Critical Cardiac Emergencies

A Structured Approach to High-Risk Cardiovascular Presentations | 2026

Educational resource for SASEM training. Not a substitute for clinical judgment, current AHA/ESC/ACC guidelines, or hospital protocols.

ABDULRAHMAN ALZAHRANI, MD, SBEM

Emergency Medicine Consultant

Important Notice

This presentation is for education only and does not replace clinical judgment, local protocols, or official guidelines. Use patient-specific assessment and institutional policies for care decisions.

Start Here

Core Categories of Cardiovascular Collapse

Ischemia

ACS, Myocardial Injury

Electrical

Arrest, Tachy, Brady

Pump Failure

Heart Failure, Cardiogenic Shock

Mechanical

Tamponade, Valve Rupture

Valvular

Acute Valve Failure

Vascular

Dissection, AAA, PE

Pressure

Hypertensive Crisis

Syncope

Cardiogenic Causes

Summary

Key Takeaways & Review

The First 10 Minutes & Beyond

Priority Actions

ABC's & Stability: Secure airway, ensure adequate breathing, and assess for shock (pulse, perfusion).
IV Access & Monitor: Two large-bore IVs, place on continuous cardiac monitor and pulse oximetry.
ECG within 10 minutes: Essential for all high-risk presentations (Chest Pain, Syncope, Dyspnea).

Focused Workup

POCUS: Rapidly assess for tamponade, severe RV strain, or LV dysfunction.
Labs: Troponin, BNP, D-dimer, Electrolytes, Hgb.
Serial Reassessment: Symptoms and ECGs are dynamic. Repeat evaluation is key.

🔍 What is an Acute Coronary Syndrome?

Acute Coronary Syndrome (ACS) is a spectrum of conditions compatible with acute myocardial ischemia and/or infarction, usually due to coronary artery disease.

🚨

STEMI

ST-Elevation MI

Complete coronary occlusion

⚠️

NSTEMI

Non-ST-Elevation MI

Partial coronary occlusion

🔔

UA

Unstable Angina

Ischemia without necrosis

📊 ACS Epidemiology

Global Burden

8.9 million deaths annually worldwide
Leading cause of death globally
30% of all deaths in adults >35 years
Increasing incidence in young adults

Time is Muscle

Each hour delay = 1% mortality increase
Door-to-balloon goal: ≤90 minutes
First medical contact: ≤10 minutes
Early recognition saves lives

🔬 Pathophysiology of Myocardial Ischemia

 The Ischemic
                            Cascade
                        
                                    1
Reduced Coronary Blood Flow → Myocardial oxygen demand exceeds
                                    supply

                                    2
Anaerobic Metabolism → Lactic acid accumulation, cellular
                                    dysfunction

                                    3
Diastolic Dysfunction → Impaired relaxation, increased LVEDP
                                

                                    4
Systolic Dysfunction → Reduced contractility, cardiogenic
                                    shock
                                

                                    5
Irreversible Injury → Myocardial necrosis, scar formation
                                

⚡ Clinical Presentation

Typical Chest Pain

Retrosternal pressure/discomfort
Radiates to left arm, jaw, neck
Duration >20 minutes
Not relieved by rest or NTG
Associated with diaphoresis, nausea, dyspnea

Atypical Presentations

Women: Epigastric pain, fatigue, nausea
Diabetics: Silent ischemia, atypical symptoms
Elderly: Weakness, confusion, syncope
Post-op: Incisional pain masking cardiac pain

                     Key Learning
                        Points
                    ACS is a spectrum: STEMI → NSTEMI → Unstable Angina (increasing
                            severity)
                        
Time-critical diagnosis: ECG within 10 minutes of presentation
Chest pain ≠ cardiac pain: Consider differential diagnosis
High clinical suspicion: Better to over-treat than miss ACS
Patient factors matter: Age, gender, comorbidities affect presentation
                        

                

MI Type	Cause	Description
Type 1	Atherosclerotic Plaque Rupture	Spontaneous MI due to primary coronary artery disease.
Type 2	Supply-Demand Imbalance	MI due to increased oxygen demand or decreased supply (e.g., hypotension, anemia, arrhythmias).
Type 3	MI leading to Death	Cardiac arrest or death before troponin samples are available.
Type 4	PCI Related	MI occurring during or shortly after percutaneous coronary intervention.
Type 5	CABG Related	MI occurring during or shortly after coronary artery bypass grafting.

STEMI Criteria (Key Takeaways)

New ST-elevation in ≥ 2 contiguous leads. Contemporary guidelines recommend: ≥ 1.5 mm in V2-V3 (anterior leads); ≥ 1 mm in other leads. Gender-specific thresholds are no longer recommended as they may delay treatment.

STEMI Localization & ECG Patterns

Click on each territory to see ECG characteristics and clinical pearls.

Anterior STEMI

LAD Artery (V1-V4)

Lateral STEMI

Circumflex Artery (I, aVL, V5-V6)

Inferior STEMI

RCA (85%) or LCx (15%)

Posterior STEMI

Posterior Descending (V7-V9)

STEMI ECG Gallery

Anterior STEMI - ST elevation V1-V4

Inferior STEMI - ST elevation II, III, aVF

Posterior STEMI - ST depression V1-V3 + tall R waves

                    
                        Critical
                        Reminders
                    Women & Diabetics: May have atypical presentations
Right-sided ECG: For inferior STEMI with hypotension
Posterior leads: V7-V9 if posterior STEMI suspected
ST criteria: ≥1mm in most leads, ≥1.5mm in V2-V3

                

🔍 NSTEMI vs Unstable Angina

                             NSTEMI
                                (Non-ST-Elevation
                                MI)
                            Myocardial necrosis with elevated troponins
ECG changes: ST depression, T-wave inversion
Partial coronary occlusion
Risk of progression to STEMI
Requires urgent intervention

                        

                             Unstable Angina
                            Ischemia without necrosis (normal troponins)
ECG changes: May be normal or nonspecific
Coronary plaque disruption
High risk of progression
Requires risk stratification

                        

📊 ECG Changes in NSTEMI

 Common
                            ECG
                            Findings
                                ST Depression
                                • ≥1mm in ≥2 contiguous leads
• Often in leads I, aVL, V5-V6 (lateral)
• May be reciprocal to ST elevation elsewhere
• More common in inferior NSTEMI

                            

                                T-Wave Inversion
                                • ≥1mm deep in ≥2 contiguous leads
• Often precedes ST depression
• Most common finding in NSTEMI
• May persist after resolution

                            

