Welcome to the QUB CardioSoc weekly peer-to-peer teaching series! Our talk this week will focus on cardiac emergencies, aimed toward preclinical students and clinical students who would like a refresher we will walk you through how to handle critical situations such as cardiac arrest!
Cardiac Emergencies
Summary
This on-demand teaching session is relevant to medical professionals and is an excellent opportunity to learn about the signs and symptoms, initial assessments, pharmacological and non-pharmacological management of common cardiac emergencies like Acute Coronary Syndrome, Acute Heart Failure, Aortic Dissection, Ruptured Abdominal Aortic Aneurysm, Arrhythmias and Cardiac Arrest. Learners will be able to develop their skills in these acute presentations with the help of MCQ's at the end to test their knowledge and understanding. Participants will also learn about the ABCDE for diagnosis and management. Don't miss this opportunity to sharpen your knowledge in cardiac emergencies!
Description
Learning objectives
Learning Objectives:
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Recognize the signs and symptoms of cardiac emergencies.
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Understand the initial assessments/investigations required for successful response to cardiac emergencies.
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Explain the pharmacological and non-pharmacological management of cardiac emergencies.
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Describe the steps for performing CPR and demonstrating the use of an AED.
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Summarize the risk factors and management of common cardiac emergencies such as Acute Coronary Syndrome, Acute Heart Failure, Aortic Dissection, Ruptured Aortic Aneurysms, Arrhythmias, and Cardiac Arrest.
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th By Carlo Ferrazzano,4 year QUB1. Identify the signs and symptoms of common cardiac emergencies. 2. Describe the initial assessments/investigations necessary for a successful response to a cardiac emergency. 3. Outline the pharmacological and non-pharmacological management of common cardiac emergencies. 4. Outline the steps for performing CPR and the use of an AED.§ Acute coronary syndrome § Acute heart failure § Aortic dissection § Ruptured abdominal aortic aneurysm (AAA) § Arrhythmias § Cardiac arrest § Not an exhaustive list! Just the most commonly seen in clinical practice.Others to look up would be hyperkalaemia and cardiac tamponade. § MCQs at the end to test knowledge/understanding§ Always start with history and examination if possible! § AGED acronym for D § AVPU § Glucose § Eyes § Drugs§ Build up of an atheromatous plaque in arterial wall § Risk factors include: § Smoking § Hypertension § Diabetes § Hyperlipidaemia § Male sex § Physical inactivity § Obesity § Poor nutrition§ Central crushing chest pain associated with: § Radiation to left arm or jaw § Nausea and vomiting § Sweating and clamminess § Feeling of impending doom § Shortness of breath § Palpitations - Symptoms normally continue at rest for more than 20 minutes - Diabetic patients can experience atypical symptoms during an acute MI e.g.epigastric pain.Important not to miss this and investigate accordingly.Chest X ray:Normal for all unless obvious underlying pathology visible e.g.heart failure§ Obtain a quick history if possible – AMPLE (Allergies, Medication, PMH, Last ate/drank, Events leading up to admission) § Serial ECGs 15 mins apart § Chest X ray to exclude other causes of chest pain e.g. pneumothorax § Arrange for FBC, U&Es, blood glucose, lipid panel § Serial troponins 6 hours apart §Troponin doesn’t tend to rise until 2-3 hours after MI and so the troponin needs to be repeated to identify any changes§ ABCDE!!! Investigate and manage accordingly as you go through M 2NA 2 § IV morphine and metoclopramide § Oxygen if sats <94% § Nitrate (GTN spray, if no response switch to IV) § Aspirin § *Another antiplatelet (ticagrelor, if higher bleeding risk give clopidogrel) à this action tends to depend on type of ACS§ Percutaenous coronary intervention (PCI) with LMWH and prasugrel/ticagrelor if symptom onset within 12 hours and within 90-120 mins of diagnosis § Thrombolysis if the 120 minutes have passed or where PCI is contraindicated --> repeat ECG within 6 hours and if no reduction