Nurse Perpy's Diary

One electrolyte imbalance can completely change the ECG!
Peaked T waves? Flattened T waves? Prolonged QT? These ECG clues may point you straight to an electrolyte imbalance.
Save this quick guide and learn the patterns they’re important for both NCLEX and clinical practice.

**HEART BLOCK:
What Every Nurse Should Know!**

Heart block occurs when electrical impulses travelling from the atria to the ventricles are delayed or interrupted.

**Know the key ECG differences:**

**1st Degree:** PR interval > 0.20 seconds. Every P wave is followed by a QRS complex.

**2nd Degree Type I (Mobitz I):** PR interval progressively lengthens until a QRS complex is dropped.

**2nd Degree Type II (Mobitz II):** PR interval remains constant, but some P waves are not followed by QRS complexes. This can progress to complete heart block.

**3rd Degree (Complete Heart Block):** No electrical relationship between P waves and QRS complexes. The atria and ventricles beat independently.

Remember:
- First degree = DELAYED conduction.
- Mobitz I = LONGER, LONGER, DROP!
- Mobitz II = SUDDEN DROP!
- Third degree = COMPLETE DISCONNECTION!

**Nursing priority:**

Assess the patient, not just the ECG! Monitor heart rate, blood pressure, consciousness and signs of poor perfusion. Symptomatic high-grade heart block requires urgent escalation and may require pacing.

Renin–Angiotensin–Aldosterone System (RAAS) is one of the important physiological mechanisms we need to understand, particularly when studying hypertension, heart failure, acute kidney injury (AKI), fluid balance and antihypertensive medications.

I'll explain it in a simple, NCLEX-friendly way.

How the RAAS system works

RAAS is a hormonal system that helps the body regulate blood pressure, circulating blood volume and sodium balance.

It is activated when the kidneys detect reduced blood pressure, reduced renal perfusion or reduced sodium chloride delivery.

The process, step by step

1\. Renin: The kidneys release renin in response to reduced renal perfusion, sympathetic stimulation or reduced sodium chloride delivery to the macula densa.

2\. Angiotensinogen: Renin converts angiotensinogen (produced by the liver) into angiotensin I.

3\. ACE: Angiotensin-converting enzyme (ACE), found particularly in vascular endothelium, including the lungs, converts angiotensin I into angiotensin II.

4\. Angiotensin II: Causes vasoconstriction, increasing systemic vascular resistance and blood pressure. It also stimulates aldosterone release from the adrenal cortex.

5\. Aldosterone: Acts on the kidneys to increase sodium reabsorption and potassium excretion. Water follows sodium, increasing circulating blood volume.

6\. ADH: Angiotensin II also promotes ADH release, increasing water reabsorption by the kidneys.

Remember this simple sequence:

Low BP → Renin → Angiotensin I → ACE → Angiotensin II → Aldosterone → Sodium and water retention → Increased BP.

An important medication connection:

* ACE inhibitors (e.g. ramipril) reduce the formation of angiotensin II.

* ARBs (e.g. losartan) block angiotensin II receptors.

* Aldosterone antagonists (e.g. spironolactone) reduce aldosterone activity.

Clinical pearl: ACE inhibitors, ARBs and spironolactone can increase serum potassium. Nurses should monitor potassium levels, renal function and blood pressure.

INSULIN MADE SIMPLE!

Rapid, short, intermediate, long or ultra-long acting do you know the difference?

For NCLEX, understanding insulin onset, peak and duration is essential for safe medication administration and preventing hypoglycaemia.

Save this quick reference guide!

NCLEX Reminder: The peak time is particularly important because it indicates when the risk of hypoglycaemia may be highest.

“A poor handover can put a patient at risk. Here’s how SBAR keeps communication safe and clear.” 🩺

“Safe handover starts with SBAR.”