Stable Angina pectoris, Vasospastic angina [Dx and treatment]; Pulmonary HTN Flashcards
Stable Angina basic definition
Angina aka pain or pressure that is felt retrosternal, lasting about 8-10 mins or less that occurs during physical activity or emotional stress situations and dessipates at rest is called a Stable Angina
This occurs mainly due to ~70% lumen constriction of coronary artery, called stenosis. In situations of increased myocardial oxygen demand, the stenotic vessel cannot appropriately supply heart with adequate blood, thus causing ischemic pain [reversible damage]
Vasosplastic Angina basic definition
It is also refered to as Prinzmetal Angina. This occurs due to vasospasms of coronary arteries which causes short lasting complete occlusion [ST elevations on ECG] at random points of time [irrespective of rest or physical activity]
Dx of Stable and Prinzmetal Angina
Stable Angina:
- ECG rest [normal, but can show signs of previous MI like pathologic Q waves if any]
- Cardiac enzyme levels like Troponins [normal]
- Exercise Stress Test
- Pharmacological Stress Test [using dobutamine for patients not compliant or compatable with Exercise]
- Exercise Stress imaging [CMRI, CCTA]
- Coronary Angiography [GOLD standard but invasive, only use when no other test gives successful result or doesnt match with clinical presentation]
- Xray/CTA/Echo for Ddx
Prinzmetal Angina:
- Coronary Angiography in presence of Ergonovine or Acetylcholine to provoke vasospasm
Treatment options for Stable and Prinzmetal Angina
Idea - Reduce Oxygen demand and Increase Oxygen delivery
Stable Angina:
- Treatment of comorbidities
- Risk factor management
- Aspirin and Beta blockers [shows reduced mortality]
- Nitroglycerine helpful during angina bouts
- Antiplatelet aggregation therpay could be useful to prevent clot formation or preogression to Unstable Angina or plaque rupture
- Revascularization via PCI
Prinzmetal Angina:
- Calcium Channel Blockers [reduces cardiac oxygen demand] with or without nitrates
- DO NOT give aspirin or Beta blockers
- Long acting Nitrates
- Short acting Nitroglycerine to help during attacks
- Alpha blockers + Long acting Nitrates may reduce occurence of spasms
Pre and post capillary, Pulm Arterial HTN
Pulmonary Hypertension definition
Pulmonary Hypertension is defined as > 20 mmHg mean Pulmonary arterial pressure [mPAP] at rest [2009 guidelines suggested > 25 mmHg mPAP]. Normal mPAP is between 10-14 mmHg
PH can be divided based on location of problem:
- Precapillary PH - pulmonary vascular remodelling leading to increased pulmonary vascular resistance | Typically caused by PAH, chronic lung diseases, chronic thromboembolism or multifactorial in nature
- Postcapillary PH - increased pulmonary venous pressure typically due to Left heart diseases and blood backup [ex. Aortic, Mitral regurgitations, LHF or CHF] | Pulmonary vascular resistance is however, usually normal and not elevated as in Precapillary PH
Pulmonary Arterial Hypertension:
- It is a subtype of Precapillary PH and not a separate type of PH
- It is a cause and not a consequence of PH
- It occurs due to loss and obstructive remodelling of pulmonary vascular beds
Divided into 5 groups based on WHO classification
Etiologies of Pulmonary Hypertension
WHO classifies Pulmonary Hypertension into 5 groups based on etiology
Group 1 PH: Pulmonary Arterial Hypertension
- Idiopathic
- Hereditary [BMPR2 loss-of-function mutation; encodes inhibitors for vascular smooth muscle cell proliferation]
- Drug induced [Methamphetamines, Sympathomimetic appetite suppressors, Chemo drugs]
- Connective Tissue disorders [SS]
- Portopulmonary HTN
- Congenital heart disease [Left-to-right shunts, Eisenmenger syndrome]
