73 Y/O Male Patient with H/O DM, CHF, and COPD Presenting with C/O 4 Days of Nasal And

Resident Version

Hypoxia Module

Created by Dr. Wendy Gerstein

(with help from Dr. Neal Gerstein and Dr. Helen Busby)

Updated 5/09

Objectives:

1) Understand and identify three different mechanisms for hypoxia.

2) Recognize severity of hypoxia by calculating A-a gradient.

3) Know three indications for intubation.

References:

1) Nunn’s Applied Respiratory Physiology. Andrew B. Lumb. 5th edition, 2003. Butterworth Heinemann.

2) Facts and Formulas. Robert C. Rollings. Copyright 1984.

3) “Interpretation of arterial oxygen tension”

CASE

HPI:

73 y/o male patient with h/o DM, CHF, and COPD presenting with c/o 4 days of nasal and chest congestion with cough productive of white sputum and yellow post nasal discharge. Patient is on continuous home O2 at 2L by nasal cannula and reports some worsening of shortness of breath that slightly improved with home nebulizer treatment at ~ 0900 day of admission. Patient denies fever but had chills intermittently for 6 days. He also has chronic chest tightness for 4 years that is worse for the past 3 days. He also has a history of intermittent bilateral lower extremity edema. Per his son, his legs are more edematous today than in the previous week. His son also reports that he appeared confused today without LOC or near syncopal episodes. Upon arrival in the ED the patient had a pulse ox of 57% on 2L NC. He was increased to 6L by NC. Patient was given dilaudid 2 mg IV for his chronic hip pain and became confused, CBG 182. He was placed on NRB 100% with O2 sat of 88% then given NTG SL, ASA, and Lasix 100mg. His blood pressure decreased to 87/42. The patient was bolused 250 cc NS with adequate response and started on bipap. He was given solumedrol 125 mg and albuterol nebs with some improvement in his O2 sat, then changed to 50% ventimask. Patient is DNR/DNI.

Pmhx:

Diabetes Mellitus: last HgA1C 6.5 H

HTN

CHF due to hypertensive cardiomyopathy. Echo 2 years ago with moderate-severe global hypokinesis, EF 30-35%

h/o Renal insufficiency in past when aggessively diuresed, baseline cr 1.0

Morbid Obesity

Mixed hyperlipidemia: recent lipids CHOL-176 dHDL-55 TG1-38 LDL-94

Chronic Obstructive Pulmonary Disease – on 2 liters at home, FEV1 1.42 liters, 45% predicted (6 yrs ago)

Osteoarthrosis, severe DJD with chronic pain

Chronic anemia: responsive to B12

Outpatient medications:

1) Combivent inhaler

2) felodipine 5m po q day

3) lovastatin 40 mg po q day

4) methadone 5 mg po q 12 hours

5) trazodone 50 mg po q hs prn

6) Vitamin B 12 injection 1 gm q month

7) lasix 80 mg po bid

8) Toprol xl 100 mg po q day

9) lisinopril 40 mg po daily

10) Previously on Glyburide 10mg qam and 5 mg qpm, expired.

Family history:Mother had CHF;

Social history:Patient lives in ABQ, alone. Tobacco discontinued 35 years ago, ETOH:denies, Drugs:denies. Unclear medication compliance.

Allergies:

MEROPENEM, HYDROCODONE, OXYCODONE-> N/V

PE:

P 62-80, Temperature 37.2 C, bp 125/57->87/42->117/47, rr 30’s, 84% on 50% facemask

General: Obese male in respiratory distress, wearing mask and snoring while asleep with O2 sat of 84%. Pausing mid sentence to breath. Arousable by loud voice with return in O2 sat to 96 %

on mask. Patient intermittently falling asleep during interview and exam. Fully oriented when awake.

HEENT: NC/AT. Pupils 2MM briskly reactive. EOMI. No sinus tenderness. Conversation hearing diminished. Neck plethoric. OP clear. JVP poorly visualized. No apparent JVD. carotids 2+ without bruits.

Chest (general): Rises evenly with use of intercostals. Bibasilar crackles with decreased BS to middle lung fields. No wheezing. Expiratory time about 1.5 x inspiratory time.

Cardiovascular:Distant heart sounds. RRR. No M/G/R

Abdomen: Obest. NT, decreased Bowel sounds. No HSM. No palpable masses.

Extremities: 2+ pitting LE edema to knees with R>L. PT pulses 1+ bilaterally. Chronic venous stasis changes on both lower legs R>L Oncomycosis of fingernails and toe nails. No cyanosis or clubbing

Neurological: Patient with myclonic jerking of both arms when dozing off. Slight intention tremor of both hands. 5/5 strength in upper and lower extremities. DTR's 1+

Labs/studies:

UA: notable for only small amount of protein, otherwise wnlexcept for 5-10 hyaline casts/hpf

BNP= 885

Troponin negative x 1

Chem 7 notable for bun 40, creatinine 1.6, chloride 93, bicarb 35, potassium 4.1, sodium 140

Mg 2.2, calcium 7.8

Wbc 8.9, 89%neutrophils, hct 43.6, platelets 213,

LFT’s wnl including alb 3.8, inr 1.0

ABG in ER on non-rebreather:

7.26/95/73/33.7/91%

pH/pco2/p02/hco3/oxygenation

CXR: peribronchial cuffing. Poor inspiratory effort. No effusion. ? patchy LLL infiltrate

EKG: No significant changes. No ST-segment or Twave changes concerning for

ischemic disease.