🖼️ NSTEMI ECG Gallery

NSTEMI - ST depression in lateral leads

NSTEMI - T-wave inversion

⚠️ High-Risk ECG Features

                            Urgent Cath Lab Activation
                            • ST depression ≥2mm in multiple leads
• ST depression in anterior leads (V1-V4)
• Dynamic ECG changes (new vs old)
• ST depression with positive troponins

                            • Modified Sgarbossa criteria in LBBB
• Posterior ECG changes (tall R waves)
• ECG changes in patients with prior CABG
• Persistent symptoms despite medical therapy

                        

                     Clinical
                        Pearls
                    
                    Normal ECG doesn't rule out ACS: Up to 20% of NSTEMI have normal ECG
                            initially
Serial ECGs are crucial: Compare with old ECGs when available
ST depression ≠ STEMI: But may indicate severe ischemia requiring
                            urgent
                            cath
T-wave inversions evolve: May appear before ST depression in evolving
                            ischemia
Right-sided ECG: Consider for inferior NSTEMI with hypotension

                

🧪 Cardiac Biomarkers Overview

Troponin I/T

🎯

Gold standard for myocardial injury

CK-MB

📊

Historical marker, less specific

Myoglobin

⚡

Early marker, low specificity

🔬 High Sensitive Troponin (hs-Tn) - Worldwide Standard

 Why
                            High
                            Sensitive Troponin Matters
                                🌍 Global Recommendation
                                ESC 2023 ACS Guidelines: hs-cTn preferred for diagnosis and 0/1h–0/2h algorithms
AHA/ACC 2021 Chest Pain: hs-cTn for early rule-out/rule-in pathways
Universal adoption: Most labs worldwide use hs-Tn

                                ⚡ Clinical Advantages
                                Earlier detection: Detects injury 1-2 hours after onset
                                    
Higher sensitivity: 10-100x more sensitive than
                                        conventional
                                    
Better risk stratification: Detects minor myocardial injury
                                    
Faster discharge: Enables 1-2 hour protocols

📊 hs-Tn Reference Ranges & Interpretation
                            
                                            hs-Tn
                                                Level
                                            
                                                Interpretation
                                            
                                                Clinical
                                                Action
                                        
                                                Normal
(<
                                                        URL)
                                            
                                            No myocardial injury detected
                                            Low suspicion: Consider discharge with
                                                outpatient follow-up
                                        
                                                Elevated
(>
                                                    URL
                                                    but < 52 ng/L)
                                            
                                            Possible myocardial injury or chronic
                                                elevation
                                            Serial testing required, assess delta
                                                change
                                            
                                                Rising
                                                    Pattern
(>20%
                                                    delta
                                                    increase)
                                            
                                            Acute myocardial injury likely
                                            Treat as NSTEMI, cardiology consultation
                                            
                                                Markedly
                                                    Elevated
(>52
                                                    ng/L)
                                            
                                            Significant myocardial injury
                                            Urgent cardiology evaluation, possible
                                                STEMI
                                                equivalent
                                        
                             Key
                                Points
                                for hs-Tn Use
                            Gender-specific cutoffs: Women have lower normal ranges than
                                    men
                                
Serial testing: Compare to baseline when available; look for rising
                                    trend
                                
Delta change: >20% increase indicates acute injury
1-2 hour protocols: Normal hs-Tn at 0h + 1-2h = rule-out MI
                                
Interference: Hemolysis, biotin supplements can falsely elevate
                                
Chronic elevations: CKD, HF patients may have baseline
                                    elevations

hs-Tn Level	Interpretation	Clinical Action
Normal (< URL)	No myocardial injury detected	Low suspicion: Consider discharge with outpatient follow-up
Elevated (> URL but < 52 ng/L)	Possible myocardial injury or chronic elevation	Serial testing required, assess delta change
Rising Pattern (>20% delta increase)	Acute myocardial injury likely	Treat as NSTEMI, cardiology consultation
Markedly Elevated (>52 ng/L)	Significant myocardial injury	Urgent cardiology evaluation, possible STEMI equivalent

📈 Troponin Kinetics

                            
                                
                                        Biomarker
                                        
                                        Onset
                                        Peak
                                        Return to
                                            Normal
                                        Clinical
                                            Use
                                        
                                    

                                
                                        Troponin I
                                        3-6 hours
                                        12-24 hours
                                        5-10 days
                                        Diagnosis of MI
                                    

                                        Troponin T
                                        3-6 hours
                                        12-24 hours
                                        10-14 days
                                        Diagnosis of MI
                                    

                                        CK-MB
                                        3-6 hours
                                        12-24 hours
                                        2-3 days
                                        Historical use
                                    

                                        Myoglobin
                                        1-2 hours
                                        6-12 hours
                                        24 hours
                                        Early detection
                                    

                            
                        

Biomarker	Onset	Peak	Return to Normal	Clinical Use
Troponin I	3-6 hours	12-24 hours	5-10 days	Diagnosis of MI
Troponin T	3-6 hours	12-24 hours	10-14 days	Diagnosis of MI
CK-MB	3-6 hours	12-24 hours	2-3 days	Historical use
Myoglobin	1-2 hours	6-12 hours	24 hours	Early detection

🔬 Pathophysiology of Myocardial Ischemia

 The Ischemic
                            Cascade
                        
                                    1
Reduced Coronary Blood Flow → Myocardial oxygen demand exceeds
                                    supply

                                    2
Anaerobic Metabolism → Lactic acid accumulation, cellular
                                    dysfunction

                                    3
Diastolic Dysfunction → Impaired relaxation, increased LVEDP
                                

                                    4
Systolic Dysfunction → Reduced contractility, cardiogenic
                                    shock
                                

                                    5
Irreversible Injury → Myocardial necrosis, scar formation
                                

⚡ Clinical Presentation

Typical Chest Pain

Retrosternal pressure/discomfort
Radiates to left arm, jaw, neck
Duration >20 minutes
Not relieved by rest or NTG
Associated with diaphoresis, nausea, dyspnea

Atypical Presentations

Women: Epigastric pain, fatigue, nausea
Diabetics: Silent ischemia, atypical symptoms
Elderly: Weakness, confusion, syncope
Post-op: Incisional pain masking cardiac pain

                     Key Learning
                        Points
                    ACS is a spectrum: STEMI → NSTEMI → Unstable Angina (increasing
                            severity)
                        
Time-critical diagnosis: ECG within 10 minutes of presentation
Chest pain ≠ cardiac pain: Consider differential diagnosis
High clinical suspicion: Better to over-treat than miss ACS
Patient factors matter: Age, gender, comorbidities affect presentation
                        

                

📊 Risk Stratification Scores

TIMI Risk Score for NSTEMI/UA

1 point each for:

