• Musculoskeletal: • GERD - Costochondritis • Pancreatitis • Peptic ulcer • Panic attack - pneumonia: cough, fever, pleuritic chest pain - Pneumothorax: SOB, risk factor: COPD, chronic smoker, young and tall gentleman - Pulmonary embolism: SOB, unilateral leg swelling and edema DVT and its risk factor. History/ presenting - GERD: obese, acid brash, heartburn sensation, any scope done complaints - Gastritis: hunger pain, resolved with antacid - Pancreatitis: pain radiating to back, underlying gallstone disease
- aortic dissection: uncontrolled BP, chest pain radiating to the back
- Pericarditis/ myocarditis: history of URTI symptoms/ SOB/ palpitations
- Chest X ray: pneumonic changes, pleural effusion,
- ECG: ST elevation, abnormal conduction/ AV block - Echocardiogram Investigations - Cardiac biomarker: high sensitivity Troponin I - Inflammatory marker - OGDS ▪ Clinical symptoms due to myocardial ischaemia. ▪ Unstable angina, Non-ST elevation and ST elevation myocardial infarct ▪ Typical symptoms: ▪ Left sided chest pain (restrosternal, heaviness pain), radiating to left arm, diaphoresis, shortness of breath, nausea/ vomiting ▪ Atypical symptoms: epigastric pain, back pain, fatigue ▪ Silent ischaemia: Asymptomatic ▪ Modifiable ▪ Smoking, DM, Dyslipidaemia, HPT, Obesity, Lifestyle
▪ Non-modifiable ▪ Family history of CAD, Male, Age (Male >55, Female >65) ▪ Result from imbalance between myocardial oxygen supply and demand and often involve pre-existing atherosclerosis plaque rupture, fissure/ ulceration with acutely superimposed thrombosis
Other proposed mechanisms
▪ Coronary artery spasm ▪ Progressive severe atherosclerotic: narrowing without thrombus formation ▪ Systemic inflammatory processes ▪ Systemic conditions that alter oxygen supply/demand ▪ Stable angina
- Angina during exertion and resolves at rest
▪ Unstable angina
- New onset (<2 months)
- Accelerated angina: more frequent, severe, prolonged precipitated with less exertion - Angina at rest Unstable Angina/ NSTEMI ▪ ECG features suggestive of USA/ NSTEMI: ▪ ST segment depression >0.05mV
▪ T-wave inversion - marked >0.2mV symmetrical T- wave inversion especially in
precordial leads.
▪ Cardiac marker: Detected/ positive in NSTEMI but not USA.
▪ STEMI is diagnosed when there is - ST elevation of >1mm in 2 contiguous leads or - New onset LBBB in the resting ECG - In a patient with ischaemic type of chest pain of >30minutes - Rise in cardiac biomarkers. ▪ Left anterior descending artery Anterior wall of LV, anterior part of interventricular septum ▪ Left circumflex artery Lateral and posterior wall of LV ▪ Right coronary artery Posterior and inferior wall of LV, right ventricles, posterior par of interventricular septum. “Type a quote here.”
–Johnny Appleseed Case 1 Case 2 Case 3
- Inferior STEMI with right ventricular infarct
- ST elevation in lead II, III and aVF with - ST elevation in V1 and STE in lead III> II, - Reciprocal changes/ ST depression in lead I and aVL. - Do a right sided ECG! ▪ Right ventricular infarct ▪ V4R is the most sensitive and specific precordial lead for RV infarct. ▪ Hypotension is significant in this case as they are pre-load dependant. Nitrates should be avoided. ▪ Observation and close monitoring ▪ Anti-anginal: nitrate, IV Morphine ▪ Antithrombotic therapy: Antiplatelet, Anticoagulant ▪ Reperfusion therapy: ▪ Fibrinolytic, percutaneous coronary intervention.
▪ Beta-blocker, ACE-inhibitor, Statin.
