Intensive Caring

15/02/2026

Sodium bicarbonate application for the
treatment of acute metabolic acidosis: what we
know and what we still don’t know


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13/02/2026

🗣️ "Calcium stabilizes the cardiac membrane."

You've probably heard this many times in classes or discussions regarding hyperkalemia, but what does it really mean?

The concentration of potassium is much higher inside the cell than outside the cell, adn that gradient is crucial to how cardiac cells (pacemaker and ventricular) operate.

When a patient's extracellular potassium increases beyond the normal parameter (~3.5-5.5mEq/L), the cardiac cell's resting membrane potential becomes less negative, but the depolarization threshold doesn't. This means that the diastolic action potential is super close to the depolarization threshold.

The long-lasting calcium channels barely have time to rest before they have to depolarize again, and for that reason, the pacemaker cells may stop. This is why P waves flatten or disappear in hyperkalemia. The cardiac myocytes rely more on fast sodium channels, which run into the same problem when the membrane doesn't spend enough time at a negative potential for them to rest.

Calcium increases the voltage requirement to depolarize, bumping the threshold and giving the sodium and calcium channels time to rest before the next beat. It only lasts for about 20 minutes though - so you may need to administer multiple doses if your transport is long.

12/02/2026

Helpful revisit of definitions and categories of physiological shock!

🩸 Shock: Types and Treatment

Shock is not a feeling.
It is a life-threatening failure of circulation resulting in inadequate oxygen delivery to tissues.

In simple terms:
Oxygen in + Blood flow = Life
If either part fails → shock develops.

The Four Main Types of Shock

Think of shock as a plumbing problem.
Something in the system has gone wrong.

1. Hypovolaemic Shock
The tank is empty
Cause: Loss of circulating volume
Haemorrhage
Dehydration
Burns
Vomiting/diarrhoea
Trauma
Signs:
Rapid pulse
Low blood pressure
Cool, pale, clammy skin
Reduced urine output
Confusion

Treatment:
Control bleeding
IV fluids
Oxygen
Rapid transport
Blood products if available

👉 Fix the leak and refill the tank.

2. Cardiogenic Shock
The pump has failed
Cause: The heart cannot pump effectively
Myocardial infarction
Arrhythmias
Heart failure
Valve problems

Signs:

Chest pain
Pulmonary oedema
Hypotension
Raised JVP
Cold peripheries

Treatment:

Oxygen
Treat the underlying cause
Aspirin / ACS pathway
Diuretics if fluid overloaded
Inotropes in hospital
👉 The pipes are fine, but the engine is broken.

3. Distributive Shock
The pipes are too wide
Blood volume is normal, but vessels dilate and pressure collapses.
Includes:
a) Septic Shock
Infection causing widespread vasodilation
b) Anaphylactic Shock
Severe allergic reaction
c) Neurogenic Shock
Spinal cord injury causing loss of vascular tone

Signs:

Warm flushed skin (early sepsis)
Low blood pressure
Tachycardia
Altered mental state

Treatment:

Oxygen
IV fluids
Adrenaline for anaphylaxis
Antibiotics for sepsis
Vasopressors in hospital
👉 The fluid is there, but it’s sloshing around in oversized pipes.

4. Obstructive Shock
Something is blocking the system
Causes:
Tension pneumothorax
Cardiac tamponade
Massive pulmonary embolism
Signs:
Sudden collapse
Distended neck veins
Chest pain
Severe breathlessness
Treatment:
Relieve the obstruction
Needle decompression (if indicated)
Rapid transport
Specialist intervention
👉 The pump works, the fluid is there, but the flow is blocked.

The Universal Management of Shock
Regardless of type, the initial approach is the same:

ABCDE – every time
Airway: maintain patency
Breathing: high-flow oxygen
Circulation: control bleeding, IV access, fluids
Disability: check GCS
Exposure: look for causes

Plus:

Keep the patient warm
Lie them flat if possible
Monitor vitals
Rapid transport to definitive care

The Golden Rule
Treat the patient, not just the monitor.
Shock is a dynamic process.
Early recognition saves lives.

Memory Aid
H.O.D.C
Hypovolaemic
Obstructive
Distributive
Cardiogenic

Bottom Line
If tissues don’t get oxygen, they die.
If shock isn’t reversed, the patient follows.
Recognise it early.
Treat it aggressively.
Find and fix the cause.

23/01/2026

This

22/01/2026

The Curve That Explains How Oxygen Is Released to Life

The oxygen–hemoglobin dissociation curve shows how strongly hemoglobin binds to oxygen at different oxygen concentrations. It has a unique S-shape, which is the secret of efficient oxygen transport. In the lungs, where oxygen level is high, hemoglobin binds oxygen tightly. In body tissues, where oxygen is low, hemoglobin releases it easily.

This curve shifts based on temperature, carbon dioxide, and pH. During exercise, when muscles produce more heat and CO₂, the curve shifts right, helping more oxygen get released. In calm conditions, it shifts left, holding oxygen more tightly.

