RAAS in Anaesthesiology — Integrated Module

Part 1

🧠 Cognitive Domain

RAAS1a

RAAS Physiology: The Complete Pathway

The Renin-Angiotensin-Aldosterone System is a hormonal cascade critical for cardiovascular and renal homeostasis, regulating blood pressure, electrolyte balance, and vascular tone. Understanding this pathway is essential for appreciating the effects of RAAS-modifying drugs used by millions of surgical patients.

RAAS Cascade

Liver
Angiotensinogen → Angiotensin I ← Kidney
Renin → Angiotensin II ← Lung ACE

AT1 Receptors

Vasoconstriction · Aldosterone release · Fibrosis · Cardiac hypertrophy · Oxidative stress

AT2 Receptors

Vasodilation · Anti-proliferation · Natriuresis · Tissue repair (counter-regulatory)

Aldosterone

Na⁺ retention · K⁺ excretion · H₂O retention · H⁺ excretion

Component	Source	Stimulus	Primary Actions
Renin	Juxtaglomerular cells	↓ Renal perfusion, ↓ Na⁺, ↑ SNS	Cleaves angiotensinogen → Angiotensin I
Angiotensinogen	Liver	Constitutive; ↑ by estrogen, inflammation	Substrate for renin
ACE	Vascular endothelium (lung)	Constitutively expressed	Ang I → Ang II; degrades bradykinin
Angiotensin II	Systemic (from ACE)	Formed from Ang I	Primary RAAS effector
Aldosterone	Adrenal zona glomerulosa	Ang II, ↑ K⁺, ACTH	Na⁺ reabsorption, K⁺ excretion

RAAS1b

RAAS in Cardiovascular Homeostasis and Pathophysiology

RAAS plays a dual role: essential for maintaining blood pressure and perfusion in normal physiology, but when chronically activated, it becomes maladaptive, driving hypertension, heart failure progression, and end-organ damage.

Condition	Mechanism of RAAS Activation	Consequences
Hemorrhage/Dehydration	↓ Renal perfusion → ↑ Renin	Appropriate: maintains BP, conserves Na⁺
Essential Hypertension	Genetic predisposition, sympathetic overactivity	Sustained vasoconstriction, vascular remodeling, end-organ damage
Heart Failure	Reduced renal perfusion, sympathetic activation	Vasoconstriction (↑ afterload), Na⁺ retention, myocardial fibrosis, arrhythmias
CKD	Reduced nephron mass, glomerular hypertension	Intraglomerular hypertension, proteinuria, glomerulosclerosis
Cirrhosis	Splanchnic vasodilation, effective hypovolemia	Hyperdynamic circulation, ascites, hepatorenal syndrome

Heart Failure: The Vicious Cycle

↓ Cardiac Output → ↓ Renal Perfusion
↑ Renin → ↑ Ang II → Vasoconstriction
+ Aldosterone ↑ → ↑ Afterload + Na⁺
Retention → ↓ CO

RAAS1c

ACE Inhibitors — Pharmacology and Clinical Applications

ACE inhibitors are among the most widely prescribed cardiovascular medications. They inhibit conversion of Angiotensin I to Angiotensin II and prevent bradykinin degradation — with both therapeutic and adverse consequences.

Drug	Prodrug	Half-life	Elimination	Key Notes
Captopril	No	2h	Renal	Short-acting, SH group, taste disturbance
Enalapril	Yes → Enalaprilat	11h	Renal	Twice daily dosing
Lisinopril	No	12h	Renal	Once daily, not a prodrug
Ramipril	Yes → Ramiprilat	13–17h	Renal	High tissue ACE affinity
Perindopril	Yes → Perindoprilat	30–120h	Renal	⚠️ Very long T½ — 24h hold may be insufficient
Fosinopril	Yes → Fosinoprilat	12h	Renal + Hepatic	Safer in CKD (dual elimination)