▪ Secondary prevention. ▪ Fibrinolytic therapy ▪ Percutaneous Cardiac Intervention (PCI) ▪ Best reperfusion strategy depends on - Time from onset of symptoms - Contraindication to fibrinolytic therapy - High risk patients
▪ Primary PCI is preferred choice if short duration of
presentation to FMC from onset of symptoms, contraindicated to fibrinolytic therapy and high risk patients. ▪ Tiny flexible catheter usually inserted via radial artery to achieve revascularisation of occluded/ atherosclerotic coronary artery with stent insertion ▪ Drug eliciting stent/bare metal stent. ▪ BMS - required DAPT for 1 month ▪ DES - required DAPT for 1 year ▪ Very late presentation (>12 hours): ▪ reperfusion therapy not recommended except for high risk patients. ▪ High risk features: Large/ extensive/ anterior infarct Left ventricular failure hemodynamically/ electrically instability Cariogenic shock Elderly patients Post-revascularisation (history of CABG/ PCI) Post-infarct angina Previous MI ▪ Streptokinase: 1.5Mega units in 100cc of N/ D5 over 1 hour ▪ Tenecteplase/ Metalyse: single IV bolus 30-50mg over 5 secs, depending on body weight streptokinase is given within 2 years, allergic to streptokinase, BP lowish *an alternative if
activator) and Anistreplase (anisoylated plasminogen streptokinase activator complex) ▪ Following fibrin specific agent, anticoagulant is recommended. Contraindication of Fibrinolytics ▪ Indicator of successful reperfusion: resolution of chest pain, early return of ST segment elevation to isoelectric line or decrease in height of ST elevation, early peaking of CK/ CK-MB, restoration/ maintenance of haemodynamical stability.
▪ Complications of thrombolytics: ▪ hypotension, allergic reaction (streptokinase), uncontrollable bleeding, repercussion arrhythmia ▪ Acetylsalicylic acid ▪ initial loading dose of 300mg of soluble/ chewable
eptifibatide ▪ For USA/ NSTEMI patient (usually duration 3-5 days) ▪ For STEMI patient who received fibrinolytic therapy but did not undergo PCI.
▪ Heparin (UFH, LMWH), subcutaneous anti Xa inhibitors
▪ Oral anticoagulant :
▪ Vitamin K antagonist (warfarin), Novel oral
anticoagulants (Dabigatran, Rivaroxaban)
- Indicated for atrial fibrillation, LV thrombus ▪ Relaxation of vascular musculature, vasodilatation of coronary arteries. Reducing preload/ afterload. ▪ Indicated in: continuing chest pain/ ischaemia. Hypertension, heart failure. ▪ Contraindicated in: hypotension, RV infarct ▪ Role: symptomatic relief, not shown to improve Long term cardiac outcome ▪ Helps to reduce cardiac demand by reducing cardiac inotropic and chronotropic effect. ▪ Contraindicated if: hypotensive/ carDiogenic shock, - pulse rate< 60, - pulmonary congestion with crepitations beyond lung bases, - signs of peripheral hypoperfusion, - 2nd or 3rd degree AV block. - bronchial asthma ▪ Contraindicated in: ▪ Hypotension ▪ Bilateral renal artery stenosis ▪ Should be stopped or reduced dosage if evidence of serum creatinine increase 30% from baseline) within 2 weeks of initiation or persistent hyperkalemia ❖ Arrhytmias: tachyarrhythmia/ bradyarrhythmia ❖ Acute heart failure ❖ LV dysfunction and cardiogenic shock ❖ RV infarction ❖ Mechanical problem, ie: mitral regurgitation, free wall rupture, ventricular septal rupture ❖ Chest pain post-STEMI - Reinfarction/Recurrent MI (reinfarction - within 28 days; recurrent MI - after 28days) - Post infarct angina ❖ Pericarditis: Dressler’s syndrome, which happened 2-10 weeks post MI, pericarditis, fever and pericardial effusion. ❖ LV thrombus ❖ Left ventricular aneurysm ❖ Prolonged hospitalisation - DVT Killip I No sign of LV failure 2-3%
Mild-moderate heart failure.
Killip II Bibasal crepitation or S3 5-12% gallop on auscultation
Killip Acute pulmonary oedema III 10-20% Killip Cardiogenic shock IV ▪ For prognostication: predict probability of ischaemic event and mortality. ▪ Age >65yo ▪ 3 or more CAD risk factors (family history, hypertension, dyslipidaemia, DM and smoking) ▪ Known CAD ( stenosis > 50%) ▪ ASA use in past 7 days ▪ Recent (<24 hours) severe angina 2 or less Low risk ▪ Increased cardiac marker 3-4 Moderate risk
▪ ST deviation >0.5mm 5 or more High risk
▪ Echocardiogram: Ejection fraction, regional wall motion abnormalities/ hypokinetic area. ▪ Coronary angiography: diagnostic and therapeutic ▪ Cardiac stress test ▪ CT Coronary ▪ Cardiac MRI ▪ Radionuclide studies: pyrophosphate scan ▪ Smoking cessation ▪ Weight reduction ▪ Exercise: 30-60minutes/ day of moderate intensity exercise for at least 3 times/ week ▪ Low cholesterol/ salt diet ▪ Aim LDL-C<2 ▪ Optimal hypertension/ diabetes control. Case 1 Case 2 Case 3
- Inferior STEMI with right ventricular infarct
- ST elevation in lead II, III and aVF with - ST elevation in V1 and STE in lead III> II, - Reciprocal changes/ ST depression in lead I and aVL. - Do a right sided ECG! ▪ Right ventricular infarct ▪ V4R is the most sensitive and specific precordial lead for RV infarct. ▪ Hypotension is significant in this case as they are pre-load dependant. Nitrates should be avoided. ▪ Observation and close monitoring ▪ Anti-anginal: Nitrate, IV Morphine ▪ Antithrombotic therapy: Antiplatelet, Anticoagulant ▪ Reperfusion therapy: ▪ Fibrinolytic, Percutaneous Coronary Intervention.
▪ Beta-blocker, ACE-inhibitor, Statin.
▪ Secondary prevention. DEFINITION
A subjective experience of breathing discomfort that consists
of qualitatively distinct sensations that vary in intensity (By American Thoracic Society) 1)Respiratory causes
2)Cardiovascular causes
3)Dyspnea with normal cardiorespiratory function
RESPIRATORY CAUSES 1. Diseases of the airway 2. Diseases of the pleura and lung parenchyma 3. Diseases of the chest wall DISEASES OF THE AIRWAY e.g. Asthma and COPD Characterised by expiratory airflow obstruction
Hyperinflation of lung and chest wall
Increased resistive and elastic load on the ventilatory muscles and
increased work of breathing
Hypoxia DISEASES OF THE PLEURA AND LUNG PARENCHYMA ▪ Pleural effusion ▪ Infective diseases of parenchyma - Pneumonia -Pneumonia occuring over existing parenchymal infective diseases-Bronchiectasis,lung abscess ▪ Interstitial lung disease – caused by -occupational exposures - autoimmune disorders DISEASES OF THE CHEST WALL a)Diseases that stiffens the chest wall -Kyphoscoliosis
b)Diseases that weakens the chest wall
-Myasthenia Gravis and Guillain - Barre Syndrome CARDIOVASCULAR CAUSES ▪ Diseases of left heart ▪ Diseases of pulmonary vasculature ▪ Diseases of pericardium DISEASES OF LEFT HEART e.g. Coronary heart diseases Valvular heart diseases Dilated cardiomyopathy
Greater end diastolic volume and incresed LV end diastolic and
pulmonary capillary pressure
Interstitial edema and stimulation of pulmonary receptors leading to
Increased pulmonary artery pressure and stimulation of
pulmonary receptors leading to dyspnea DISEASES OF PERICARDIUM ▪ Constrictive pericarditis ▪ Cardiac tamponade
Dyspnea caused by -incresased pulmonary vascular pressure -decreased cardiac output stimulation of metaboreceptors and chemoreceptors DYSPNEA WITH NORMAL CARDIORESPIRATORY FUNCTION ANEMIA- stimulation of metaboreceptors
OBESITY-impaired ventilatory pump function and high cardiac output
This Photo by Unknown Author is licensed under CC BY This Photo by Unknown Author is licensed under CC BY-SA-NC Stages Definition and Criteria
Stage A: At Risk for HF At risk for HF but without symptoms, structural heart disease, or cardiac biomarkers of stretch or injury (e.g., patients with hypertension, atherosclerotic CVD, diabetes, metabolic syndrome and obesity, exposure to cardiotoxic agents, genetic variant for cardiomyopathy, or positive family history of cardiomyopathy). Stage B: Pre-HF No symptoms or signs of HF and evidence of 1 of the following: Structural heart disease* • Reduced left or right ventricular systolic function o Reduced ejection fraction, reduced strain • Ventricular hypertrophy • Chamber enlargement • Wall motion abnormalities • Valvular heart disease Evidence for increased filling pressures* • By invasive hemodynamic measurements • By noninvasive imaging suggesting elevated filling pressures (e.g., Doppler echocardiography) Patients with risk factors and • Increased levels of BNPs* or • Persistently elevated cardiac troponin in the absence of competing diagnoses resulting in such biomarker elevations such as acute coronary syndrome, CKD, pulmonary embolus, or myopericarditis Structural heart disease with current or previous symptoms of HF. Stage C: Symptomatic HF
Marked HF symptoms that interfere with daily life and with
Stage D: Advanced HF recurrent hospitalizations despite attempts to optimize GDMT. Type of HF According to LVEF Criteria • LVEF ≤40% HFrEF (HF with reduced EF) • Previous LVEF ≤40% and a follow-up measurement of LVEF >40% HFimpEF (HF with improved
EF) • LVEF 41%–49% HFmrEF (HF with mildly • Evidence of spontaneous or provokable increased LV filling pressures (e.g., elevated natriuretic peptide, noninvasive and invasive hemodynamic reduced EF) measurement) • LVEF ≥50% HFpEF (HF with preserved EF) • Evidence of spontaneous or provokable increased LV filling pressures (e.g., elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement) This Photo by Unknown Author is licensed under CC BY- SA
This Photo by Unknown Author is licensed under CC BY-SA-NC
▪ Group of conditions in which the electrical activity of the heart is irregular or is faster or slower than normal ▪P : Atria Depolarization ▪ QRS : Ventricle Depolarization ▪ PR : Conduction A-V ▪T : Ventricle Repolarization ▪ QT : Duration of ventricle Repolarization • Sinus bradycardia
• Junctional bradycardia
• 1st Degree AV block
• 2nd Degree AV block
• Ventricular escape rhythm and complete heart block
• Tachy-brady syndrome This Photo by Unknown Author is licensed under CC BY-NC This Photo by Unknown Author is licensed under CC BY-NC This Photo by Unknown Author is licensed under CC BY-SA BRADI • BRASH/hyperkalemia • Isolated hyperkalemia • BRASH syndrome (Bradycardia, Renal failure, AV node blockade, Shock and Hyperkalemia) • Reduced vital signs • Hypoxia • Hypoglycemia • Hypothermia +/- hypothyroid • Acute coronary occlusion • Inferior MI: nodal ischemia and vagal response, self-limiting or responds to atropine • Anterior MI: infranodal ischemia, often requires pacing • Drugs: withdraw if stable, reverse if unstable • Beta-blockers • Calcium channel blockers • Digoxin • Intracranial pressure, Infection (Lyme, endocarditis): treat underlying This Photo by Unknown Author is licensed under CC BY-SA-NC (<0.12s) (>0.12s)
(0.12s = small squares)
91 ECG findings: ▪ P waves have normal morphology ▪ 100-200 bpm ▪ Regular ventricular rhythm ▪ One P wave precedes every QRS complex
92 ▪ Sinus tachycardia is usually a response to physiological stress, such as exercise, or an increased sympathetic tone with increased catecholamine release, such as stress, fright, flight, and anger •• Exertion Physiological Anxiety • Pain
93 ECG findings: ▪ Regular ventricular rhythm ▪ Narrow QRS complex <0.12s ▪ May not see any P-wave ▪ Widespread ST depression — this is a common electrocardiographic finding and does not necessarily indicate myocardial ischaemia, provided the changes resolve once the patient is in sinus rhythm 94 Sync. Unstable Cardioversio n 50-100 J
Stable Non Pharmacological Pharmacological ▪ Carotid massage 1. IV adenosine 6mg rapid push with 20cc NS ▪ Modified valsalva manoeuvre via cubital fossa, then raise arm above heart level (slows AV node conduction) , followed by 12mg , up to 2 times • Side effects: Flushing, chest pain/tightness, bradycardia, brief asystole • Contraindication: Heart block, asthma, COPD, hx allergy 2. IV Verapamil 2-5mg run 1mg/min, up to 20mg 3. IV Diltiazem 2.5mg/min (max 50mg) 4. IV amiodarone 300mg rapid bolus, followed by 150mg if persists 95 ECG findings: ▪ Sawtooth appearance ▪ Regular ventricular rhythm ▪ Narrow QRS
96 Sync. Unstable Cardioversio n 50-100 J ▪ Often unstable rhythm, usually degenerate to atrial fibrillation
Rate control CCB 1. IV Verapamil 2-5mg run 1mg/min, up to 20mg
2. IV Diltiazem 2.5mg/min (max 50mg)
Pharmacological Betablockers Cardioversion IV Ibutilide >60 kg: 1 mg IV 1. IV esmolol 500mcg /kg over 1min, followed by infusion 50- in 10 min; <60 kg: 0.01 200mcg/kg/min mg/kg IV in 10 min 2. IV metoprolol 2-5mg every 5 min, up to 15mg Others: flecainide, procainamide, amiodarone 3. IV propranolol 100mcg/kg in 3 divided dose (2-3 mins interval) and propafenone 4. IV Sotalol 1 mg/kg IV in 10 min
97 IV amiodarone 300mg rapid bolus, followed by 150mg if persists ▪ Long term management ▪ 1st episode & stable : cardioversion alone ▪ Recurrent & stable : catheter ablation or maintenance of normal sinus rhythm with either dofetilide, amiodarone or sotalol ▪ Unstable : catheter ablation
▪ Antithrombotic therapy ▪ For patients with atrial flutter, the recommendations for antithrombotic therapy(eg warfarin) are according to the same risk profile used for those with AF
100 Sync. Unstable Cardioversio n 120-200 J ▪ Stable – Aim for rate control If no evidence of Heart Failure CCB 1. IV Verapamil 2-5mg run 1mg/min, up to 20mg 2. IV Diltiazem 2.5mg/min (max 50mg) Betablockers 1. IV esmolol 500mcg /kg over 1min, followed by infusion 50-200mcg/kg/min 2. IV metoprolol 2-5mg every 5 min, up to 15mg 3. IV propranolol 100mcg/kg in 3 divided dose (2-3 mins interval)
Any evidence of Heart Failure
1. IV amiodarone 300mg in 1H, followed by 900mg in 24H 2. IV digoxin 0.5mg in 100cc NS in 1H 3. IV Procainamide in 20mg/min until arrhythmia suppression
101 ▪ Anticoagulant ▪ Thromboembolic event risk is greatest when AF has been present for longer than 48 hours ▪ Effective anticoagulation in patients with AF reduces the risk of stroke 3-fold after 4-6 weeks
102 Regular Irregular
Ventricular Ventricular fibrilation
tachycardic Torsades de points
polymorphic ventricukar tachy
103 Ventricular tachycardia 104 Management of Ventricular tachycardia
Unstable Stable - Cardioversion 1. IV Amiodarone 150mg over 10min (repeat as needed) • Start at 200J (mono)/ followed by maintenance 1mg/kg for 6hrs 100J (biphasic) 2. IV Lidocaine 1-1.5mg/kg over 10min , repeated once at half dose after 10min (max 3mg/kg) or IV Procainamide 100mg in 5min , 20-50mg/min until arrhythmia suppresed or IV Satolal 100mg or 1.5mg/kg over 5min ( Avoid 105 prolonged QT) Torsades De Points
