The 3-Step Approach to Acute Hyperkalemia

1. Stabilize: the Heart (If ECG changes) → Calcium

2. Shift: K+ Into Cells → Insulin + Glucose, Albuterol, Bicarb (if acidotic)

3. Send-it: Remove K+ From Body → Diuretics (if making urine), Kayexalate (if GI motility intact), Dialysis (if severe/refractory)

I – IV Fluids

C – Calcium

B – Beta-2 Agonists

B – Bicarbonate

I – Insulin & Glucose

K – Kayexalate (Sodium Polystyrene Sulfonate)

D – Diuretics

D – Dialysis

1. First Step: Assess ECG & Risk of Arrhythmia

• Peaked T waves, QRS widening, sine wave = Give Calcium ASAP

• Calcium doesn’t lower K+, but it prevents cardiac arrest.

2. Temporary vs. Definitive Treatments

• Shifting K+ into cells (Beta-agonists, Bicarb, Insulin) buys time.

• Excreting K+ (Diuretics, Dialysis, Kayexalate) removes K+.

3. Timing of Interventions:

• Calcium: Immediate (stabilizes heart).

• Insulin/Albuterol/Bicarb: 15–30 min (shifts K+).

• Diuretics/Kayexalate: 1–6 hours (removes K+).

• Dialysis: Immediate, definitive.

4. Common Pitfalls & Pro Tips

• Insulin can cause hypoglycemia – recheck glucose in 30 minutes.

• Albuterol requires high doses – typical 2.5 mg nebs won’t cut it.

• Bicarb only works if acidotic – don’t rely on it in normotensive patients.

• Kayexalate is slow & controversial – consider patiromer or zirconium cyclosilicate instead in chronic cases.

• If oliguric or ESRD → Straight to dialysis.

USED CARS mnemonic for non-anion gap metabolic acidosis (NAGMA):

Why “USED CARS”?

• Ureterosigmoidostomy

• Saline & Chloride infusion (excessive).. chloride offsets AG

• Endocrine disorders (Addison’s disease aka adrenal insufficiency, hypoaldosteronism)

• Diarrhea

• Carbonic anhydrase inhibitors

• Ammonium chloride

• Renal tubular acidosis

• Spironolactone

⸻

U – Ureteroenteric fistula (or diversion surgery)

• Why NAGMA?

• Ureter attached directly to colon; bicarbonate lost into bowel, chloride absorbed, causing hyperchloremic acidosis.

• Symptoms:

• History of bladder/colon surgery, urine-like smell from stool, chronic acidosis.

• Labs: Normal AG, elevated chloride, chronic metabolic acidosis.

• ED Management:

• Identify, refer to urology or general surgery for definitive repair.

• Correct electrolyte disturbances (usually potassium, bicarbonate).

⸻

S – Saline Infusion (Excessive)

• What: Excessive infusion of normal saline (0.9% NaCl).

• Why (Pathophysiology): High chloride content of NS dilutes bicarbonate → hyperchloremic metabolic acidosis (common in hospitalized patients).

• Symptoms: Usually subtle (fatigue, mild confusion, fluid overload signs).

• Labs: Normal AG, hyperchloremia, normal renal function initially.

• ED Management:

• Switch to balanced solutions (Lactated Ringer’s, Plasmalyte).

• Monitor fluid and electrolyte balance.

⸻

E – Endocrine Disorders (Addison’s Disease/Adrenal Insufficiency):

• Why: Lack of aldosterone = inability to excrete acid & retain sodium.

• Clinical Clues: Weakness, fatigue, low BP, dizziness, hyperpigmentation (skin darkening), abdominal pain.

• Labs: Low sodium, high potassium, normal anion gap, metabolic acidosis.

• ED Management:

• IV fluids (Normal saline), hydrocortisone, monitor electrolytes closely.

• Admit for adrenal crisis management.

⸻

D – Diarrhea

• Pathophysiology: Loss of bicarbonate-rich fluids via stool → bicarbonate depletion.

• Clinical Clues: Frequent watery stools, dehydration signs (tachycardia, low BP).

• Labs: Normal anion gap, hypokalemia common, hyperchloremia.

• ED Management:

• Aggressive fluid resuscitation (often NS or LR).

• Electrolyte replacement (especially potassium).

⸻

C – Carbonic Anhydrase Inhibitors (Acetazolamide)

• Mechanism: Prevent bicarbonate reabsorption → bicarbonate loss → acidosis.

• Clinical clues: Medication history (glaucoma treatment, altitude sickness prophylaxis, idiopathic intracranial hypertension).

