Cardiology Flashcards
AF Management Acute Setting
- DC Cardioversion if <48hrs.
- Rate Control: B-Blocker (bisoprolol) or CCB (Diltiazem/verapamil; AVOID IN HF).
- Rhythm control (DC Cardioversion or Pharmacologically with Amiodarone).
- Be aware Amiodarone has a range of side-effects - given to older sedentary patients.
Specific drugs used in AF
- Flecainide“pill in the pocket” when symptoms come on. Favourable in Young patients.
- Amiodarone. Significant side-effects so should normally only be given to older, sedentary patients.
- Sotalol (beta blocker with additional K channel blocker action). Used for those that don’t meet the demographics for either flecainide or amiodarone.
Antiocoagulation options in AF
Warfarin
- Requires cover with LMWH for 5 days when initiating treatment (because warfarin is initially prothrombotic).
- INR monitoring.
- INR can be affected by a whole host of drugs and foods. Has 40 hour half-life therefore anticoagulant effect lasts days.
- Is the only oral anticoagulant licenced for valvular AF.
Direct oral anticoagulants (DOACs) for AF
- Examples of DOACs are edoxaban, apixaban, rivaroxaban & dabigatran Do not require monitoring Generally associated with less bleeding risks than warfarin.
- Most have approximately 12 hour half-lives therefore if patients miss doses they are not covered. Low Molecular Weight Heparin (LMWH) for AF
- An example of a LMWH is enoxaparin. A rare option in patients who cannot tolerate oral treatment. Involves a daily treatment dose injections.
Causes of LAD (ECG)
- Left anterior fascicular block
- Left bundle branch block
- Left ventricular hypertrophy
- Inferior MI
- Ventricular ectopy
- Paced rhythm
- Wolff-Parkinson White syndrome
Causes of RAD
- Left posterior fascicular block
- Lateral myocardial infarction
- Right ventricular hypertrophy
- Acute lung disease (e.g. Pulmonary Embolus)
- Chronic lung disease (e.g. COPD)
- Ventricular ectopy
- Hyperkalaemia
- Sodium-channel blocker toxicity
- WPW syndrome
- Normal in children or thin adults with a horizontally positioned heart
STEMI Management
- Targeted oxygen therapy (aiming for sats >90%)
- Loading dose of PO aspirin 300mg Note that some hospital protocols will also call for a loading dose of a second anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)
- For those going on to have PCI, NICE guidance suggests adding Prasugrel (if not on anti-coagulation) or clopidogrel (if on anti-coagulation)
- Sublingual GTN spray - for symptom relief IV morphine/diamorphine - in addition this causes vasodilation reducing preload on the heart
- Primary percutaneous coronary intervention (PPCI) for those who: Present within 12 hours of onset of pain AND Are <2 hours since first medical contact
NSTEMI Management
- Targeted oxygen therapy (aiming for sats >90%)
- Loading dose of PO aspirin 300mg and fondaparinux
- Patients should have their 6 month mortality score (often the GRACE score) calculated as early as possible - all those who are anything other than lowest risk should also be given prasugrel or ticagrelor unless they have a high risk of bleeding where PO clopidogrel 300mg is more appropriate.
- Sublingual GTN spray - for symptom relief
- IV morphine/diamorphine - in addition this causes vasodilation reducing preload on the heart
- Start antithrombin therapy such as treatment dose low molecular weight heparin or fondaparinux if they are for an immediate angiogram
- Patients with high 6 month risk of mortality should be offered an angiogram within 96 hours of symptom onset.
Post-MI Management
Post-MI management
- ALL patients post-MI patients should be started on the following 5 drugs:
- Aspirin 75mg OM + second anti-platelet (clopidogrel 75mg OD or ticagrelor 90mg OD)
- Beta blocker (normally bisoprolol)
- ACE-inhibitor (normally ramipril)
- High dose statin (e.g. Atorvastatin 80mg ON)
- All patients should have an ECHO performed to assess systolic function and any evidence of heart failure should be treated.
- All patients should be referred to cardiac rehabilitation.
- Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia.
