Acid and Base Lecture Flashcards

1
Q

Normal Arterial Blood Gases

A

– pH 7.35 – 7.45 (7.4)

– PaCO2 35 – 45 (40)

– PaO2 80 – 100 (90)

– HCO3 22 – 26 (24)

– O2 Sat 92‐100%

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2
Q

Arterial Blood Gases

A
  • Gas Concentrations and pH: Provide information about LUNG FUNCTION, OXYGENATION, and VENTILATION
  • pH, paCO2, paO2, HCO3
  • pH: Hydrogen Ion Concentration
  • paCO2: Carbon Dioxide
  • PaO2: Oxygen
  • HCO3: Bicarbonate
  • O2Sat: Oxygen Saturation
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3
Q

Hypoxemia with ABGs

A
  • HYPOXEMIA is SUBNORMAL OXYGENATOIN in BLOOD
  • Normal O2:
    = 104 - (0.27 x Age)
    = 100 - (1/3 x Age)
    = DECREASE with AGE!!!!!
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4
Q

Causes of Hypoxia

A

1) HYPOVENTILATION
2) V/Q (Ventilaiton/ Perfusion) mismatch as seen in PULMONARY EMBOLISM
3) Shunting Ex Cardiac Anomalies
4) LOW INSPIRED FRACTION of O2 (FiO2)
5) HIGH ALTITUDE
6) Diffusion Abnormalities (Ex Alveolar Hemorrhage, Connective Tissue Disorder)

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5
Q

ABG Terms

A
  • Acidosis pH 7.35 or LOWER
  • Alkalosis pH 7.45 or HIGHER

• Hypoxia pO2 LESS THAN 60!!!!! (Arterial)

  • Hypercapnia pCO2 GREATER THAN 45
  • Hypocapnia pCO2 LESS THAN 35
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6
Q

Metabolic Acidosis (WINTER EQUATION)

A

Expected PCO2 = 1.5 x (measured HCO3) + 8 +/- 2

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7
Q

Bicarbonate in Kindeys

A
  • Kidney starts to RETAIN HCO3 in 12 to 16 hours; MAX CONCENTRATION in 1 Week!!!
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8
Q

ABG Analysis 3 Step Approach

A

1) Does patient have ACIDOSIS or ALKALOSIS?
pH High or Low?

2) Is the Acidosis/ Alkalosis a RESPIRATORY or METABOLIC PROCESS
3) If it is a Respiratory Acidosis/ Alkalosis, is it a PURE RESPIRATORY or is there a METABOLIC COMPONENT?

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9
Q

ABG Analysis

A

1) If pH and pCO2 are BOTH UP or DOWN in the SAME DIRECTION, the process is METABOLIC!!!!!!!
2) If One is UP while the Other is DOWN (OPPOSITE) the process is RESPIRATORY!!!!!

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10
Q

ABG Analysis Step 1 and 2 Recap

A

• Step1:
– If pH 7.45 alkalosis

• Step2:
– If the pCO2 and pH move in SAME direction a METABOLIC process is occurring

– If the pCO2 and pH move in OPPOSITE direction there is a primary RESPIRATORY process

• (as pCO2 INCR, then pH DECR; as pCO2 DECR, then pH INCR)

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11
Q

ABD Analysis Step 3

A

In a PURE RESPIRATORY PROCESS:

- For each 10 mmHG CHANGE in PaCO2, the pH should move in the OPPOSITE DIRECTION by o.8 (+/- 0.2)!!!!!!!!!!

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12
Q

ABG Analysis- Step 3A Examples

A

– If PaCO2 is 30 ( a DECREASE of 10 mmHg from 40) the pH should be 7.48 (7.4 + .08)!!!!!!!

– If PaCO2 is 60 (an increase of 20 mmHg) the pH should be 7.24 (7.4 – 2 x .08 or .16) a DECREASE of .16 or .08 for each 10 mmHg RISE in pCO2!!!!!!