Adverse Effect	Incidence	Mechanism	Management
Cough	5–20%	↑ Bradykinin	Switch to ARB
Angioedema	0.1–0.7%	Bradykinin-mediated	Emergency airway management
Hyperkalemia	Dose-dependent	↓ Aldosterone	Monitor K⁺, dietary counseling
Hypotension	Common (1st dose)	↓ Angiotensin II	Start low, anticipate intraoperatively
AKI	In renal artery stenosis	Efferent arteriolar dilation	Hold in suspected RAS
Fetal toxicity	Contraindicated in pregnancy	Fetal renal development	FDA Category D — avoid

RAAS1d

Angiotensin Receptor Blockers (ARBs) — Pharmacology and Clinical Applications

ARBs selectively block AT1 receptors, providing more complete RAAS blockade than ACE inhibitors by preventing angiotensin II effects regardless of production pathway. They lack bradykinin-mediated side effects.

Parameter	ACE Inhibitors	ARBs
Mechanism	Inhibit Ang II production	Block AT1 receptor
AT2 stimulation	↓ (less Ang II for AT2)	↑ (Ang II shunted to AT2)
Bradykinin	↑ (cough, angioedema)	Unchanged
Cough rate	5–20%	Placebo-equivalent
Angioedema	0.1–0.7%	Very rare (<0.1%)
Evidence in HFrEF	CONSENSUS, SOLVD	Val-HeFT, CHARM

ARB	Half-life	Elimination	Notable Feature
Losartan	6–9h (active metabolite)	Renal + Hepatic	Uricosuric effect
Valsartan	6h	Hepatic 83%	High protein binding
Candesartan	9h	Renal 33% / Hepatic 67%	Insurmountable antagonism
Telmisartan	24h	Hepatic 99%	PPAR-γ agonist activity; long T½
Irbesartan	11–15h	Hepatic 80%	Once daily
Olmesartan	13h	Renal 40% / Hepatic 60%	Enterohepatic recirculation

RAAS1e

Newer RAAS Agents — ARNI, Direct Renin Inhibitors, Aldosterone Antagonists

The landscape of RAAS-targeted therapy has expanded beyond ACE inhibitors and ARBs. ARNI (sacubitril/valsartan) has revolutionized heart failure treatment; aldosterone antagonists and direct renin inhibitors play roles in specific populations.

ARNI: Sacubitril/Valsartan (Entresto®)

Mechanism: Sacubitril inhibits neprilysin → ↑ natriuretic peptides → vasodilation + natriuresis; Valsartan blocks AT1

Key Trial: PARADIGM-HF — 20% relative mortality reduction vs enalapril; 21% ↓ hospitalization

Indication: HFrEF NYHA II–IV, EF ≤40% — now preferred over ACEi/ARB

Perioperative: Greater hypotension than ACEi/ARB alone; angioedema risk possible; same hold/continue principles

Agent	Spironolactone	Eplerenone
Mechanism	Non-selective MR antagonist (also progesterone/androgen)	Selective MR antagonist
Half-life	Active metabolites 12–20h	4–6h
Indications	HFrEF, resistant HTN, cirrhosis, primary aldosteronism	HFrEF post-MI, hypertension
Key side effects	Gynecomastia (10%), menstrual irregularities	Hyperkalemia — monitor closely
Periop concern	⚠️ Highest hyperkalemia risk of all RAAS blockers — especially in combination therapy

RAAS1f

2024 ACC/AHA Perioperative Guidelines — The "Hold vs Continue" Controversy

The 2024 ACC/AHA guidelines provide updated recommendations for ACEi/ARB management. The controversy centres on balancing intraoperative hypotension risk (continuation) against postoperative cardiovascular event risk (withdrawal).

