

Cardiac examination shows tachycardia and an S 4. Breath sounds are 

normal. Serum creatinine concentration is 1.1 mg/dL (185.6 µmol/L). 

Chest radiograph is negative for infiltrates, widened mediastinum, and 

pneumothorax.

EKG

PE protocol CT

What happened? 

4:45 

pm 

History 

6:45 

pm 

Physical 

Exam 

7:05 

pm 

Diagnostic 

tests 

9:10 

am 

HD 

Monitor Treatment 

#5

Why? 

4:45 

pm 

History 

6:45 

pm 

Physical 

Exam 

7:05 

pm 

Diagnostic 

tests 

9:10 

am 

HD 


#5

What historical elements increase the 

pretest probability of PE? 

4:45 

pm 

History 

A 54-year-old man is evaluated in the emergency 

department for a 1-hour history of chest pain with mild 

dyspnea. The patient had been hospitalized 1 week ago 

for a colectomy for colon cancer. His medical history also 

includes hypertension and nephrotic syndrome secondary 

to membranous glomerulonephritis, and his medications 

are furosemide, ramipril, and pravastatin. 

On physical examination, the temperature is 37.5 °C (99.5 

°F), the blood pressure is 110/60 mm Hg, the pulse rate 

is 120/min, the respiration rate is 24/min, and the BMI is 

30. Oxygen saturation is 89% with the patient breathing 

ambient air and 97% on oxygen, 4 L/min. Cardiac 

examination shows tachycardia and an S 4. Breath sounds 

are normal. Serum creatinine concentration is 1.1 mg/dL 

(185.6 µmol/L). Chest radiograph is negative for 

infiltrates, widened mediastinum, and pneumothorax.



4:45 

pm 

History 

* Ann Intern Med 2001;135:98-107 

**JAMA. 2006;295:172-179 

N Engl J Med 2008;358:1037-52. 

1.3% had PE 

16.2% had PE 

37.5% had PE* 

12.1% had PE: +D-dimer 23.2% had PE, -D-dimer 0.5% PE 

37.1% had PE**



4:45 

pm 

History 

A 54-year-old man is evaluated in the emergency 

department for a 1-hour history of chest pain with mild 

dyspnea. The patient had been hospitalized 1 week ago 

for a colectomy for colon cancer. His medical history also 

includes hypertension and nephrotic syndrome secondary 

to membranous glomerulonephritis, and his medications 

are furosemide, ramipril, and pravastatin. 

On physical examination, the temperature is 37.5 °C (99.5 

°F), the blood pressure is 110/60 mm Hg, the pulse rate 

is 120/min, the respiration rate is 24/min, and the BMI is 

30. Oxygen saturation is 89% with the patient breathing 

ambient air and 97% on oxygen, 4 L/min. Cardiac 

examination shows tachycardia and an S 4. Breath sounds 

are normal. Serum creatinine concentration is 1.1 mg/dL 

(185.6 µmol/L). Chest radiograph is negative for 

infiltrates, widened mediastinum, and pneumothorax.



4:45 

pm 

History 

* Ann Intern Med 2001;135:98-107 

**JAMA. 2006;295:172-179 

37.1% had PE** 

N Engl J Med 2008;358:1037-52. 

37.5% had PE*

Why? 

4:45 

pm 

History 

6:45 

pm 

Physical 

Exam 

7:05 

pm 

Diagnostic 

tests 

9:10 

am 

HD 


#5

6:45 

pm 

Mechanisms of Hypoxemia 

Physical 

Exam 

Decreased Inspired Oxygen 

Hypoventilation 

V/Q mismatch 

Shunt 

Venous Admixture

6:45 

pm 


Physical 

Exam 

PI O2= 

FI O2 x (P atm –P H2O ) 

PAO2= FIO2 x (Patm –PH2O ) – PCO2/R Mason: Murray and Nadel's Textbook of Respiratory Medicine, 5th ed. 

A decrease in 

inspired oxygen (PI O2) 

leads to a decrease 

in the PA O2. 

As a result the driving 

pressure of oxygen 

through the alveolarcapillary 

membrane 

(ie the Aa gradient) is 

reduced and 

hypoxemia occurs.

6:45 

pm 


Physical 

Exam 



V/Q mismatch 

Shunt 

Venous Admixture

6:45 

pm 


Physical 

Exam 

When you hypoventilate, what happens to your P CO2 ? 

PA O2= FI O2 x (P atm –P H2O ) - 

Drive 

CNS Drive 

1. Narcotics 

2. Mass lesions 

Metabolic Drive 

1. Alkalosis 

2. Acidosis 

Respiratory Muscles 

• Muscular dystrophy 

• Myositis 

• Diaphragm weakness 

• Hypothyroidism 

Neurologic conditions 

• Myasthenia Gravis 

• Spinal cord injury 

• ALS/MS/GBS 

P CO2/R 

Strength Load 

Chest wall 

•Kyphosis, Obesity 

Lungs 

•Fibrosis 

Airways 

•Asthma, COPD 

Metabolic demands 

•Exercise, sepsis

6:45 

pm 


Physical 

Exam 



V/Q mismatch 

Shunt 

Venous Admixture

6:45 

pm 

V/Q mismatch 

Physical 

Exam 

Low V/Q: 

Open alveoli, but low 

airflow (atelectasis, 

bronchospasm, partial 

obstruction of airway) 

Mason: Murray and Nadel's Textbook of Respiratory Medicine, 5th ed. 

