Cardiology Flashcards
Define Acute coronary syndrome
A set of symptoms and signs that occur due to decreased blood flow to the heart at rest, this happens when there is sudden plaque rupture and clot formation w/in diseased coronary arteries leading to either partial occlusion and ischaemia (unstable angina) or complete occlusion, hypoperfusion and infarction (NSTEMI and STEMI)
Define Unstable angina
Partial occlusion of the coronary artery leading to troponin -ve chest pain (myocardial ischaemia) at rest w/ normal/abnormal ECG signs (ST depression and T wave inversion)
Define Non-ST elevating myocardial infarction
Severe but incomplete occlusion of a coronary artery leading to troponin +ve chest pain (myocardial death) w/out ST elevation (but w/ ST depression and T wave inversion)
Define ST elevating myocardial infarction
Complete occlusion of a coronary artery leading to troponin +ve chest pain (myocardial death) and ST elevation on ECG
Define Type 2 myocardial infarction
Myocardial infarction due to cardiac hypoperfusion for reasons other than ACS - e.g. severe sepsis, hypotension, hypovolaemia or coronary artery spasm
Don’t require the usual treatment for MI’s
Acute coronary syndrome features
- Central/left sided, sudden onset, crushing chest pain which may radiate to the left arm and jaw
- Associated nausea, sweating, clamminess, SOB, syncope
- Occurs are rest but is worsened by exercise/exertion and may be improved by GTN
- Inferior infarcts can present atypically w/ epigastric pain
Diabetic pts may have silent MI’s:
- NO pain
- Acute SOB
- Palpitations
- Acute confusion
- Hyperglycaemic crisis
- Syncope
Acute coronary syndrome investigations
- Troponin at least 3 hours after onset of pain and then 6 hours later
- ECG - STEMI = ST elevation >2cm in adjacent chest leads, ST elevation >1cm in adjacent limp leads, new LBBB
- CXR to rule out other causes/complications
Changes in which ECG leads demonstrate an inferior MI, and what coronary artery is affected?
Leads II, III and aVF
RCA affected
Changes in which ECG leads demonstrate a septal MI, and what coronary artery is affected?
Leads V1 and V2
Proximal LAD affected
Changes in which ECG leads demonstrate an anterior MI, and what coronary artery is affected?
Leads V3 and V4
LAD affected
Changes in which ECG leads demonstrate an apical MI, and what coronary artery is affected?
Leads V5 and V6
Distal LAD, LCx and RCA affected
Changes in which ECG leads demonstrate a lateral MI, and what coronary artery is affected?
Leads I and aVL
LCs affected
Changes in which ECG leads demonstrate a posterolateral MI, and what coronary artery is affected?
Leads V7-V9 show ST elevation, V1-V3 show ST depression
RCA/LCx affected
Causes of a raised troponin
- MI
- Pericarditis
- Myocarditis
- Arrhythmias
- Defibrillation
- Acute HF
- PE
- Type A aortic dissection
- CKD
- Prolonged strenuous exercise
- Sepsis
STEMI management
Offer 300mg loading dose of aspirin ASAP, sublingual GTN and IV morphine/diamorphine and continue aspirin indefinitely unless contraindicated, then offer reperfusion therapy (PCI or fibrinolysis) if possible, or medical management if not:
Percutaneous coronary intervention:
- Offer if presenting w/in 12 hrs of symptoms and PCI can be done w/in 2 hrs
- Give prasugrel w/ the aspirin if not already taking oral anticoagulants, and less than 75
- Give Clopidogrel/ticagrelor w/ the aspirin if taking an oral anticoagulant
- PCI involves endovascular stenting or complete revascularisation
Fibrinolysis:
- Offer if presenting w/in 12 hrs of symptoms and PCI cannot be giving w/in 2 hours
- Give ticagrelor w/ the aspirin
- Give an antithrombin
- Do not repeat, offer a PCI if still not resolving
Medical:
- Give ticagrelor w/ aspirin
- Asses LV function
NSTEMI/unstable angina management
- Loading dose of 300mg aspirin and fondaparinux
- Calculate GRACE score (6 mon mortality risk) and all pts who aren’t low risk should be given prasugrel or ticagrelor
- Sublingual GTN
- IV morphine/diamorphine
- Antithrombin e.g. Enoxaparin or fondaparinux
Post-MI secondary management
ALL pts post-MI should be started on the following 5 drugs:
1) Aspirin 75mg OD + a second anti platelet (Clopidogrel 75mg or ticagrelor 90mg OD)
- Beta blocker (normally bisoprolol)
- ACEi (normally Ramipril)
- High dose statin (normally atorvastatin 80mg ON)
All pts should have an echo to assess systolic function, as well as being referred for cardiac rehabilitation
MI complications
DARTHVARDER:
Death
Arrhythmia
Rupture
Tamponade
HF
Valve disease
Aneurysm
Dressler’s syndrome = post-infarction pericarditis 2-3 wks later
Embolism
Recurrence
Define Pericarditis
Inflammation of the pericardium (the fibroelastic sac surrounding the heard)
Causes of Pericarditis
- Idiopathic
- Infective = coxsackie B viruses (echovirus, CMV, HSV, HIV), bacteria (staphs, streps, pneumococcus, haemophilus, TB), rarely fungi and parasites
- Malignancies = lung, breast and Hodgkin’s lymphoma
- Cardiac = HF, Dressler’s syndrome
- Radiation
- Drugs = doxorubicin chemo, hydralazine, isoniazid, methyldopa, phenytoin, penicillin allergy
- Rheumatological = SLE, RA, Sarcoidosis, Takayasu’s, Behcet’s
- Uraemic renal failure
- Hypothyroidism
- IBD
- Ovarian hyperstimulation
Pericarditis features
- Pleuritic chest pain worse on inspiration
- Worse lying flat and relieved by sitting forwards
- Fever
- Pericardial friction rub = high-pitched scratching noise, best heard over the left sternal border during inspiration
Pericarditis investigations
- Serial troponins
- ECG - Widespread saddle ST elevation (not following vascular territories) and PR depression
- Echo
Pericarditis management
Idiopathic or viral:
- 1st line = exercise restriction and NSAIDs + PPI for 1-2 wks
- 2nd line = colchicine
- 3rd line = corticosteroids
Bacterial:
- IV abx +/- pericardiocentesis if purulent exudative present
Non-infective causes
- Corticosteroids
Pericarditis complications
- Pericardial effusions
- Cardiac tamponade
Define Acute pulmonary oedema