Patient Group	Recommendation	Class	Rationale
HFrEF	Reasonable to continue	IIa	Benefits of RAAS blockade outweigh hypotension risk
Hypertension (well-controlled)	Withhold 24h preoperatively	IIa	Reduces intraoperative hypotension
Hypertension (poorly controlled)	Consider continuing	IIb	Risk of perioperative hypertension
Diabetic Nephropathy / CKD	Individualize	—	Based on K⁺, Cr, volume status
Unknown indication	Consult primary care / cardiology	—	Clarify indication first

Practical Decision Algorithm

1Identify indication: HFrEF vs Hypertension vs CKD/DM vs Unknown

2HFrEF: Consider continuing (Class IIa) — coordinate with cardiologist

3Hypertension-only, well-controlled: Withhold 24h (Class IIa) — verify drug half-life

4Assess drug-specific half-life: Perindopril (30–120h), Aliskiren (40h) — may need longer hold

5Document and communicate: Record indication, decision, rationale, and restart plan

6Emergency surgery: Proceed — prepare vasopressin, arterial line, enhanced monitoring

RAAS1g

RAAS and Electrolyte / Acid-Base Implications

RAAS blockers significantly impact electrolyte homeostasis through aldosterone inhibition. Hyperkalemia is the most clinically important disturbance, and can progress to life-threatening arrhythmia.

Mild

5.5–6.0

Usually no ECG changes

Moderate

6.1–6.5

Peaked T waves possible

Severe

6.6–7.0

Peaked T waves · Widened QRS

Life-threatening

>7.0

Sine wave · VF · Asystole

Risk Factor	Odds Ratio	Mechanism
CKD (eGFR <30)	5–10×	Reduced renal excretion
Combination RAAS therapy	3–5×	ACEi + ARB + aldosterone antagonist
Volume depletion	3×	Reduced distal Na⁺ delivery
Diabetes	2–3×	Hyporeninemic hypoaldosteronism
Heart failure	2–3×	Reduced renal perfusion + comorbidities
Elderly	2×	Age-related GFR decline

Part 2

✋ Psychomotor Domain

RAASs1

Preoperative RAAS Medication Reconciliation & Timing Verification

Basic Skill

Drug Class	Common Names	Half-life Range	24h Hold Sufficient?
ACE Inhibitors (short)	Captopril, Enalapril, Lisinopril	2–12h	✓ Yes
ACE Inhibitors (long)	Ramipril, Perindopril	13–120h	⚠️ May need longer hold
ARBs (most)	Losartan, Valsartan, Candesartan	6–15h	✓ Yes
ARBs (long)	Telmisartan	24h	⚠️ Consider 48h
ARNI	Sacubitril/Valsartan (Entresto)	~12h sacubitril	✓ 24h likely sufficient
Aldosterone antagonists	Spironolactone, Eplerenone	12–20h (metabolites)	✓ Yes
Direct Renin Inhibitors	Aliskiren	40h	✗ Consider 48–72h hold

Critical Information to Gather

1Indication: HFrEF vs Hypertension vs CKD/DM — drives hold/continue decision

2Last dose time + drug half-life: Calculate whether 24h hold is sufficient

3Concurrent diuretics / aldosterone antagonists: Multiplies K⁺ and volume risk

4Recent K⁺ and creatinine: Baseline for electrolyte and renal monitoring

5Document and communicate plan to surgical team and PACU/ward nursing

RAASs2

ACEi/ARB Withholding Decision Algorithm (2024 ACC/AHA)

Intermediate Skill

Decision Pathway

HFrEF

→ Consider continuing (Class IIa)
Coordinate with cardiologist
Arterial line recommended
Vasopressin available

Hypertension only

Well-controlled → Hold 24h (Class IIa)
Poorly controlled → Individualize
Restart when hemodynamically stable

CKD / Diabetic Nephropathy

Check K⁺, Cr, volume status
K⁺ normal + Cr stable → consider continuing
K⁺ elevated or Cr rising → hold

Emergency Surgery

Proceed regardless
Prepare vasopressin 0.01–0.04 units/min
Invasive monitoring strongly advised

RAASs3

Vasopressin Administration Protocol for RAAS-Associated Hypotension

Advanced / Crisis Skill

Patients on RAAS blockers have impaired compensatory vasoconstriction via Angiotensin II. Vasopressin is often more effective than catecholamines because it acts through V1 receptors independent of the RAAS pathway.

Preparation: 20 units in 100 mL NS = 0.2 units/mL

Intraoperative hypotension 0.01–0.03 units/min ↑ by 0.005–0.01 units/min q10min | Max: 0.04 units/min

Septic shock (adjunct) 0.01–0.03 units/min Fixed dose — do not titrate

Vasoplegic syndrome 0.02–0.04 units/min Post-CPB; may need up to 0.06 units/min (rare)

Adverse Effect	Mechanism	Monitoring
Cardiac ischemia	V1-mediated coronary vasoconstriction	ECG: ST changes
Mesenteric ischemia	Splanchnic vasoconstriction	Abdominal pain, lactate
Digital ischemia	Peripheral vasoconstriction	Skin mottling, capillary refill
Hyponatremia	V2 receptor stimulation (high doses)	Serum sodium

RAASs4

Hyperkalemia Management Algorithm

Advanced / Crisis Skill

Emergency Drug Dosing

Calcium gluconate 10%10–20 mL IV over 2–5 minMembrane stabilization — onset 1–3 min

Calcium chloride 10%5–10 mL IV over 2–5 min3× Ca²⁺ of gluconate — use centrally if possible

Regular insulin10 units IVGive with Dextrose 50% 50 mL — intracellular shift

Albuterol nebulized10–20 mgBeta-2 mediated shift — onset 30 min

Sodium bicarbonate50–100 mEq IVIf metabolic acidosis present

Furosemide40–80 mg IVPromotes renal excretion

Stepwise Management: K⁺ >6.5 or ECG Changes

1Immediate IV Calcium — membrane stabilization, buy time for definitive therapy

2Insulin + Glucose — shifts K⁺ into cells (effect ~15–30 min, duration 4–6h)

3Albuterol nebulized — additive to insulin; do not use as sole therapy

4Recheck K⁺ in 1–2h — if still elevated, consider dialysis or K⁺-binding resin

5Cancel elective surgery if K⁺ >6.0 with ECG changes — this is a safety issue

RAASs5

Postoperative RAAS Medication Re-initiation Protocol

Intermediate Skill

Criterion	Target Before Restart
Hemodynamic stability	No vasopressors >12–24h; SBP >90 mmHg without support
Volume status	Euvolemic (not dehydrated or overloaded)
Renal function	Stable or improving creatinine — no active AKI
Potassium	K⁺ <5.5 mmol/L (checked within 24h)
Oral intake	Tolerating oral medications

Scenario	Recommendation
Postoperative AKI	Hold until renal function recovers; restart at reduced dose
Postoperative hypotension	Hold until vasopressors weaned; consider half-dose restart
Hyperkalemia (K⁺ >5.5)	Hold, treat cause; restart when K⁺ <5.0
Combination RAAS therapy	Restart one agent at a time; monitor K⁺ after each

Part 3

❤️ Affective Domain

RAASa1

Shared Decision-Making — The "Hold vs Continue" Discussion

Patients on RAAS blockers often have strong beliefs about their medications. Explaining the perioperative plan requires clear communication, respect for patient autonomy, and genuine shared decision-making.

Script: Hypertension-only (holding)

"You take lisinopril for your blood pressure. For surgery, the safest approach is to skip your morning dose. This reduces the risk of your blood pressure dropping too low during anaesthesia. We'll restart it once you're stable after surgery — usually within a day or two. Your blood pressure will be monitored closely throughout."

Script: Heart Failure (continuing)

"I see you take Entresto for your heart failure. This medication is critical for your heart function. The latest guidelines suggest it's safer to continue it through surgery, even though it may cause some blood pressure changes. We'll monitor you very closely with an arterial line and have medications ready to support your blood pressure if needed. Your cardiologist agrees with this plan."