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13
Q

ABG Analysis- Step 3B

A
  • If this rule is violated a SECOND Metabolic process is ALSO PRESENT and this is referred to as a MIXED PROCESS!!!!
  • Step 3 – COMPARES the “should be” (aka expected or calculated) pH to the ACTUAL measured pH reported
  • If the actual pH is not what it should be, is it HIGHER or LOWER? If it is HIGHER there must be a concomitant METABOLIC ALKALOSIS – If it is LOWER, there must be a concomitant METABOLIC ACIDOSIS
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14
Q

ABD Example #1

pH 7.58 pCO2 20

A

• Step 1
pH > 7.45 – ALKALOSIS

• Step 2
pCO2 & pH OPPOSITE direction – RESPIRATORY PROCESS

• Step 3
- For each 10 change in pCO2 the pH moves in opposite direction by .08. pCO2 is  by 20

  • pH should be elevated by 2 x .08 or .16 +.02

*** 7.40 + .16 = 7.56 so this is PURE RESPIRATORY ALKALOSIS

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15
Q

ABG Example #2

pH 7.16 pCO2 70

A

• Step 1

pH PURE RESPIRATORY ACIDOSIS

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16
Q

ABG Example #3

pH7.5 pCO2 50

A

• Step 1
pH > 7.45 ALKALOSIS

• Step 2
- pCO and pH in SAME direction – METABOLIC PROCESS

• Step 3
- Does not apply since this is not a respiratory process

** METABOLIC ALKALOSIS!!!

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17
Q

ABG Example #4

pH 7.25 pCO2 20

A

• Step 1
pH less than 7.35 = ACIDOSIS

• Step 2
pH and pCO2 are in the SAME DIRECTION therefore METABOLIC

METABOLIC ACIDOSIS!!!!!!

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18
Q

ABG Example #5

pH 7.49 pCO2 20

A

• Step 1
pH > 7.45 ALKALOSIS

• Step 2
pCO2 and pH OPPOSITE – RESPIRATORY PROCESS

• Step 3
- pCO2 is DECREASED by 20; pH SHOULD BE increased by .08 x 2 or .16;

  • 7.40 + .16 = 7.56

– The measured 7.49 is lower than the calculation says it should be i.e. a secondary process is present; there must be a metabolic process causing the pH to stay down

**RESPIRATORY ALKALOSIS and METABOLIC ACIDOSIS**

19
Q

ABG Example #6

pH6.8 pCO2 60

A

• Step 1
pH LESS THAN 7.35 = ACIDOSIS

• Step 2
pCO2 and pH OPPOSITE= RESPIRATORY

• Step 3
pH should be DOWN by 0.16 from 7.4
** pH of 6.8 is too low therefore must have METABOLIC ACIDOSIS too

*** RESPIRATORY ACIDOSIS and METABOLIC ACIDOSIS

20
Q

Case 1

  • A 70‐year‐old male presents to the emergency department with INCREASING DYSPNEA (respiratory rate 25 breaths/min.)
  • Physical Exam: JVD at 45°, estimated CVP 11mm H2O
  • Lungs – bilateral crackles in bases and scattered wheezes
  • Heart – grade 3/6 systolic murmur at apex with radiation into left axilla, S3 gallop heard, no S4
  • Bilateral peripheral edema of the legs; cool extremities
  • BP 100/68, P 115/min, irregular, R 25 breaths/min
  • Afebrile, O2 sat 78%!!!!!

VENOUS LAB RESULTS:
• Na: 128(135‐148)

  • K: 5.8 (3.5‐5.5)
  • Cl: 92 (96‐112)
  • HCO3: 12 (22‐28)
  • BUN: 42 (8‐25)
  • Creatinine: 2.1 (0.6‐1.5)
  • BNP: 500 (0‐100)
A

Anion Gap for Case #1:
• = Na – (Cl+HCO3)
• 128 – (92 + 12) = 24 (HIGH)

** METABOLIC ACIDOSIS with a HIGH ANION GAP!!!!!!

Diagnosis:

  • Heart Failure
  • Atrial Fibrillation with Rapid Ventricular Response
  • Hyponatremia
  • Azotemia
  • Metabolic Acidosis
  • Mitral Regurgitation

TREATMENT:
• Oxygen 2‐4 liters/min N/C

  • IV–loop diuretic
  • Fluid Restriction 1‐ 1.5 L/day

• Na HCO3 – cautiously (why?)
- It would take HCO3 a long time to balance out the pH and therefore also take a long time to DISSIPATE if you give too much

• ACEI – cautiously(why?)
- Can help kidneys, but have to watch POTASSIUM and CREATININE

21
Q

Anion Gap

A

• NORMAL ELECTROLYTES
– Na 135 – 145 (140)