The sudden accumulation of fluid in the lungs, specifically the alveoli and interstitial spaces, leading to severe dyspnoea and hypoxia - caused by increased left heart pressure which in turn leads to a backlog of pressure into the lungs via in the pulmonary veins. This increases the hydrostatic pressure in the lungs forcing fluid out of the pulmonary capillaries
Causes of Acute pulmonary oedema
- Left ventricular HF (most common)
- Posterior-inferior MI leading to mitral regurgitation
- HTN crisis
- Iatrogenic fluid overload
Acute pulmonary oedema features
- Severe dyspnoea
- Orthopnoea and paroxysmal nocturnal dyspnoea
- Sitting upright, leaning forwards and tripoding
- Pink frothy sputum
- Widespread crackles and wheeze
- Raised JVP
- Tachycradia
- Pulsus alternans and S3 gallop
Define Pulsus alternans
An arterial pulse w/ alternating strong and weak beats - indicates severe LV dysfunction
Acute pulmonary oedema management
- A-E
- O2 therapy
- Loop diuretic = IV furosemide 400mg STAT+ close fluid balance
- CPAP (reduced hypoxia and recruits more alveoli, thus improving V/Q mismatch)
- Furosemide infusion over 24 hrs
- IV dopamine for vasopression
- Intra-aortic balloon pump if pt in cardiogenic shock
- Intubation and ventilation
Define Acute bradycardia
HR <60bpm + adverse features (shock, syncope, HF or evidence of myocardial ischaemia) - usually caused by sick sinus syndrome
Causes of bradycardia
- Physiological
- Sick sinus syndrome
- Heart block
- Post-MI
- Aortic valve disease
- Vasovagal
- Hypothyroidism
- Hypothermia
- Electrolyte abnormalities
- Raised ICP
- Medication = beta blockers, CCBs, digoxin
Acute bradycardia management
- A-E
- 1st line = 500 micrograms atropine IV (atropine blocks the vagus nerve which increases firing rate of the SAN) - can give repeat doses up to a total of 3mg
- 2nd line = Transcutaneous pacing, isoprenaline, adrenaline
Causes of Myocarditis
Viral:
- Cocksackie B viruses (echovirus, CMV, HSV, HIV)
- COVID-19
- Adenovirus
- EBV
Bacterial:
- Diphtheria
- Clostridia
- N. Gonorrhoea
Protozoa = Trypanosoma cruzi
AI:
- Kawasaki disease
- Scleroderma
- SLE
- Sarcoid
- Systemic vasculitides
Drug reactions:
- Antipsychotics e.g. clozapine
- Immune-checkpoint inhibitors
- Mesalazine
Myocarditis features
- Chest pain = sharp, stabbing
- SOB
- Palpitations
- Light-headedness
- Syncope
- Fever and viral prodrome
- Severe cases can cause unexplained cardiac death
- Dull heart sounds
Myocarditis investigations
- ECG = non-specific changes, arrhythmias, tachycardia, ectopic beats
- Bloods = raised troponin and CK-MB
- Echo
- Cardiac biopsy = gold standard (shows inflammatory infiltrates and myocardial necrosis)
Myocarditis management
- Treat underlying cause
- ITU support
- Corticosteroids if viral
- Limit activity for a few months post-recovery
Myocarditis complications
- HF
- Arrhythmias
- Dilated cardiomyopathy
Define Aortic dissection
When a tear in the tunica intima of the aorta creates a false lumen where blood can flow between the inner and outer layers of the walls of the aorta
Aortic dissection risk factors
- HTN
- Marfan’s
- Valvular heart disease
- Cocaine/amphetamine use
Aortic dissection Stanford classifications
- Type A = involves the ascending aorta and/or arch of the aorta
- Type B = involves the descending aorta
Aortic dissection features
Symptoms:
- Sudden onset tearing chest pain or interscapular pain which radiates to the back
- Bowel/limp ischaemia
- Renal failure
- Syncope
Signs:
- Radio-radial delay
- Radio-femoral delay
- BP difference between arms
Aortic dissection investigations
CT angiogram to diagnose
Aortic dissection management
Initial:
- Resuscitation if necessary
- Cardiac monitoring
- Strict BP control e.g. IV metoprolol infusion
Definitive:
- Type A = Surgical management e.g. aortic graft
- Type B = conservatively w/ BP control - endovascular/open repair if signs of end organ damage
Causes of aortic regurgitation
Acute:
- Infective endocarditis
- Aortic dissection (due to dilation of the aortic root)
- Blunt/penetrating trauma to the valve leaflets
- Iatrogenic (balloon valvotomy)
- Non-native aortic valve regurgitation
Chronic:
- Rheumatic heart disease
- Age-related calcification
- Congenital bicuspid aortic valve
- CTD e.g Marfan’s, Ehler’s Danlos
- Infective endocarditis
- Rheumatological = RA, ankylosing spondylitis, APLS, GCA
Aortic regurgitation features
Symptoms:
- Exertional dyspnoea
- Orthopnoea
- Stable angina in the absence of coronary artery disease (due to reduction in diastolic coronary perfusion)
Signs:
- Early diastolic murmur heard best at the aortic region, leaning forwards and on expiration
- De Quicke’s sign = nail bed pulsations
- Waterhammer pulse
- De Musset’s sign = head bobbing in time to heart beat
- Corrigan’s sign = dancing carotids
- Muller’s sign = pulsation of the uvula
- Traube’s sign = femoral bruit
- Widened pulse pressure
Aortic regurgitation investigations
Transthoracic echo + investigate for infective endocarditis and Group A strep
Aortic regurgitation management
- Conservative = no treatment for mild-moderate AR
- Medical = Beta blockers +/- losartan to lower BP in higher risk pts (e.g Marfan’s or bicuspid valves)
- Surgical = for pts with symptomatic AR, asymptomatic w/ LVEF <=50%, refractory IE, significant enlargement of ascending aorta
Aortic stenosis causes
- Age-related calcification
- Congenital bicuspid valve
- Rheumatic heart disease
- William’s syndrome (supravalvular stenosis)
Aortic stenosis features
Symptoms:
- Severe = syncope, angina, dyspnoea
- Palpitations
- Signs of left ventricular failure
- Sudden cardiac death
Signs:
- Ejection systolic murmur heard best at the second intercostal space in the mid clavicular line, which radiates to the carotids
- Slow-rising carotid pulse
- Narrow pulse pressure
- Heaving, non-displaced apex beat
- Soft S2
Aortic stenosis investigations
Echo is definitive - CXR may show cardiomegaly in severe cases
Aortic stenosis management
- Conservative = for asymptomatic and stable cases - echo monitoring every 6 months for severe cases, and yearly for mild-moderate cases