Heart Block Management
Various levels of heart block are common - particularly following inferior infarcts (because the right coronary artery supplies the SA node).
These may be treated with:
- Simple observation (as many will revert back to sinus rhythm)
- Transcutaneous/venous pacing (if symptomatic)
- Permanent pacing (if failing to resolve)
Left ventricular thrombus/aneurysm
- Aneurysm can occur following an anterior MI where the myocardium can be susceptible to wall stress leading to an aneurysm.
- It may be silent, cause arrhythmias or embolic events.
- It is definitely diagnosed on ECHO but ECG may show persisting ST elevation.
- Thrombus can form either within an above described aneurysm or around hypokinetic regions of the myocardium.
- Thrombi can embolise causing complicaitons such as stroke, acute limb ischaemia and mesenteric ischaemia.
Left/right ventricular free wall rupture
- Necrosis of the free walls of either ventricle can lead to rupture allowing blood into the pericardial space.
- This leads to a rapid tamponade and normally leads to cardiac arrest/death within seconds.
- Treatment includes pericardiocentesis and surgery but prognosis is extremely poor.
Acute mitral regurgitation
This can occur because of papillary muscle rupture and carries a poor prognosis.
This presents with:
- Pansystolic murmur heard best at the apex
- Severe and sudden heart failure
- It is diagnosed on Echocardiogram and may require surgical correction.
VSD Features
- Interventricular septal rupture is a short-term complications of myocardial infarction.
- Rupture caused by an anterior infarct is generally apical and simple.
- Rupture caused by an inferior infarct is generally basal and more complex.
- Without reperfusion, septal rupture typically occurs within the first week after the infarction
Features of septal rupture include:
- Shortness of breath
- Chest pain
- Heart failure
- Hypotension
- Harsh, loud pan-systolic murmur along the left sternal border.
- Palpable parasternal thrill.
- Diagnosis is with echocardiogram.
- Patients are managed with emergency cardiac surgery.
Dressler’s syndrome
- Dressler’s syndrome or post-infarction pericarditis typically presents with persistent fever and pleuritic chest pain 2-3 weeks or up to a few months after an MI.
- Note that patients can get pericarditis immediately following MI which is NOT considered Dressler’s syndrome.
- Symptoms usually resolve after several days.
- Occasionally it can also present with features of pericardial effusion and has become relatively uncommon since the introduction of PCI.
Management:
- High dose aspirin
Narrow-Complex Tachycardias i.e. AF, Atrial Flutter, VT
Management of narrow complex tachycardias
Management is according to the Resuscitation Council adult tachycardia algorithm.
- Patients should be assessed using the ABCDE approach.
- If the patient shows adverse features (shock, syncope, heart failure, or myocardial ischaemia), emergency synchronised direct current (DC) cardioversion is indicated.
In haemodynamically stable patients management differs according to whether there is a broad (QRS duration >120 ms) or narrow (QRS duration <120 ms) QRS complex.
If the tachycardia is narrow complex, the next step is to determine whether the rhythm is regular or irregular:
- In regular narrow complex tachycardias (SVTs) the first step is to trial vagal manoeuvres (carotid sinus massage or Valsalva manoeuvre).
- If vagal manoeuvres fail, adenosine should be administered (initially as a 6 mg intravenous bolus, and if this fails 12 mg followed by a further 12 mg is trialled).
- In irregular narrow complex tachycardias the most likely diagnosis is atrial fibrillation.
- Atrial fibrillation with onset <48 hours is typically managed with rhythm control (LMWH followed by flecainide if there is no structural heart disease, or amiodarone if there is structural heart disease).
- Atrial fibrillation with onset >48 hours is typically managed with rate control (i.e. metoprolol or bisoprolol or verapamil, or digoxin if there are signs of heart failure) and anticoagulation.
Malignant Hypertension
Malignant Hypertension Definition
Malignant hypertension is a syndrome involving severe elevation of arterial blood pressure, resulting in end-organ damage.