– K 3.5–5 (4)

– CL 98 – 106 (103)

–CO2 21–28 (24)

* (Mid‐range number for calculations)*

ANION GAP = Na – (CL + HCO3)

= (12 +/- 2)
From 10 to 14*

  • Anion gap – reflects concentration of ANIONS that AREN’T routinely measured. (Sulfates, phosphates, acetoacetic acid, beta hydroxybutric acid)
22
Q

Metabolic Acidosis

A

1) Metabolic Acidosis: DECREASE in EXTRACELLULAR pH caused by a DECREASE in HCO3!!!!
a) LOSS of HCO3: Gastrointestinal Tract (GIT), Renal

b) INCREASE HYDROGEN Load: DKA or Lactic Acid
c) DECREASE HYDROGEN EXCRETION by Kidney: UREMIC ACIDOSIS or RTA
2) Two (2) Types: ELEVATED ANION GPA or a NORMAL ANION GAP with HYPERCHLOREMIA!!!!!

23
Q

Causes of HIGH ANION GAP

A

” MUDPILES”

• M ‐ METHANOL – formic A

• U ‐ UREMIA (renal failure)
–  BUN, Creatine
–  Sulfates, phosphate as UNMEASURED ANIONS

• D ‐ DIABETIC KETOACIDOSIS
– Glucose; Starvation, Alcohol abuse
– Acetoacetic acid, B‐hydroxybutyric acid

  • P ‐ PARALDEHYDE
  • I ‐ INH, IRON
  • L ‐ LACTIC ACID – Shock, sepsis, low perfusion, marathon runners
  • E ‐ ETHYLENE GLYCOL (Glycolic Acid)
  • S ‐ SALICYLATES
  • CCAT- CO, Cyanide, Alcohol, Toluene
24
Q

Lactic Acidosis

A

1) TYPE A (TISSUE HYPOXIA)- Shock, Severe Anemia, Heart Failure, CO Poisoning
2) TYPE B1 (Associated with SYSTEMIC DISORDERS) DM, Liver Failure, Sepsis, Seizures
3) TYPE B2 (Associated with DRUGS/ TOXINS) Ethanol, Methanol, Ethylene Glycol, ASA
4) TYPE B3 (Associated with INBORN ERRORS OF METABOLISM) G6PD Deficiency

25
Q

Other Tests for Lactic Acidosis

A

1) Echocardiogram
2) Lactic Acid Level
3) Cardiac Enzymes (Troponin I, CK MB)

26
Q

Case #2

  • 68‐year‐old African American female presents to the emergency department in a lethargic state. History from the family is for the past 3‐4 weeks, she has developed anorexia, CONFUSION, edema and weight gain.
  • PMH is positive for POORLY CONTROLLED HYPERTENSION
    and DIABETES MELLITUS, DJD and hypothyroidism.
  • Medications – HCTZ 50mg daily, Lantus insulin 20 units hs, NSAID for arthritis and Synthyroid .05 mg orally daily.
  • Arousable, but lethargic.
  • BP 158/88, P – 90/min., R 10 breaths/min., Temp. 98°F, O2 sat 88%
  • Neck veins mildly distended at 45°

• Heart – 2/6 systolic murmur 2nd ICS, RSB with slight
radiation into R carotid

  • Lungs – Basilar crackles, R > L
  • Abdomen – Tenderness RUQ, edge of liver is three (3) fingers below costal margin. Percussion span of liver is eight (8) centimeters (normal span)
  • Extremities – markedPITTING EDEMA of feet, calves and thighs

Tests:
• CBC–Hgb 9 grams, Hct 27%

  • CMP BUN 110mg/ Creatine 8.0mg, Na 150, K7.0, CL 115, HCO3 10
  • TSH–10
  • HbA1C‐ pending

ABG:
– pH 7.1, pCO2 45, pO2 68, HCO3 8

A

What is your Diagnosis?
- Metabolic ENCAPHALOPATHY - R/O HYPOTHYROID (Myxedema)

  • Likely Ischemic Cerebral Vascular Disease due to POORLY CONTROLLED HYPERTENSION
  • Electrolyte/ Acid- Base Disorder
  • Fluid Overload

What is you DIFFERENTIAL DIAGNOSIS?
- Myxedema

  • Ischemic Cerebral Vascular Disease
  • Valvular Heart Disease
  • Heart Failure
  • Hypertension

ABG’s:
- METABOLIC and RESPIRATORY ACIDOSIS

Anion Gap:
= Na - (Cl + HCO3)
= 150 - (115 + 10)
= 25 (HIGH!!!!)