- Medical = symptom management of LV failure = diuretics, beta blockers, ACEi
- Surgical = Transcatheter/surgical aortic valve replacement - for all symptomatic pts, or asymptomatic pts with LVEF <=50%
Define Aortic sclerosis
Thickening and calcification of the aortic valve, but without obstruction of ventricular outflow - causes an ejection systolic murmur that DOESN’T radiate to the carotids
Define Atrial flutter
A common supraventricular tachycardia characterised by an abnormal cardiac rhythm w/ an atrial rate of 300 bpm and a ventricular rate that can be fixed or variable - caused by an aberrant re-entrant circuit w/in the right atrium which cycles at 300 bpm - produces a classical saw-tooth appearance of ECG
Causes of Atrial flutter
- Pulmonary diseases = COPD, OSA, PE, pulmonary HTN
- Ischaemic heart disease
- Sepsis
- Alcohol
- Cardiomyopathy
- Thyrotoxicosis
Atrial flutter management
In haemodynamically unstable pts:
- Synchronised DC cardioversion +/- amiodarone
In haemodynamically stable pts:
- 1st line = bisoprolol or CCB (dilitiazem, verapamil)
- 2nd line = cardioversion
- 3rd line = ablation of the aberrant circuit
Use CHADVASC to decide on giving anticoagulation
Define Atrial fibrillation
Irregular, uncoordinated contractions at a rate of 300-600 bpm - delays at the AVN means that only some of the irregular impulses are conducted resulting in an irregularly irregular ventricular response
Atrial fibrillation classifications
- Acute = lasts <48 hrs
- Paroxysmal = lasts <7 days and is intermittent
- Persistent = lasts >7 days but is amendable to cardioversion
- Permanent = lasts >7 days and is not amendable to cardioversion
Also can be fast (>=100bpm) or slow (<=60bpm)
Causes of Atrial fibrillation
Cardiac:
- IHD
- HTN
- Rheumatic heart disease
- Peri/myocarditis
Non-cardiac:
- Dehydration
- Endocrine causes e.g. hyperthyroidism
- Sepsis and other infections
- Pulmonary causes = PE, pneumonia
- Alcohol abuse
- Electrolyte disturbances e.g. hypokalaemia, hypomagnesaemia
Atrial fibrillation features
Symptoms:
- Palpitations
- Chest pain
- SOB
- Syncope
- Light-headedness
Signs:
- Irregularly irregular pulse
- A single waveform on JVP (due to loss of a-wave which signifies atrial contraction)
- ECG changes = absent P waves, irregularly irregular rhythm
Atrial fibrillation acute management
Acute unstable pt:
- Synchronised DC cardioversion +/- amiodarone
Stable pt w/ onset <48 hrs:
- Rhythm control w/ DC cardioversion or anti-arrhythmics (flecainide if no heart disease, amiodarone otherwise)
- Heparin if DC cardioversion is delayed
- Alternatively can use rate control (below)
Stable pt w/ onset >48hrs:
- Rate control only w/ bisoprolol, diltiazem or digoxin
- Can try cardioversion later if its persisting, but need to anticoagulated for 3 wks prior to this due to the risk of throwing off a clot
Atrial fibrillation chronic management
Rate control:
- 1st line = bisoprolol or rate limitng CCB (diltiazem or verapamil)
- 2nd line = dual therapy
- Digoxin monotherapy in sedentary pts w/ non-paroxysmal AF, who are hypotensive or who have HF
Rhythm control:
- Either DC cardioversion or medical w/ flecainide, amiodarone or sotalol
- For pts who have AF secondary to a reversible cause, HF associated w/ AF, new-onset AF
Catheter ablations
CHADVASC to calculate the need for anticoagulation (DOAC 1st line)
Define Broad complex tachycardias
Dysrhythmias that have a heart rate greater than 100bpm and a QRS complex that is greater than 120ms
Examples:
- VT
- VF
- Torsade’s de pointes
- SVT w/ aberrancy
Ventricular Tachycardia features
A regular broad complex tachycardia that occur w/ or w/out a pulse
ECG features:
- Tachycardia >100bpm
- Absent P waves
- Monomorphic regular QRS complexes >120ms
Pulseless Ventricular Tachycardia management
- This is a shockable rhythm = 200J bi-phasic unsynchronised shock should be administrated
- IV adrenaline (1mg in 10ml of 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock
- Adrenaline should be administered every 3-5 min thereafter
Pulsed Ventricular Tachycardia management
With adverse features:
- Synchronised DC shocks (up to 3) - need to sedate the pt if their awake
- 300mg IV amiodarone over 10-20 min, followed by 900mg infusion over 24 hrs
With no adverse features:
- 300mg IV amiodarone over 10-60 min
- If that doesn’t work, the synchronised DC shocks (up to 3)
Ventricular fibrillation features
An irregular broad complex tachycardia - this is always pulseless
ECG features:
- Tachycardia >100bpm
- QRS complexes are polymorphic and irregular (>120ms)
Ventricular fibrillation management
- This is a shockable rhythm = 200J bi-phasic unsynchronised shock should be administrated
- IV adrenaline (1mg in 10ml of 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock
- Adrenaline should be administered every 3-5 min thereafter
Define Brugada syndrome
A genetic condition caused by a sodium channelopathy that predisposes pts to ventricular fibrillation/tachycardia - most common in SEA males
Brugada syndrome triggers
- Sleep
- Eating heavy meals
- Dehydration
- Excess alcohol
- Drugs = flecainide, verapamil, TCAs
- Electrolyte abnormalities
- Fevers
Brugada syndrome investigations
Characteristic ECG changes + at least 1 clinical criterion
ECG changes = RBBB and ST elevation in V1-V3
Criteria:
- VF or polymorphic VT
- FHx of sudden cardiac death under 45 yrs
- Syncope or ECG signs in family
- Inducible VT
- Nocturnal agonal breathing (gasping or grunting in sleep)
Brugada syndrome management
Conservative = lifestyle measures and avoiding triggers
Definitive = insertion of an ICD to reduce risk of sudden cardiac death from VT/VF - can add quinidine (anti-arrhythmic) in pts who still have arrhythmias
Define Bundle branch block
When the electrical impulses to the ventricles are slower than normal, leading to a widened QRS complex >120ms
Can be left or right BBB
Incomplete BBB is when there is a partial delay and the QRS complex is between 110-120ms
How do you identify right vs left BBB?