Script: Patient wants to take medication against advice

"I understand you're used to taking your medication every day. I want to explain why we recommend holding it — it's not because it's a bad medication, but because anaesthesia can temporarily lower blood pressure, and this medication increases that effect significantly. If you're very concerned, we can discuss this with your cardiologist together. Ultimately, we respect your decision, but we need to plan for enhanced monitoring if you choose to take it."

A patient once told me: "No one ever explained why I should hold my blood pressure pill. I just took it anyway because I thought they forgot to tell me to take it." Clear communication prevents misunderstandings and builds trust.

RAASa2

Team Communication About RAAS Medication Status

Multiple team members — preop nurse, surgeon, anaesthesiologist, PACU nurse, ward nurse — need to know the RAAS medication plan. Communication failures lead to errors and missed doses.

SSituation

"This is Dr. [name]. I'm handing over Mr. Smith, post-op day 1 after laparoscopic cholecystectomy. He's on lisinopril for hypertension."

BBackground

"Lisinopril 20mg daily. It was held preoperatively per guidelines. He's been haemodynamically stable, eating and drinking."

AAssessment

"K⁺ yesterday was 4.2, creatinine stable. BP 115/75 without vasopressors. Ready to restart."

RRecommendation

"Restart lisinopril this morning. Hold if BP <100/60. Continue daily K⁺ monitoring for 2 days. Document in notes."

A patient once missed 3 days of ACE inhibitor postoperatively because the plan wasn't communicated to the ward nurse. Now I always include "restart RAAS blocker" in my postoperative orders and handover.

RAASa3

Speaking Up About Hyperkalemia Risk — The CUS Tool

Hyperkalemia is often asymptomatic until life-threatening. Early recognition requires speaking up — even across hierarchical boundaries.

I am Concerned

"I'm concerned about this patient's potassium. He's on lisinopril, spironolactone, and has CKD stage 3. Preop K⁺ is 5.8."

I am Uncomfortable

"I'm uncomfortable proceeding with elective surgery with K⁺ 5.8. The risk of intraoperative arrhythmia is significant."

This is a Safety Issue — Stop the Line

"This is a safety issue. We need to cancel the case and manage hyperkalemia before proceeding. I'm stopping the line."

A junior resident once said: "K⁺ is 6.2 but the surgeon really wants to do the case." Speaking up prevented a potential cardiac arrest. Psychological safety saves lives.

RAASa4

Patient Education About RAAS Medications

Topic	Key Message for Patient
Why hold	"Anaesthesia can lower blood pressure, and your blood pressure medication adds to this effect. Holding it makes anaesthesia safer."
When to restart	"We'll restart it once you're awake, eating, and your blood pressure is stable — usually the next day."
Warning signs	"If you feel dizzy, lightheaded, or unusually tired after restarting, let your nurse know immediately."
Long-term importance	"This medication protects your heart and kidneys. It's important to restart it — just at the right time."

A patient once told me: "I've been on this pill for 10 years and no one ever explained why I take it." Taking 2 minutes to explain builds partnership and improves adherence.

RAASa5

Debriefing After RAAS-Related Complications

Phase	Plus / Delta Format
Plus (What went well?)	"What did we do well in managing this patient's RAAS medications?" — "What should we sustain?"
Delta (What could improve?)	"What would we do differently?" — "Was the medication plan clearly communicated at all handover points?"

3-Phase Debriefing	Focus Questions
Reaction	"How did that feel when the patient became hypotensive?" Allow emotional processing first.
Analysis	"What happened? Why did this patient develop severe hypotension? Could earlier vasopressin have helped?"
Summary	"What are our takeaways? Should we update our RAAS protocol? What do we change tomorrow?"

After a patient with HFrEF developed severe hypotension when her ACE inhibitor was held for 3 days postoperatively, we debriefed. We now have a protocol for early restart in heart failure patients. Debriefing turns complications into system improvement.