• Labs: Normal AG, mild hypokalemia, mild hyperchloremia.

• ED Management:

• Stop offending medication, supportive care, and electrolyte replacement.

⸻

A – Ammonium Chloride Ingestion

• Mechanism: Direct chloride ingestion overwhelms bicarbonate buffers.

• Rare cause today, often historical or industrial exposure.

• Clinical clues: History of ingestion, occupational exposures, metabolic symptoms (nausea, vomiting, confusion).

• Labs: Normal AG, hyperchloremia.

• ED Management:

• Supportive care, stop exposure.

• Correct metabolic acidosis if severe (sodium bicarbonate IV if severe).

⸻

R – Renal Tubular Acidosis (RTA)

• Mechanism: Kidneys fail to reabsorb bicarbonate or excrete acid properly.

• Bicarbonate replacement.

• Potassium correction (careful monitoring).

• Referral to nephrology.

⸻

R – Renal Tubular Acidosis (Already covered above)

• Included in detail in the “A” section, given its complexity.

⸻

S – Spironolactone (and other Aldosterone Antagonists)

• Mechanism: Blocks aldosterone receptors → reduced acid and potassium excretion.

• Clinical clues:

Use in CHF, cirrhosis, hypertension treatment.

• Hold spironolactone, manage hyperkalemia aggressively (calcium gluconate, insulin/dextrose, albuterol, kayexalate).

• Consider bicarbonate if severely acidotic.

The GOLD MARK causes are divided into three major pathophysiologic groups based on the source of the acid production:

1. Alcohols (Toxic Ingestions) → Emergency Toxins

• Glycols → Ethylene glycol (antifreeze) and propylene glycol

• Methanol → Windshield washer fluid, homemade alcohol substitutes

• Why grouped together?

• Common in suicide attempts, accidental ingestions, or chronic alcoholics.

• Key labs: Serum osmolality, anion gap, osmolar gap.

• Imaging: Calcium oxalate crystals on urine microscopy (ethylene glycol).

• Treatment: Fomepizole or ethanol (blocks alcohol dehydrogenase), hemodialysis in severe cases.

2. OTCs & Medication-Related Causes → Common but Easily Missed

• Oxoproline → Chronic acetaminophen (Tylenol) use, often in malnourished patients

• Aspirin → Salicylates, including bismuth subsalicylate (Pepto-Bismol)

• Why grouped together?

• Often overlooked in chronic users or the elderly.

• Key signs: Tachypnea (respiratory alkalosis), tinnitus (aspirin), altered mental status.

• Key labs: Salicylate level, ABG (mixed acid-base disorder).

• Treatment: Alkalinization (sodium bicarb drip), dialysis for severe cases.

3. Metabolic Causes → Endogenous Acid Production

• L-lactate → Type A (ischemia), Type B (mitochondrial dysfunction)

• D-lactate → Short gut syndrome, bacterial overgrowth

• Renal Failure → Uremia, organic acids

• Ketones → Starvation, alcohol, diabetic ketoacidosis (DKA)

• Why grouped together?

• These involve internal production of acids due to organ dysfunction.

• Key labs:

• Lactate level (for sepsis, ischemia).

• BHB (beta-hydroxybutyrate) for DKA.

• BUN/Cr for renal failure.

• Urinalysis (ketones, glucose, uremia markers).

• Treatment:

• Fluids, treat underlying cause (DKA → insulin drip, renal failure → dialysis).

Clinically Important Considerations for EM Physicians

In the ED, when a patient has metabolic acidosis with an elevated anion gap, think:

1. What is the patient’s history?

• Suicide attempt or confusion? → Alcohols, aspirin

• Chronic Tylenol use or malnourished? → Oxoproline

• Sepsis, shock, ischemia? → L-lactate

• Short gut, diarrhea, recent antibiotics? → D-lactate

• Known diabetes, alcoholism, or fasting? → Ketones

• Chronic kidney disease? → Uremia

2. What tests should I order immediately?

• ABG/VBG → Confirms metabolic acidosis.

• Anion gap calculation → Determines if the acidosis is anion gap or non-anion gap.

• Serum osmolality & osmolar gap → Alcohol toxicity (ethylene glycol, methanol).

• Lactate level → Sepsis, ischemia, mitochondrial dysfunction.

• BHB (Beta-hydroxybutyrate) → DKA vs. alcoholic/starvation ketosis.

• Salicylate level & acetaminophen level → Toxic ingestion screening.