First question – how do you interpret the blood gas? Go through the steps listed…

1) acidosis or alkalosis?

2) Primary process respiratory or metabolic?

3) Is it acute or chronic?

Second question – what is your initial assessment and plan for this patient’s presentation?

Third question – what precipitated this patient’ssubsequent decline after hospitalization, and discuss further assessment/management issues.

Outline for discussion:

1) Definition of hypoxia: “cessation of oxidative phosphorylation leading to critical fall in mitochondrial PO2 levels.” Usually defined when PaO2<60mmHg, or SaO2<90% (correlate to each other based on oxygen saturation curve).

2) Causes of hypoxia (there are 5 general categories)

A) R to L shunt physiology: perfusion without ventilation (blood, pus, or water in alveolar space).

B) V/Q mismatch: abnormal ventilation/perfusion ratio (normal is .8)

C) Hypoventilation: Guillain-Barre, heroin overdose, CNS depression

D) Low FiO2 (meth lab blows up in closed space, or patient intubated) or decreased barometric pressure (top of Everest).

E) Decreased diffusion (DLCO): lung disease

ShuntV/Q mismatchDead Space

V/Q = 0This is a continuumV/Q=infinity

Perfusion with Ventilation

no ventilationwith no perfusion

3) Calculating degree of hypoxia

A) Calculate Aa gradient (normal is 10-15 mmHg). Equation: PAO2-PaO2 (PaO2 from blood gas. PAO2 = (barometric pressure – partial pressure H2O) x FiO2 – PaCO2/respiratory quotient. Barometric pressure here is 660 mmHg, PH2O is 47 mmHg, and respiratory quotient is .8. Calculate for case patient.

B) Although the FiO2 can be variable based on the patient’s minute ventilation, it is important to have some understanding of how much oxygen you are delivering:

- FiO2 of room air is 21% (regardless of altitude).

- Every liter of oxygen increases FiO2, on average, by 5%, so 6 liters of oxygen by nasal cannula gives you an average FiO2 of 51%.

- Venti- mask (not used very often anymore) – can titrate FiO2 (if 50%, then FiO2=50%).

- Non rebreather mask (NRB)- if reservoir kept inflated, can titrate FiO2 up to 100%, but usually maximum is 60% due to design flaw (bag crimps).

- Gin mask – can titrate up to almost 100% FiO2.

C) Normal PO2 on room air is 80 mmHg here in Albuquerque. If you put a normal person on 100% FiO2, their PO2 will be over 500 mmHg when measured on a blood gas.

4) Initial evaluation of a patient with hypoxia:

A) Is it a real reading? Repeat it, does it match clinical picture of patient, do they have PVD or Raynauds…

B) Physical exam. Focus on vitals, assessment of airway, circulation (evidence of hypoperfusion), lung exam, LE edema, etc. Review recent events in hospital, recent medications and procedures; are they an aspiration risk, what is their LV function, h/o COPD?

C) Labs: GET ABG – underutilized, can give valuable information about PCO2, degree of hypoxemia (calculate Aa gradient). Also need basic labs such as CBC, chem 7. Consider BNP, d-dimer and troponin based on clinical suspicion.

D) Initial studies: CXR, EKG. CT if thinking pulmonary embolus.

5) Indications for intubation (assuming patient full code – otherwise consider bipap):

A) Unable to protect airway

B) Significant problem with oxygenation (PO2 <60 mmHg on 100%NRB)

C) Significant problem with ventilation (PCO2>55 with pH < 7.25, ie acidosis)

D) Anticipated clinical course (progressive pneumonia, shock, severe burns)

Review Questions:

1) Which of the following represents a primary dead space problem?

A) Interstitial lung disease

B) CO poisoning

C) Aspiration pneumonia

D) Pulmonary Embolus

.

2) Cardiac arrest physiology is best described by:

A) V/Q mismatch

B) R to L Shunt physiology

C) Dead space

D) Change in FiO2

3) Acetazolamide was used in the case patient presented primarily because:

A) It inhibits the Na+/Cl/K+ cotransport system in the loop of Henle.

B) It increases HCO3 reabsorption in the proximal convoluted tubules.

C) It decreases HCO3 reabsorption in the proximal convoluted tubules.

D) It blocks reabsorption of Na+ in the distal tubule of the kidneys.

E) It inhibits the aldosterone-sensitive Na+ channels in the collecting tubules.

4) Which of the following will not show significant improvement in the Aa gradient when you give 100% FiO2?

A) V/Q mismatch

B) R-L Shunt

C) Diffusion defect (decreased DLCO)

D) Hypoventilation

Post Module Evaluation

Please place completed evaluation in an interdepartmental mail envelope and address to Dr. Wendy Gerstein, Department of Medicine, VAMC (111).

1) Topic of module:______

2) On a scale of 1-5, how effective was this module for learning this topic? ______

(1= not effective at all, 5 = extremely effective)

3) Were there any obvious errors, confusing data, or omissions? Please list/comment below:

______

4) Was the attending involved in the teaching of this module? Yes/no (please circle).

5) Please provide any further comments/feedback about this module, or the inpatient curriculum in general:

6) Please circle one:

Attending Resident (R2/R3)Intern Medical student