** HIGH ANION GAP METABOLIC ACIDOSIS because of RENAL FAILURE (Retention of Hydrogen Ions) in UREMIC ACIDOSIS

AND

**RESPIRATORY ACIDOSIS because the Lungs haven’t compensated as you’d expect for the Metabolic Acidosis by DECREASING the pCO2

TREATMENT:

  • Dialysis: Hemodialysis
  • Na HCO3
  • Synthyroid
  • Aerosol treatments with NEBULIZERS
27
Q

Case #3

  • A 37‐year‐old female presents to the emergency department with a six (6) day history of DIARRHEA.
  • She has approximately seven (7) stools per day and she is up 3‐4 times through the night with watery, non‐bloody stools.
  • She is able to drink fluids, soups and jello. She hasn’t traveled out of the country, camped outdoors, or ingested spring or river water.
  • She states her aunt has Crohn’s disease. She hasn’t been on any antibiotics over the past four (4) months.

PHYSICAL EXAM:
• BP 80/50, P 110/min., R 18/min., Temp. 100°F, O2 Sat 94%

  • General – PALE, poor skin turgor, dry mucous membranes
  • Neck veins are flat
  • Heart – no murmur, S3 or S4 ; tachycardia at 110 p/min.
  • Lungs – clear
  • Abdomen – Hyperactive bowel sounds, mildly tender diffusely, no organomegalia
  • Extremities – COOL TO TOUCH. Tattoo R ankle
  • Neurologic ‐ normal

TESTS:
• CBC Hb16, Hct 50%, WBC 14,000

  • CMP– Na 148, K 2.6, CL 114, HCO3 20
  • Stools–culture for enteric pathogens, ova parasites, WBC’s/hemoccult of stool
  • ABG’s – pH 7.1, pCO2 34, pO2 92, HCO3 20
A

Diagnosis:

1) DIARRHEA
a) Secretory
b) Infectious
c) Consider Inflammatory Bowel Disease

2) HYPOVOLEMIA: Volume contracted, possibly electrolyte/ Acid Base Disturbance
3) HYPOTENSION

Anion Gap:
= Na - (Cl + HCO3)
= 148 - (114 + 20)
= 14 (Upper Normal)

  • ** METABOLIC ACIDOSIS with Normal Anion Gap
  • LOW HCO3 and ELEVATED CL!!!!!!

TREATMENT:
1) IV FLUIDS for VOLUME RESTORATION (Careful not to give too much NaCl or N/S)

2) Could give fluids of 1/2 STRENGTH N/S with Na HCO3 and K!!!!!!!!

28
Q

Normal Anion Gap Met METABOLIC ACIDOSIS (HCO3 Falls and CL RISES)

aka HYEPRCHLOREMIC MET ACID

“HARDUPS”

A

“HARDUPS”

  • H: HYPERALIMENTATION
  • A: ACID INFUSION, Acetazolamide
  • R: RENAL TUBULAR ACIDOSIS (RTA) - Renal loss of HCO3/ or DECREASED H Secretion
  • D: DIARRHEA, losing HCO3, DECR K
  • U: URETERAL SIGMOID or ILEAL DIVERSION, Losing HCO3/ INCR Cl and H Resorption
  • P: PANCREATIC FISTULA, losing HCO3, and DECR K+
  • S: SPIRONOLACTONE
29
Q

Renal Tubular Acidosis (RTA)

A

1) DISTAL: Decreased SECRETION of H+, so NOT GETTING RID of ACID, “ Failure to Acidify Urine” aka TYPE I**

2) PROXIMAL: Decreased ABSORPTION of HCO3, so not absorbing Buffer aka TYPE II**
- Possible causes: Multiple Myeloma, Heavy Metal Poisoning, Wilson’s Disease, Amyloidosis

3) HYPERKALEMIC RTA: HYPORENIN and HYPOALDOSTERONE, DECR NH4 Excretion and DECR HCO3 Production aka TYPE IV*****
- Possible causes: Analgesic Nephropathy, Sickle Cell Disease and SLE