of ST elevation consider rescue PCI§ Already administered aspirin § All patients usually receive IV fondaparinux (anticoagulant), unless the patient is undergoing immediate coronary angiography, or has a high bleeding risk. Unfractionated heparin may be used as an alternative in patients with significant renal impairment. § Establish GRACE score (predicts 6 month mortality risk and adverse events) § Patients with intermediate-high 6 month risk of mortality should be offered an angiogram within 96 hours of symptom onset with potentially a PCI (if undergoing PCI, give unfractionated heparin and prasugrel/ticagrelor). Patients undergoing PCI should be offered heparin in the cardiac catheter lab regardless of whether or not they have already received fondaparinux. § Patients with low risk should receive ticagrelor/clopidogrel depending on bleeding risk.§ Coronary artery disease and previous ACS § Diabetes • Hypertension • Obesity • Congenital heart problems e.g.hypertrophic cardiomyopathy • Valvular heart disease e.g.aortic stenosis§ Note:HF can be chronic and well controlled.These are symptoms mostly related to an acute exacerbation.Surprise surprise, ABCDE!!! Investigate and manage as you go through: Obtain a quick history if possible – AMPLE (Allergies, Medication, PMH, Last ate/drank, Events leading up to admission) A – Check if patient is maintaining own airway. If not, maintain airway. If unsuccessful call anaesthetist for intubation support B - Obtain SpO2, give O2 if sats <94%. Arrange CXR and look for pulmonary oedema/cardiomegaly (next slide) C – Obtain IV access, BP, HR, capillary refill, ECG, FBC, U&E, troponin and BNP. If BP (thrombophylaxis) GTN spray. Also prescribe, morphine, furosemide and enoxaparin D + E – AGED + monitor sats, urine output and obs Mnemonic for management à LMNOP (Loop diuretic, Morphine, Nitrate, Oxygen, Position)An aortic dissection is caused by a weakened area of the aorta's wall. Some risk factors: • Hypertension • Atherosclerosis • Aneurysm • Valvular defects e.g. aortic regurgitation/stenosis • Marfan syndrome • A narrowing of the aorta at birth (aortic coarctation) • Drug use e.g. cocaine especially• Sudden onset, ‘ripping/tearing’ chest pain radiating through the back • Hypotension, tachycardia • Signs and symptoms of tamponade e.g. Beck’s triad: muffled heart sounds, elevated JVP and low BP • Absent pulse or increased BP differential in both armsObtain a quick history if possible – AMPLE (Allergies, Medication, PMH, Last ate/drank, Events leading up to admission) A – Check if patient is maintaining own airway. If not, maintain airway. If unsuccessful call anaesthetist for intubation support B - Obtain SpO2, give O2 if sats <94%. Arrange CXR à normally shows a increased mediastinal width (next slide) C - Obtain IV access, BP, HR, capillary refill, ECG, FBC, U&E, troponin, coag screen, crossmatch (mixing patient blood with donor blood to see if any reactions à important to do when risk of blood loss is high). Prescribe morphine and IV labetalol (beta blocker) if hypertensive. Note: important to closely monitor BP and keep within tight limits as increased BP can lead to a bigger size vessel haematoma D + E – AGED + monitor sats, urine output, obs. When stable, arrange a CT aorta to confirm diagnosis.• Type A • Treated with open surgery (midline sternotomy) to remove the section of the aorta with the defect in the wall and replace it with a synthetic graft. The aortic valve may need to be replaced during the procedure. • Type B • Haemodynamically stable patients usually only require beta blockers and analgesia • May be treated with thoracic endovascular aortic repair (TEVAR), with a catheter inserted via the femoral artery inserting a stent graft into the affected section of the descending aorta. Complicated cases may require open surgery.§ Hypertension § Smoking § Atherosclerosis § Ageing § Marfan syndrome § Similarly to aortic dissection,there is a weakness in the aortic wall.However, there is no actual breakage.So the aortic pressure pushes the three aortic layers laterally,creating a bulge.