• CMP (BUN/Cr, glucose, liver enzymes, electrolytes) → Renal failure, DKA, liver dysfunction.

Takeaway: What’s an Emergency?

• Dialysis Emergencies → Methanol, ethylene glycol, severe aspirin toxicity, uremia.

• Toxin Emergencies → Alcohols (treat with fomepizole), salicylates (alkalinization & dialysis).

• Septic Shock / Tissue Hypoxia → Elevated L-lactate = immediate resuscitation with fluids & source control!

• DKA → Fluids, insulin drip, and monitor for electrolyte shifts (esp. potassium).

Mister Ronald McDonald (MR RM) is a helpful flowchart for interpreting acid-base disorders, specifically for determining whether a patient’s condition is due to a metabolic (M) or respiratory (R) cause:

1. Check the pH (7.4 is the cutoff)

• pH > 7.4 → Alkalosis

• pH < 7.4 → Acidosis

2. Assess Carbon Dioxide (CO₂) Levels (PaCO₂)

• The key threshold is 40 mmHg:

• If CO₂ > 40 mmHg, this suggests respiratory acidosis or metabolic alkalosis.

• If CO₂ < 40 mmHg, this suggests respiratory alkalosis or metabolic acidosis.

3. Determine the Cause

• In Alkalosis:

• If CO₂ > 40, the cause is Metabolic (M) Alkalosis.

• If CO₂ < 40, the cause is Respiratory (R) Alkalosis.

• In Acidosis:

• If CO₂ > 40, the cause is Respiratory (R) Acidosis.

• If CO₂ < 40, the cause is Metabolic (M) Acidosis.

Key Takeaway

• The chart helps determine whether a patient’s acid-base imbalance is due to a metabolic or respiratory cause by analyzing pH and CO₂ levels.

To determine if the patient requires admission or can be discharged, the Glasgow-Blatchford Score (GBS) is used.

Here’s the ABCDEF mnemonic and why these factors increase the risk of an upper GI bleed:

• ​ A - Active: Conditions like syncope or melena indicate ongoing or significant bleeding, increasing risk severity.

• ​ B - Blood Urea Nitrogen: Levels ≥ 7 mg/dL suggest impaired kidney function, which is often associated with poor systemic clearance and bleeding risk.

• ​ C - Circulation: A systolic blood pressure ≥ 110 mm Hg may reflect hemodynamic instability or stress response to bleeding.

• ​ D - Drop in Hemoglobin: Hemoglobin levels ≤ 12.9 g/dL (men) or ≤ 11.9 g/dL (women) indicate anemia, suggesting significant blood loss.

• ​ E - Elevated Pulse: A pulse rate ≥ 100/min signals compensatory tachycardia, often a response to blood loss.

• ​ F - Failure: Cardiovascular or liver disease impairs clotting and hemodynamic stability, exacerbating bleed risk.

Developed in Scotland, the GBS is a risk assessment tool for upper GI bleeds and considers symptoms, vital signs, and lab values on admission. Key factors in the score include melena, syncope, liver disease, heart failure, heart rate, blood pressure, hemoglobin, and BUN levels. Points are assigned based on these variables to assess the severity of bleeding and volume loss.

For example:

• ​Melena suggests significant GI bleeding, whereas isolated hematemesis (like coffee-ground emesis) has no scoring points.
• ​Syncope, tachycardia, hypotension, and changes in Hb/BUN levels suggest volume loss.
• ​Comorbid conditions (e.g., liver disease) may indicate a need for admission, especially if variceal bleeding is suspected.

Discharge criteria also include access to follow-up care, a support system, and a nearby hospital for emergency returns if symptoms worsen.

For more on current recommendations, consult the 2021 American Journal of Gastroenterology guidelines on upper GI bleeding.

CENTOR criteria Fever PAIN: Strep Throat mnemonic

The “H’s and T’s” refer to a mnemonic used in medicine to help healthcare professionals quickly recall the most common causes of cardiac arrest during a code (a medical emergency requiring CPR). Memorizing these is crucial because identifying and addressing these causes rapidly can improve the chances of saving a patient’s life.

Here’s a breakdown:

The H’s: OK TV

Hypoxia - Lack of oxygen to tissues can lead to a heart stopping, so ensuring proper oxygenation is key.

Hypo-/Hyperkalemia - Abnormal potassium levels affect the heart’s electrical activity, potentially causing it to stop.

Hypothermia - Low body temperature can slow heart function and lead to cardiac arrest.

Hypovolemia - Loss of blood or fluids can lead to insufficient circulation and cardiac arrest.