30
Q

Treatment of Metabolic Acidosis

A

1) Treat UNDERLYING CAUSE
2) Treat of CV Compromise; pH Less than 7.2, HCO3 less than 10

3) HCO3 DEFICIT:
= Desired HCO3 - Measured HCO3 x (0.5 x wt in kg)****

4) Treat NaHCO3:
- 1 amp 8.5%, 50 mEq/ 50cc
- Tablets, 650 mg

31
Q

Case #4

A 46‐year‐old Hispanic male presents to your office with WEAKNESS and a one week history of VOMITING. He states he is NOT BEEN ABLE TO DRINK water, tea or soup without vomiting. HE HASNT EATEN ANY SOLID FOOD for the past six (6) days. He denied diarrhea, or hematemesis. He did admit to CHILLS, malaise and “FELT HOT”, but didn’t take his temperature. His past medical history in unremarkable. Medications and allergies – none

PHYSICAL EXAM:
• BP 90/52, P 118/min., R 20/min.

  • Temp 101 °F, O2 Sat 90%
  • General appearance – DRY MUCOUS MEMBRANES, poor skin turgor with mild tenting
  • Neck veins are flat
  • Lungs – clear
  • Heart – no murmur, S3 or S4. Normal S1 and S2 splits on inspiration.
  • Abdomen – vitiligo areas on abdomen, no distention or organomegaly
  • Extremities – no edema, normal temperature to touch, no rashes
  • Neurologic ‐ normal

TESTS:
• CBC, Hb 16.5, Hct 49%, WBC 11,500

  • CMP: Na 130, CL 88, K 3.0, HCO3 31
  • Urine CL 10 meq/L
  • Stool hem occult negative
  • Blood cultures – pending
  • ABGs: pH 7.5, pCO2 45, pO2 90, HCO3 31
A

Differential Diagnosis?
1) VOMITING complicated by VOLUME CONTRACTION

2) HYPOTENSION, TACHYCARDIA Secondary VOLUME LOSS
3) FEVER: R/O Intestinal Infection

ABG Interpretation:
- METABOLIC ALKALOSIS (Due to Vomiting with CONTRACTION ALKALOSIS aka VOLUME LOSS)

TREATMENT:
- IV Fluids (0.9% N/S with KCl) to replenish VOLUME LOSS and DEHYDRATION

32
Q

Metabolic Alkalosis

A
  • INCR pH, INCR (Greatly) HCO3, INCR paCO2
  • Compensate paCO2 INCR 0.7 for every 1 INCR in HCO3 ****
  • Causes “CLEVER PD” !!!!!!!!!!!
  • Cl LOSS or HCO3 EXCESS
  • Volume Contraction
  • Cl LOSS: VOmiting, N/G Suction, Villous Adenoma, Diuretics
  • HCO3 EXCESS: Enhanced HCO3 Resorption (Hyperaldosterone, LICORIDE EXCESS)
33
Q

Metabolic Alkalosis

“CLEVER PD”

A

C: CONTRACTION of Volume

L: LICORICE

E: Endocrine (CONNS, Cushing’s, Bartters)

V: VOMITING

E: Excess Alkali

R: Refeeding ALKALOSIS

P: Post HYPERCAPNIA

D: DIURETICS

34
Q

Metabolic Alkalosis 2 Types

A

1) CHLORIDE RESPONSIVE:
- Urine Cl is LESS THAN 10 to 20 mEq/ L

  • Improves with NaCl and Volume
  • DECR Serum Cl and Volume Contraction
  • Vomiting, NG Suction, Diuretics

2) CHLORIDE UNRESPONSIVE:
- Urine Cl GREATER THAN 10 to 20 mEq/ L

  • UNRESPONSIVE to saline
  • Endocrine Causes: Cartters, Severe K+ Depletion, HYPERAldosteronism, Cushing’s
35
Q

Treatment for Metabolic Alkalosis

A

1) Treat UNDERLYING CAUSE
2) NaCl, KCl, and Magnesium
3) SPIRONOLACTOEN for Mineralcorticoid Excess

36
Q

Case #5

A 52‐year‐old female, who is an established patient of yours, presents to the office with a chief complaint of “I FEEL WEAK ALL OVER”. She has had this complaint on other office visits. She is being followed for treatment of HYPERTENSION, however, her BP has been more RESISTANT TO CONTROL despite medications. She is taking a BETA BLOCKER, an ACEI and a VASODILATOR. She does not smoke, or take hormones or use NSAID. She drinks 1‐2 glasses of wine every 2‐3 weeks.

