Coronary Artery Disease, Angina and Myocardial Infarction - Concept Map
Coronary Artery Disease and Acute Coronary Syndrome
Related concepts
Pathophysiology of CAD
Sub concepts
- Atherosclerosis and plaque formation
- Endothelial injury and inflammation
- LDL deposition in arterial intima
- Progressive luminal narrowing
- Myocardial ischemia when demand exceeds supply
- Plaque rupture and thrombosis
Relationship to central
Foundation of disease process
Risk Factors
Sub concepts
- Non-modifiable: age, sex, family history, ethnicity
- Modifiable: hypertension, dyslipidemia, diabetes mellitus, smoking
- Lifestyle factors: obesity, physical inactivity, stress
- DOH PhilPEN screening targets
- Prevention as pillar of NCD program
Relationship to central
Modifiable and non-modifiable causes
Angina Pectoris
Sub concepts
- Stable angina: exertional, predictable, relieved by rest and nitroglycerin
- Unstable angina: at rest, frequent, not relieved by rest, form of ACS
- Variant angina: coronary spasm, nocturnal
- Normal cardiac biomarkers
- Clinical presentation: substernal pressure, radiation to arm/jaw/back
Relationship to central
Reversible myocardial ischemia presentation
Myocardial Infarction
Sub concepts
- Complete coronary occlusion
- Prolonged ischemia leading to permanent damage
- STEMI: ST-segment elevation, full-thickness injury
- NSTEMI: ST depression or T-wave inversion, partial occlusion
- Elevated troponin and CK-MB
- Severe, crushing chest pain lasting over 20 minutes
- Atypical presentations in women, elderly, diabetics
- Silent MI in diabetics due to neuropathy
Relationship to central
Irreversible myocardial necrosis
Acute Coronary Syndrome Management
Sub concepts
- MONA framework with modern nuance
- Aspirin: chewable 160-325 mg, first-priority drug
- Nitroglycerin: sublingual, up to 3 doses, contraindications
- Oxygen: only for hypoxia, SpO2 below 90-94%
- Morphine: reserved for pain unrelieved by nitroglycerin
- Reperfusion therapy: PCI vs thrombolytics
- Adjunct pharmacology: antiplatelets, anticoagulants, beta-blockers, ACE inhibitors, statins
Relationship to central
Treatment and intervention strategies
Reperfusion Therapy
Sub concepts
- PCI: preferred first-line, door-to-balloon under 90 minutes
- Thrombolytic therapy: alteplase, reteplase, tenecteplase, streptokinase
- Door-to-needle time under 30 minutes
- Time window: ideally within 6 hours, up to 12 hours
- Bleeding risk and absolute contraindications
- Reperfusion signs and dysrhythmias
Relationship to central
Critical for restoring coronary blood flow
Nursing Management and Priorities
Sub concepts
- Pain relief and anxiety reduction
- 12-lead ECG within 10 minutes
- IV access and cardiac marker draw
- Continuous cardiac monitoring for dysrhythmias
- Position upright to reduce oxygen demand
- Bed rest and workload reduction
- Vital signs and rhythm monitoring
- Patient reassurance
Relationship to central
Evidence-based nursing interventions
Complications
Sub concepts
- Dysrhythmias: ventricular fibrillation (leading cause of early death)
- Cardiogenic shock
- Heart failure and pulmonary edema
- Pericarditis and Dressler's syndrome
- Papillary muscle rupture
- Ventricular aneurysm
- Cardiac rupture
Relationship to central
Adverse outcomes requiring intervention
Cardiac Rehabilitation and Patient Teaching
Sub concepts
- Structured, progressive exercise programs
- Phases: inpatient, early outpatient, long-term maintenance
- Nitroglycerin use and storage
- Warning signs recognition and response
- Risk factor modification: smoking cessation, BP control, diabetes management
- Heart-healthy diet: low-saturated fat, low-sodium
- Sexual activity and driving resumption
- Medication adherence
Relationship to central
Long-term recovery and prevention
Diagnostic Tools
Sub concepts
- 12-lead ECG: ST elevation, ST depression, T-wave inversion, Q waves
- Troponin: most specific and sensitive cardiac biomarker
- CK-MB: rises in myocardial necrosis
- Serial biomarker measurement
- Angiography for determining anatomy and stenosis severity
Relationship to central
Confirmation and assessment methods
Angina vs MI Differentiation
Sub concepts
- Cause: reversible ischemia vs irreversible necrosis
- Duration: under 15 minutes vs over 20-30 minutes
- Relief: rest/nitroglycerin responsive vs non-responsive
- Cardiac markers: normal vs elevated troponin/CK-MB
- ECG changes: transient vs persistent ST-T changes
Relationship to central
Clinical distinction for management decisions
Concept connections
- AtherosclerosisMyocardial IschemiaProgressive atherosclerotic plaque narrows coronary artery lumen, reducing blood flow and oxygen supply to myocardium
- Risk FactorsAtherosclerosisModifiable and non-modifiable risk factors accelerate atherosclerotic plaque formation and progression
- Myocardial IschemiaStable AnginaTransient reversible ischemia triggered by exertion or stress results in anginal chest pain
- Plaque RuptureThrombosisRupture of atherosclerotic plaque exposes thrombogenic material, triggering platelet aggregation and thrombus formation
- ThrombosisMyocardial InfarctionComplete coronary artery occlusion by thrombus causes prolonged myocardial ischemia leading to irreversible necrosis
- Unstable AnginaMyocardial InfarctionUnstable angina is a form of ACS that signals impending MI; biomarkers remain normal but tissue damage may occur
- STEMIReperfusion TherapyST-elevation MI requires immediate reperfusion via PCI or thrombolytics to minimize myocardial damage and mortality
- NSTEMIMedical TherapyNSTEMI is managed initially with aggressive medical therapy including dual antiplatelets and anticoagulation before angiography
- AspirinAntiplatelet EffectAspirin irreversibly inhibits platelet aggregation, reducing thrombus formation and improving outcomes in ACS
- NitroglycerinSymptom ReliefNitroglycerin causes vasodilation, reduces preload, and relieves ischemic chest pain in angina
- Contraindications to NitroglycerinRight Ventricular MIRV MI patients are preload-dependent; nitroglycerin-induced vasodilation can cause profound hypotension
- Thrombolytic TherapyBleeding RiskThrombolytic agents dissolve fibrin clots but carry significant risk of hemorrhage including intracranial bleeding
- Continuous Cardiac MonitoringDysrhythmia DetectionContinuous monitoring enables early detection and treatment of potentially fatal dysrhythmias like VF occurring in MI
- DysrhythmiasMI ComplicationsVentricular dysrhythmias are the leading cause of death in the early hours of MI
- Cardiac RehabilitationRisk Factor ModificationStructured rehabilitation includes patient teaching and supervised exercise to modify cardiovascular risk factors
- Patient TeachingMedication AdherenceEducation on nitroglycerin use, antiplatelet therapy, and long-term medications improves compliance and outcomes
- TroponinMI DiagnosisElevated troponin is the most specific and sensitive marker for myocardial necrosis and confirms MI diagnosis
- ECG ChangesSTEMI vs NSTEMIST elevation indicates full-thickness transmural MI; ST depression or T-wave inversion suggests subendocardial or partial MI
- Door-to-Balloon TimeMyocardial SalvageRapid PCI within 90 minutes of arrival maximizes myocardial salvage and reduces infarct size and mortality
- Door-to-Needle TimeThrombolytic EfficacyThrombolytic administration within 30 minutes of arrival improves clot dissolution and clinical outcomes
- Atypical MI PresentationsWomen and ElderlyWomen, older adults, and diabetics often present with fatigue, dyspnea, or indigestion rather than classic chest pain
- Silent MIDiabeticsDiabetic neuropathy masks typical MI pain symptoms, leading to delayed recognition and treatment
- ACE InhibitorsVentricular RemodelingACE inhibitors reduce afterload and prevent pathologic ventricular remodeling following MI
- Beta-blockersMyocardial Oxygen DemandBeta-blockers decrease heart rate, blood pressure, and contractility, reducing myocardial oxygen consumption
- StatinsPlaque StabilizationStatins lower LDL cholesterol and stabilize atherosclerotic plaques, reducing rupture risk
- Cardiogenic ShockMI MortalityCardiogenic shock develops when MI damages a large area of myocardium, impairing cardiac output and perfusion
- Papillary Muscle RuptureAcute MIAcute MI can cause necrosis of papillary muscles, leading to acute mitral regurgitation and pulmonary edema
- PericarditisPost-MI InflammationPost-MI pericarditis and Dressler's syndrome occur as inflammatory responses to myocardial necrosis
- Heart FailureMI ComplicationsSystolic heart failure develops when MI impairs left ventricular contractility and ejection fraction
- Oxygen Saturation MonitoringOxygen TherapySupplemental oxygen is indicated only when SpO2 falls below 90-94%, reflecting current evidence-based practice
Diagrams
Coronary Artery Disease, Angina and MI - Complete Concept Hierarchy
Comprehensive mind map showing the complete hierarchy of concepts related to coronary artery disease, angina, and myocardial infarction. Organizes pathophysiology, risk factors, clinical presentations, management strategies, nursing care, complications, and rehabilitation into interconnected branches.
Acute Coronary Syndrome Recognition and Initial Management Flow
Flowchart depicting the clinical decision pathway for recognizing acute coronary syndrome and implementing appropriate management. Shows the critical distinction between STEMI and NSTEMI, reperfusion strategies, MONA application, and progression to rehabilitation. Emphasizes time-critical interventions and monitoring priorities.
Angina versus Myocardial Infarction Clinical Differentiation
Clinical decision tree for differentiating angina from myocardial infarction based on duration, response to treatment, cardiac biomarkers, and ECG findings. Demonstrates the critical pathway to diagnosis and appropriate management strategy selection.
Pathophysiology of Myocardial Ischemia to Infarction Timeline
Sequence diagram illustrating the temporal progression from stable atherosclerotic disease through angina to acute myocardial infarction. Shows the cascade of events including plaque formation, rupture, thrombus development, and myocardial necrosis, with critical time windows noted.
Nitroglycerin Administration Protocol and Contraindications
Detailed protocol flowchart for safe sublingual nitroglycerin administration in acute coronary syndrome. Emphasizes critical contraindications including hypotension, right ventricular MI, and recent phosphodiesterase inhibitor use. Shows the sequential dosing schedule with vital sign checks between doses, consistent with modern NLE expectations.
MONA Framework - Modern Evidence-Based Application
Modern interpretation of the MONA framework reflecting current evidence-based practice. Highlights the critical nuances: aspirin as first-priority drug, oxygen only for hypoxia, nitroglycerin contraindications and dosing protocol, and morphine reserved for pain unrelieved by nitroglycerin. This reflects changes emphasized in current NLE preparation materials.
Thrombolytic Therapy - Screening and Considerations
Comprehensive screening flowchart for thrombolytic therapy eligibility in STEMI when PCI is unavailable. Details absolute contraindications, time windows, drug selection, and critical monitoring parameters. Emphasizes the major risk of bleeding and the importance of careful patient selection.
Relative Distribution of Early MI Complications
Pie chart showing the relative frequency of major complications occurring in the early phase of myocardial infarction. Demonstrates that dysrhythmias, particularly ventricular fibrillation, are the leading cause of death, emphasizing the critical importance of continuous cardiac monitoring and ACLS readiness in acute MI management.
Cardiac Rehabilitation Phases and Patient Teaching
Comprehensive flowchart of cardiac rehabilitation phases from acute MI through long-term maintenance. Shows the three-phase progression from inpatient stabilization through early supervised outpatient recovery to sustained long-term lifestyle modification and prevention. Includes key teaching topics that address modifiable risk factors and medication management.