In both, the QRS complex will b > 120ms
Look at V1 and V6 - then use WiLLiaM and MaRRoW:
- In LBBB, V1 QRS complexes will look like W, and V6 will look like an M
- In RBBB, V1 complexes will look like an M and V6 will look like a W
Causes of LBBB
- Aortic stenosis
- IHD
- Hyperkalaemia
- Digoxin toxicity
- MI - new LBBB can indicate STEMI
Causes of RBBB
- RB hypertrophy
- PE
- IHD
- Atrial septal defect
- Normal variant
Define Cardiac tamponade
When pericardial fluid accumulates and intrapericardial pressure rises compressing the IVC and heart chambers - this compromises ventricular filling and leads to reduced cardiac output
Caused by the accumulation of:
- Blood
- Fluid
- Purulent exudate
- Air
Cardiac tamponade features
Symptoms:
- SOB
- Tachycardia
- Confusion
- Chest pain
- Abdo pain
Signs:
- Beck’s triad = hypotension, quiet heart sounds, raised JVP
- Pulsus paradoxus (pulse fades on inspiration)
Cardiac tamponade investigations
- ECG = low voltage QRS
- CXR = may show large globular heart
- Echo = will demonstrate the amount of fluid and quantify the level of ventricular compromise
- Pericardiocentesis = will allow for sampling of the fluid to find the underlying cause and treat the immediate problem
Cardiac tamponade management
If haemodynamically unstable = pericardiocentesis
If stable = careful observation w/ repeat echo’s and IV fluid treatment to maintain ventricular filling
Most common reversible causes of cardiac arrest
4 H’s:
1) Hypoxia
2) Hypovolaemia
3) Hypo/hyperkalaemia
4) Hypo/hyperthermia
4T’s:
1) Tamponade
2) Toxins
3) Tension pneumothorax
4) Thrombosis
Indications for cardiac catheterisation
- Imaging = inject contrast dye into the coronary vessels to image anatomy and blood supply
- Angioplasty = balloon dilatation and stenting (PCI)
- Valvuloplasty = transcatheter aortic valve implantation (TAVI)
- Repair = transcatheter repair of septal defects
- Electrophysiology = studies and catheter ablations
- Measurements = accurate measures of pressures w/in heat and great vessels
- Biopsy
Define Cardiac myxoma
Benign tumours of the cardiac cells composed of unspecialised mesenchymal cells w/in a mucopolysaccharide stroma - this causes it to look smooth and gelatinous
Cardiac myxoma features
Symptoms:
- Fever
- WL
- Dyspnoea
- Orthopnoea
- Cough
- A. fib
- Can rarely embolize and cause ACS
Signs:
- Tumour plop on auscultation
Cardiac myxoma investigations
- Raised inflammatory markers
- Echo = mobile mass
- Cardiac MRI
Cardiac myxoma management
Surgical resection
Define Carney complex
A genetic condition of benign connective tissue tumours - characterised by cardiac/cutaneous myxomas, schwannomas, endocrine tumours and abnormal skin pigmentation
What is the purpose of temporary cardiac pacing?
To restore haemodynamic stability to a pt
How is temporary pacing done?
Transcutaneous = using electrode pads on the skin - used as a bridge to transvenous pacing
Transvenous pacing = inserting a pacemaker wire into a vein and then passing it to the right atrium or ventricle - wire is then connected to an external pacemaker box and may be kept in place until a permanent pacemaker is inserted, or its no longer required
Indications for permanent pacemaker insertion
- Complete heart block
- Mobitz type 2 heart block
- Symptomatic Mobitz type 1 heart block
- Symptomatic sick sinus syndrome
- Permanent bradyarrhythmias due to MI
- Tachyarrhythmias resistant to therapy
Define Constrictive pericarditis
The loss of elasticity in the pericardial sac due to scarring - this prevents normal cardiac filling and leads to restriction of ventricular volume, stroke volume and cardiac output
Constrictive pericarditis features
Symptoms = symptoms of HF:
- Fatigue
- Reduced exercise tolerance
- Exertional dyspnoea
- Peripheral oedema
Signs:
- Raised JVP
- Kussmaul’s sign = paradoxical rise in JVP w/ inspiration
- Pulsus paradoxus
- Quiet heart sounds (if pericardial effusion present)
- Pericardial knock = high pitched, early diastolic sound that occurs when stiff pericardium results in sudden arrest of ventricular filling
Constrictive pericarditis investigations
- CXR = small heart +/- pericardial calcifications
- Echo = ventricular filling defect and heart failure w/ preserved ejection fraction
- Cardiac MRI = helps differentiate from restrictive cardiomyopathy
Constrictive pericarditis management
Surgical excision of the fibrosed pericardium (pericardiectomy)
Define Cor pulmonale
Right ventricular failure as a result of long standing lung disease
Chronic arterial vasoconstriction occurs due to hypoxia, in order to overcome this increased pressure in the pulmonary circulation, the right side of the heart has to work harder - when it can no longer compensate this leads to right HF
Cor pulmonale features
Symptoms:
- Fatigue
- Peripheral oedema
- Ascites
- Symptoms of chronic lung condition
Signs:
- Cyanosis
- Raised JVP w/ prominent a and v waves
- RV heave
- Loud P2
- Pansystolic murmur w/ tricuspid regurgitation
- Pulsatile hepatomegaly
- Graham-Steel murmur = functional pulmonary regurgitation as the chronic HTN stretches the valvular attachments, whilst the valve itself is healthy
Cor pulmonale investigations
- ECG = Right axis deviation
- CXR = enlarged right atrium and ventricle w/ prominent pulmonary arteries
- Echo = diagnostic - look to see right ventricular function
Cor pulmonale managemet
No specific treatments other than optimise management of respiratory condition w/ O2 therapy to reduce pulmonary HTN- can give diuretics for symptomatic relief
Define Coronary artery bypass graft
A revascularisation technique used to treat coronary artery disease - a healthy vein (usually harvested from the leg or chest) is attached to the heart so blood can get around the narrowed coronary artery
Coronary artery bypass graft indications
In pts with:
- Symptoms of CAD that are not controlled by optimal medical management
- Complex 3 vessel disease and/or significant left main stem on CTCA
PCI is more cost effective than CABG, but CABG confers a mortality benefit in pts >65, with DM or complex 3 vessel disease
Define Pansystolic murmur
A systolic murmur that is of uniform intensity, as opposed to the crescendo-decrescendo ejection systolic murmurs - they start at S1 and extend up to, and may merge with, S2
Causes of pansystolic murmurs
- Mitral regurgitation (most common) = loudest at the axilla and on expirations, radiates to the axilla
- Tricuspid regurgitation = loudest at the left lower sternal edge and on inspiration
- Ventricular septal defect = loudest at the lower sternal edge
Define Ejection systolic murmurs
A systolic murmur that is described as a high-pitched, crescendo=decrescendo mid-systolic murmur
Causes of ejection systolic murmurs
- Aortic stenosis (most common) = loudest in aortic region and on expiration, radiates to the carotids
- Aortic sclerosis = loudest in aortic region and on expiration, no radiation
- Pulmonary stenosis = loudest in pulmonary region and on inspiration
