Angina
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"angina pectoris"[MeSH Terms] AND management
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Angina Pectoris - Complete Overview
Definition
Angina pectoris is intermittent chest discomfort or pain caused by transient, reversible myocardial ischemia that is insufficient to cause myocyte necrosis. Pain results from ischemia-induced release of adenosine, bradykinin, and other molecules that stimulate sympathetic and vagal afferent nerves, producing the characteristic chest discomfort.
Not all ischemic events are perceived as pain. Silent ischemia is particularly common in the elderly and in diabetic neuropathy, manifesting as dyspnea, nausea, palpitations, diaphoresis, fatigue, or no symptoms at all.
- Robbins & Kumar Basic Pathology, Robbins, Cotran & Kumar Pathologic Basis of Disease
Types of Angina
1. Stable (Typical) Angina
- The most common form
- Caused by chronic stenosing coronary atherosclerosis creating an oxygen supply/demand mismatch
- Predictable, reproducible episodes triggered by increased cardiac demand: physical exertion, emotional stress, anemia, tachycardia, environmental cold
- Does not occur at rest
- Classic presentation: crushing or squeezing substernal chest pain radiating to the left arm or jaw (referred pain)
- Relieved by rest or nitroglycerin (within minutes)
Canadian Cardiovascular Society (CCS) Classification:
| Class | Description |
|---|---|
| I | No angina with ordinary physical activity |
| II | Minimal limitation - angina with exertion or emotional stress |
| III | Severe limitation - angina with ordinary physical activity |
| IV | Unable to perform any activity without angina; symptoms at rest or minimal exertion |
- Rosen's Emergency Medicine
2. Unstable Angina (UA)
- Part of the Acute Coronary Syndrome (ACS) spectrum
- Three presentations:
- Rest angina: occurs at rest, lasts >20 minutes, within 1 week of presentation
- New-onset angina: CCS class II or higher, onset within 2 months
- Progressive (crescendo) angina: previously stable pattern becomes more frequent, longer, or more easily provoked (within 2 months, reaching at least CCS class III)
- Pathophysiology: plaque rupture/erosion + superimposed thrombosis + vasospasm + distal thrombus embolization
- Also called: preinfarction angina, accelerating angina, intermediate coronary syndrome, pre-occlusive syndrome
- ECG findings: T-wave and ST-segment changes (ST depression or T-wave inversion, unlike STEMI)
- Associated with evidence of myocyte injury in the majority of cases
- A harbinger of MI - must be treated aggressively
3. Prinzmetal (Variant) Angina
- Caused by coronary artery vasospasm at rest
- Can occur in vessels with or without significant atherosclerosis
- Episodes are unrelated to physical activity, heart rate, or blood pressure
- ECG: ST-segment elevation (transient) - can be indistinguishable from STEMI on presentation
- Responds promptly to vasodilators (nitroglycerin, calcium channel blockers)
- Beta-blockers are NOT effective (and may worsen spasm)
Pathophysiology Summary
The core mechanism across all angina types is myocardial oxygen supply < demand:
| Factor | Supply | Demand |
|---|---|---|
| Determinants | Coronary blood flow, O₂ content | Heart rate, contractility, wall stress (preload + afterload) |
| Disruption | Atherosclerosis, spasm, thrombosis | Exertion, tachycardia, hypertension, anemia |
- In stable angina: fixed atherosclerotic narrowing limits maximum coronary flow reserve
- In unstable angina: acute plaque disruption + thrombus formation
- In variant angina: dynamic spasm reduces coronary blood flow
Clinical Features & Diagnosis
| Feature | Stable | Unstable | Variant (Prinzmetal) |
|---|---|---|---|
| Onset | With exertion | At rest or minimal exertion | At rest (often nocturnal) |
| Duration | 2-10 min | >20 min | 5-30 min |
| ECG | Normal or ST depression with exercise | ST depression / T-wave inversion | Transient ST elevation |
| Troponin | Negative | May be elevated (NSTEMI overlap) | Usually negative |
