Title | Cardio - Collated from sources such as Passmed, Zero to Finals, AMBOSS, BMJ best practice |
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Course | Medicine |
Institution | Cardiff University |
Pages | 25 |
File Size | 1.6 MB |
File Type | |
Total Downloads | 110 |
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Collated from sources such as Passmed, Zero to Finals, AMBOSS, BMJ best practice...
CARDIOVASCULAR DISEASE Normal ECG variants In an athlete: Sinus brady 1st degree HB Wenckebach phenomenon T wave inversion in V1, aVR and III In children: Partial RBB
Reference ranges: PR = 120-200 ms – 3-5 small squares QRS = 160/100 Severe = >180/110 If clinic reading is >140/90 take another reading and record whichever’s lowest If BP is >140/90 Ambulatory blood pressure monitoring to confirm dx. Assess for end organ damage. Assess CV risk If >180/120 same day specialist assessment if there’s papilloedema, confusion, chest pain, HF signs, AKI. If not assess for end organ damage - start anti-HTN if present, if not repeat reading in 7 days Ix for target end organ damage: Urine dipstick for haematuria Urinary ACR HbA1c U+E’s, creatinine, eGFR (CKD) Fundoscopy ECG (any LV hypertrophy?) Ix for CV risk: Total Cholesterol and HDL cholesterol QRISK tool - >10% Mx If men) Commonest cause of palpitations in pt’s with structurally normal hearts Causes: o Unknown (#1) o Toxins e.g. caffeine, alcohol, recreational drugs o Drugs e.g. Theophylline, Salbutamol, amphetamines o Stress o Thyroid disorders Px Palpitations SOB Anginal chest pain if there’s underlying CAD Syncope or presyncope Polyuria (due to release of ANP causing diuresis) ECG signs -
AVRT
Sinus tachy ~140-280 bpm Narrow QRS 150 bpm)
AF Most common sustained arrhythmia - occurs in 1-2% of the population, usually in >75 yrs Paroxysmal AF = stops spontaneously within 7 days, usually within 48hrs. But can recur Persistent AF = continuous for >7 days (so unlikely to self-terminate) Long standing AF = >1 year Permanent AF = fails to terminate with cardioversion, or does terminate but relapses 100bpm (usually 160-180) Rate = 96 bpm Rhythm = irregularly irregular Down sloping ST depression and flattened/inverted T waves seen in V6, II, III and aVF suggests Digoxin effect
Complications STROKE VTE Heart failure Mx of AF Was the onset within the last 48 hrs? YES Urgent admission for electrical cardioversion NO…
Conservative: o Pt education on AF - written information, discuss causes o Stroke awareness o Support groups o Advise on how it will impact life:
DRIVING: can drive once cause has been identified and controlled for 4 weeks for normal drivers or 3 months for lorry/bus drivers Need to stop driving if the arrhythmia causes incapacity (disqualified if type 2 driver) Don’t need to tell DVLA
Medical: o Rate control with Bisoprolol or Non-dihydropyridine CCB (usually diltiazem) Digoxin if sedentary with non-paroxysmal AF Rhythm control with Amiodarone is only really used for AF + HF pt’s o Assess stroke Vs bleeding risk
Anticoagulate men with a score >1, women with a score >2 DOAC e.g. Apixaban, Dabigatran “aban” = Xa inhibitor Dabigatran = Direct thrombin inhibiter **UNLESS THERE’S VALVULAR HEART DISEASE** Warfarin o Refer for cardioversion if tx doesn’t work Surgical: o Left atrial ablation o Pace and ablate
Follow-up Within 1 week after starting tx Annually
Atrial Flutter *Narrow complex tachy at 150bpm Atrial Flutter until proven otherwise ECG signs - Narrow complex tachy (150 bpm) - Saw tooth pattern best seen in II, III, aVF - Loss of isoelectric baseline
Mx Conservative: o Pt education o Talk about reducing risk factors Medical: o Acute - DC cardioversion (70-120J) o Long term - Ablation of the accessory pathway o Assess stroke risk using CHADSVASC and Anticoagulate
Broad complex Tachycardia *Broad QRS is VT until proven otherwise Main DDx for BCT = VT, SVT with aberrancy, VF, Torsade de pointes Sounds like VT No prior hx of tachy Structural cardiac disease, pacemaker or ICD Unstable pt Very broad QRS - >140ms (normal is 140) - QRS are similar morphology - Concordance (all chest leads are +’ve, or all -‘ve)
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VF Needs a precipitating stimulus e.g. ischaemia, electrolyte abnormalities Ventricles suddenly start contracting at rates up to 500 bpm This is too fast for them to contract in a synchronised way, so there’s loss of CO which will become fatal - (asystole) ECG changes in VF Chaotic, irregular deflections of varying amplitude No P waves, QRS complexes or T waves
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Amplitude decreases with duration (as myocardial stores are depleted, and it gets closer to asystole)
Causes of VT or VF Ischaemia Cardiomyopathies Structural heart disease Post-infarction Iatrogenic o Digoxin o TCA’s Electrolyte disturbance o Hypokalaemia o Hypocalcaemia o Hypomagnesaemia Infection e.g. myocarditis Mx - SYSTEM 1. ABCDE CHECK FOR ADVERSE SIGNS o YES ALS - GET HELP (2222) 1) Chest compressions & DC cardiovert if shockable (VT or VF) (non-shockable - PEA, asystole) Up to 3 shocks 120-150J 1st Then 150-360J 2) IV Adrenaline 1mg (1 in 10,000) repeated every 3-5 mins as needed 2) IV Amiodarone 300mg over 20-60 mins 3) IV Amiodarone 900mg over 24 hrs o Non-shockable = chest compressions + adrenaline only o NO 1) IV Amiodarone 300mg over 20-60 mins 2) IV Amiodarone 900mg over 24 hrs Once corrected, look for cause Consider maintenance anti-arrhythmic’s If there’s recurrent episodes of VT consider surgical input - ICD **For VF you can use NON-SYNCHRONISED DC cardioversion - because there’s no R wave to trigger defibrillation
Torsades de Pointes (TdP)
Aka Polymorphic VT o Need VT + QT prolongation (>11 small squares) (start of Q wave to end of T wave) “Twisting peaks” - QRS complexes have varying amplitudes and durations Can be self-terminating, but often px with haemodynamic instability and collapse Can degenerate into VF (esp if HR is >220 bpm)
Causes #1 = myocardial ischaemia ALL THE HYPO’s o Hypokalaemia o Hypomagnesaemia o Hypocalcaemia o Hypothermia ^ICP Congenital long QT
Drugs causing Long QT Anti-psychotics Type IA and IC antiarrhythmic’s Sotalol Amiodarone TCA’s Antihistamines Macrolides Antidepressants e.g. Citalopram, Venlafaxine
Drugs Myocardial disease e.g. cardiomyopathy Complete HB TdP 2o to Hypokalaemia Initially: Rate = ~100 bpm Sinus rhythm U wave + T wave inversion indicating Hypokalaemia Developing into TdP
Mx of TdP Rule out congenital long QT o Congenital long QT Mx: High-dose B-blockers for LQT1, Na channel blockers for LQT3 Consider other causes o Check U+E’s for electrolyte abnormalities o Look at drug chart for iatrogenic causes Otherwise: IV Mg
CHEST PAIN DDx: Cardiac disorder Dissecting Thoracic aneurysm Definition: >1.5x normal diameter - >5cm for ascending aorta - >4cm for descending Ix: CT with contrast Mx: Conservative e.g. reduce risk factors, monitoring - if small. Surveillance: - Annually if 4.5cm Surgical - if rapidly expanding, symptomatic at all, any aortic valve pathology of CT disorder hx, or ‘large’: >5.5cm - Growing >0.5cm/yr Surgical options: - Open repair for ascending or arch - Endovascular repair (TEVAR) for descending Pericarditis Causes: - Infection (coxsackie #1, usually
Signs Pt profile: 65 y/o male smoker with HTN & atherosclerosis HTN BP discrepancy between arms Unequal pulses New diastolic murmur (AR) Neurological deficits
Sx
Pericardial friction rub Evidence of pericardial effusion e.g. faint heart sounds
Sudden tearing pain if ruptured --> back, inter-scapular Chest ‘pressure’ if not Back pain Signs of compression e.g. dysphagia, SVC syndrome, hoarseness (recurrent laryngeal nerve compression), horners (sympathetic trunk compression) BUT can be asymptomatic & incidental finding
Sharp, pleuritic, retrosternal pain --> L shoulder or arm, into abdomen
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viral, can be bacterial e.g. TB or fungal) Trauma Post-MI (Dressler’s syndrome) Post-cardiac surgery Post-radiotherapy SLE Rheumatic fever Iatrogenic (cyclosporin, penicillin)
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If it’s constrictive - fluid overload signs, kussmaul sign Saddle ST elevation & PR depression with reciprocal changes Sinus tachy
Better when sitting forward Worse when lying down, on inspiration, when coughing or swallowing Fever Cough Arthralgia
Mx: Often self-limiting - NSAID’s + PPI - Colchicine 500mcg for 3 months for prevention
Cardiac tamponade Definition: pericardial effusion which ends up compressing heart Causes: Bloody = trauma, aortic dissection, cardiac surgery, ventricular free wall rupture post-MI Serous = idiopathic, acute pericarditis, malignancy, autoimmune disorders, HF, renal failure
1. 2. 3. -
Pulsus paradoxus Beck’s triad: Hypotension JVP distension Muffled heart sounds Low voltage QRS Sinus tachy Possibly electrical alternans (QRS voltages vary)
Sharp, sternal pain SOB Compressive sx e.g. Dysphagia, cough, hoarseness
^JVP S3 Gallop Inspiratory crackles Wheeze
Tachycardia
Ankle swelling Orthopnoea Fatigue Severe breathlessness Cough Palpitations Breathlessness Syncope or pre-syncope
Ix: Echo Mx: ABCDE Pericardiocentesis or surgery to drain fluid Fluid resus +/- inotropes e.g. dobutamine Identify underlying cause Heart failure
Arrhythmia
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Non-cardiac DDx o MSK Rib fracture Costochondritis o GI Pancreatitis PUD
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GORD Oesophageal rupture Cholecystitis o Psychosomatic o Respiratory problems e.g. PE Pneumothorax Asthma Lung collapse CAP
Investigations Hx - assess if they need admitting Examination Bloods - FBC, U+E, TFT’s, LFT’s, CRP, lipids, BM, troponin ECG CXR
CVD = any condition that affects the heart or blood vessels Caused by thrombosis, or atherosclerosis NHS Health check is used to identify people at high risk of CVD o 40-74 y/o are invited every 5 yrs for a health check involving (basically health MOT): - CVD risk assessment with QRISK3 tool (variables are shown) -
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Assessing alcohol consumption and physical activity Cholesterol BMI Dementia check for 65-74 y/o DM screening CKD screening Mx of QRISK3 results 10% - (Conservative +) Medical: o Atorvastatin 20mg OD (evening) *If CVD develops - increase to 80mg OD (2o prevention dose)
Not for use if >85 y.o Not for people who already have CVD, CKD or T1DM Calculates a 10-year estimated risk
Starting Statins: CI in pregnancy LFT’s before starting, at 3 months and 12 months Initial review after 4 weeks - check compliance, SE’s etc *Then review every 6-12 months Side effects: o GI - nausea, vomiting, diarrhoea, abdo pain o Headache o Itching o **Muscle pain - Statins can cause RHABDOMYOLYSIS - tell pt they have to see Dr if they develop sudden muscle pain (esp with simvastatin + clarithromycin) o Can interact with grape-fruit juice
Angina = pain in the chest, neck, shoulders, jaw or arms caused by insufficient blood supply to the myocardium
Causes #1 = CAD Valvular disease HCOM HTN
To classify as ‘stable’ angina, the pain needs to be: On exertion or emotional stress Last 10 minutes Relieved by rest and GTN spray
Atypical angina has extra sx e.g. o GI pain o Breathlessness o Nausea
Prinzmetal’s angina is pain at rest caused by coronary artery spasm o Women > men o ST elevation during pain
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Investigations 12-lead ECG o May be normal o Evidence of ischaemia e.g. Pathological Q waves LBBB T wave flattening, elevation or inversion Mx Conservative: o Pt education o Discuss possible triggers e.g. exertion, stress, big meals, cold o Lifestyle advice to manage cardiovascular RF o DRIVING: For normal drivers - don’t need to tell DVLA, can drive if there’s sx control (STOP if sx are at rest or with emotion) For T2 drivers - must tell DVLA, licence may be taken away but might be permitted later if sx free for 6 wks
Should always check with insurer that they’re still covered Medical: o GTN for rapid sx relief during activities *Can take 2nd dose after 5 mins if pain hasn’t subsided If it’s still not gone after a further 5 mins Call 999 o B-blocker or dihydropyridine CCB (nifedipine, amlodipine) 2nd line: Long-acting nitrate (isosorbide mononitrate) Nicorandil (vasodilator) 10mg BD o CI if using with Sildenafil Ivabradine (funny current (If) inhibitor) 5mg BD or 2.5 mg BD if >75 o NOT if resting HR is 20 mins o “silent ACS” = no chest pain - seen in DM or elderly pt’s Nausea Sweating Dizziness Palpitations Investigations Bloods: FBC, U+E, LFT’s, CRP, Glucose, lipids, Mg o Keep checking electrolytes regularly Troponin at baseline, repeat at 6hrs and again at 12 hrs o T & I are the most sensitive ECG (8% = high risk coronary angiography...