- Flow murmur = in anaemia, pregnancy and thyrotoxicosis
- HOCM
- Pulmonary stenosis
- Supravalvular aortic stenosis (Williams syndrome)
Indications for digoxin
Atrial fibrillation/flutter who may be in HF or hypotensive
Digoxin mechanism of action
Inhibits Na/K/ATPase ion pump inhibitor in the myocardium and has parasympathetic affects on the AV node - its negatively chronotropic and positively ionotropic (slows down the heart but increases contractility)
Risk factors for digoxin toxicity
- Hypokalaemia
- Hypomagnesaemia
- Hypercalcaemia
- Elderly pts
Digoxin toxicity features
- N&V
- Diarrhoea
- Blurred vision
- Yellow/green discolouration of vision
- Haloes in vision
- Confusion
- Fatigue
- Palpitations
- Syncope
ECG changes:
- Down sloping ST depression - reverse tick
- T wave inversion
- Biphasic/flattened and shortened QT interval
- Slight PR prolongation
Digoxin toxicity manegement
- Stop digoxin
- Correct electrolyte imbalance
- Administer digifab = digoxin-specific antibody)
ECG changes in hyperkalaemia
Typically occurs w/ levels => 6
-Tall tented T waves (that would hurt to sit on)
- PR prolongation
- P wave flattening
- Bradyarrhythmia - sinus bradycardia, high-grade AV block or slow AF
- QRS broadening w/ unusual morphology
ECG changes in hypokalaemia
Typically occurs w/ levels < 2.7
- Widened P wave
- Prolonged PR interval
- ST depression
- T wave inversion
- U waves ( a second wave after the T wave due to repolarisation of the perkinje fibres)
- Long QT/U interval
- Supraventricular complexes
- Supraventricular arrhythmias - atrial fibrillation/flutter
- Ventricular arrhythmias - Torsade’s de pointes, VT, VF
Hypokalaemia management
- 3-3.5 = replace w/ oral K if
- < 3 = replace w/ IV K over 10-12 hours if pt asymptomatic and there are no ECG changes
- < 3 = IV K over 3-4 hrs if pt symptomatic and there are ECG changes
Examples of supraventricular (narrow complex) tachycardias
Atrial fibrillation/flutter, AV re-entry tachycardia (AVRT), AV nodal re-entry tachycardia (AVNRT)
What are the adverse features of SVT?
HISS
- Heart failure
- Ischaemia
- Shock
- Syncope
Management of SVT with adverse features
Synchronised DC shock
Management of stable SVT
Depends on if the rhythm is regular or irregular
Regular:
- Vagal manoeuvres = carotid sinus massage or Valsalva manoeuvre
- If those don’t work - give 6mg IV adenosine (temporarily blocks conduction through the AV node)
Irregular:
- Go down Atrial fibrillation/flutter management pathway
How is adenosine given?
Given IV rapidly over 1-3 seconds, followed by 20ml of normal saline bolus
Pts should be warned that they might have difficulty breathing, chest tightness and flushing - but this should resolve w/in seconds
Contraindications for giving adenosine
- Pts with a central line
- Pts on dipyridamole or carbamazepine as these can potentiate its effects
- Pts w/ asthma - use verapamil instead
1st degree Heart block definition and features
Prolonged conductivity through the AVN - can be identified by PR interval of >200ms
Causes of 1st degree Heart block
- High vagal tone (e.g. athletes)
- Acute inferior MI
- Electrolyte abnormalities e.g. hyperkaelemia
- Drugs = NHP-CCB, beta blockers, digoxin, cholesterase inhibitors
1st degree Heart block management
Mostly benign and doesn’t need treating - but treat any underlying pathologies
Mobitz type I heart block definition and features
A type of 2nd degree heart block due to reversible conduction block at the AVN - characterized by progressive lengthening of the PR interval until a QRS complex is skipped
Causes of Mobitz type I heart block
- Inferior MI
- Drugs = beta blockers, CCBs, digoxin
- High vagal tone (e.g. athletes)
- Myocarditis
- Cardiac surgery
Mobitz type I heart block management
It’s generally asymptomatic and thus doesn’t require treatment - if there are symptoms (e.g. bradycardia) then monitor ECGs and if they have adverse features give atropine
Mobitz type II heart block definition and features
A type of 2nd degree heart block usually caused by a block in the His-Perkinje system - characterized by intermittent non-conductive P waves, the PR interval is constant (normal or prolonged) and there is commonly a fixed ration of P waves to QRS complexes (e.g. 2:1 or 3:1)
Causes of Mobitz type II heart block
- Anterior MI
- Surgery = mitral valve repair or septal ablation
- Inflammatory = rheumatic heart disease, SLE, systemic sclerosis, myocarditis
- Lenegre’s disease = progressive fibrosis of the conduction system
- Infiltrations = sarcoidosis, haemochromotosis, amyloidosis
- Drugs = beta blockers, CCBs, digoxin, amioderone
Mobitz type II heart block management
Permanent pacemaker as these pts are at risk of complete heart block
3rd degree heart block definition and features
This is complete heart block where the atrial impulses are not conducted to the ventricles, cardiac output is due to a ventricular or junctional escape impulses - ECG shows bradycardia and a complete dissociation between P waves and QRS complexes
What are the risks of 3rd degree heart block
- Asytole
- VT
- Cardiac arrest
Causes of 3rd degree heart block
- MI’s (esp inferior)
- Drugs acting at the AVN = beta blockers, dihydropyridine CCBs, adenosine
- Idiopathic fibrosis
3rd degree heart block management
Manage acute bradycardia and then insert a permanent pacemaker
Define Heart failure
The failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body
What are the 3 classification systems for Heart failure ?
1) Low-output vs High-output
2) Systolic VS Diastolic
3) New York Heart Association symptom severity
Low-output vs High-output heart failure
Low-output HF occurs when cardiac output is reduced due to a primary problem in the heart (more common)
High-output HF occurs when there is a normal cardiac output , but there is an increased peripheral metabolic demand that the heart is unable to meet
Causes of high-output HF
AAPPTT
- Anaemia
- AV malformations
- Paget’s disease
- Pregnancy
- Thyrotoxicosis
- Thiamine deficiency
Systolic VS Diastolic heart failure
Systolic HF occurs when the ventricles fill well, but are unable to sufficiently pump blood around the body due to impaired myocardial contractility during systole - this leads to HF with reduced ejection fraction
Diastolic HF occurs when the ventricles are unable to properly relax and fill during diastole, thus it is able to pump blood normally, but pumps out less blood per contraction - this leads to HF with preserved ejection fraction
Causes of HF with reduced ejection fraction
Anything which reduces the ventricles ability to contract
- IHD
- Dilated cardiomyopathy
- Myocarditis
- Infiltrates = sarcoidosis, haemochromatosis
Causes of HF with preserved ejection fraction
Anything which stops the ventricles filling properly
- Uncontrolled chronic HTN = leads to LV hypertrophy
- Hypertrophic cardiomyopathy
- Cardiac tamponade
- Constrictive pericarditis
What is a normal ejection fraction?