• Abdominal pain radiating to the back, or back pain alone • Hypotension, tachycardia, collapse • Pulsatile abdominal mass • If not ruptured, it can be an incidental finding on CT or MRI. These patients tend to be asymptomaticObtain a quick history if possible – AMPLE (Allergies, Medication, PMH, Last ate/drank, Events leading up to admission) A – Check if patient is maintaining own airway. If not, maintain airway. If unsuccessful call anaesthetist for intubation support. Most importantly, immediate vascular surgery referral B - Obtain SpO2, give O2 if sats <94%. C - Obtain IV access, BP, HR, capillary refill, ECG, FBC, U&E, troponin, coag screen, crossmatch 10 units and activate major haemorrhage protocol. Fluid resuscitation to achieve around 80mmHg systolic (permissive hypotension). Prescribe morphine. D + E – AGED + monitor sats, urine output, obs. Send to theatre ASAP.§ Bradyarrhythmias (slow) § Bradycardia § Heart block § Tachyarrhythmias (fast) § Narrow complex § AF § SVT § Broad complex § Ventricular tachycardia § Ventricular fibrillation Again, not exhaustive, just the most commonHeart rate under 60 BPM • Older age • Hypertension • Smoking • Heavy alcohol use • Illegal drug use - Several causes e.g. weak SA node signal (heart’s intrinsic pacemaker), ACS, hypothyroidism, hypothermia, drugs (beta blockers, calcium channel blockers) - Not necessarily worrisome, unless it’s under 50 BPM and symptomatic (next slide) - Heart block is when there is a partial or complete blockage of SA node signalling§ Majority of patients have no symptoms when in sinus bradycardia (ECG coming up) § Symptomatic bradycardia/heart block: §Fatigue §Exercise intolerance §Lightheadedness §Dizziness §Syncope §Worsening of anginal symptoms §Worsening of heart failureObtain a quick history if possible – AMPLE (Allergies, Medication, PMH, Last ate/drank, Events leading up to admission) A – Check if patient is maintaining own airway. If not, maintain airway. If unsuccessful call anaesthetist for intubation support. B - Obtain SpO2, give O2 if sats <94%. C - Obtain IV access, BP, capillary refill, ECG, FBC, U&E, troponin, Fluid resuscitation if low BP. Consider atropine first line to increase HR. D + E – AGED + monitor sats, urine output, obs. 24 hrs observation with Holter monitor if no underlying cause found (checks ECG continuously) § If patient has repetitive symptomatic episodes of bradycardia and/or heart block, the definitive management is a pacemaker§ Remember,AF affects Mrs SMITH (causes): § Sepsis § Mitral valve pathology § Ischaemic heart disease § Thyrotoxicosis § HypertensionThis leads to a narrow complex tachycardia and an irregularly irregular rhythm.What does that even mean?!§ Regular – normal rhythm, QRS complexes are equidistant § Regularly irregular - every beat not equally spaced but there is a distinct pattern e.g. Mobitz 1 § Irregularly irregular – sporadic pattern of beats with no clear spacing e.g. AF § A narrow QRS complex (<120 ms) reflects rapid activation of the ventricles via the normal His-Purkinje system, which in turn suggests that the arrhythmia originates above or within the His bundle (ie a supraventricular tachycardia). The mechanism of tachycardia may be in the sinus node, the atria, the AV node, the His bundle, or some combination of these sites. § A widened QRS (≥120 ms) occurs when ventricular activation is abnormally slow. The most common reason that a QRS is widened is because the arrhythmia originates below the His bundle in the bundle branches, Purkinje fibers, or ventricular myocardium (eg ventricular tachycardia).Narrow QRS complex (less than 3 small squares) and irregularly irregular rhythm§ Shortness of breath § Palpitations § Syncope § Chest discomfort (not necessarily pain) § Stroke/TIA à irregular rhythm can lead to clot formation in the heartObtain a quick history if possible – AMPLE (Allergies, Medication, PMH, Last ate/drank, Events leading up to admission) A – Check if patient is maintaining own airway. If not, maintain airway. If unsuccessful call anaesthetist for intubation support. B - Obtain SpO2, give O2 if sats <94%. C - Obtain IV access, BP, capillary refill, ECG, FBC, U&E, TFTs, troponin. Fluid resuscitation if low BP. Urgent sedation and synchronised cardioversion (next slide) if haemodynamically unstable e.g. low BP, symptoms of HF, chest pain. If haemodynamically stable usually a beta blocker works well. D + E – AGED + monitor sats, urine output, obs. 24 hrs observation with Holter monitor and treat underlying cause if any§ Not as common as AF § In AF, atria contract sporadically causing an irregularly irregular rhythm § In other SVTs, generally atria contract quickly but regularly, causing a much higher HR usually (>150 BPM). § Management in hemodynamic instability is the same --> synchronized cardioversion § Management in hemodynamic stability à vagal maneuvers, if unsuccessful, adenosine (don’t use in asthmatic as it can cause bronchoconstriction)(next slide). § Example: atrioventricular nodal re-entry tachycardia (AVNRT) à episodes are due to an extra pathway — called a reentrant circuit — located in or near the AV node that causes the heart to beat prematurely.