Part 4

🔗 Three-Domain Integration

Core Curriculum Integration

Domain	Key Principles	Integration Point
Preoperative Assessment	Identify RAAS medications, timing, indication (HFrEF vs hypertension)	Pharmacology Reconciliation Shared decision-making
Intraoperative Management	Anticipate vasoplegia; first-line vasopressin; goal-directed therapy	Physiology Vasopressin titration Closed-loop communication
Complication Prevention	Hyperkalemia recognition and treatment; avoid AKI	Electrolyte pathophysiology ECG interpretation Speaking up
Postoperative Care	Safe re-initiation timing; monitoring for hypotension and hyperkalemia	Pharmacology Electrolyte monitoring Patient education

Cross-Domain Connections

Connection 1: Guidelines → Algorithm → Communication

2024 ACC/AHA Guidelines
(individualize by indication) → Withholding Algorithm
(HFrEF continue; HTN hold) → Shared Decision-Making
(discussing plan with patient)

Connection 2: Physiology → Protocol → Handover

Impaired Ang II response
(RAAS blockade) → Vasopressin Protocol
(0.01–0.04 units/min) → SBAR Handover
(vasopressor infusion status)

Connection 3: Electrolyte Pathophysiology → Management → Speaking Up

K⁺ risk with ACEi +
aldosterone antagonist → Hyperkalemia Algorithm
(calcium → insulin/glucose) → Speaking Up (CUS)
("K⁺ 6.2 — cancel elective case")

Module Progress Dashboard

Cognitive Domain

RAAS Physiology

90%

ACEi Pharmacology

90%

ARB Pharmacology

85%

2024 Guidelines

85%

Newer Agents

75%

Psychomotor Domain

Medication Reconciliation

95%

Withholding Algorithm

80%

Vasopressin Protocol

70%

Hyperkalemia Algorithm

80%

Re-initiation Protocol

80%

Affective Domain

Shared Decision-Making

★★★★★

Team Communication

★★★★

Speaking Up (CUS)

★★★★★

Patient Education

★★★★

Debriefing

★★★★★

Summary

💡 10 Key Evidence-Based Insights

The RAAS cascade: Renin (kidney) cleaves angiotensinogen (liver) → Angiotensin I → ACE (lung/endothelium) → Angiotensin II → AT1 receptors (vasoconstriction, aldosterone, fibrosis) and AT2 receptors (counter-regulatory vasodilation).

ACE inhibitor cough in 5–20% via bradykinin accumulation — angioedema in 0.1–0.7% is life-threatening. ARBs are alternatives with placebo-level cough rate. Perindopril has exceptionally long T½ (30–120h): 24h hold may be insufficient.

Newer agents (ARNI): Sacubitril/valsartan reduces mortality by 20% in HFrEF (PARADIGM-HF). These patients have the most to lose from unnecessary RAAS blockade interruption. Aldosterone antagonists (spironolactone, eplerenone) carry the highest perioperative hyperkalemia risk.

2024 ACC/AHA perioperative guidelines: Individualise ACEi/ARB management — continue in HFrEF (Class IIa), withhold 24h in hypertension-only (Class IIa). There is no one-size-fits-all answer; indication drives decision.

Vasopressin 0.01–0.04 units/min is first-line for RAAS-associated hypotension because it bypasses the blocked RAAS pathway, acting through V1 receptors independent of angiotensin II. Do not wait for catecholamines to fail.

Hyperkalemia risk factors (multiplicative): CKD (5–10×), combination RAAS therapy (3–5×), volume depletion (3×), diabetes (2–3×). A patient with CKD + spironolactone + ACEi is extremely high risk perioperatively.

Hyperkalemia ECG progression: Peaked T waves (K⁺ 6.0–7.0) → widened QRS (7.0–8.0) → sine wave (8.0–9.0) → VF/asystole (>9.0). Treatment: calcium (membrane stabilisation) → insulin/glucose (intracellular shift) → albuterol. Cancel elective surgery for K⁺ >6.0 with ECG changes.