Right to Left Shunt: 

passage of venous blood into 

the arterial circulation w/o 

passing ventilated alveoli 

Pa O2≈Mv O2 

High V/Q: 

Increasing 

dead space 

(PE, 

hypovolemia) 

Dead Space: 

alveolar units are 

fully ventilated 

but not perfused 

Pa O2≈ Pi O2

6:45 

pm 


Physical 

Exam 



V/Q mismatch 

Shunt 

Venous Admixture

Shunt 

Passage of 

venous blood 

into the arterial 

circulation w/o 

passing 

ventilated 

alveoli 

6:45 

pm 

Physical 

Exam 

Kliegman: Nelson Textbook of Pediatrics, 18th ed. 

Hypoxemia caused by shunt is characterized by the failure 

of PaO 2 to rise despite inhalation of pure oxygen (100%). 

Intrapulmonary Shunt Extrapulmonary Shunt 

Pulmonary arteriovenous 

malformations 

hepatopulmonary 

syndrome 

+/- alveolar 

consolidation or collapse 

Atrial septal defect 

Ventricular septal defect 

Patent ductus arteriosis 

Anomalous pulmonary 

venous circulation 

Due to deoxygenated blood returning to the left atrium from the 

thebesian veins and from the bronchial circulation of the airways, 

there is a normal (anatomic) shunt of 5% in normal individuals.

6:45 

pm 


Physical 

Exam 



V/Q mismatch 

Shunt 

Venous Admixture

6:45 

pm 

Venous Admixture 

Physical 

Exam 

Kliegman: Nelson Textbook of Pediatrics, 18th ed.

6:45 

pm 

Venous Admixture: heart failure 

Physical 

Exam 

60% 

60% 

60% 

85% 65% 75%

6:45 

pm 

What is the primary mechanism of 

Hypoxia for PE? 

Physical 

Exam 

V/Q mismatch 

Increases the amount of dead space 

How can PE cause shunt physiology? 

Acquired PFO 

Atelectasis in infarcted segment

Why? 

4:45 

pm 

History 

6:45 

pm 

Physical 

Exam 

7:05 

pm 

Diagnostic 

tests 

9:10 

am 

HD 


#5

7:05 7:05 

pm 

pm 

Comparison of tests 

Diagnostic 

tests 

CLEVELAND C.LINIC JOURNAL OF MEDICINE 2002; 69: 721-29.

7:05 

pm 

What about a V/Q scan? 

Diagnostic 

tests 

JAMA 1990; 263:2753–2759. 

CLEVELAND C.LINIC JOURNAL OF MEDICINE 2002; 69: 721-29.

7:05 7:05 

pm 

Diagnostic 

tests 

pm 

N Engl J Med 2008;359:2804-13. 

Pre-test Probability: 

important in 

choosing your next 

diagnostic test

Why? 

4:45 

pm 

History 

6:45 

pm 

Physical 

Exam 

7:05 

pm 

Diagnostic 

tests 

9:10 

am 

HD 


#5

Why are PE’s so deadly? 

9:10 

am Monitor 

Hypoxemia 

RV dysfunction

S1Q3T3: a 

sign of acute 

cor pulmonale 

EKG DDx: PE, acute bronchospasm, pneumothorax, and other acute lung 

disorders. 

− An S wave in lead I signifies a complete or more often incomplete RBBB 

− In lead III, look for a Q wave, slight ST elevation, and an inverted T wave. These 

findings are due to the pressure and volume overload over the right ventricle 

which causes repolarization abnormalities.

9:10 

am 

How does RV dysfunction cause shock? 

Monitor 

As the right ventricle 

dilates, the interventricular 

septum shifts toward the 

left, resulting in left 

ventricular underfilling and 

decreased left ventricular 

diastolic distensibility. 

Consequently, systemic 

cardiac output and systolic 

arterial pressure decline, 

thereby impairing coronary 

perfusion and causing 

myocardial ischemia.

How does PE cause Myocardial 

ischemia? 

Myocardial 

ischemia occurs 

whenever 

demand 

exceeds 

supply… 

9:10 

am Monitor 

Elevated right ventricular wall tension reduces right coronary artery blood flow, 

increases right ventricular myocardial oxygen demand, and causes coronary 

arterial ischemia. 

Hypoxemia further diminishes limited myocardial oxygen supply. 

Ultimately, right ventricular infarction, circulatory collapse, and death may 

ensue. 

Demand 

1. Heart Rate 

2. Systolic Blood pressure 

3. Wall Tension 

• LVEDP/Preload 

• Wall thickness 

4. Contractility 

Supply 

1. O2 carrying capacity 

• PaO2 tension 

• Hemoglobin 

2. O2 extraction 

3. Coronary blood flow

Terminology 

9:10 

am Monitor 

Massive PE: presence of cardiogenic shock, 

persistent arterial hypotension, or both. 

accounts for 5% of all cases of pulmonary embolism 

Submassive PE: normotensive patients who 

may have an elevated risk of death because 

of right ventricular dysfunction or injury to the 

myocardium 

Among hemodynamically stable PE patients, 

elevated troponin levels were associated with a 

6-fold increased mortality.

9:10 

am Monitor 

Risk factors for mortality 

Age >70 

Cancer 

Clinical CHF 

COPD 

SBP20 

RV Hypokinesis 

Lancet 1999;353:1386–1389 

Circulation 2005;112;e28-e32

Why? 

4:45 

pm 

History 

6:45 

pm 

Physical 

Exam 

7:05 

pm 

Diagnostic 

tests 

9:10 

am 

HD 


#5

HD 

#5 Treatment 

Treatment of Acute PE 

1. Active cancer 

2. Unprovoked 

Pulmonary Embolism 

3. Recurrent venous 

thromboembolism 

N Engl J Med 2010;363:266-74.

HD 

#5 Treatment

afternoon delight - The University of Chicago Department of Medicine

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