§ With ventricular arrhythmias, the electrical signals originate within the ventricles. In other words, they do not start in the SA node and move along the usual route of the heart muscle. Twisting of the points à gradual change in amplitude and twisting of QRS complexes at the isoelectric point.Often coupled with QT prolongation Ventricular fibrillation§ Heart failure § Ischaemic heart disease § Structural heart disease e.g.valve pathology or cardiomyopathies § Infiltrative heart disease e.g.sarcoidosis § Myocarditis § Advanced age § Sepsis § Electrolyte disturbances• Chest pain (angina) • Dizziness. • Palpitations • Lightheadedness. • Shortness of breath. • Cardiac arrest (will cover shortly)Obtain a quick history if possible – AMPLE (Allergies, Medication, PMH, Last ate/drank, Events leading up to admission) A – Check if patient is maintaining own airway. If not, maintain airway. If unsuccessful call anaesthetist for intubation support. B - Obtain SpO2, give O2 if sats <94%. C - Obtain IV access, BP, capillary refill, ECG, FBC, U&E, troponin. Fluid resuscitation to maintain BP. Urgent sedation and synchronised cardioversion if haemodynamically unstable e.g. low BP, symptoms of HF, chest pain. If not, manage medically with amiodarone if sustained VT or MgSO if To4sades de pointes. If in pulseless VT or VF, manage as a cardiac arrest (see later). D + E – AGED + monitor sats, urine output, obs. 24 hrs observation with Holter monitor and treat underlying cause if any§ Sometimes sustained VT, especially if not managed promptly, can transform into VF and/or cardiac arrest Initial assessment: unconscious, unresponsive, pulseless patient, accompanied by respiratory arrest, apnoea or gasping A – Check if patient is maintaining own airway. Most often it will have to be maintained. If unsuccessful call anaesthetist for intubation support. B - Assess for breathing and check the pulse simultaneously; if no pulse or breathing, start CPR. Compressions at the lower sternum to at least a depth of 5cm, at a rate of ≥100 compressions per minute. Ventilation: mouth-to-mouth or bag-mask ventilation (8-10 breaths per minute). Guidelines recommend performing ventilation only in the presence of other personnel, as disruption of CPR can significantly reduce chances of survival. If no mask, can give 2 rescue breaths after 30 compressions. C - Assess cardiac rhythm and determine whether it is a shockable rhythm (SVT, VT, VF) or unshockable (pulseless electrical activity, asystole). Obtain intravenous access and administer IV adrenaline as appropriate: 0.1mg/ml IV adrenaline should be given after the second shock and every 3–5 minutes subsequently. D + E – AGED + monitor sats, urine output, obs. At least 24 hrs observation with Holter monitor and treat underlying cause if any (next slide).§ There are a multitude of causes, no need to list them all § However, look out for these potentially reversible causes: § 4 Hs: hypokalaemia, hypoglycaemia, hypothermia, hypoxia § 4 Ts: tension pneumothorax, tamponande (cardiac), toxins, thromboembolism§ Secondary prevention § Safety netting § Counselling about medication and co-morbiditiesA 45-year old man presents to the Emergency Department with acute central, crushing chest pain. He is a known Type-2 diabetic with a 30-year smoking pack history. Physical examination shows no abnormalities. His serial troponin tests taken after four hours and repeated hourly are normal. His ECG shows ST segment depression in leads II, III and aVF. Which of the following is the most likely diagnosis? A - Pericarditis B - NSTEMI C – Unstable angina D – Pulmonary embolism E - STEMIA 40 year old female patient presents to the emergency department with a 2 hours history of palpitations and malaise. Her pulse rate is 140 beats per minute, but other vital signs are within normal range. Physical examination shows no abnormalities. ECG