- HIV infection; Schistosomiasis
- Persistent Pulmonary HTN of newborns
Group 2 PH: Left Heart Diseases
- Congestive HF
- Valvular Heart Diseases [Aortic and Mitral stenosis]
- Hypoplastic heart, Aortic coarctation, HCM, LVOT obstruction which all can lead to postcapillary PH
Group 3 PH: Chronic Lung Diseases
- Includes conditions causing chronic hypoxemia
- Obstructive Lung Diseases [COPD, Emphysema, Sleep Apnea]
- Restrictive Lung Diseases [ILD]
- High altitude
- Developmental lung disorders, mixed obstructive and restrictive diseases
Group 4 PH: Pulmonary Artery Obstruction
- Chronic Thromboembolic Pulmonary HTN [recurrent microthrombi]
- Extrinsic compression due to tumours, Arteritis, Congenital PA stenosis, Fibrosing Mediastinitis
Group 5 PH: Unclear Multifactorial Mechanisms
- Hematologic [Sickle cell, chronic hemolytic anemia]
- Systemic [Sarcoidosis, Neurofibromatosis, Langerhans cell histiocytosis]
- Metabolic [CKD, Gauchers Disease]
- Multiple Congenital heart diseases at once
Conditions at high risk of Pulmonary Hypertension
- Family History
- Positive BMPR2 in 1st-degree relative
- Exposure or usage of drugs inducing PH
- Scleroderma
- MCTD
- HIV
- Portal Hypertension
- Recent surgical history [3-6 months] for congenital Left-to-Right shunt repair
Require regular checkups for PH symptoms
Increased Pulm vascular resistance, venous pressure, blood flow
Basic Pathophysio of Pulmonary Hypertension
Increased Pulmonary Vascular Resistance:
- Occlusive vasculopathy [idiopathic PAH; connective tissue disorders]
- COPD, Obstructive Sleep Apnea [causing chronic hypoxic vasoconstriction and thickening of vessle wall]
- Right heart hypertrophy and failure, arrhythmias
- Inflammation causing intimal fibrosis
- Arteriosclerosis from high endothelin and low vasodilators of vessel walls
Increased Pulmonary Venous Pressure:
- Volume or Pressure overload from Left heart diseases
- Mitral and Aortic Regurgitations
- CHF
Increased Pulmonary Blood Flow:
- Left-to-Right shunting [ASD, VSD, PDA]
- Portopulmonary HTN
- Sickle cell Anemia [Anemia induced increase in CO]
Clinical Features of Pulmonary Hypertension
- Dyspnea and/or Syncope on exertion
- Chest pain [does not respond to nitrates]
- Fatigue
- Cyanosis
- Symptoms of underlying etiologies
- Hoarsness [less common]
- Cough, Hemoptysis [less common]
- Clubbing of Fingers
- Lound and Palpable second heart sound [often split]
- Jugular vein distention
- Palpitations, Pulmonary edema, hepatojugular reflex [signs of right heart failure]
- Parasternal heave
Dx approach for Pulmonary Hypertension
- Screen and Monitor patients with conditions of high risk for pulmonary hypertension
- Transthoracic Echocardiography for high clinical suspecion of PH
- If TTE shows high mPAP and arterial pressures, find underlying etiology [NT-proBNP | Arterial Blood gas, PFTs, DLco, CT chest and Sleep studies | V/Q scan | Drug screen, Genetic testing, Connective tissue screening panel]
- Confirmatory Right heart Catheterization if etiology is unclear but PH is evident from TTE and/or severe PH is identified
- ECG typically shows non-specific signs [Right axis deviation, RV Hypertrophy, P Pulmonale, Incomplete or Complete RBBB, S1Q3T3, Ischemic heart disease signs]
Treatment approch to Pulmonary Hypertension
- Conduct a Severity Assessment to guide treatment plans [WHO-FC modelled from NYHA functional capacity for symptomatic HF]
- Group 1 PH get CCBs and Pulmonary vasodilators like PDE5i + Endothelin Antagonists for WHO-FC I/II or Parenteral prostaglandins for WHO-FC III/IV
- Groups 2, 3 and 4 are focused on treating underlying causes
- Group 5 get both underlying etiology treatment plus vasodilator therapy on case-by-case basis
