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Medical and surgical emergencies
Advanced cardiac life support (ACLS): Clinical (To be retired)
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Coronary artery disease: Clinical (To be retired)
Heart failure: Clinical (To be retired)
Syncope: Clinical (To be retired)
Pericardial disease: Clinical (To be retired)
Valvular heart disease: Clinical (To be retired)
Chest trauma: Clinical (To be retired)
Shock: Clinical (To be retired)
Peripheral vascular disease: Clinical (To be retired)
Leg ulcers: Clinical (To be retired)
Aortic aneurysms and dissections: Clinical (To be retired)
Cholinomimetics: Direct agonists
Cholinomimetics: Indirect agonists (anticholinesterases)
Muscarinic antagonists
Sympathomimetics: Direct agonists
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Loop diuretics
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Positive inotropic medications
Antiplatelet medications
Blistering skin disorders: Clinical (To be retired)
Bites and stings: Clinical (To be retired)
Burns: Clinical (To be retired)
Diabetes mellitus: Clinical (To be retired)
Hyperthyroidism: Clinical (To be retired)
Hypothyroidism and thyroiditis: Clinical (To be retired)
Parathyroid conditions and calcium imbalance: Clinical (To be retired)
Adrenal insufficiency: Clinical (To be retired)
Neck trauma: Clinical (To be retired)
Insulins
Mineralocorticoids and mineralocorticoid antagonists
Glucocorticoids
Abdominal pain: Clinical (To be retired)
Appendicitis: Clinical (To be retired)
Gastrointestinal bleeding: Clinical (To be retired)
Peptic ulcers and stomach cancer: Clinical (To be retired)
Inflammatory bowel disease: Clinical (To be retired)
Diverticular disease: Clinical (To be retired)
Gallbladder disorders: Clinical (To be retired)
Pancreatitis: Clinical (To be retired)
Cirrhosis: Clinical (To be retired)
Hernias: Clinical (To be retired)
Bowel obstruction: Clinical (To be retired)
Abdominal trauma: Clinical (To be retired)
Laxatives and cathartics
Antidiarrheals
Acid reducing medications
Blood products and transfusion: Clinical (To be retired)
Venous thromboembolism: Clinical (To be retired)
Anticoagulants: Heparin
Anticoagulants: Warfarin
Anticoagulants: Direct factor inhibitors
Antiplatelet medications
Thrombolytics
Fever of unknown origin: Clinical (To be retired)
Infective endocarditis: Clinical (To be retired)
Pneumonia: Clinical (To be retired)
Tuberculosis: Pathology review
Diarrhea: Clinical (To be retired)
Urinary tract infections: Clinical (To be retired)
Meningitis, encephalitis and brain abscesses: Clinical (To be retired)
Bites and stings: Clinical (To be retired)
Skin and soft tissue infections: Clinical (To be retired)
Protein synthesis inhibitors: Aminoglycosides
Antimetabolites: Sulfonamides and trimethoprim
Antituberculosis medications
Miscellaneous cell wall synthesis inhibitors
Protein synthesis inhibitors: Tetracyclines
Cell wall synthesis inhibitors: Penicillins
Miscellaneous protein synthesis inhibitors
Cell wall synthesis inhibitors: Cephalosporins
DNA synthesis inhibitors: Metronidazole
DNA synthesis inhibitors: Fluoroquinolones
Herpesvirus medications
Azoles
Echinocandins
Miscellaneous antifungal medications
Anthelmintic medications
Antimalarials
Anti-mite and louse medications
Hypernatremia: Clinical (To be retired)
Hyponatremia: Clinical (To be retired)
Hyperkalemia: Clinical (To be retired)
Hypokalemia: Clinical (To be retired)
Metabolic and respiratory acidosis: Clinical (To be retired)
Metabolic and respiratory alkalosis: Clinical (To be retired)
Toxidromes: Clinical (To be retired)
Medication overdoses and toxicities: Pathology review
Environmental and chemical toxicities: Pathology review
Acute kidney injury: Clinical (To be retired)
Kidney stones: Clinical (To be retired)
Adrenergic antagonists: Alpha blockers
Stroke: Clinical (To be retired)
Seizures: Clinical (To be retired)
Headaches: Clinical (To be retired)
Traumatic brain injury: Clinical (To be retired)
Neck trauma: Clinical (To be retired)
Lower back pain: Clinical (To be retired)
Spinal cord disorders: Pathology review
Anticonvulsants and anxiolytics: Barbiturates
Anticonvulsants and anxiolytics: Benzodiazepines
Nonbenzodiazepine anticonvulsants
Migraine medications
Osmotic diuretics
Antiplatelet medications
Thrombolytics
Opioid agonists, mixed agonist-antagonists and partial agonists
Opioid antagonists
Asthma: Clinical (To be retired)
Chronic obstructive pulmonary disease (COPD): Clinical (To be retired)
Venous thromboembolism: Clinical (To be retired)
Acute respiratory distress syndrome: Clinical (To be retired)
Pleural effusion: Clinical (To be retired)
Pneumothorax: Clinical (To be retired)
Chest trauma: Clinical (To be retired)
Bronchodilators: Beta 2-agonists and muscarinic antagonists
Pulmonary corticosteroids and mast cell inhibitors
Joint pain: Clinical (To be retired)
Anatomy clinical correlates: Clavicle and shoulder
Anatomy clinical correlates: Axilla
Anatomy clinical correlates: Arm, elbow and forearm
Anatomy clinical correlates: Wrist and hand
Anatomy clinical correlates: Median, ulnar and radial nerves
Anatomy clinical correlates: Bones, joints and muscles of the back
Anatomy clinical correlates: Hip, gluteal region and thigh
Anatomy clinical correlates: Knee
Anatomy clinical correlates: Leg and ankle
Anatomy clinical correlates: Foot
Acetaminophen (Paracetamol)
Non-steroidal anti-inflammatory drugs
Glucocorticoids
Opioid agonists, mixed agonist-antagonists and partial agonists
Antigout medications
Metabolic and respiratory alkalosis: Clinical (To be retired)
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of complete
Elizabeth Nixon-Shapiro, MSMI, CMI
Kaia Chessen, MScBMC
Anca-Elena Stefan, MD
In metabolic alkalosis, the blood pH is above 7.45, and it’s due to a bicarbonate or HCO3 concentration in the blood over 27 mEq/L.
Individuals with metabolic alkalosis can be asymptomatic or can cause hypoventilation, due to respiratory compensation.
Associated symptoms are related to the underlying cause.
For example, if there’s a history of vomiting, nasogastric suction, laxative abuse or use of loop or thiazide diuretics, then there may be symptoms of dehydration.
The diagnosis is usually based on an ABG, and in addition to a pH above 7.45, and HCO3 levels above 27 mEq/L, if there’s respiratory compensation, the pCO2 is usually above 45 mm Hg.
Generally, for every 1 mEq/L elevation in HCO3 above the normal level of 27 mEq/L, pCO2 increases by about 0.7 mm Hg above the normal level of 45 mm Hg, but pCO2 doesn’t usually rise above 55 mm Hg, regardless of HCO3 levels.
Let’s take an example and say that HCO3 level is 30 mEq/L - so it’s 3 mEq/L above the baseline.
This means that our pCO2 should be 45- which is the baseline for pCO2- plus 3 times 0.7, which equals 47.1 mm Hg.
In addition, electrolytes are also done to see if there’s any imbalances, like hypokalemia.
Now, if the cause of metabolic alkalosis isn’t obvious from the history, then a spot urine chloride is measured.
If the urine chloride is below 20 mEq/L, that suggests volume depletion from a variety of causes like vomiting which leads to loss of hydrochloric acid, so the treatment is really aimed at addressing the underlying cause of vomiting.
A related cause is aggressive nasogastric suction, so the treatment is stopping or slowing the removal of gastric secretions.
Another cause is loop or thiazide diuretics which block hydrogen ion and chloride ion reabsorption in the kidney.
Chloride is a negatively charged ion, so loss of chloride leads to increased reabsorption of bicarbonate to compensate for the loss.
The loss of chloride causes the urine chloride to go above 20 mEq/L, and a lot of hydrogen is lost-leading to metabolic alkalosis.
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