PHYSICAL EXAM:
• BP 168/ 104, P 84/min., R 14/min
• Temp 98.6°F, O2 sat 94%
• DIFFUSE MUSCLE WEAKNESS is noted in hands,arms, and legs
• The remainder of the exam is normal
TESTS:
• CMP – Na 140 meq, K 2.7 meq., CL 102 meq
• HCO3 30 meq
• Mg, Ca – Normal
• BUN 20 mg creatinine 1.0 meq
• ECG (slide)
• CBC – normal
• TSH – normal

ABGs:
- pH 7.5, PCO2 48, pO2 90, HCO3 29

Other Tests:;
• Urine Chloride – HIGH >20
• Aldosterone level – HIGH
• Plasma Renin level‐ LOW

A

Differential Diagnosis:

1) DIFFUSE MSUCLE WEAKNESS:
a) HYPOTHYROIDISM

b) ELECTROLYTE DISORDER- LOW levels of :
- Na
- K
- Magnesium
- Calcium

2) HYPERTENSION becoming RESISTANT TO TREATMENT

ABGs:

  • METABOLIC ALKALOSIS
  • ** HYPOKALMEIA

New Diagnosis after OTHER TESTS:
1) Combination fo HYPERTENSION, HYPOKALEMIA

2) METABOLIC ALKALOSIS
3) HYPERALDOSTERONISM (CONN’S SYNDROME)

37
Q

Conn’s Syndrome

A
  • Primary HYPERALDOSTERONISM
  • MINERALCORTICOID EXCESS
  • Saline RESISTANT (Urine Cl GREATER THAN 20)
  • INCREASED HCO3 EXCRETION in URINE
38
Q

Treatment for Conn’s Syndrome

A

1) CT of Adrenals
2) ADENOMA (Solitary) 85%————-> LAPAROSCOPIC EXCISION
3) BILATERAL HYPERPLASIA (15%)—–> SPIRONOLACTONE!!!!!!
4) CORRECT HYPOKALEMIA!!!!!

39
Q

Case #6

A 74‐year‐old who presents to the emergency department with DYSPNEA, COUGH and FEVER. Onset of problems was six (6) days ago. Cough is productive of YELLOW-GREENISH SPUTUM. The DYSPNEA IS AT REST and on any exertional activity. He states his temperature has been up to 101°F, with accompanying shaking chills.
• PMH is pertinent for COPD, oxygen dependent, DJD and IBS. He continues to SMOKE 1⁄2 ppd of cigarettes!!!!!!

• Medications – Spiriva inhaler two (2) puffs daily, Symbicort MDI two (2) puffs BID, aerosol nebulizer with albuterol with N/S 3‐4x/day and Prednisone 20 mg po daily for past six (6) months

PHYSICAL EXAM:
• Generally appears to have RESPIRATORY DISTRESS, using accessory muscles of respiration. Breathing is RAPID (26‐28 x/min.) and SHALLOW, lips are pursed.

  • BP 110/70, P 120 irregular/min., R 28/min., Temp 101F, O2 sat 70% (on ambient aka room air)
  • Neck veins DISTENDED

• Lungs ‐ ↓ breath sounds bilaterally with suspected
crackles left lung lower lobe

  • Heart – IRREGULAR rhythm, RAPID RATE (approx 120/min) no obvious murmur
  • Abdomen – thin, no organomegaly, decreased bowel sounds, non‐distended, scar RLQ
  • Extremities – nicotine stain on fingers. Feet are cool with bluish colored toes, no pulses in either foot are palpable.
  • Neuro – Brisk reflexes arms and legs.
  • No cranial nerve deficit. Alert and oriented

TESTS:
• CXR (Incr AP Diametet)

  • EKG (Peaked T Waves)
  • CBC – WBC 17,500, Hb 12, Hct 36
  • CMP – Na 130, K 3.8, CL 102, HCO3 29, BUN 54, creatinine 1.4
  • Sputum – epithelial cells, no WBC’s
  • Blood cultures ‐ pending

