Acid base disorders
Steps for interpretation:1. Acidemia or Alkalemia?2. Respiratory or Metabolic?3. Compensated? Acute or chronic?4. Anion gap? Delta-delta?5. Differentials?
ABG and BMP Normal values
pH 7.35-7.45
PaCO2 35-45 mmHg
PaO2 80-100 mmHg
HCO3 (on BMP) 22-26 mmol/L
Step 1: pH <7.35= Acidemia >7.45=Alkalemia
Step 2:
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pH pCO2
Metabolic Acidosis
Metabolic alkalosis
Resp Acidosis
Resp Alkalosis
Step 3:
Step 4: Anion Gap (AG) = {Na – (Cl + HCO3)} Normal = 12 +/- 2Corrected Anion Gap = AG + 2.5(4-albumin)Delta: Delta = AG-12
24-HCO3Delta: Delta Interpretation for metabolic acidosis
<0.4 Pure Normal AG metabolic acidosis
0.4-0.8 Normal + High AG metabolic acidosis
0.8-2.0 Pure High AG metabolic acidosis
>2.0 Metabolic acidosis with superimposed Metabolic alkalosis/Resp acidosis
Respiratory compensation Metabolic acidosis Metabolic alkalosis
Expected PCO2 (ABG) 1.5(HCO3) + 8 (+/-2) 40 + (HCO3-24)X0.7 (+/-5)
Additional disorder If PCO2 is greater than expected = additional respiratory acidosisIf PCO2 is lower than expected = additional respiratory alkalosis
Causes of High Anion Gap Metabolic acidosis
G Glycols - ethylene glycol “antifreeze” and propylene glycol (present in IV benzodiazepines)
O Oxoproline (associated with acetaminophen dosing)
L L-lactate (common form of lactate)
D D-lactate (short bowel syndrome, intestinal bacterial overgrowth, propylene glycol)
M Methanol
A Aspirin (salicylates)
R Renal failure (uremia)
K Ketoacidosis (starvation, diabetic)
Step 5:
Causes of Normal Anion Gap Metabolic acidosis
Diarrhea
Renal tubular acidosis/Chronic renal failure
Adrenal insufficiency
Rapid saline infusion
Acetazolamide
Causes of Metabolic Alkalosis
Vomiting, NG suction
Volume depletion (diuresis)
Mineralocorticoid excess
Causes of Respiratory acidosis
CNS depression (sedation, narcotics, CVA)
Neuromuscular weakness (GBS, Myasthenia gravis)
Obstructive or restrictive lung disease (COPD, OSA, Asthma, Obesity hypoventilation)
Airway obstruction (foreign body, aspiration)
Causes of Respiratory alkalosis
Hyperventilation (Anxiety, pain, fever, hypoxia)
“Classically” noted with pulmonary embolism (with associated hypoxia)
Salicylates
M. Daniyal Hashmi, MD@MDaniyalHashmi1 (twitter)
Troubleshooting
Basics of Mechanical Ventilation
Positive End Expiratory Pressure
M. Daniyal Hashmi, MD
ARDS - overview
Ven
tilator settin
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M. Daniyal Hashmi, MD
APRV - OverviewAirway pressure release ventilation (APRV) uses prolonged periods of high continuous positive airway pressures interrupted by brief episodes of pressure release to a lower pressure• Intended as a rescue therapy for severe ARDS (low lung compliance with
high oxygenation requirements)
Description• Two levels of airway pressure: P(high) and
P(low)• P(high) set at desired plateau pressure
(hence dictates arterial oxygenation and risk of alveolar baro/volutrauma)
• P(low) set to prevent de-recruitment of alveoli during pressure release
• T(high) (>85% of cycle time) determines time spent at P(high) to maintain alveolar recruitment
• T(low) determines time spent at P(low), very brief to prevent alveolar de-recruitment
P high
T high
Control Mean Airway Pressure
Pressure gradient
T low
Control ventilation
Improving oxygenation • Increase P(high) and T(high) to increase Mean airway pressure (pay attention to hemodynamics as increased thoracic pressures can decrease cardiac output)
• Increase Fio2• Ensure minimal de-recruitment (decrease T(low) and/or
increase P(low)
Improving Ventilation
• Increase pressure gradient: P(high) – P(low) to increase alveolar volume
• Adjust T(low) to allow for adequate expiratory time
• Increase frequency of pressure release
• Titrate sedation to allow for spontaneous breathing (allows for ventilation even during T high)
Suggested Initial settings
P(high) = Plateau pressure (Keep <30cmH20)
P(low) = 0-5 cmH20
T(high) = 4.5 – 6 seconds
T(low) = 0.5-0.8 seconds
-Modrykamien A, Chatburn RL, Ashton RW. Airway pressure release ventilation: an alternative mode of mechanical ventilation in acute respiratory distress syndrome. Cleve Clin J Med. 2011 Feb;78(2):101-10. doi: 10.3949/ccjm.78a.10032. Review. Erratum in: Cleve Clin J Med. 2011 Apr;78(4):240-Myers TR, MacIntyre NR. Respiratory controversies in the critical care setting. Does airway pressure release ventilation offer important new advantages in mechanical ventilator support? Respir Care. 2007 Apr;52(4):452-8; discussion 458-60-Putensen C, Wrigge H. Clinical review: biphasic positive airway pressure and airway pressure release ventilation. Crit Care. 2004 Dec;8(6):492-7
Advantages: Alveolar recruitment and improved oxygenation, preservation of spontaneous breathing, lower sedation requirements
Disadvantages: Risk of volutrauma, increased work of breathing and energy expenditure, consistently increased intrathoracic pressures may adversely affect hemodynamics
References:
M. Daniyal Hashmi, MD@MDaniyalHashmi1 (twitter)
Shock• Syndrome of impaired oxygen delivery to tissues• Mechanisms-Absolute/relative decrease in oxygen delivery-Ineffective tissue perfusion-Ineffective utilization of delivered oxygen
Septic shock
Cardiogenic shock
ExaminationManagement of Hypotension
M. Daniyal Hashmi, MD
General factsSpread: Droplet spread, survives 2-3 hours on most surfaces, 2 days on smooth metal/plastic
Incubation: 2-14 days1st week: Fever, cough, headache, fatigue, myalgias, pharyngitis2nd week: Resolves in 80%, Viral pneumonia 20%Risk increased: Heart/lung disease, immunosuppression, poorly controlled DMExam: Non specificLabs: Lymphopenia with normal WBC count or relative leukopenia, Elevated Ferritin/CRP/D-Dimer is negative prognostic indicatorMortality: Due to oxygenation failure or septic shock/multiorgan failureImaging:
Testing: CBC, CMP, ABG, Troponin, G6PD, Rapid flu testing and bacterial sputum and blood cultures (coinfection with BACTERIAL respiratory pathogens unlikely), Coronavirus PCR testing, CRP, Ferritin, D-DimerTreatment: Symptomatic support for stable patients otherwise refer to guidelines for critical care support-Currently under investigation (Plaquenil, Azithromycin and Remdesivir)
M. Daniyal Hashmi, MD
Per présentation by Dr. Leon Liang-Yu Lai, MD
Concerning levels on ABG
M. Daniyal Hashmi, MD