It is not just a graph. It is the reason your blood knows when to carry oxygen and when to give it away. The dissociation curve proves that life depends on smart chemistry, not random binding.

22/01/2026

Cytokine storm


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16/01/2026

Icu colleagues.
The sodium anion

🧊 Chloride (Cl⁻): The Unsung Backup Dancer That Keeps the Rhythm

Normal Range: 98–106 mEq/L
Low: Hypochloremia
High: Hyperchloremia

⚡ Charge & Type

Charge: Negative → Anion
Type: Major extracellular anion

💃 Dancing Partner

Main Partner: Sodium (Na⁺), sometimes Potassium (K⁺).
They stick together to keep plasma electrically neutral and osmotic pressure balanced.

If Cl⁻ loses its partner: the acid–base balance goes sideways — you’ll see shifts in bicarbonate and hydrogen ions that can swing a patient from alkalosis to acidosis before you can find your ABG kit.

🔬 Pathophysiology Deep Dive

Chloride isn’t flashy, but it’s everywhere. It rides with sodium and helps control extracellular fluid volume, osmotic pressure, and pH. It’s part of hydrochloric acid in the stomach, helps CO₂ move as chloride shift (Hamburger phenomenon), and balances every positive charge in the blood.

Low Cl⁻ (Hypochloremia):
• Causes: vomiting, NG suction, loop diuretics, metabolic alkalosis.
• Lose chloride → kidneys hold bicarbonate → alkalosis worsens.
• Cells get confused; neurons start firing weirdly; patient gets twitchy or weak.

High Cl⁻ (Hyperchloremia):
• Causes: aggressive normal saline resuscitation, renal tubular acidosis, dehydration, or diarrhea.
• Excess chloride displaces bicarbonate → metabolic acidosis.
• You’ll see Kussmaul respirations, low pH, and maybe vasodilation-related hypotension.

❤️ Cardiac, Neuro & Systemic Effects
• Cardiac: Chloride indirectly affects rhythm through acid–base shifts. Hyperchloremic acidosis = decreased contractility and hypotension.
• Neuro: Acid–base imbalances alter neuronal firing; alkalosis → confusion, acidosis → lethargy.
• Muscle: Hypochloremia can cause weakness from pH-driven calcium shifts.
• Renal: Chloride’s the kidney’s barometer. If it’s off, tubular transport’s off acid–base regulation fails.
• GI: Chloride helps make stomach acid; low levels reduce gastric acidity, altering digestion.

💀 What Happens Without Its Partner

Without sodium or potassium to neutralize its negative charge, Cl⁻ floats free and the body scrambles to compensate. Hydrogen and bicarbonate ions shift to balance the pH, often leading to metabolic disturbances. It’s like pulling the drummer out of the band — everyone else starts missing the beat.

🧠 Why We Care

Because chloride’s the quiet stabilizer that nobody charts until it’s screaming.
Too low, and alkalosis sneaks up. Too high, and perfusion drops while acid builds.
Every liter of 0.9 NS you hang has 154 mEq/L of chloride you can literally cause acidosis trying to fix dehydration.
If sodium is the headline act, chloride’s the rhythm section keeping the patient’s chemistry from falling apart.

01/12/2025

Rapid sequence intubation (RSI) is a method for emergency tracheal intubation that involves the quick, successive administration of a sedative and a paralytic agent. It is the preferred method for critically ill or injured patients, especially those at risk of aspiration, to secure the airway quickly and safely. Key components include preoxygenation, a sedative agent for unconsciousness, and a neuromuscular blocking agent for muscle paralysis, followed by rapid laryngoscopy and endotracheal tube placement.

13/11/2025

14/09/2025

Very detailed and concise explanation of the Triad during Spinal coning
Important so you understand what you’re looking at
Elements of focus
Monroe Kellie Hypothesis
Increased intracranial pressure after cerebral auto regulation has been exhausted causes direct effect on Medulla….the primal cerebral functions of heart rate and respiratory rate.
Cardiac response of widening blood pressures (systolic rise with diastolic drop) - NEecessary cerebral perfusion pressure of 60 at least (equation is MAP - ICP = CPP)
Bradycardia due to systolic rise and or pressure on medulla or both. Remember if you are tachycardia with good ventricular stroke volume, your BP will rise, thus why some BP meds work by dropping heart rate, if that’s the source.
Finally, the altered breathing called Cheyne Stokes breathing. Deep irregular and infrequent breaths before coning of brain tissue through the Foramen Magnum, where spinal cord begins…… this triad in a remote area setting is the most challenging and mostly fatal event.
Mechanisms that cause this clinical crisis range from blunt force head injuries, to end stage liver failure, to sepsis, amongst other possible triggers.
For more detail on management of this often fatal scenario, look into the use of sedation and inotropic support used to flatten out cerebral activity , use of diuretic mannitol and manipulation of MAP to facilitate higher BP to counter the resistance from high ICPs.

06/08/2025

Best practice for Supraventricular Tachycardia

06/08/2025

RPAH ICU days….