50%
Anything less than 40% is heart failure
New York Heart Association (NYHA) Classification of HF
- Class I - no limitation in physical activity, and activity does not cause undue fatigue, palpitations or dyspnoea
- Class II - slight limitation of physical activity, and comfort at rest. Ordinary physical activity causes fatigue, palpitations 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
Left HF features
Left HF causes pulmonary congestion (pressure builds up on the left side of the heart leading to back pressure into the pulmonary circulation and lungs) and hypoperfusion
Symptoms:
- SOB on exertion
- Orthopnoea
- Paroxysmal nocturnal dypnoaea
- Nocturnal cough +/- pink frothy sputum
- Fatigue
Signs:
- Tachyapnoea
- Bibasal crackles on the lungs
- Cyanosis
- Prolonged CRT
- Hypotension
Right HF features
Right HF causes venous congestion (back pressure through the vena cava) and pulmonary hypoperfusion (reduced right ventricle output)
Symptoms:
- Peripheral oedema
- Weight gain
- Ascites
- Anorexia and nausea
- Fatigue
Signs:
- Raised JVP
- Pitting oedema
- Tender, smooth hepatomegaly
- Ascities
- Transudative pleural effusion (usually bilaterally)
Define Congestive cardiac failure
When left-sided HF causes significant enough pulmonary congestion that the right-side of the heart can no longer overcome the pressure and goes into failure
Pts present w/ signs of both LHF and RHF
Heart failure investigations
- 1st line = NT-pro-BNP levels =a molecule released by the ventricles in reponse to myocardial stretch
- ECG
- Echo = to assess ejection fraction
- CXR
- Bloods = U&E, LFT, TFT, glucose and lipid profile
What are the key CXR findings in a pt w/ heart failure?
ABCDEF
- Alveolar oedema = bat wing perihilar shadowing
- Kerley B lines = interstitial oedema
- Cardiomegaly
- Upper lobe blood Diversions
- Plueral effusions
- Fluid in the horizontal fissure
Heart failure management
Conservative:
- WL if BMI >30
- Smocking cessation
- Salt and fluid restriction
- Exercise
- Annual and one-off influenza vaccines
Medical:
- Loop diuretics (furosemide or bumetanide) for fluid overload
- For mortality benefits in HFrEF BASH = beta blockers, ACEi/ARBs, spirinolactone, hydralazine
- There are no medical treatments to improve mortality in HFpEF
- Can concider gicing SGLT2 inhibitors in pts with optomised meds
Surgical:
- Implantable cardiac defibrillators if at risk of sudden cardiac death, or with wide QRS complexes
Define Hypertrophic obstructive cardiomyopathy
An autosomal dominant condition resulting in asymmetrical septal hypertrophy which leads the LV hypertrophy and diastolic dysfunction w/out an obvious cause
HOCM features
Symptoms:
- Asymptomatic
- Exertional syncope
- Syncope
- Sudden cardiac death
- Exertional dyspnoea
- Fatigue
- Chest pain - anginal or atypical
Signs:
- Jerky pulse
- Double apex beat
- Harsh ejection systolic murmur
- Apical thrill
- A wave in JVP
HOCM investigations
ECG
Echo (definitive) = signs can be remembered usiuing MR SAM ASH:
-Mitral regurgitation
- Systolic anterior motion of the mitral valve leaflets
- Asymmetrical septal hypertrophy
Cardiac MRI = if echo is clear but still suscpect HOCM (20% of cases missed on echo)
HOCM management
Conservative:
- Avoid especially strenuous activity or competitive sports
Medical:
- Beta blockers 1st line
- Verapamil
- Amiodarone
Surgical (for those w/ severe LV outflow obstructions, or serve symptoms):
- Surgical septal myectomy
- Alcohol septal ablation
- ICD insertion
Hypothermia classification
- Mild = 32-35 degrees - tachyapnoea, tachycardia, vasoconstriction and shivering
- Moderate = 28-32 degrees - cardiac arrhythmias, hypotension, respiratory distress, confusion, stop shivering
- Severe = <28 degrees - markedly reduced consciousness/coma, apnoea, arrythmias, fixed and dilated pupils
ECG features of hypothermia
- Bradyarrhythmias
- Osborne waves (J waves) = positive deflection points between the end of the QRS complex and beginning of the ST segment
- Prolonged PR, QRS and ST
- Shivering artifacts
- Ventricular ectopics
- Cardiac arrest
Infective endocarditis classification
- Acute = symptoms for < 6 wks (usually Staph. A)
- Subacute = symptoms for 6 wks - 3 months
- Chronic = sumptoms for > 3 months
Common organisms in Infective endocarditis
- Staph aureus = most common
- Strep viridans = in pts w/ poor dentition
- Enterococci
- Staph epidermidis = common in prosthetic valves
- Strep bovis = linked w/ colorectal cancer - pts need endoscopy
- Fungal
- HACEK organisms = culture negative IE
- Non-infective = marantic endocarditis (pancreatic cancer), Libman-Sacks (SLE)
Infective endocarditis features
Symptoms:
- Fever
- NS
- Anorexia and WL
- Myalgia
- Other signs of systemic unwellness
Signs:
- New murmur
- Vascular phenomenon = spetic emboli, Janeway lesions (palms and soles)
- Immune phenomenon = splinter haemorrhages, Osler’s nodes (end of fingers), Roth spots (retinal haemorrhages), glomerulonephritis
Infective endocarditis investigations
Use modified Dukes criteria - need 2 majors, 1 major and 3 minor or all 5 minor to have IE
Pneumonic = BE FIVE PM
Major:
- Blood cultures (2x positive)
- Evidence of vegetation on echo
Minor:
- Fever
- Immune phenomena
- Vascular phenomena
- Electrocardiogram suggestive but not definitive
- Predisposing features
- Microbiology suggestive but not definitive
Infective endocarditis management
6 wks IV antibiotics
- Native valve S. aureus = fluclox or vanc + rif
- Prosthetic valve S. aurues = fluclox + rif + gent
- Strep viridans = benzylpen or vanc + gent
- HACEK = ceftriaxone
- Surgery if indicated
What are the indications for surgical management in Infective endocarditis?
- Haemodynamic instability
- Severe HF
- Refractory severe sepsis
- Valve obstruction
- Infected prosthetic valve
- Persistent bacterameia
- Repeated emboli
- Aortic root abscess (will give new PR prolongation)
Define Long QT syndrome
Individuals with persistent prolonger QT intervals
This is >440ms in men and >460ms in women
QT prolongation predisposes pts to Torsade’s de Pointes ad VF
Causes of QTc prolongation
Congenital = Romano-Ward syndrome, Jervell and Lange-Nielson syndrome
Acquired = TIMES
- Toxins (clarithromycin, anti-arrhythmics, anti-psychotics, TCAs)
- Ischaemia
- Myocarditis/mitral valve prolapse
- Electrolyte abnormalities (hypokalaemia, hypocalcaemia, hypomagnesaemia)
- Subarachnoid haemorrhage
Long QT syndrome management
Acquired = adress underlying cause
Congenital:
- 1st line = beta blockers if no bradycardia
- 2nd line = ICD insertion or cardiac pacing
Define Malignant hypertension
A medical emergency where there is a relatively rapid increase in BP that leads to end organ damage - there is a rapid increase in systemic vascular resistance by vasoconstriction leading to hypoperfusion of organs
Occurs at SBP =>180 and DBP =>120
Causes of Malignant hypertension
- Anti-hypertensive non-compliance
- Drugs = cocaine, amphetamines, sympathomimetics
- Renovascular disease = renal artery stenosis or Takayasu arteritis
- Renal parenchymal disease = glomerulonephritis, SLE, systemic sclerosis
- Endocrine = pheochromocytoma, Cushing’s, Conn’s
- CNS = head injury, stroke
Malignant hypertension features
SBP =>180 and DBP =>120 + evidence of end organ damage:
- Papilledema and/or retinal haemorrhages
- New onset confusion )encephalopathy)
- Occipital pulsatile headache +/- visual disturbance
- Seizures
- Chest pain
- Signs of HF
- AKI
Malignant hypertension management
- Aim for a controlled drop in BP to around 160/100 over at least 24hrs
- 1st line = CCBs e.g. amlodipine or nifedipine
PO is preferred to IV unless there is evidence of encephalopathy, HF or aortic dissection
An uncontrolled drop can result in ischaemic stroke due to poor cerebral autoregulation and perfusion
Hypertensive encephalopathy management
IV labetalol or IV sodium nitroprusside
What are the shockable rhythms?
- VT w/out a pulse
- VF
What are the non-shockable rhythms?
- Pulseless electrical activity
- Asystole
Management of non-shockable rhythms
- CPR 30:2
- Give 1mg IV adrenaline as ASAP
- Give further adrenaline very 3-5 min (after 2 2-min loops of CPR)
Define Mitral valve prolapse
Abnormal systolic displacement of one or both leaflets of the mitral valve into the left atrium - over time this leads to mitral regurgitation
Specifically displacement >2mm above the annular plane or echo
Mitral valve prolapse classifications
Primary = caused by the degeneration of the valve leaflets in the absence of an identifiable cause
Secondary = occurs due to a CTD e.g. Marfan’s, Ehlers-Danlos, Turner’s
Mitral valve prolapse features
Symptoms:
- Mostly assymtomatic
- Palpitaions - development of AF due to dilated L atium
- Lightheadedness
- SOB
- Fatigue
Signs:
- Mid systolic click on auscultation = results from the sudden tensing of the mitral valve apparatus as the leaflets prolapse into the L atrium
- Pansystolic mitral regurgitation murmur
Mitral valve prolapse management
Conservative = if asymptomatic it requires no treatment, can council on increased risk of IE
Medical and surgical - only if mitral regurgitation develops:
- Loop diuretics and management of HF
- Valve replacement
Define Mitral regurgitation
Back flow of blood into the L atrium during systole die to the incompetence of the mitral valve
Overtime this leads to enlargement of the L atrium, volume overload in the left side of the heart and leads to LV failure
Causes of acute Mitral regurgitation
- Papillary muscle rupture secondary to a posterio-inferior MI
- Rupture of the chordae tendinea = due to myoxomatous disease, IE, rheumatic heart disease, trauma
- Damage to a prosthetic valve
Causes of chronic Mitral regurgitation
Leaflet causes:
- Mitral valve prolapse
- Degenerative causes
- Rheumatic fever
- IE
- SLE/scleroderma
- CTD
- Congenital causes e.g. mitral valve clefts
- Hypertrophic cardiomyopathy
- Drug-related damage
Chordae causes:
- Myxomatous disease
- Trauma
Papillary muscle causes:
- MI
- Dilated cardiomyopathy
Annular causes:
- Calcification
- Dilation due to cardiomyopathy or CTD
Mitral regurgitation features
Acute symptoms = sudden onset:
- SOB
- Exertional dyspnoea
- Fatigue
- Weakness
- Signs of pulmonary oedema, hypotension and cardiogenic shock
Chronic symptoms:
- Asymptomatic until significant systolic dysfunction then pulmonary HTN or symptomatic AF
- Fatigue
- Exertional dyspnoea
Signs:
- Pansystolic murmur, loudest at the apex, radiates to the axilla, louder on exertion and on rolling to the left
- S1 may be quiet or absent
- Signs of LHF
Mitral regurgitation management
Conservative = if asymptomatic then regular echo’s for monitoring
Medical = treatment of complications:
- AF w/ rate control and anticoagulation
- HF w/ diuretics, ACEi and beta blockers
Surgical:
- Mitral valvuloplasty = repair of the valve (preferred)
- Mitral valve replacement
Define Mitral stenosis
The narrowing of the mitral valve resulting in reduced blood flow to the left ventricle, usually due to calcification and thickening
The leads to increased volume in the left atrium, atrial dilation (which predisposes to AF), pulmonary congestion and RHF
Causes of Mitral stenosis
Rheumatic heart disease
Mitral stenosis features
Asymptomatic until valve area falls to < 1.5cm^2
Symtpoms:
- Gradual exertional dyspnoea
- Haemoptysis due to pulmonary congestion
- AF
- Chest pain
- Hoarseness - large L atrium can compress the recurrent laryngeal nerve (Ortner’s syndrome)
- Peripheral oedema due to RHF
Signs:
- Malar flush due to CO2 retention
- Mid-to-late diastolic murmur, most prominent at the apex, loudest on expiration, heard best when pt lying on left side and with the bell
Mitral stenosis management
Conservative = no treatment if asymptomatic
Medical = symptomatic management
Surgical:
- Balloon valvuloplasty if valve pliable and not calcified
- Percutaneous mitral valvotomy if moderate disease
- Valve replacement