| Cause | Fixed stenosis | Plaque rupture + thrombus | Vasospasm |
| Relief | Rest, NTG | NTG (partial), requires treatment | NTG, CCBs |
Management
Stable Angina
Acute relief:
- Sublingual nitroglycerin (NTG) - releases NO → increases cGMP → smooth muscle relaxation → venodilation reduces preload, reduces O₂ demand
Prophylaxis (anti-anginal drugs):
| Drug Class | Examples | Mechanism | Notes |
|---|---|---|---|
| Nitrates | Isosorbide dinitrate/mononitrate, transdermal NTG | Vasodilation, reduce preload | Nitrate tolerance - require nitrate-free interval |
| Beta-blockers | Propranolol, atenolol, metoprolol | Decrease HR, CO, BP → reduce O₂ demand | First-line for stable angina; avoid in variant angina |
| Calcium channel blockers (CCBs) | Verapamil, diltiazem, amlodipine, nifedipine | Reduce vascular resistance, HR, contractility | Useful when beta-blockers contraindicated; dihydropyridines preferred if heart failure concerns |
| Ranolazine | Ranolazine | Late sodium current inhibitor | For refractory angina; does not affect HR or BP |
Disease-modifying / risk-reduction therapy:
- Aspirin (antiplatelet) + statin (plaque stabilization, LDL lowering)
- ACE inhibitor if coexisting HF, diabetes, or hypertension
- Control of risk factors: hypertension, diabetes, dyslipidemia, smoking cessation
Unstable Angina (ACS Management)
- Dual antiplatelet therapy: aspirin + clopidogrel (P2Y12 inhibitor)
- Anticoagulation: IV heparin or LMWH
- Nitroglycerin + beta-blockers
- CCBs for refractory ischemia
- GP IIb/IIIa inhibitors (e.g., abciximab) if proceeding to PCI
- Statin therapy and ACE inhibitor
- Coronary angiography + PCI/CABG in high-risk patients
Variant (Vasospastic) Angina
-
Nitrates + calcium channel blockers - first-line combination; ~70% complete abolition of attacks, ~20% marked reduction
-
All CCBs appear equally effective
-
Beta-blockers are not indicated (may worsen spasm)
-
Surgical revascularization and angioplasty are not indicated unless significant fixed stenosis is also present
-
Katzung's Basic and Clinical Pharmacology, 16th Edition
Key Drug Toxicities to Remember
| Drug | Main Adverse Effects |
|---|---|
| Nitroglycerin | Orthostatic hypotension, reflex tachycardia, headache; contraindicated with PDE-5 inhibitors (sildenafil, etc.) |
| Beta-blockers | Bronchospasm (avoid in asthma), AV block, acute HF exacerbation |
| Verapamil/Diltiazem | AV block, acute HF, constipation |
| Nifedipine (short-acting) | Excessive hypotension, reflex tachycardia; prompt-release form contraindicated in angina |
Recent Evidence (2024-2026)
- A 2024 systematic review (PMID: 39353703) found that ischemia with no obstructive coronary artery disease (INOCA) - which includes microvascular angina - carries worse long-term outcomes than previously appreciated, reinforcing the need for active investigation beyond standard coronary angiography.
- A 2025 meta-analysis (PMID: 39980940) found stellate ganglion block to be effective and safe for refractory angina pectoris.
- A 2025 meta-analysis (PMID: 40684096) assessed the coronary sinus reducer device for refractory angina - showing efficacy and safety, relevant for patients failing medical therapy.
Sources: Robbins & Kumar Basic Pathology | Robbins, Cotran & Kumar Pathologic Basis of Disease | Rosen's Emergency Medicine | Katzung's Basic and Clinical Pharmacology, 16th Edition | Goldman-Cecil Medicine
Dyspnea
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"dyspnea"[MeSH Terms] AND diagnosis
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Dyspnea - Complete Overview
Definition
Dyspnea is an uncomfortable awareness of breathing - the subjective sensation of breathlessness or shortness of breath. Common synonyms include "air hunger" and "breathlessness." It is one of the most frequent complaints prompting patients to seek medical evaluation and is alarming to most patients, who often fear a dire underlying cause.
Dyspnea is a subjective complaint with no single objective correlate - it does not always correlate with tachypnea, oxygen saturation, or pulmonary function test results.
- Fishman's Pulmonary Diseases and Disorders | Guyton and Hall Textbook of Medical Physiology
Pathophysiology - How Dyspnea Is Generated
Three major factors contribute to the sensation of dyspnea:
1. Abnormal Respiratory Gases
- Hypercapnia (elevated CO₂) is the most potent driver - stimulates central and peripheral chemoreceptors
- Hypoxia is a less potent direct stimulus but contributes indirectly
- Acid-base disturbances (metabolic acidosis → compensatory hyperventilation = Kussmaul breathing) can produce "air hunger" that is visually obvious but not always consciously experienced by the patient
2. Increased Respiratory Muscle Work
- Even with normal blood gases, if the respiratory muscles must work excessively to maintain ventilation (e.g., severe airflow obstruction, stiff lungs, neuromuscular weakness), the sense of effort itself generates dyspnea
- The motor cortex sends a "corollary discharge" signal simultaneously to the sensory cortex and to the respiratory muscles - if the actual ventilation achieved is less than expected (efferent-afferent mismatch), dyspnea intensifies
3. Psychological and Neurogenic Factors
- Anxiety heightens the perception of breathlessness
- Psychogenic dyspnea can occur with entirely normal blood gases and respiratory mechanics
- Blunting of sensorium (narcotics, acute hypercapnia) can suppress the sensation even with abnormal breathing
Afferent pathways involved:
-
Upper airway and face receptors (mechanoreceptors)
-
Lung and airway receptors (via vagus nerve) - irritant receptors cause chest tightness
-
Chest wall mechanoreceptors
-
Peripheral chemoreceptors (carotid bodies) - detect O₂ and CO₂
-
Central chemoreceptors (medulla) - primarily CO₂/pH-sensitive
-
Fishman's Pulmonary Diseases and Disorders | Guyton and Hall Textbook of Medical Physiology
Quality of Dyspnea - Diagnostic Clues
Different underlying causes produce qualitatively distinct sensations:
| Sensation Described | Likely Cause |
|---|---|
| "Hunger for air," "urge to breathe" | Heart failure, hypercapnia |
| "Increased work/effort to breathe" | Airway obstruction (COPD, asthma), neuromuscular disease |
| "Chest tightness or constriction" | Bronchoconstriction (asthma, COPD), pulmonary edema |
| "Heavy breathing," "rapid breathing," "need to breathe more" | Deconditioning |
| Breathing discomfort that worsens at rest but improves with activity | Anxiety/psychogenic dyspnea |
- Goldman-Cecil Medicine
Special Patterns of Dyspnea
| Pattern | Definition | Most Common Cause(s) |
|---|---|---|
| Orthopnea | Dyspnea in the recumbent (supine) position | Left ventricular failure, severe COPD; instant orthopnea = bilateral diaphragm paralysis |
| Paroxysmal nocturnal dyspnea (PND) | Severe dyspnea waking the patient from sleep, forcing upright position | Left ventricular failure; also COPD (pooled secretions), nocturnal aspiration |
| Platypnea | Dyspnea in the upright position (relieved by lying down) | Intracardiac or intrapulmonary shunts (e.g., hepatopulmonary syndrome) |
| Trepopnea | Dyspnea in one lateral decubitus position | Unilateral pleural effusion, heart disease |
| Exertional dyspnea | Dyspnea with physical activity | Broad - cardiac, pulmonary, deconditioning, anemia |
- Murray & Nadel's Textbook of Respiratory Medicine
Causes of Dyspnea - Organized by Onset
Acute Dyspnea (minutes to hours)
| Cardiovascular | Pulmonary | Other |
|---|---|---|
| Myocardial ischemia / MI | Pulmonary embolism | Severe anemia |
| Acute heart failure / pulmonary edema | Pneumothorax | Metabolic acidosis (DKA, salicylates) |
| Pericardial tamponade | Acute severe asthma | Anaphylaxis (upper airway) |
| Hypertensive emergency | Pneumonia | Anxiety/panic attack |
| Aortic dissection | Upper airway obstruction | Drug overdose (salicylates) |
Subacute / Chronic Dyspnea (days to months/years)
| Cardiac | Pulmonary | Other |
|---|---|---|
| Chronic heart failure (left-sided) | COPD | Chronic anemia |
| Valvular heart disease | Asthma | Obesity / deconditioning |
| Pulmonary hypertension | Interstitial lung disease (ILD) | Neuromuscular disease (ALS, myasthenia) |
| Pleural effusion | Thyroid disease (hyperthyroidism) | |
| Lung cancer | Psychogenic dyspnea |
- Goldman-Cecil Medicine | Murray & Nadel's Textbook of Respiratory Medicine
Clinical Assessment
History Key Points
- Onset: sudden (pneumothorax, PE, MI) vs. gradual (COPD, HF)
- Timing: at rest, nocturnal (PND), exertional only, postural (orthopnea)
- Severity quantification: How many stairs before stopping? Walking distance on flat ground? Dyspnea with talking, eating, or dressing?