Malignant Hypertension features
- Blood pressure ≥180 mm Hg systolic and ≥120 mm Hg diastolic
- Evidence of end-organ damage
- Papilloedema and/or retinal haemorrhages
- New-onset confusion (encephalophathy)
- Seizure
- Chest pain
- Signs of heart failure
- Acute kidney injury
Malignant Hypertension Management
Guidelines in treatment suggest aiming for controlled drop in blood pressure, to around 160/100mmHg over at least 24 hours.
Uncontrolled drops can lead to ischaemic stroke due to poor cerebral autoregulation and perfusion.
Oral medication is preferred to IV, unless there is encephalopathy, heart failure or aortic dissection. Oral calcium channel blockers such as amlodipine or nifedipine are often used first line.
Hypertension Pharmacologic Management
Indications to start pharmacological management of essential hypertension
- Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >20%
OR
- Anyone with Stage 2 hypertension
Step 1 of Pharmacological management
ACE-inhibitor (e.g. Ramipril) if <=55 years old
DHP-Calcium Channel Blocker (e.g. Nefedipine) if >55 years old OR African or Caribbean ethnicity
If unable to tolerate ACE-inhibitor then switch to Angiotensin Receptor Blocker (e.g. Candesartan)
Step 2 of Pharmacological management
(If maximal dose of Step 1 has failed or not tolerated)
Combine CCB and ACE-I/ARB
Step 3 of Pharmacological management
(If maximal doses of Step 2 has failed or not tolerated):
Add thiazide-like diuretic (e.g. Indapamide)
Step 4 of Pharmacological management
If blood potassium <4.5mmol/L then add Spironolactone
If >4.5mmol/L increase thiazide-like diuretic dose
Other options at this point include:
Alpha blocker (e.g. Doxacosin)
Beta blocker (e.g. Atenolol)
Referral to cardiology for further advice
HT Investigations
Patients with a two measured BP >140/90 should be offered either ambulatory BP monitoring or home blood pressure monitoring.
Assess for end organ damage including:
- Urine dip and albumin:creatinine level
- Blood glucose, lipids and renal function
- Fundoscopy for evidence of hypertensive retinopathy
- ECG - look for evidence of LV hypertrophy
HT Classification
Severity is classified by three stages:
- Single reading >140/90 mmHg and average ambulatory readings >135/85 mmHg
- Single reading >160/100 mmHg and average ambulatory readings >150/95 mmHg
- Single reading with systolic >180 mmHg or diastolic >110 mmHg.
Causes of Secondary Hypertension
Primary intrinsic kidney disease (most common)
Glomerulonephritis
Chronic pyelonephritis
Polycystic kidney disease
Renovascular disease (second most common)
Atheromatous renal artery stenosis in older co-morbid patients
Fibromuscular dysplasia in a younger patient group
Coarctation of the aorta is a potential cause of secondary hypertension in young children and adolescents.
Endocrine disease
Cushing’s syndrome (raised cortisol)
Conn’s syndrome(raised aldosterone)
Phaeochromocytoma (catecholamine producing tumour)
Secondary HT Investigations
Renal function (sodium, potassium, urea, creatinine)
Hypernatraemia and hypokalaemia in Conn’s syndrome
Raised urea and creatinine in intrinsic renal disease
Aldosterone:renin ratio - raised in Conn’s syndrome
24 hour urinary cortisol or dexamethasone suppression test - raised in Cushing’s syndrome
24 hour metanephrine collection - raised in pheochromocytoma
Renal ultrasound - looking for evidence of kidney abnormalities (e.g. polycystic kidneys)
CT/MR angiography - renovascular disease
Renal biopsy - intrinsic kidney disease
General Management (modifiable RFs) HT
- Weight loss
- Healthy diet (reduce salt and saturated fats)
- Reduce alcohol and caffeine
- Reduce stress
- Stop smoking
Management of Acute Bradycardia
Definition
Bradycardia is define as a heart rate of <60 beats per minute (Other sources state <50bpm)
Causes of acute bradycardia
- Sinus/AV nodal disease
- Drug induced such as beta blockers, calcium channel blockers
- Electrolyte abnormalities
- Hypothyroidism
- Clinical features
- Dizziness
- Syncope
- Tiredness
Initial management of acute bradycardia
DR ABCDE, ECG monitoring and any reversible causes should be identified and treated.
If there are any adverse features (shock, syncope, myocardial ischaemia or heart failure) then atropine 500 mcg IV is given.
Atropine blocks the vagus nerve activity on the heart, which increases the firing rate of the SA node. Repeat boluses can be given up to 3mg
Factors increasing the risk of asystole in bradycardia
Mobitz type II block
Complete heart block + broad QRS
Recent asystole
Ventricular pause >3 seconds
If any of these features are present in a patient with bradycardia and no adverse features then atropine should also be administered. If there is an inadequate response to atropine, alternative drugs include isoprenaline, adrenaline, aminophylline, dopamine, glucagon (in beta blocker/ calcium channel blocker overdose) or glycopyrrolate
Further management after initial measures attempted
Transcutaneous pacing can also be used as an interim measure whilst awaiting expert help for transvenous pacing/ permanent pacemaker insertion.
Coronary Artery Involved - Leads II, III & aVF
Inferior regiona - RCA
Coronary Artery Involved - V1-2
Septal - Proximal LAD
Coronary Artery Involved - V3-4
Anterior - LAD
Coronary Artery Involved - V5-6
Apex - Distal LAD/LCx/RCA
Coronary Artery Involved - I & aVL
Lateral - LCx
Coronary Artery Involved - V7-9 (ST Depression V1-3)
Posterolateral - RCA/LCx
Troponin Interpretation
Troponin is a myocardial protein released into the bloodstream when cardiac myocytes are damaged. Serum levels typically rise 3 hours after myocardial infarction begins.
Different hospitals have differing guidelines (and assays) for interpretations of results. In general there are three groups of troponin levels:
- Low - definitely no myocardial cell death. The patient is not having an MI although they may be experiencing unstable angina.
- Mildly raised - This is an equivocal result and may be due to other non-MI related factors (see below). These patients usually need a 6-12 hour repeat test.
- If repeat troponin is raised on the repeat they are having an MI
- If repeat troponin is stable or falling then they are unlikely to be having an MI.
- Definitely raised - MI confirmed (be aware of the possibility of a Type 2 MI)
Initial Management of acute heart failure (pulmonary oedema)
- Sit the patient up
- Oxygen therapy (aiming saturations >94% in normal circumstances)
- IV furosemide 40mg or more (with further doses as necessary) and close fluid balance (aiming for a negative balance)
- SC morphine - this is contentious with some studies suggesting that it might increase mortality by suppressing respiration
HF Pharmacologic Management
- ACE-inhibitor and beta-blocker (these improve mortality)
- Consider angiotensin receptor blocker (ARB) if intolerant to ACE inhibitors
- Consider hydralazine and a nitrate intolerant to ACE-I and ARB.
- Loop diuretics such as furosemide or bumetanide improve symptoms (but NOT mortality)
- If symptoms persist and NYHA Class 3 or 4 consider:
- Aldosterone antagonists such as spironolactone or eplerenone. These drugs also improve mortality.
- Hydralazine and a nitrate for Afro-Caribbean patients
- Ivabradine if in sinus rhythm and impaired ejection fraction
- Angiotensin receptor blocker
- Digoxin - useful in those with AF. This worsens mortality but improves morbidity.
HF Lifestyle modification
- Smoking cessation
- Salt and fluid restriction (this improves mortality)
- Supervised cardiac rehabilitation
Interpretation of NT-proBNP in HF
BNP is released by the ventricles in response to myocardial stretch.
BNP has a high negative predictive value, so if the BNP is not raised the diagnosis of congestive cardiac failure is highly unlikely.
If the BNP is raised, the patient should be referred for trans-thoracic echocardiogram.
- If BNP>2000ng/L the patient needs an urgent 2 week referral for specialist assessment and an ECHO.
- If BNP 400-2000ng/L the patient should get a 6 week referral for specialist assessment and an ECHO.
New York Heart Association Classification of Heart failure
The NYHA Classification system is used to classify severity of cardiovascular disability through severity of exertional dyspnoea limiting activity, or discomfort at rest. It runs from Class I (no limitation) to Class IV (discomfort at rest).
- Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitation or dyspnoea.
- Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitation and/or dyspnoea.
- Class III - marked limitation in physical activity, but comfort at rest. Minimal physical activity causes fatigue (less than ordinary).
- Class IV - inability to carry on any physical activity without discomfort, with symptoms occurring at rest. If any activity takes place, discomfort increases.
Diastolic vs. Systolic HF Causes
Systolic vs diastolic heart failure
Low output heart failure can be further classified into that caused by: pump failure, arrhythmias, excess after-load or excess pre-load.
Pump failure may be caused by diastolic dysfunction (impaired ventricular filling during diastole) or systolic dysfunction (impaired myocardial contraction during systole).
Causes of systolic heart failure
- Ischaemic heart disease
- Dilated cardiomyopathy
- Myocarditis
- Infiltration (e.g. in haemochromatosis or sarcoidosis)
Causes of diastolic heart failure
- Hypertrophic obstructive cardiomyopathy
- Restrictive cardiomyopathy
- Cardiac tamponade
- Constrictive pericarditis
Tetralogy of Fallot (TOF)
Tetralogy of Fallot (TOF) is the most common cause of cyanotic congenital heart disease*. It typically presents at around 1-2 months, although may not be picked up until the baby is 6 months old
TOF is a result of anterior malalignment of the aorticopulmonary septum. The four characteristic features are:
- ventricular septal defect (VSD)
- right ventricular hypertrophy
- right ventricular outflow tract obstruction, pulmonary stenosis
- overriding aorta
Other features
- cyanosis
- causes a right-to-left shunt
- ejection systolic murmur due to pulmonary stenosis (the VSD doesn’t usually cause a murmur)
- a right-sided aortic arch is seen in 25% of patients
- chest x-ray shows a ‘boot-shaped’ heart, ECG shows right ventricular hypertrophy
VF
An irregular broad complex tachycardia on the electrocardiogram is assumed to be ventricular fibrillation. This is always a pulseless rhythm.
ECG features of VF
The QRS complexes are polymorphic and irregular
Management of VF
- Ensure the airway is patent, check for signs of life (pulse and breathing), and commence CPR.
- Ventricular fibrillation is a shockable rhythm: the next step is to administer defibrillation (unsynchronised cardioversion using a 200 J biphasic shock).
- Chest compressions should then be resumed.
- 1 mg adrenaline (10 ml 1:10 000) plus 300 mg amiodarone should be administered after the 3rd shock. Adrenaline should subsequently be administered every 3-5 mins (after every alternate shock).
VT
ECG features of Ventricular tachycardia (VT)
- Tachycardia (>100 beats per minute), plus
- Absent P waves, plus
- Monomorphic regular broad QRS complexes (>120 ms).
Management of pulseless Ventricular tachycardia (VT)
If there is no pulse the patient should be managed according to the Advanced Life Support algorithm:
- VT is a shockable rhythm so a 200 J bi-phasic (unsynchronised) shock should be administered.
- CPR should be resumed for 2 minutes before re-checking the rhythm.
- Intravenous adrenaline (1 mg of 10 ml 1:10 000 solution) and amiodarone (300 mg) should be administered after delivery of the 3rd shock.
- Adrenaline should be administered every 3-5 minutes thereafter (after every alternate shock).
Management of Ventricular tachycardia with a pulse with adverse features
If there is a pulse but the patient shows adverse features (shock, syncope, myocardial ischaemia, or heart failure) the patient should be managed according to the Resuscitation Council tachyarrhythmia algorithm:
- Synchronised DC shock (up to 3 attempts).
- After seeking expert help Amiodarone (300 mg intravenously over 10-20 minutes followed by 900 mg over 24 hours) should be administered.
Management of Ventricular tachycardia with a pulse with no adverse features
- Amiodarone (300 mg intravenously over 20-60 minutes followed by 900 mg over 24 hours).
Torsades de pointes
Torsades de pointes (TdP) is a form of polymorphic ventricular tachycardia caused by QT prolongation.
ECG features of Torsades de pointes
The electrocardiogram characteristically shows QRS complexes ‘twisting’ around the isoelectric line.
Causes of Torsades de pointes
- Congenital Long QT syndromes such as Romano Ward syndrome and Jervell and Lange-Nielsen syndrome
- Medication (antiarrhythmics, antibiotics such as erythromycin, tricyclics, antipsychotics, ketoconazole )
- Myocardial infarction
- Renal/liver failure
- Hypothyroidism
- AV block
- Toxins
Management of TdP in haemodynamically unstable patients
If the patient displays adverse features (shock, syncope, myocardial ischaemia, or heart failure) emergency synchronised direct current shock should be administered, followed by intravenous amiodarone.
Management of TdP in haemodynamically stable patients
In haemodynamically stable patients, initial management is with intravenous magnesium sulphate (2 g over 10 minutes).
Offending drugs such as drugs that prolong the QT interval should be stopped and electrolyte abnormalities (particularly hypokalaemia and hypomagnesaemia) should be corrected.
Isoprenaline infusion and temporary or permanent pacing may be considered. These may be used in patients with recurrent TdP despite initial therapy with magnesium sulphate.
ECG
Sinus Arrhythmia
- ECG meets all criteria of sinus rhythm but the rhythm is irregular (R-R interval)
- Irregularity caused by physiological changes in the cardiac timing caused by respiration
- Considered to be a normal variant
- P wave for every QRS complex
ECG
Atrial Fibrillation
Disorganised electrical activity in the atria (impulses no longer travel from SA to AV node). AV node receives continuing electrical impulses and conducts some of these to the ventricle. Can occur at any ventricular rate (anywhere between 30 - 200 bpm)
Characterised by: No P Waves and Irregular QRS Complex (R-R intervals) and Ragged Baseline
Treatment:
https://litfl.com/atrial-fibrillation-ecg-library/
ECG
Atrial Flutter
A regular, usually narrow-complex (QRS <120ms/3 small squares) tachycardia
Caused by a re-entry circuit within the atria, resulting in an atrial rate of 300 bpm.
Characterised by: ‘Saw-Tooth’ Baseline appearance (lead V1 or Lead II, III and aVF), Ventricular Rate is a division of 300 (3F:1 QRS ratio or variable) and F Waves.
Treatment:
https://litfl.com/atrial-flutter-ecg-library/
ECG
Junctional Rhythm
Originates at the AV junction instead of SA node, therefore electrical impulse travels to atria and ventricles simultaneously. Rate may be normal, bradycardic or tachycardic.
Characteristics: Regular Rhythm. Retrograde (inverted) P waves can be seen in the ST segment (seen as negative deflection) with narrow QRS-Complex unless co-existing LBBB/RBBB.
ECG
Supraventricular Tachycardia (SVT)
- Originates above or involves the AV node. Exclude Sinus, Atrial Fibrillation and Atrial Flutter. Generally involves an accessory pathway i.e. WPW. No obvious flutter waves.
- Characteristics: Regular, Narrow-Complex (QRS <120ms/3 small squares) Tachycardia. Often no clear P Waves. Notch on ST-Segment (retrograde p-wave).
- Treatment:
- https://litfl.com/supraventricular-tachycardia-svt-ecg-library/
ECG
Supraventricular Ectopics
Sinus rhythm. Differing morphologies of P waves on beats 3, 6 and 9.
Characteristics: Regular, Early P waves on beat 3, 6 and 9, Narrow QRS Complex (<120ms/3 small squares). Varying PR and R-R intervals.
ECG
Ventricular Premature Complexes (VPCs)
A premature beat arising from an ectopic focus within the ventricles.
Characteristics: Broad QRS complex (≥ 120 ms) with abnormal morphology. Unifocal — Arising from a single ectopic focus; each PVC is identical or Multifocal — Arising from two or more ectopic foci; multiple abnormal QRS morphologies.
Features:
- Broad QRS complex (≥ 120 ms) with abnormal morphology.
- Premature — i.e. occurs earlier than would be expected for the next sinus impulse.
- Discordant ST segment and T wave changes.
- Usually followed by a full compensatory pause.
- Retrograde capture of the atria may or may not occur.
ECG
Ventricular Tachycardia
Monomorphic: Most common form. Regular broad-complex tachycardia (QRS >120ms/3 small squares). May be associated with haemodynamic compromise. Always abnormal and must be acted upon.
ECG
Ventricular Fibrillation
Characteristics: Irregular Random baseline. No clear discernable waveforms. Chaotic irregular deflections of varying amplitude. Rate 150 to 500 bpm.
No identifiable P waves, QRS complexes, or T waves. May be subtle.
Always associated with LOC
Treatment: DC Cardioversion
ECG
1st Degree HB
Characteristics: PR Interval prolonged (>200ms/1 large square) but constant - no progressive lengthening. Stable rhythm. No haemodynamic disturbance.
No specific treatment required
Causes: Increased vagal tone, Athletic training, Myocarditis, Normal Variant.
ECG
Mobitz I (Wenckebach Phenomenon)
Characteristics: Progressive PR Interval prolongation (>200ms/1 large square). Cyclical. 1st PR Normal. PR then lengthens. Eventually P wave with No QRS Complex i.e. Eventual ‘Missed Beat’ - ‘Drops a beat’.
Due to time taken for the AV node to repolarise in order to ‘accept’ the next impulse.
May be a normal variant, especially with high vagal tone (athletes).
Not treated unless severe or accompanied with collapse/haemodynamic compromise.
Causes: Drugs (BBs, CCBs, Digoxin, Amiodarone)
Treatment: Asymptomatic patients do not require treatment. Symptomatic patients usually respond to atropine. Permanent pacing is rarely required.
ECG
Mobitz II (Hay)
Characteristics: PR Constant. P Wave with No QRS Complex. Subsequent missed beat/QRS.
Failure of conduction at the level of the His-Purkinje system (i.e. below the AV node). May deteriorate into CHB/Asystole.
Causes: Structural damage to the conducting system (e.g. infarction, fibrosis, necrosis).
Treatment: Immediate admission for cardiac monitoring, backup temporary pacing and ultimately insertion of a permanent pacemaker.
ECG
3rd Degree HB (Complete HB/AV Block)
No functioning electrical connection between Atria & Ventricles. Complete absence of AV conduction – none of the supraventricular impulses are conducted to the ventricles.
P Waves & QRS Complexes Present.
Characteristics: No relationship between P wave and QRS complex. Broad QRS Complex (>120ms/3 small squares) - ventricular escape* rhythm. Typically the patient will have severe bradycardia with independent atrial and ventricular rates, i.e. AV dissociation.
Tip: Mark P Wave Positions, Move along to QRS - P Waves & QRS will be dissociated
Treatment: They require urgent admission for cardiac monitoring, backup temporary pacing and usually insertion of a permanent pacemaker. In the event of circulatory collapse with complete HB, IV Atropine and Isoprenaline may be indicated as stabilising measures until trans venous pacing wire insertion can be undertaken.
ECG
Pulseless Electrical Activity
Cardiac Arrest occurring with any rhythm which would usually be associated with a pulse is termed pulseless electrical activity.
Treatment: Prompt CPR is indicated and identification of a potential reversible cause.
ECG Territories
ECG
Pericarditis
Important cause of ST-Elevation
Symptoms include: Pleuritic Chest Pain (worse on inspiration), Fever, Pericardial Friction Rub
ECG Changes: UPWARD CONCAVE ST Elevation
Changes do not evolve
Widespread changes involving >1 vascular territory i.e. Inferior and anterior ST Elevation
Can be difficult to differentiate from ST elevation MI
PR depression is a useful diagnostic tool
Characteristically:
Widespread concave ST elevation and PR depression throughout most of the limb leads (I, II, III, aVL, aVF) and precordial leads (V2-6).
Reciprocal ST depression and PR elevation in lead aVR (± V1).
Sinus tachycardia is also common in acute pericarditis due to pain and/or pericardial effusion.
https://litfl.com/pericarditis-ecg-library/
Steps to distinguish pericarditis from STEMI:
Is there ST depression in a lead other than AVR or V1? This is a STEMI
Is there convex up or horizontal ST elevation? This is a STEMI
Is there ST elevation greater in III than II? This is a STEMI
Now look for PR depression in multiple leads… this suggests pericarditis (especially if there is a friction rub!)
Causes: Infectious – mainly viral (e.g. coxsackie virus); occasionally bacterial, fungal, TB. Immunological – SLE, rheumatic fever. Uraemia. Post-myocardial infarction / Dressler’s syndrome. Trauma. Following cardiac surgery (post pericardiotomy syndrome). Paraneoplastic syndromes. Drug-induced (e.g. isoniazid, cyclosporin). Post-radiotherapy.
Treatment: NSAIDS and Colchicine
Differentiating Pericarditis, BER and LBBB
Saddle-shaped ST Elevation (pericarditis)
BER; high take off in ST - normal in young individuals
LBBB; ST elevation - new-onset
ECG
Ventricular Hypertrophy
Thickening of the ventricular walls. Increase in LV mass, not volume. Left Ventricular Hypertrophy is more common, but can occur in either ventricle. Healthy Cardiac Hypertrophy is the normal response to healthy exercise or pregnancy which results in an increase in the heart’s muscle mass. Pathological Hypertrophy is the response to stress or disease such as HT, MI, HF or Neurohormones.
Characteristics: Markedly increased LV voltages: huge precordial R and S waves that overlap with the adjacent leads (SV2 + RV6 >> 35 mm). R-wave peak time > 50 ms in V5-6 with associated QRS broadening. LV strain pattern* with ST depression and T-wave inversions in I, aVL and V5-6. ST elevation in V1-3. Prominent U waves in V1-3. LAD.
*ST segment depression and T wave inversion in the left-sided leads: AKA the left ventricular ‘strain’ pattern
Be careful, severe LVH such as this appears almost identical to LBBB — the main clue to the presence of LVH is the excessively high LV voltages
ECG
Left Bundle Branch Block
In LBBB the left ventricle is activated from the right bundle.
Results in injury to both L. Ant. Hemibundle and L. Post. Hemibundle.
Best seen in V6
Characteristics: W-shaped QRS in V1. M-shaped QRS in V6. WilliaM MorroW. rSR complex (small R wave, deep S wave) in V1.
ECG Criteria: Broad QRS (>120ms/3 small squares). Wide, notched QRS (M-Shaped) I, aVL, V5 and V6. Wide, notched QS complexes and Dominant S Wave in V1 with no preceding R wave. R wave in V2/V3.
With MI: Cannot reliably diagnose the presence of MI with LBBB. See Sgarbossa Criteria.
Causes: IHD, MI, Cardiomyopathy and HT.
ECG
Right Bundle Branch Block
The right ventricle is stimulated by the impulse from the left ventricle
Characteristics: Broad QRS Complex. M shaped QRS in V1. W shaped QRS in V6. rSR pattern. WilliaM MorroW
ECG Criteria: Broad QRS (>120ms/3 small squares). rSR complex in V1-V3. M-Shaped QRS Complex in V1. W-shaped QRS Complex in V6. Delayed S wave in I, aVL, V4, V5, V6 (>120ms). Best seen in V1.
With MI: if abnormal Q waves are present, they will not usually be masked by the BBB pattern. There is no alteration of the initial part of the complex RS (in V1) and abnormal Q waves can usually still be seen.
STEMI Management
NSTEMI Management
Cardiac Rehab
Heart Murmur Locations
Listen over the 4 valve areas in turn for murmurs:
- Pulmonary: 2nd I.C.S left sternal border
- Aortic: 2nd I.C.S right sternal border
- Tricuspid: 5th I.C.S left sternal border
- Mitral: 5th I.C.S mid clavicular line (apex area)