ABGs:
- pH 7.14, pCO2 70, pO2 50, HCO3 29

A

Diagnosis:
1) Probable PNEUMONIA, CAP (Community Acquired Pneumonia): Immunosuppressed DUE TO Chronic Steroid Use

2) EXACERBATION of COPD Secondary to INFECTION
3) TOBACCO ADDICTION
4) Peripheral Vascular Disease SECONDARY to ARTERIAL SCLEROSIS OBLITERATIONS (PVD Secondary to ASO)

ABGs:
- RESPIRATORY ACIDOSIS (Acute) with HYPOXIA

40
Q

Respiratory Acidosis

A
  • DECR pH, INCR (Greatly) paCO2, INCR HCO3
  • Anything that causes HYPOVENTILATION or CNS DEPRESSIOn: Drugs, CVA, Neuromuscular Airway Obstruction, Pneumonia, Pulmonary Edema, Pneumothorax, Pleural Disease, COPD, Restrictive Disease (Disorders of the Chest Wall, Resp Muscles)
41
Q

Treatment for Respiratory Acidosis

A

1) ADMIT to the Hospital (ICU) Cardiac Monitor and CONTINUOUS OXIMETRY
2) AEROSOL Treatments, every 4 hr around the Clock (Beta Agonists, Inhaled Steroids)
3) NASAL and ORAL Tracheal Suction Prn
4) If AIRWAY compromised or gases worsen, BiPAP or CPAP, may need INTUBATION and Mechanical Ventilation
5) IV Steroids: Methylprednisolone 125 mg. IV
6) Sputum for Gram Staina dn C&S
7) Blood Cultures: Pending
8) Begin IV Antibiotics with coverage AGAINST Community Acquired Pathogens

42
Q

Case #7

A 21‐year‐old female college student presents to the emergency department with a history of RIGHT FLANK PAIN, FEVER, CHILLS and dyspnea. She has biochemistry test in the morning.

No significant PMH

PHYSICAL EXAM:
• BP 100/68, P 110/min., R 28/min., Temp 100°F, O2 sat 89%

  • Neck – THYROID ENLARGED, non tender, no JVD
  • Lungs – clear
  • Heart – no murmur, S3 or S4. Soft 1/6 systolic murmur over apex
  • Abdomen – soft, no guarding or rigidity. Decreased bowel sounds. TENDERNESS to light percussion/palpation over the RIGHT COSTOVERTEBRAL ANGLE (Right flank)
  • Extremities – warm, but no rash
  • Neurologic – Brisk DTR’s (2+/4) bilaterally; slight tremor of hands
What TESTs?
• CBC
• CMP
• Blood cultures
• UAwithC&S
• TSH,freeT4
• Renalultrasound,CTofabdomen 
• ABG’s

Interpretation of TESTS:
• CBC – Hb 15, Hct 45, WBC 21,000 – INFECTION

  • CMP – normal
  • Blood cultures – pending
  • TSH DECR, free T4 INCR
  • UA – TNTC WBC’s in urine, CLOUDY and NITRATE POSITIVE
  • C & S pending
  • Renal Ultrasound:
  • L Kidney normal
  • R kidney mildly ENLARGED!!!!

ABGs:
- pH 7.56, pCO2 20, pO2 89, HCO3 20

A

Diagnosis:
1) Probably UTI (Pyelonephritis)

Differentail Diagnosis:

  • Sepsis
  • Renal Abscess
  • HYPERVENTIALTION
  • R/O Hyperthyroidism

ABGs:
- RESPIRATORY ALKALOSIS (Acute)

Why is she Breathing so fast?
- ? Septic: Pyelonephritis, Renal Abscess

  • ? Hyperthyroid
  • ? Anxiety: Biochemistry Test
  • Pain/ Fever

TREATMENT:
- IVs to HydrateN/S

  • IV Antibiotics
  • CT of Abdomen and Pelvis
  • NOTE: Respiratory HYPERVENTILATION may also be DUE TO INFECTION (Sepsis)
  • Other factors include HYPERTHYROIDISM and ANXIETY
43
Q

Respiratory Alkalosis

“CHAMPS”

A
  • INCR pH
  • DECR (Greatly) paCO2
  • DECR HCO3

C: CNS Disease

H: HYPOXIA

A: ANXIETY

M: Mechanical Ventilation

P: PROGESTERONE

S: Salicylates/ Sepsis/ Stress