Hydrogen ion (acidosis) - A build-up of acid in the blood (often due to respiratory failure or shock) can disrupt heart function.

The T’s: THROW TEN TOXIC TAMPONS

Thrombosis (pulmonary or coronary) - Blood clots in the lungs (pulmonary embolism) or heart (myocardial infarction) can obstruct blood flow, leading to cardiac arrest.

Tension Pneumothorax - Air trapped in the chest cavity compresses the heart and lungs, affecting circulation.

Toxins - Certain substances (medications, drugs, poisons) can disrupt heart rhythms.

Tamponade (cardiac) - Accumulation of fluid around the heart prevents it from pumping effectively.

Importance of Memorizing the H’s and T’s:

These causes cover many reversible conditions that may lead to cardiac arrest. During a code, time is critical, so having these potential causes at the top of your mind helps quickly assess and treat the patient. Remembering the “H’s and T’s” mnemonic ensures that a healthcare provider methodically works through possible causes and provides the best chance of resuscitation.

These are the adventitious lung sounds Mneumonics.

Strider:

Everyone can take in stride.

Crackles:

A fine chap with firecrackers.

Wheezing:

Just ask any whale: Can you HAC the wheeze?

Rhonchi:

I BOPped the wrong guy

Plural friction rub:

PPP (3 words 3 P’s)

The “KEEP” mnemonic is a tool to remember the most common organisms causing urinary tract infections (UTIs). Here’s how the mnemonic breaks down, followed by key information relevant for emergency medicine boards:

K - Klebsiella species

• Relevance: Klebsiella is the second most common organism causing UTIs, especially hospital-acquired infections.

• Key Points:

• Gram-negative rod.

• Often seen in patients with underlying conditions like diabetes, or those with urinary catheters.

• Resistant to many antibiotics, so susceptibility testing is important.

• Treatment Options: Cephalosporins (like ceftriaxone), carbapenems in resistant cases.

E - Escherichia coli (E. coli)

• Relevance: The most common organism causing both community-acquired and some hospital-acquired UTIs.

• Key Points:

• Gram-negative rod.

• Responsible for approximately 70-90% of uncomplicated UTIs.

• Often originates from the gut.

• Can exhibit antibiotic resistance, particularly to trimethoprim-sulfamethoxazole.

• Treatment Options: Trimethoprim-sulfamethoxazole (Bactrim), nitrofurantoin, fosfomycin, or ciprofloxacin based on resistance patterns.

E - Enterococcus species

• Relevance: More common in complicated UTIs, particularly in hospital settings.

• Key Points:

• Gram-positive cocci.

• Often found in patients with catheters, immunocompromised status, or structural abnormalities in the urinary tract.

• Can be resistant to many antibiotics, including vancomycin-resistant Enterococcus (VRE).

• Treatment Options: Ampicillin or amoxicillin when susceptible; for resistant cases, vancomycin or linezolid.

P - Proteus species

• Relevance: Known for causing complicated UTIs and is associated with kidney stones.

• Key Points:

• Gram-negative rod.

• Produces urease, which increases urine pH and can lead to the formation of struvite stones.

• Can cause upper UTIs and is known to colonize catheters.

• Treatment Options: Ciprofloxacin, trimethoprim-sulfamethoxazole, cephalosporins; nitrofurantoin is usually not effective.

Summary of the Mnemonic ‘KEEP’

• Klebsiella: Second most common UTI organism; hospital-acquired; antibiotic resistance common.

• E. coli: Most frequent cause of UTIs; community-acquired; potential resistance to some antibiotics.

• Enterococcus: Complicated and hospital-acquired UTIs; often found in patients with urinary abnormalities.

• Proteus: Associated with kidney stones; catheter-related UTIs; produces urease.

By remembering “KEEP,” you can recall the key organisms responsible for UTIs and their relevance to diagnosis and treatment in emergency settings.

The **SPIT** mnemonic is used to help remember common causes of **altered mental status in children**. Here's what each letter stands for:

- **S**eizures: Includes both febrile and non-febrile seizures that can cause confusion or unconsciousness.

- **P**oisoning: Exposure to toxins or ingestion of substances like medications, household chemicals, or recreational drugs.

- **I**nfections: Infections such as meningitis, encephalitis, sepsis, or any systemic infection that can lead to altered mental status.

- **T**rauma: Head injuries, concussions, or other physical trauma leading to changes in consciousness.

This mnemonic helps quickly identify potential life-threatening causes of altered mental status in a pediatric patient.