reveals a regular tachycardia with QRS complex duration of 80 ms. Which of the following management options is the most appropriate next step? A – IV adenosine B – Carotid sinus massage C – IV adrenaline D – IV amiodarone E – Synchronised cardioversionA 75 year old male is admitted to the emergency department after suffering His ECG is taken (left). What does the. ECG show? A – Torsades de Pointes B – Ventricular tachycardia C – Atrial fibrillation D – STEMI E – Ventricular fibrillationA 54-year-old male patient presents to A&E with atrial fibrillation. On admission, he has a heart rate of 143 and a blood pressure of 89/63. What is the most appropriate treatment of choice? A - Verapamil B – Synchronised cardioversion C - Amiodarone D - Digoxin E – Beta blockerA 23 year old man with a past medical history of cocaine abuse presents to the ED with sudden, central tearing chest pain. On examination, his vitals are: RR 24, SpO2 97% RA, BP 190/100 mmHg, HR 120 bpm, T 36.9 degrees Celsius. A CT thorax showed a widened mediastinum. What is the next best step in management? A - Amlodipine B – Labetalol C - Nifedipine D - Ramipril E – Percutaneous coronary interventionA 68-year-old man presents to his GP with worsening leg swelling. He explains he is finding it difficult to put on his shoes and socks. He denies breathlessness or chest pain. His past medical history includes chronic obstructive pulmonary disease (COPD), gout and osteoarthritis. On examination, he has a raised JVP and bilateral pitting oedema up to the knees. There are no crepitations on auscultation of his lungs. What is the most likely diagnosis? A – Acute coronary syndrome B – Pulmonary oedema C – Left sided heart failure D – Right sided heart failure E – Pleural effusionA 70 year old man presents to the emergency department with a 2 hour history of crushing central chest pain radiating to his jaw and left arm. He has a past medical hypertension and obesity. His current medications are atorvastatin, metformin and ramipril. On examination he is sweating profusely and clutching at heart rate is 88bpm with a blood pressure of 110/72nd his mmHg. His ECG is shown. Which of the following treatment options will confer the greatest long prognostic benefit? A - Thrombolysis B – Aspirin C – Percutaneous coronary intervention D - Morphine E - ClopidogrelA 64-year-old patient on the cardiology ward is ECG monitor which is shown. No pulse is detected. What is the single most appropriate management for this patient? A - Chest compressions and Amiodarone 300mg IO/IV B - Synchronised DC cardioversion C - Start chest compressions at a rate of 200-250 per minute and deliver an unsynchronised shock D - Start chest compressions at a rate of 100-120 per minute and deliver an unsynchronised shock E - Start chest compressions (give 15 compressions: 2 rescue breaths) and deliver an unsynchronised shockA 56 year old man presents to A&E brought by ambulance with sudden onset severe abdominal pain. On examination, there is a pulsatile expansile abdominal mass and the patient looks extremely pale. Observations show a heart rate of 107, blood pressure of 84/52, saturations of 95%, he is V on the AVPU scale and has a respiratory rate of 26. He has a past medical history of hypertension. Given the most likely diagnosis, what is the single most useful action to take for the initial management? A – Give fluid resuscitation B – High flow oxygen C – Call vascular surgeon on call D – Admit to ICU E – Try to wake him up and take a full history§ https://www.grepmed.com/images/3707/diagnosis-angina-nstemi-definitions-acs § https://pathologia.ed.ac.uk/topic/atherosclerosis-and-atheroma/ § https://en.wikipedia.org/wiki/Electrocardiography § https://bnf.nice.org.uk/treatment-summaries/acute-coronary-syndromes/ § https://newportcts.com/aortic-dissection/ § https://www.rwjbh.org/treatment-care/heart-and-vascular-care/diseases-conditions/aortic-dissection/ § https://greek.doctor/third-year/pathology-1/theoretical-exam-topics/57-types-and-clinicopathology-of-the- aneurysms/ § https://app.pulsenotes.com/medicine/cardiology/notes/atrial-fibrillation § https://healthandwillness.org/vagal-maneuvers-for-svt/ § https://www.uptodate.com/contents/narrow-qrs-complex-tachycardias-clinical-manifestations-diagnosis-and- evaluation § https://www.ncbi.nlm.nih.gov/books/NBK459388/ § Medicine in a minute (great book)