Postoperative re-initiation criteria: Haemodynamically stable, euvolemic, stable renal function, K⁺ <5.5, tolerating oral intake. Restart at preoperative dose unless new contraindication. Monitor K⁺ daily for 2–3 days after restarting aldosterone antagonists.

Patient education prevents errors: "No one told me to hold my blood pressure pill so I just took it." Clear communication — explaining WHY, WHEN, and WHAT to watch for — builds trust and prevents perioperative incidents from avoidable misunderstandings.

Speaking up (CUS) prevents cardiac arrests: Using "Concerned → Uncomfortable → Safety issue" structures assertive communication across hierarchies. A K⁺ of 6.2 is a reason to cancel elective surgery — regardless of who is in the room or how the surgeon feels about it.

Module Summary by Domain

🧠 Cognitive

RAAS cascade: renin → Ang I → ACE → Ang II → AT1/AT2
AT1: vasoconstriction, aldosterone, fibrosis
AT2: counter-regulatory vasodilation
ACEi: cough 5–20%, angioedema 0.1–0.7%
ARBs: no cough, selective AT1 blockade
ARNI: 20% mortality reduction in HFrEF
Aldosterone antagonists: highest K⁺ risk
2024 guidelines: individualise by indication
Hyperkalemia: ECG progression + treatment

✋ Psychomotor

Medication reconciliation: indication + timing + half-life
Withholding algorithm: HFrEF continue / HTN hold
Vasopressin 0.01–0.04 units/min: first-line for vasoplegia
Hyperkalemia: calcium → insulin/glucose → albuterol
Re-initiation: criteria + timing + monitoring
ECG interpretation: peaked T → widened QRS → sine wave
SBAR handover for RAAS status at every handover
POCUS for volume assessment

❤️ Affective

Shared decision-making: scripts for hold and continue
SBAR communication across the perioperative team
CUS tool: speak up about K⁺ 6.2 regardless of hierarchy
Patient education: WHY we hold, WHEN we restart
Debriefing: Plus/Delta after RAAS complications
Ethical balance: perioperative risk vs long-term benefit
Complications are learning opportunities for the system

Renin-Angiotensin-Aldosterone Systemin Anaesthesiology

Cognitive Domain

Psychomotor Domain

Affective Domain

🧠 Cognitive Domain

RAAS Physiology: The Complete Pathway

RAAS in Cardiovascular Homeostasis and Pathophysiology

ACE Inhibitors — Pharmacology and Clinical Applications

Angiotensin Receptor Blockers (ARBs) — Pharmacology and Clinical Applications

Newer RAAS Agents — ARNI, Direct Renin Inhibitors, Aldosterone Antagonists

2024 ACC/AHA Perioperative Guidelines — The "Hold vs Continue" Controversy

Practical Decision Algorithm

RAAS and Electrolyte / Acid-Base Implications

✋ Psychomotor Domain

Preoperative RAAS Medication Reconciliation & Timing Verification

Critical Information to Gather

ACEi/ARB Withholding Decision Algorithm (2024 ACC/AHA)

Decision Pathway

Vasopressin Administration Protocol for RAAS-Associated Hypotension

Hyperkalemia Management Algorithm

Stepwise Management: K⁺ >6.5 or ECG Changes

Postoperative RAAS Medication Re-initiation Protocol

❤️ Affective Domain

Shared Decision-Making — The "Hold vs Continue" Discussion

Team Communication About RAAS Medication Status

Speaking Up About Hyperkalemia Risk — The CUS Tool

Patient Education About RAAS Medications

Debriefing After RAAS-Related Complications

🔗 Three-Domain Integration

Core Curriculum Integration

💡 10 Key Evidence-Based Insights

🧠 Cognitive

✋ Psychomotor

❤️ Affective

Renin-Angiotensin-Aldosterone System
in Anaesthesiology