Define Narrow complex tachycardia
A dysrhythmia with a HR > 100pbm and QRS complexes <120ms
Can be:
- Supraventricular = starts suddenly and then stays at the same rate until it ends
- Sinus = frequently changes rate and speeds up/slow down over seconds-minutes
Types of Narrow complex tachycardia
Regular NCT’s:
- Sinus tachycardia = physiological or pathological
- Focal atrial tachycardia
- Atrial flutter
- Atrioventricular re-entry tachycardia (AVRT)
- Atrioventricular nodal re-entry tachycardia (AVNRT)
- Junctional tachycardia
Irregular NCT’s:
- Atrial fibrillation
- Atrial flutter w/ variable block
- Multifocal atrial tachycardia
Define Focal atrial tachycardia
When there is autonomous atrial cells acting like the SAN
Causes abnormal p wave morphology
Define Atrioventricular re-entry tachycardia
Where there is an accessory pathway between the atria and the ventricles that is not filtered by the AVN
Associated w/ Wolff-Parkinson White
Define Atrioventricular nodal re-entry tachycardia
Where there is are re-entry circuits w/in or near the AVN causing a supraventricular tachycardia
Define Junctional tachycardia
When the AVN becomes the pacemaker and causes ventricular contraction >100bpm
Define Multifocal atrial tachycardia:
Where there are multiple groups of autonomous atrial cells acting as the SAN leading to an irregular rhythm
Commonly found in pts w/ severe COPD
Narrow complex tachycardia management
- A-E
- If adverse signs = synchronised DC cardioversion +/- amiodarone
- If no adverse signs, consider if its regular or irregular
Regular:
- 1st line = vagal manoeuvres
- 2nd line = IV adenosine 0 initially a 6mg bolus, if that’s unsuccessful give 12mg, if that’s unsuccessful give 18mg
- 3rd line = verapamil or beta-blocker
- 4th line = synchronised DC cardioversion
Irregular:
- Beta blockers
- If HF - trial digoxin
- If onset >48hrs then anticoagulated
What are the 4 main types of cardiomyopathy?
- Dilated
- Restrictive
- Arrhythmogenic
- Hypertrophic
Define Dilated cardiomyopathy
A dilated heart w/ impaired systolic function (HFrEF) - most common cardiomyopathy
Causes of Dilated cardiomyopathy
- Ischaemic changes
- Congenital
- Toxin-related = excessive alcohol, cocain use, doxorubicin chemo, cyclophosphamide, chloroquine, clozapine
- Infiltrative = haemochromatosis, amyloidosis, sarcoidosis
- Peripartum
- Thyrotoxicosis
- Secondary to myocarditis
- HIV
- Lyme disease
- Chagas disease
- Idiopathic
Dilated cardiomyopathy features
Symptoms = signs of HF
Signs:
- Displaced apex beat
- S3 gallop rhythm (rapid ventricular filling)
- Mitral regurgitation
- Signs of HF
Dilated cardiomyopathy investigations
- ECG = poor R wave progression
- Echo (diagnostic) = globular, dilated heart w/ reduced EF
Dilated cardiomyopathy management
- Address underlying issue
- HF management = loop diuretics, beta blockers, ACEi
Define Restrictive cardiomyopathy
Non-dilated, non-hypertrophied ventricles w/ impaired diastolic filling but w/ near-normal systolic function
Causes of Restrictive cardiomyopathy
- Familial non-infiltrative cardiomyopathy
- Infiltrative = amyloidosis, sarcoidosis, fatty infiltration
- Storage = haemochromatosis, Fabry disease, glycogen storage disorders
- Diabetic cardiomyopathy
- Scleroderma
- Radiation
- Doxorubicin chemo
Restrictive cardiomyopathy features
Signs and symptoms of RHF
Most will have associated AF
Difficult to distinguish between this and constrictive pericarditis clinically
Restrictive cardiomyopathy investigations
- Echo = shows thickened ventricular walls and valves, w/ impaired ventricular filling and preserved systolic function
- Cardiac MRI to distinguish from contractive pericarditis
Restrictive cardiomyopathy management
- Resolve underlying cause
- Loop diuretics and anticoagulation for symptomatic relief
Define Arrhythmogenic Right Ventricular Cardiomyopathy
When fatty, fibrous material replaces the myocardium due to a a. dominant defect in the desmosomes
Primarily involves the right ventricle and can be seen on echo w/ hypokinetic segments of the free wall of the RV
Arrhythmogenic Right Ventricular Cardiomyopathy features
- Palpations
- Syncope
- Sudden cardiac death
All due to development of dangerous arrhythmias
Define Takotsubo cardiomyopathy
Non-ischaemic cardiomyopathy associated w/ transient apical ballooning of the myocardium usually due to stress
Suspect in pts w/ troponin +ve chest pain, ST elevation but normal coronary angiography with a Hx of a significant stressor
Self resolves in around 2 months
Define Pericardial effusion
Accumulation of fluid w/in the pericardial sac of >50mL - results in compression of the ventricles, possible haemodynamic compromise and cardiac tamponade
Causes of Pericardial effusion
Any cause of pericarditis can cause pericardial effusion
The fluids can be:
- Serous = in acute viral pericarditis
- Blood = in hemopericardium from a penetrating chest wound
- Pustulent = secondary to a bacterial infection
Pericardial effusion features
Symptoms:
- Can be asymptomatic and picked up on echo
- Dyspnoea
- Chest pain
- Local structure compression = phrenic nerve causing hiccups, diaphragmatic pressure causing nausea
Signs:
- Ewarts sign = bronchial breathing at L lower base
- Muffled heart sounds
- Signs of cardiac tamponade = Becks triad, hypotension, raised JVP
Pericardial effusion management
- Address the underlying cause
- Pericardiocentesis to remove fluid = either for further diagnostic reasons, or to treat symptoms in a large volume effusion
Causes of Essential hypertension
Physiological:
- Reduction of elasticity of large arteries
- Age/atherosclerosis-related calcifications
- Degradation of arterial elastin
Pathological = conditions associated w/ increased CO:
- Anaemia
- Hyperthyroidism
- Aortic regurgitation
Essential hypertension classification
- Stage 1 = Clinic => 140/90, ABPM => 135/85
- Stage 2 = Clinic =>160/100, ABPM => 150/95
- Stage 3 = Clinic systolic => 180, or diastolic =>120
Essential hypertension investigations
24hr halter to establish HTN
Do a QRISK2 and assess for signs of end organ damage:
- Urine dip and albumin:creatinine level
- Blood glucose, lipids and renal function
- Fundoscopy
- ECG to look for evidence of LV hypertrophy
Refer for same-day specialist assessment in pts with:
- