Angina Pectoris 1

Angina Pectoris
Chest pain due to myocardial ischemia 2° to coronary artery narrowing or spasm; no necrosis.
1. Retrosternal chest pain radiating to the chest, jaw, neck, shoulders or arms.
2. Sx worse with exertion (exercise or dobutamine).
3. Sx relieved within 5min by rest or GTN.
4. Angina NOT likely if ➝ Pain is pleuritic OR associated with sweatiness, SOB, palpitations.
Types
 Vasospastic (Prinzmetal)
o Cause: Occurs at rest 2o to coronary artery spasm.
o Symptoms:
 Young pt. with chest pain at night (NO depleted ➝ ↑ vagal tone).
 Sx NOT relieved by rest BUT resolves with GTN.
 ECG during pain shows transient ST segment elevation.
o RF:
 Tobacco smoking increases risk.
 HT & hypercholesterolaemia does not.
o Triggers: (cat) Cocaine, alcohol, amphetamine, triptans (pt. with headache).
o Treatment: Stop smoking + CCB ± nitrates. Avoid triptans.
 Stable angina:
o Cause: 2o to atherosclerosis (≥70% occlusion) ➝ NO infarction.
o Sx: Induced by effort, relieved by rest or GTN. Good prognosis.
 Unstable angina:
o Atheroma plaque rupture ➝ thrombosis + incomplete occlusion ➝ NO infarction.
o Sx: Induced by minimal exertion or at rest.
o ECG: ST depression or T-wave inversion (NO cardiac biomarker elevation).
 NSTEMI:
o Atheromatous plaque rupture ➝ Incomplete occlusion ➝ Subendocardial infarction.
o ECG: ST-segment depression and T-wave inversion.
 STEMI:
o Atheromatous plaque rupture ➝ Complete occlusion ➝ Transmural infarction.
o ECG: Peaked T-waves ➝ ST-elevation (minutes) ➝ deep Q-waves (hours).
o New LBBB can be suggestive of STEMI.
Management: Raisin (ranolazine, atenolol, amlodipine, isosorbide mononitrate, ivabradine, nicorandil)
Coronary Artery Disease / IHD
Ischemic Heart Disease
 Stable angina & ACS (unstable angina + MI).
 Unstable angina has NO myocardial necrosis thus NOT release troponin.
 MI has ischemia + necrosis (NO blood supply + cell death ➝ releases troponin).
MI
 MOA:
o Commonly occluded arteries are LAD > RCA > circumflex artery*
o Atheromatous plaque rupture ➝ thrombus occludes lumen ➝ hypoxia (↓ O2)
o Hypoxia impairs oxidative phosphorylation ➝ ↓ ATP (reversible)
 ↓ Aerobic + ↑ Anaerobic metabolism ➝ ↑ Lactate (low pH)
 Na-K ATPase pump impaired ➝ ↑ intracellular Na + water ➝ cell + RER swelling
 SARCA impaired ➝ ↑ intracellular Ca ➝ activates proteases + pro-apoptotic.
 Ischemic insult ➝ ↓ Contractility ➝ HF, cardiogenic shock.
 CF:
o Acute retrosternal chest pain >20min radiating to left arm or jaw.
o NO precipitating factors.
o NOT respond to sublingual GTN or rest.
o Associated with palpitations, nausea, sweatiness, SOB, fatigue.
 LV Dysfunction
o Anterolateral MI (I, aVL, V1-V6) ➝ Left main, LCX and/or LAD
o Left-sided HF
 ↓ Contractility ➝ ↓ CO ➝ Cardiogenic shock.
 ↑ PCWP ➝ PHTN ➝ Pulmonary edema ➝ ↑ CVP i.e., RAP.
 RV Dysfunction
o Inferior wall MI (II, III, aVF) ➝ PDA (RCA in right-dominant circulation).
o Electrical conductivity defects.
o Right-sided HF
 preload-dependency thus AVOID ↓ preload (venodilators like GTN, diuresis)
 ↑ CVP with normal or ↓ PCWP
 Myocardial Stunning
o Acute ischemia ➝ transient LV systolic HF ➝ delayed return to N fxn even after reperfusion.
 Myocardial Hibernation
o Chronic ischemia ➝ reversible LV systolic HF ➝ CM (eccentric hypertrophy).
 Reperfusion injury
o Ischemia ➝ reperfusion ➝ O2 derived free radicals ➝ tissue damage (↑ troponins)
Anti-Anginal Drugs
 Ranolazine: Inhibits late inward Na current ➝ ↓ Ca influx ➝ ↓ intracellular Ca ➝ ↓ diastolic wall
tension + ↓ O2 use).
 Atenolol (βB) + Amlodipine (CCB) ➝ NOT combine BB + non-DHP CCB (verapamil & diltiazem).
 β Blockers
o Use: SVT, ventricular rate control for AFib and atrial flutter.
o BB Overdose: saline, atropine, glucagon.
o Mechanism:
 BB block β R’ ➝ inhibit Gs pathway ➝ ↓ cAMP ➝ ↓ PKA ➝ ↓ intracellular calcium:
 Ventricular cells ➝ ↓ Ca-induced Ca release ➝ ↓ contractility.
 ↓ Pacemaker cell activity (SAN/AVN) ➝ ↓ Phase 4 & 0 slope (L-Ca channels).
o SAN ➝ ↓ HR (↓ phase 4 slope)
o AVN esp. sensitive ➝ ↑ PR interval (↓ phase 0 slope)
o SE:
 Impotence, CNS (sedation), CVS (Bradycardia, HF, AV block already have ↑ PR)
 Metoprolol ➝ dyslipidaemia
 Propranolol ➝ exacerbate vasospasm in vasospastic angina.
o CI: (Hack)
 Hypoglycaemia masks symptoms like tachycardia.
 COPD or Asthma (BAN ➝ BB, aspirin, NSAIDs)
 Cocaine/Pheochromocytoma
 unopposed ⍺1 agonism if BB alone (ALL β R’ blocked ➝ cocaine goes to ⍺ R’)
 Exceptions ➝ labetalol, carvedilol (non-selective ⍺ & β antagonist)
 Isosorbide Mononitrate (Nitrates)
o Drugs: Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
o Uses: angina, ACS, pulmonary edema
o MOA:
 ↑ NO in vascular smooth muscle ➝ ↑ cGMP ➝ smooth muscle relaxation
(vasodilation).
 Dilate veins >> arteries ➝ ↑ O2 supply.
 ↓ preload ➝ ↓ O2 demand.
o SE
 Reflex tachycardia (treat with β-blockers), hypotension, flushing, headache.
 Methemoglobinemia.
 “Monday disease” in industrial nitrate exposure:
 Tolerance for vasodilating action develops during work week.
 Loss of tolerance over weekend ➝ tachycardia, dizziness, headache upon re-
exposure.
 Thus, maintain nitrate-free intervals to prevent Monday Disease.
o CI:
 HOCM
 Nitrates with PDE-5 inhibitor is CI (excess cGMP)
 RV infarction (inferior MI; RV is preload dependent ➝ AVOID nitrates as ↓ preload)
 Ivabradine: prolongs phase 4 by selectively inhibiting funny Na channels (If)
 Nicorandil: K+ channel activator.

Angina Pectoris 1

Uploaded by

Copyright:

Available Formats

Angina Pectoris 1

Uploaded by

Document Information

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Angina Pectoris 1

Uploaded by

Copyright:

Available Formats

Angina Pectoris

You might also like

Pfad - The Proxy pFad of © 2024 Garber Painting. All rights reserved.