• Age ≥65 years
• ≥3 CAD risk factors
• Known CAD (stenosis ≥50%)
• ST deviation ≥0.5mm
• ≥2 anginal episodes in 24h
• ASA use in past 7 days
• Elevated cardiac markers

0-1: Low risk

2-3: Intermediate

4-5: High risk

6-7: Very high

HEART Score

Points (0-2 each):

History: Highly suspicious (2), Moderately (1), Slightly (0)
ECG: Significant ST depression (2), Nonspecific (1), Normal (0)
Age: ≥65 (2), 45-64 (1), ≤44 (0)
Risk factors: ≥3 (2), 1-2 (1), None (0)
Troponin: ≥3x normal (2), 1-3x (1), Normal (0)

0-3: Low risk (2% MACE)

4-6: Intermediate (20% MACE)

7-10: High risk (65% MACE)

⚡ Management Based on Risk

 Treatment
                            Algorithms
                                High-Risk Features (Urgent Cath)
                                • TIMI ≥4 or HEART ≥7
• Recurrent ischemia at rest
• ST depression ≥1mm
• New/worsening MR
• Elevated troponins
• Hemodynamic instability
• Sustained VT

                            

                                Low-Risk Features (Medical Management)
                                
                                • TIMI 0-2 or HEART 0-3
• No recurrent symptoms
• Normal ECG
• Normal troponins
• No hemodynamic issues
• Good functional capacity

                            

💊 Anti-Ischemic Therapy

Initial Medical Therapy

Aspirin 325mg (chewed)
Nitroglycerin SL (if no contraindications)
Oxygen (if hypoxemic)
Morphine (for refractory pain)
Beta-blockers (if no contraindications)

Anticoagulation

Heparin (unfractionated or LMWH)
Timing: Start immediately if cath planned
Duration: Until PCI or discharge
Monitoring: aPTT for unfractionated heparin

🎯 Timing of Intervention

 Cath Lab
                            Activation
                            Guidelines
                            
                                        Risk Level
                                        
                                        Timing
                                        Rationale
                                        
                                        Very High Risk
                                        Immediate (<2 hours)
                                        Ongoing ischemia, hemodynamic instability
                                        
                                        High Risk
                                        Early (<24 hours)
                                        Elevated troponins, ST changes
                                    
                                        Intermediate Risk
                                        24-72 hours
                                        Ischemia-guided approach
                                    
                                        Low Risk
                                        Outpatient
                                        Stress testing first

Risk Level	Timing	Rationale
Very High Risk	Immediate (<2 hours)	Ongoing ischemia, hemodynamic instability
High Risk	Early (<24 hours)	Elevated troponins, ST changes
Intermediate Risk	24-72 hours	Ischemia-guided approach
Low Risk	Outpatient	Stress testing first

                    
                        Decision-Making
                        Framework
                    Risk stratify immediately upon presentation
Don't delay high-risk patients for "rule-out" protocols
Serial ECGs and troponins guide management
Consider patient preferences and comorbidities
Early invasive strategy for most NSTEMI patients

                

🚨 Code STEMI Activation Protocol

                            
                                Door-to-Balloon Time Goals
                            Primary PCI (PCI center): aim FMC/door-to-device ≤90 minutes (system goal)
Transfer PCI: aim device within ≤120 minutes of first medical contact when transfer pathway is used
Fibrinolysis (if PCI delayed): door-to-needle ≤30 minutes when indicated
ECG to Activation: ≤ 10 minutes

                        

                             Immediate Actions
                            Immediate action
Effective communication
Attention to detail

                        

💊 Reperfusion Strategies

Primary PCI (Preferred)

Indications: Symptom onset <12 hours when timely PCI is available (PCI-capable center; aim FMC-to-device ≤90 min, transfer pathway often ≤120 min — confirm local STEMI network targets)
Benefits: Higher patency rates, lower bleeding risk, better outcomes
Contraindications: Patient refusal, advanced comorbidities

Fibrinolysis

Indications: Symptom onset <12 hours when timely PCI is not available (commonly when expected FMC-to-device exceeds ~120 min — follow local protocol)
Agents: Alteplase, Reteplase, Tenecteplase
Monitoring: Watch for bleeding complications

📊 Risk Stratification - HEART Score

                            
                                
                                        Component
                                        
                                        Points
                                        Description
                                        
                                    

                                
                                        History
                                        0-2
                                        Highly suspicious (2), Moderately (1),
                                            Slightly
                                            (0)
                                    

                                        ECG
                                        0-2
                                        Significant ST depression (2), Nonspecific
                                            (1),
                                            Normal (0)
                                    

                                        Age
                                        0-2
                                        ≥65 years (2), 45-64 (1), ≤44 (0)
                                    

                                        Risk factors
                                        
                                        0-2
                                        ≥3 risk factors (2), 1-2 (1), None (0)
                                    

                                        Troponin
                                        0-2
                                        ≥3x normal (2), 1-3x (1), Normal (0)
                                    

                            
                        
0-3
Low Risk
Early discharge possible
4-6
Moderate Risk
Further testing needed
7-10
High Risk
Admission required

Component	Points	Description
History	0-2	Highly suspicious (2), Moderately (1), Slightly (0)
ECG	0-2	Significant ST depression (2), Nonspecific (1), Normal (0)
Age	0-2	≥65 years (2), 45-64 (1), ≤44 (0)
Risk factors	0-2	≥3 risk factors (2), 1-2 (1), None (0)
Troponin	0-2	≥3x normal (2), 1-3x (1), Normal (0)

                     Student
                        Learning
                        Points
                    Every second counts! Practice makes perfect in STEMI recognition
Don't delay for labs: ECG diagnosis trumps everything
Know your system: Understand local protocols and transport times
Document thoroughly: Times are tracked for quality improvement
Team coordination: Everyone has a role in saving lives

                

STEMI Protocol: Time is Muscle

The Golden Metric: Door-to-Balloon Time

Goal: ≤90 minutes from first medical contact to balloon inflation. Every minute of delay = 1% increase in mortality.

0-10 min

ECG, diagnosis, activation

10-60 min

Transport, prep, procedure

60-90 min

Balloon inflation target

Pre-Hospital Activation

EMS Protocol

12-lead ECG in field when possible
Pre-notification to receiving hospital
Direct transport to cath-capable center
By-pass closer hospitals if needed

ED Activation Criteria

≥1mm ST elevation in ≥2 contiguous leads
Sgarbossa criteria met in LBBB
Posterior STEMI with anterior changes
Right-sided ECG for inferior STEMI

ED Response Team

Immediate Actions

Call "Code STEMI" overhead page
Notify cardiology fellow immediately
Activate cath lab team
Prepare patient for transport

Team Composition

ED physician - diagnosis & stabilization
Cardiology fellow - immediate response
Cath lab team - procedure ready
ED nursing - prep & transport

Pre-Cath Medications

The STEMI Cocktail

Aspirin: 325mg PO chewed immediately

Heparin: 60 IU/kg IV bolus (max 5000U)

Antiplatelet: Clopidogrel 600mg or Ticagrelor 180mg

Nitroglycerin: If hypertensive (avoid RV MI)

Transport Protocol

To Cath Lab

Monitor continuously - cardiac, BP, O₂ sat
Minimize interruptions in compressions if arrest
Give report en route to cath lab
Document times meticulously
Family notification before transport

Time Documentation

Door time: Patient arrival
ECG time: First diagnostic ECG
Activation time: Code STEMI called
Balloon time: Device inflation

                        Critical Success Factors
                            System Factors
                            • Single-call activation
• Pre-established protocols
• Regular team training
• Quality improvement tracking

                        

                            Individual Factors
                            • Pattern recognition

                        

HEART Score: Guiding Disposition

For patients with suspected ACS where the initial ECG is non-ischemic, the HEART score estimates the risk of Major Adverse Cardiac Event (MACE) within 6 weeks.

History (H)

ECG (E)

Age (A)

Risk Factors (R)

Troponin (T)

                     Summary of Scores
                    Score 0-3 (Low Risk): MACE Risk < 2%. Consider early discharge
                            with
                            appropriate follow-up.
Score 4-6 (Moderate Risk): MACE Risk 12-17%. Requires admission for
                            observation and further non-invasive testing.
Score ≥ 7 (High Risk): MACE Risk 50-65%. Requires aggressive
                            management
                            and cardiology consultation.

                

ACLS Cardiac Arrest Algorithm

ACLS cardiac arrest algorithm (teaching figure): Use as a visual overview. Energy settings, airway approach, and post-ROSC targets must match your current hospital ACLS card and latest AHA/ILCOR updates — do not rely on this image alone for clinical dosing.

Shockable vs. Non-Shockable Rhythms

Why Shockable Rhythms Matter

Shockable rhythms are abnormal heart rhythms that can be treated with electrical defibrillation. These rhythms have organized electrical activity that can be "reset" by delivering an electric shock, potentially restoring normal sinus rhythm.

Early defibrillation is critical because survival decreases by approximately 10% for every minute that passes without defibrillation in shockable rhythms. The first shock should be delivered within 2 minutes of cardiac arrest recognition.

Defibrillation works by depolarizing all cardiac cells simultaneously, allowing the heart's natural pacemaker (SA node) to regain control and restore organized electrical activity.

Shockable Rhythms

Ventricular Fibrillation (VF): Chaotic electrical activity, no organized depolarization.
Pulseless Ventricular Tachycardia (pVT): Organized wide-complex, but no pulse.
Management: Immediate high-quality CPR → Defibrillation (biphasic energy per manufacturer; often 120–200 J range for first shock — confirm device) → Epinephrine 1 mg IV/IO every 3–5 min → Amiodarone or lidocaine for refractory VF/pVT → continue CPR/defibrillation cycles.
Post-ROSC care: Support airway/breathing/circulation; treat STEMI urgently; temperature control / avoid fever per current post-arrest guidance and local protocol; hemodynamic optimization and delayed neuroprognostication.

Non-Shockable Rhythms

These rhythms do not respond to electrical defibrillation because they lack organized electrical activity that can be "reset."

Pulseless Electrical Activity (PEA): Organized electrical activity on monitor, but no mechanical contraction (no pulse).
Asystole: Flatline - complete absence of electrical activity.
Management: Continuous CPR → Epinephrine (every 3-5 min) → Focus on the H's and T's (Hypovolemia, Hypoxia, Tamponade, Tension PTX, etc.).

Ventricular Fibrillation (VF)

Chaotic electrical activity with no organized depolarization - shockable rhythm requiring immediate defibrillation to restore normal cardiac rhythm

Asystole

Flatline - No electrical activity visible on ECG monitor

The Post-ROSC Algorithm

Time is Brain: The Golden Hour

The first hour after return of spontaneous circulation (ROSC) is critical for neurologic recovery. Immediate optimization of hemodynamics and oxygenation is essential.

0-5 min

Secure airway, optimize oxygenation

5-15 min

12-lead ECG, labs, imaging

15-60 min

Temperature management, cath lab

Immediate Management

Hemodynamic Goals

Mean BP: ≥ 65 mmHg (MAP)
SBP: ≥ 90 mmHg
Urine output: ≥ 0.5 mL/kg/hr
Lactate clearance as marker

Ventilation Strategy

ETCO₂: 35-45 mmHg
SpO₂: 94-98% (avoid hyperoxia)
Protective ventilation: TV 6-8 mL/kg
Sedation + analgesia for intubation

Targeted Temperature Management

TTM / temperature control: 32–37.5°C range (protocol-dependent)

Indicated for: Comatose patients post-OHCA
Goal: Prevent fever. Target 32–36°C or controlled normothermia <37.5°C (per local protocol / current AHA–ILCOR guidance)
Duration: Maintain strategy for at least 24h
Monitor: Shivering, electrolytes, glucose

Neurologic Assessment

Neuroprognostication: After 72 hours
SSEP, EEG: For prognostication
Avoid early withdrawal of care
Family support throughout

Investigations

Diagnostic Workup

ECG: STEMI? → Immediate cath lab
Echo: LV function, tamponade, aortic dissection
CT chest/abdomen: If indicated
Coronary angiogram: For OHCA with STEMI
EEG: For seizure activity

Supportive Care

Medical Management

Glycemic control: 144-180 mg/dL
Antiarrhythmics: If recurrent VF/VT
Antibiotics: If infection suspected
DVT prophylaxis: When stable
GI prophylaxis: PPI or H2 blocker

                     Key Points
                        for
                        Students
                    Don't declare brain death early! Wait at least 72 hours
                            post-rewarming
                        
STEMI post-arrest = cath lab: Even if initially comatose
Avoid hyperoxia: SpO₂ 94-98% reduces oxidative stress
Multidisciplinary approach: Cardiology, ICU, neurology involvement
                        
Family communication: Honest, compassionate, regular updates

                

The Unstable Tachycardia Protocol

If the patient is Unstable (hypotension, shock, acute heart failure, ischemic chest pain, altered mental status) due to the rhythm, proceed directly to Synchronized Cardioversion.

Wide Complex Tachycardia (WCT, QRS ≥ 120ms)

Rule: Treat as Ventricular Tachycardia (VT) until proven otherwise.
Stable VT: Amiodarone or Procainamide.
Caution: Avoid AV nodal blockers (Verapamil, Diltiazem) in WCT of unknown origin, especially if WPW is suspected (can precipitate VF).

Narrow Complex Tachycardia (NCT, QRS < 120ms)

SVT: Stable - Vagal Maneuvers → Adenosine
A-fib/A-flutter: Stable - Rate Control (Beta-blockers or Calcium Channel Blockers). Check stroke risk (CHADS2-VASc).

Ventricular Tachycardia (VT)

Wide complex tachycardia (QRS ≥ 120ms) with regular rhythm - treat as VT until proven otherwise

AF Recognition & Initial Assessment

Clinical Presentation

Irregularly irregular pulse - hallmark finding
Palpitations - most common complaint
Dyspnea, chest pain, fatigue
May be asymptomatic - discovered incidentally

ECG Features

Irregular R-R intervals
Absence of P waves
Coarse or fine atrial fibrillation waves
Variable ventricular response

Critical Initial Steps

1. ABCs

Assess stability - rate-related symptoms?

2. Duration

< 48h vs > 48h (anticoagulation implications)

3. Stroke Risk

CHA₂DS₂-VASc score

Rate vs Rhythm Control

Rate Control (Preferred for ED)

β-blockers: Metoprolol 2.5-5mg IV, or PO
CCBs: Diltiazem 10-20mg IV (avoid in HF)
Digoxin: 0.25mg IV (renal/hepatic caution)
Goal: HR < 110 bpm at rest

Rhythm Control (Selected cases)

Stable patient with recent onset
Amiodarone: 150mg IV over 10 min
Cardioversion: if unstable

Anticoagulation Strategy

CHA₂DS₂-VASc Score ≥2

New onset AF: Start anticoagulation
DOAC preferred: Apixaban or Rivaroxaban
Warfarin: If CrCl <30 or mechanical valve

AF Duration <48h

Low stroke risk: Can cardiovert without AC
Start AC: After cardioversion
TEE: If duration uncertain

                     Clinical
                        Pearls for Students
                    Don't miss the irregular pulse! Feel the radial pulse for 30
                            seconds
                        
Rate control first: Most ED patients don't need rhythm control
Stroke prevention: Address anticoagulation even if rhythm restored
                        
Follow-up: All patients need cardiology referral

                

Symptomatic Bradycardia Algorithm

The Need for Intervention

Bradycardia requires treatment only if it is causing symptoms: Shock/Hypotension, Acute Altered Mental Status, Acute Heart Failure, or Ischemic Chest Pain.
High-Grade Blocks: Mobitz Type II and 3rd Degree Heart Block are inherently unstable and often require pacing.

Management Steps

Step 1 (First Line): Atropine (1mg IV, max 3mg). Less effective for infra-nodal blocks (Type II/3rd Degree).
Step 2 (If Atropine fails): Transcutaneous Pacing (TCP). Start at 60-80 bpm, increase mA until capture.
Step 3 (Alternatives/Bridge): Dopamine or Epinephrine infusion (chronotropic agents).

Common Bradycardia ECG Patterns

Bradycardia ECG Patterns

Common Bradycardia Patterns:

Sinus Bradycardia

• Normal P waves before each QRS
• Rate < 60 bpm
• Often benign if asymptomatic

Heart Block

• P waves and QRS dissociated
• May be 2nd or 3rd degree
• Requires pacing if symptomatic

⚠️ Bradycardia requires treatment only if symptomatic. Immediate pacing may be needed for high-grade blocks or hemodynamic instability.

💔 Heart Failure: When the Pump Fails

What is Heart Failure?

Heart failure is a clinical syndrome characterized by the heart's inability to pump blood effectively to meet the body's metabolic demands. It can be acute or chronic, systolic or diastolic.

Systolic HF

Reduced ejection fraction (<40%). "Weak pump" - impaired contraction.

Diastolic HF

Preserved ejection fraction (≥50%). "Stiff pump" - impaired relaxation/filling.

                            Clinical Presentation
                                
                                    Cardinal Symptoms
                                🫁 Dyspnea: Orthopnea, PND (paroxysmal nocturnal dyspnea)
                                    
💧 Peripheral edema: Sacral, pedal edema
😮 Fatigue: Reduced exercise tolerance
💓 Tachycardia: Compensatory response

                            

                                
                                    Respiratory
                                    Signs
                                🫁 Pulmonary rales: Crackles on auscultation
💨 S3 gallop: Low-frequency extra heart sound
🫀 Jugular venous distension: Elevated JVP
📏 Hepatojugular reflux: Positive test

                            

NYHA Classification

Class I: No limitation of physical activity

Class II: Slight limitation, comfortable at rest

Class III: Marked limitation, comfortable only at rest

Class IV: Unable to carry out any physical activity

                             Management
                                Principles
                            💧 Diuretics: Loop diuretics (furosemide) for congestion
💊 Vasodilators: Nitroglycerin for preload reduction
🫀 Inotropes: Dobutamine for severe cases
📊 Monitor: Daily weights, fluid balance

                        

Red Flags: Immediate Intervention

• Hypotension: SBP <90 mmHg with symptoms
• Acute pulmonary edema: Respiratory distress
• Cardiorenal syndrome: Rising creatinine
• Arrhythmias: New-onset atrial fibrillation
• Progression to cardiogenic shock

🚨 Cardiogenic Shock: Pump Failure with Systemic Impact

What is Cardiogenic Shock?

Cardiogenic shock is a state of critical end-organ hypoperfusion due to primary cardiac dysfunction. It's characterized by inadequate tissue perfusion despite adequate preload, resulting in cellular hypoxia and organ dysfunction.

💓

Cardiac Output

↓ CO despite ↑ preload

🫀

Blood Pressure

↓ MAP (<65 mmHg)

🫁

Tissue Perfusion

↓ End-organ perfusion

                                Clinical Features
                                     Hemodynamic Criteria
                                    📊 CI <2.2 L/min/m²: Low cardiac index
💉 MAP <65 mmHg: Mean arterial pressure
🫀 PCWP >15 mmHg: Elevated wedge pressure
⚡ SVR normal or ↑: Systemic vascular resistance

                                

                                    
                                        End-Organ
                                        Effects
                                    🧠 Confusion/altered mental status
💛 Oliguria (<0.5 mL/kg/hr)
                                        
🫁 Pulmonary congestion/edema
🌡️ Cool extremities, delayed capillary refill

                                

Causes of Cardiogenic Shock

65%: Acute MI (especially anterior STEMI)

10%: Acute valvular regurgitation

10%: Cardiomyopathy exacerbation

5%: Ventricular septal defect

10%: Other (tamponade, arrhythmias, etc.)

Emergency Management

1. ABCs + Oxygen

2. Identify & treat reversible causes

3. Inotropic support: Dobutamine ± norepinephrine

4. Mechanical support: IABP, Impella, ECMO

5. Definitive therapy: PCI, CABG, valve repair

Mortality: 40-50% Despite Treatment

• Early recognition is critical - intervene before end-organ damage
• SCAI classification: A (at risk) → B (beginning) → C (classic) → D (deteriorating) → E (extremis)
• Time to intervention: Door-to-support time should be <90 minutes
• Multidisciplinary approach: Cardiology, cardiac surgery, critical care

🔒 Obstructive Shock: When the Pump Can't Fill or Empty

Cardiac Tamponade

Beck's Triad

🔽 Hypotension: Low blood pressure
🫁 JVD: Jugular venous distension
❤️ Muffled heart sounds: Distant, quiet

Pulsus Paradoxus

>10 mmHg drop in SBP during inspiration

POCUS Findings

RV diastolic collapse, swinging heart

Tamponade ECHO

Pericardial effusion causing RV collapse

                                    
                                        Emergency Management
                                    🔴 Immediate: IV fluids + vasopressors
🟡 Definitive: Pericardiocentesis (ECHO-guided)
🟢 Avoid: Positive pressure ventilation

Pulmonary Embolism (PE)

Massive PE Criteria

🔽 SBP <90 mmHg for ≥15 min
🫁 Respiratory failure (O2 sat <90%)
💙 RV dysfunction on ECHO
🏥 ICU admission required

Time is Lung

Door-to-needle: <15 min for massive PE
Thrombolytics: tPA 100mg IV over 2h

Clinical Clues

• Sudden dyspnea, chest pain
• Tachycardia, hypoxia
• Unilateral leg swelling
• Risk factors: Immobility, cancer, OCP

PE Pathophysiology

Clot obstructs pulmonary artery → RV strain → shock

Management Algorithm

1. ABCs + Oxygen

2. Assess stability:

• Stable: Anticoagulation

• Unstable: Thrombolytics

3. Consider thrombectomy if contraindications

🔥 Pericarditis: When the Heart's Wrapper is on Fire

Pericarditis Diagnostic Checklist

Pleuritic chest pain (worse with inspiration)

Better leaning forward (classic finding)

Pericardial friction rub on auscultation

Fever (>38°C)

Diffuse ST elevation on ECG

PR depression on ECG

Mild troponin elevation (≤1x URL)

Pericardial effusion on ECHO

Diagnosis: ≥2 of 4 criteria + typical chest pain. ECG changes are highly specific!

                                Clinical Presentation
                                     Chest Pain Characteristics
                                    
                                    🔥 Sharp, pleuritic (worse with inspiration)
📍 Retrosternal or left precordial
🏃‍♂️ Better with sitting/leaning forward
⏰ Can last hours to days

                                

                                    
                                        Physical Exam
                                    🔊 Pericardial friction rub: "Scratchy" sound
🌡️ Fever in infectious cases
🫁 Tachypnea if pleural effusion
💓 Distant heart sounds if effusion

                                

Classic Pericarditis ECG

Diffuse ST elevation + PR depression

Treatment Protocol

1st Line: NSAIDs (Ibuprofen 600-800mg TID) + PPI

Add-on: Colchicine 0.5mg BID (reduces recurrence)

Steroids: Only if contraindications to NSAIDs

Duration: 1-2 weeks, taper gradually

Red Flags - Seek Immediate Care

• Tamponade signs: Hypotension, JVD, pulsus paradoxus
• Large effusion: >2cm on ECHO
• Myocarditis: Elevated troponins, LV dysfunction
• Recurrent episodes: Multiple flares

💔 Myocarditis: When the Heart Muscle is Under Attack

Myocarditis Risk Stratifier

Low Risk

• Normal EF (>50%)
• No arrhythmias
• Mild symptoms
• Troponin ≤3x URL

Outpatient management

Intermediate Risk

• EF 35-50%
• Non-sustained VT
• Moderate symptoms
• Troponin 3-10x URL

Telemetry monitoring

High Risk

• EF <35%
• Sustained VT/VF
• Cardiogenic shock
• Troponin >10x URL

ICU admission

                                Causes
                                & Presentation
                                     Common Causes
                                    🦠 Viral: Coxsackie, EBV, CMV (most common)
💊 Drugs: Doxorubicin, cocaine, NSAIDs
🦠 Bacterial: Lyme, diphtheria, sepsis
⚡ Autoimmune: SLE, sarcoidosis
🔬 Hypersensitivity: Sulfa drugs, vaccines

                                

                                    
                                        Clinical Signs
                                    💔 Chest pain: Retrosternal, worse supine
😮 Dyspnea: Acute heart failure
💓 Palpitations: Arrhythmias common
🌡️ Fever: Infectious cases
⚡ Fatigue: Viral prodrome

                                

Myocarditis ECG Changes

ST changes, conduction blocks, arrhythmias

Management Strategy

🔴 Supportive Care: Rest, monitor hemodynamics

🟡 Heart Failure: ACEi/ARBs, beta-blockers, diuretics

🟢 Arrhythmias: Antiarrhythmics as needed

🔵 MCS: IABP/ECMO for refractory shock

🟣 Transplant: Bridge to recovery/transplant

Diagnostic Workup

Essential Tests:

• Troponin (elevated in 90%)
• BNP/NT-proBNP
• ECG (daily monitoring)
• ECHO (EF assessment)

Advanced Testing:

• Cardiac MRI (gold standard)
• Endomyocardial biopsy
• Viral PCR studies
• Autoimmune workup

🚪 Valvular Emergencies: When Heart Valves Fail Suddenly

                                    Decompensated Aortic Stenosis
                                         Emergency Presentation
                                        
                                        💔 Acute heart failure: Pulmonary edema
🔽 Hypotension: Fixed cardiac output
🫁 Dyspnea: LV failure symptoms
💓 Angina: Supply-demand mismatch

                                            Classic Physical Exam
                                        🔊 Harsh systolic murmur: RUSB/base
📉 Narrow pulse pressure: Fixed stroke volume
💓 Slow rising carotid pulse: "Parvus et tardus"
                                            
🫀 LV heave: Pressure overload

                                    
                                        Management
                                    🔴 Stabilize: Vasopressors for hypotension
🟡 Avoid: Nitroglycerin, beta-blockers
🟢 Definitive: Urgent surgical consultation
🔵 TAVR: Alternative for high-risk patients

                                

 Acute Mitral Regurgitation
                                         Causes
                                        🔗 Chordae rupture: Endocarditis, trauma
💔 Papillary muscle rupture: MI complication
⚡ Acute ischemia: papillary muscle dysfunction
🔄 Prosthetic valve dysfunction

                                    

                                        
                                            Presentation
                                        🫁 Acute pulmonary edema: Volume overload
💓 Holosystolic murmur: Apex, radiates axilla
🔊 S3 gallop: Rapid filling
📉 Hypotension: Low cardiac output

                                    

                                    
                                        Emergency Management
                                    🔴 Vasopressors: Maintain BP (afterload)
🟡 IABP: Reduces afterload temporarily
🟢 Definitive: Urgent surgical repair
🔵 Avoid: Excessive vasodilation

                                

                                    Prosthetic Valve Emergencies
                                         Thrombosis
                                        ❌ INR <2.5: Mechanical valves
🔊 New murmur: Regurgitation
🫁 Pulmonary edema: Acute failure
🔴 Embolic events: Stroke risk

                                    

                                        
                                            Endocarditis
                                        🌡️ Fever: Persistent bacteremia
💓 New murmur: Perivalvular leak
🔴 Emboli: Septic emboli
🫁 Abscess: Periannular complications

                                    

                                        
                                            Structural Failure
                                        🔊 Clicking sound: Leaflet fracture
💓 Regurgitant murmur: Paravalvular leak
🫁 Hemolysis: Anemia, jaundice
📉 Cardiac failure: Acute decompensation

                                    

Management

Thrombosis: Heparin + urgent surgery

Endocarditis: Broad-spectrum ABX + surgery

Structural: TEE-guided intervention

All cases: Urgent cardiac surgery consult

The Vascular Catastrophes

Aortic Dissection

Pain: Sudden, severe, tearing/ripping chest/back pain.
Exam: Look for Pulse/BP Differential (>20 mmHg difference between arms) and new Aortic Regurgitation murmur.
Tx: Aggressive Heart Rate (≤ 60 bpm) and Blood Pressure (SBP ≤ 120 mmHg) control (Esmolol, Labetalol). Emergent Type A surgery.

Ruptured AAA

Triad: Pain (abdominal/flank/back), Pulsatile abdominal mass, and Hypotension. (Only present in ~ 50% of cases).
Key: Consider in all elderly patients with back/abdominal pain and hypotension/syncope.
Tx: Immediate surgical consult. Permissive Hypotension (target SBP ~ 90 mmHg) to avoid dislodging clot.

Diagnosis and Treatment Goals

Hypertensive Emergency

Definition: Severe hypertension (≥ 180/120 mmHg) PLUS acute end-organ damage (e.g., encephalopathy, stroke, acute HF, ACS, aortic dissection, acute renal failure).
Goal: Reduce MAP by 10-15% in the first hour, and by max 25% in the first day. (Exceptions: Aortic Dissection requires *immediate* SBP ≤ 120 mmHg).
Tx: IV titratable agents (Labetalol, Nicardipine, Esmolol).

Hypertensive Urgency

Definition: Severe hypertension (≥ 180/120 mmHg) WITHOUT evidence of acute end-organ damage.
Goal: Do NOT acutely lower BP in the ED. Risk of cerebral hypoperfusion outweighs benefits.
Tx: Restart home meds or start oral agent. Discharge with close outpatient follow-up.

Three Major Categories of Syncope

Reflex (Neurally Mediated)

Vasovagal: Classic faint, triggered by stress, pain, or sight of blood. Prodrome (nausea, diaphoresis).
Situational: Triggered by cough, micturition, defecation.
Carotid Sinus: Triggered by neck compression/shaving.

Orthostatic Hypotension

Caused by failure of baroreflex → hypotension upon standing.
Etiologies: Volume depletion (dehydration), medications (diuretics, antihypertensives), autonomic dysfunction (DM, Parkinson's).
Diagnosis: Drop of SBP ≥ 20 or DBP ≥ 10 mmHg within 3 minutes of standing.

Cardiac Syncope (High Risk)

Arrhythmic: VT, high-grade blocks. Often abrupt, without prodrome.
Structural: Severe Aortic Stenosis, HOCM, Tamponade, Pulmonary Embolism (obstructive).
Key: Cardiac syncope is ~ 5 times more likely to result in adverse events than non-cardiac.

Red Flags & High-Risk Features

Cardiac Red Flags

Syncope during exertion (structural heart disease, increased risk).
Syncope while supine (arrhythmia, increased risk).
Associated symptoms: Chest pain, dyspnea, palpitations prior to LOC.
Family history of sudden cardiac death.

Essential Initial Workup

ECG: Must rule out blocks, VT/VF history, long QT, or WPW.
Orthostatic Vitals: Must be performed in all patients.
Labs: Hgb (anemia), Troponin (ischemia), B-HCG (pregnancy).
POCUS: If heart failure or structural disease is suspected.

Canadian Syncope Risk Score (CSRS)

A validated clinical decision tool to identify patients at low risk for serious outcomes within 30 days:

Low Risk (Score -3 to 0):

• No serious underlying diagnosis
• No adverse events at 30 days
• Safe for discharge with follow-up

High Risk (Score ≥1):

• 2.5% risk of serious outcome
• Requires hospital admission
• Further cardiac evaluation needed

Disposition Decision

Hospital admission is required for all patients with cardiac syncope or those with high-risk features (e.g., HF history, abnormal ECG, exertional syncope), even if the initial workup is non-diagnostic.

Essential Cardiac Drugs for Emergency Use

Vasopressors & Inotropes

Norepinephrine (Levophed)

Indication: Hypotension, septic/cardiogenic shock
Dose: 0.05-0.5 mcg/kg/min IV
Effects: α₁ > β₁ (vasoconstriction)
Caution: Monitor extremities for ischemia

Epinephrine

ACLS arrest: 1 mg IV/IO every 3–5 min (all arrest rhythms)
Anaphylaxis (adult IM): 0.3–0.5 mg IM (1:1000) — different concentration/route than arrest dosing
β₁β₂α₁ effects: Inotropy + chronotropy + vasoconstriction (dose-dependent)
Infusion: titrate (commonly started ~0.05–0.5 mcg/kg/min) per protocol

Dopamine

Second-line agent: After Norepinephrine
Medium (5-10 mcg/kg/min): Inotropy (β₁)
High (10-20 mcg/kg/min): Vasoconstriction (α₁)
Note: NO "Renal Dose" benefit

Antiarrhythmics

Amiodarone

Refractory VF/pVT: 300 mg IV/IO first, then 150 mg
Stable wide-complex / AF (selected): often 150 mg IV over 10 min — indication-specific
Multi-channel blocker (Class III predominant teaching label)
Caution: Hypotension, bradycardia, long half-life

Lidocaine

Refractory VF/pVT option: 1–1.5 mg/kg IV/IO, then 0.5–0.75 mg/kg
Class Ib agent (Na⁺ channel)
Alternative/adjunct option to amiodarone in ACLS algorithms
Caution: CNS toxicity at high cumulative doses

Adenosine

Regular narrow-complex SVT: 6 mg rapid IV push, then 12 mg (if needed)
Half-life: <10 seconds
Diagnostic for SVT vs VT
Caution: WPW (can cause VF)

Antihypertensives

Labetalol

HTN emergency: 20mg IV bolus
Aortic dissection: Preferred agent
α₁β₁β₂ blocker
Caution: Asthma, bradycardia

Nicardipine

HTN emergency: 5mg/hr IV infusion
CCB - pure vasodilator
Less reflex tachycardia
Titratable, predictable

Anticoagulants & Antiplatelets

Heparin

STEMI/NSTEMI: 60 IU/kg IV bolus
LMWH alternative: Enoxaparin
Monitor: aPTT 1.5-2x normal
Reversal: Protamine

Antiplatelets

Aspirin: 325mg PO/NG chewed
Clopidogrel: 300-600mg loading
Ticagrelor: 180mg loading
Give before cath when possible

Medication Mnemonics for Students

Pressor Order

"LED" = Levophed → Epinephrine → Dopamine

(Increasing vasoconstriction)

AF Rate Control

"BBD" = Beta-blockers → CCBs → Digoxin

(Decreasing renal function)

Antiarrhythmics

"A Dozen Little Children" = Amiodarone, Dofetilide, Lidocaine, etc.

HTN Emergency

"LIP" = Labetalol, Nicardipine, Nitroprusside

                         Critical Pearls
                        Know your doses cold! Practice ACLS algorithms regularly
Double-check calculations - medication errors kill
Monitor for side effects: Hypotension, bradycardia, torsades
Reversal agents: Know common reversal agents for anticoagulants you use
Drug interactions: Consider comorbidities and other meds

                    

Essential Points to Remember

Time-Critical Interventions

Door-to-device (STEMI): system goal often ≤90 min (transfer pathway often ≤120 min FMC-to-device)
Door-to-needle: ≤30 min when fibrinolysis is the chosen strategy
Defibrillation: biphasic energy per manufacturer (often ~120–200 J first shock); minimize delay
Post-ROSC: prevent fever / TTM per protocol (e.g. 32–36°C or <37.5°C), early PCI for STEMI-equivalent
Early recognition saves lives

Critical Assessments

ECG within 10 minutes for high-risk presentations
Beck's Triad for tamponade
Orthostatic vitals for all syncope patients
Canadian Syncope Risk Score for disposition decisions
Serial reassessment - conditions evolve

Essential Medications

AF Rate Control: β-blockers first-line
STEMI Cocktail: Aspirin + Heparin + Antiplatelets
Shock: Norepinephrine for hypotension
VT/VF: Amiodarone or Lidocaine
Know your doses! Practice prevents errors

Remember
                            the H's and T'sHypovolemia
Hypoxia
Hydrogen ion (acidosis)
Hypo/Hyperkalemia
Hypothermia
Toxins
Tamponade
Tension PTX
Thrombosis (PE)
Thrombosis (MI)

This comprehensive presentation covers the complete spectrum of critical cardiac emergencies from ACS to arrhythmias, tamponade to aortic dissection, with special focus on ED-specific management and the latest evidence-based protocols.

New topics added: Atrial Fibrillation in the ED • Post-Cardiac Arrest Care • Cardiac Medications • Code STEMI Activation

Always consult local protocols and consider patient-specific factors in clinical decision-making.

🙏

Thank you for your attention and dedication to saving lives!

You've completed the comprehensive guide to Critical Cardiac Emergencies. Remember: Every second counts in cardiac emergencies - your knowledge can make the difference between life and death.

Selected References

Educational resource only (SASEM). Algorithms and doses can change — always verify against the latest AHA/ESC/ACC publications and your hospital protocol. Content reviewed for structure 2026; re-check focused ACLS updates regularly.

🐦

Follow on X (Twitter)

@I_am_Doctor

📧

Get in Touch

[email protected]

Bookmarked Slides

Critical Cardiac Emergencies

ABDULRAHMAN ALZAHRANI, MD, SBEM

Important Notice

Start Here

Quiz 16Q

Assessment

MCQ 5

CPR Helper

Cases

Calculators

Presentation

The Cardiac Emergency Spectrum

Core Categories of Cardiovascular Collapse

Ischemia

Electrical

Pump Failure

Mechanical

Valvular

Vascular

Pressure

Syncope

Summary

Initial Approach

The First 10 Minutes & Beyond

Priority Actions

Focused Workup

ACS 1: Introduction to Acute Coronary Syndromes

🔍 What is an Acute Coronary Syndrome?

📊 ACS Epidemiology

Global Burden

Time is Muscle

🔬 Pathophysiology of Myocardial Ischemia

The Ischemic Cascade

⚡ Clinical Presentation

Typical Chest Pain

Atypical Presentations

Key Learning Points

ACS 2: STEMI ECG Patterns

STEMI Criteria (Key Takeaways)

STEMI Localization & ECG Patterns

Anterior STEMI

Lateral STEMI

Inferior STEMI

Posterior STEMI

STEMI ECG Gallery

Critical Reminders

ACS 3: NSTEMI & Unstable Angina ECG Patterns

🔍 NSTEMI vs Unstable Angina

NSTEMI (Non-ST-Elevation MI)

Unstable Angina

📊 ECG Changes in NSTEMI

Common ECG Findings

ST Depression

T-Wave Inversion

🖼️ NSTEMI ECG Gallery

⚠️ High-Risk ECG Features

Urgent Cath Lab Activation

Clinical Pearls

ACS 4: Biomarkers in ACS

🧪 Cardiac Biomarkers Overview

Troponin I/T

CK-MB

Myoglobin

🔬 High Sensitive Troponin (hs-Tn) - Worldwide Standard

Why High Sensitive Troponin Matters

🌍 Global Recommendation

⚡ Clinical Advantages

📊 hs-Tn Reference Ranges & Interpretation

Key Points for hs-Tn Use

📈 Troponin Kinetics

🔬 Pathophysiology of Myocardial Ischemia

The Ischemic Cascade

⚡ Clinical Presentation

Typical Chest Pain

Atypical Presentations

Key Learning Points

ACS 5: Risk Stratification in ACS

📊 Risk Stratification Scores

TIMI Risk Score for NSTEMI/UA