- Triggers: cigarette smoke, dusts, allergens, cold air (suggests reactive airways)
- Relieving factors: rest, sitting upright, albuterol, diuretics
- Associated symptoms:
- Wheezing → obstructive airways disease
- Productive cough, fever → pulmonary infection
- Leg edema → heart failure or DVT/PE
- Chest pain → ACS, pneumothorax, pleuritis, PE
- Palpitations → arrhythmia driving dyspnea
Patients often unconsciously adapt - they walk more slowly or avoid stairs, and attribute limitation to "aging." Probing is essential to uncover true functional limitation.
Physical Examination
- Respiratory rate, oxygen saturation (SpO₂)
- Lung auscultation: crackles (pulmonary edema, ILD, pneumonia), wheeze (obstruction), absent breath sounds (pneumothorax, effusion)
- Cardiac exam: S3 gallop, elevated JVP, peripheral edema (heart failure); loud P2 (pulmonary hypertension)
- Accessory muscle use, pursed lip breathing → severe COPD
- Cyanosis - central (SpO₂ low) vs. peripheral
Investigations
| Test | What it Answers |
|---|---|
| SpO₂ / ABG | Hypoxemia? Hypercapnia? Acid-base status? |
| CXR | Cardiomegaly, pulmonary edema, pneumonia, pneumothorax, effusion |
| ECG | Ischemia, arrhythmia, right heart strain (PE) |
| BNP / NT-proBNP | Heart failure (very sensitive) |
| Troponin | ACS |
| CBC | Anemia |
| D-dimer / CT-PA | Pulmonary embolism |
| Spirometry / PFTs | Obstructive (COPD, asthma) vs. restrictive (ILD) pattern |
| Echocardiogram | LV function, valvular disease, pericardial effusion, pulmonary HTN |
| CPET (cardiopulmonary exercise test) | Unexplained dyspnea - distinguishes cardiac vs. pulmonary vs. deconditioning |
- Goldman-Cecil Medicine
Management Principles
Management targets the underlying cause. Key principles:
| Cause | Treatment Approach |
|---|---|
| Heart failure | Diuretics, ACE inhibitors/ARBs, beta-blockers, SGLT2 inhibitors |
| COPD | Bronchodilators (LABA, LAMA), inhaled corticosteroids, pulmonary rehab |
| Asthma | Inhaled corticosteroids, SABA/LABA, avoid triggers |
| Pulmonary embolism | Anticoagulation (heparin → DOAC or warfarin) |
| Pneumothorax | Observation (small), aspiration or chest drain (large/tension) |
| Anemia | Treat underlying cause, iron/B12/folate, transfusion if severe |
| Psychogenic / anxiety | Breathing techniques, anxiolytics, CBT |
Symptomatic relief of dyspnea (irrespective of cause):
- Low-dose opioids (oral/IV morphine) - most evidence-based symptomatic treatment for refractory dyspnea in palliative/end-stage disease
- Supplemental oxygen - beneficial if SpO₂ <88-90%; does not consistently relieve dyspnea in non-hypoxemic patients
- Fan or cool airflow to the face - stimulates facial mechanoreceptors, reduces dyspnea perception
- Breathing techniques (pursed lip breathing, diaphragmatic breathing) - proven benefit in COPD and serious respiratory illness (PMID: 39477355)
Measurement Scales
| Scale | Use |
|---|---|
| Borg Scale (0-10) | Exertional dyspnea - quick clinical rating |
| MRC (Medical Research Council) Dyspnea Scale (1-5) | Chronic dyspnea in COPD and general assessment |
| NYHA Classification | Dyspnea in heart failure (Class I-IV) |
| Pulmonary Functional Status and Dyspnea Questionnaire | Validated research/clinical tool |
- Murray & Nadel's Textbook of Respiratory Medicine
Recent Evidence (2024-2026)
- A 2026 JAMA systematic review (PMID: 41729549) examined clinical examination features for volume overload - a key cause of dyspnea - refining the rational clinical examination approach.
- A 2024 systematic review (PMID: 39477355) confirmed that breathing techniques (pursed lip breathing, diaphragmatic breathing, yoga breathing) significantly reduce dyspnea symptoms in serious respiratory illness.
Sources: Fishman's Pulmonary Diseases and Disorders | Murray & Nadel's Textbook of Respiratory Medicine | Goldman-Cecil Medicine | Guyton and Hall Textbook of Medical Physiology | Rosen's Emergency Medicine
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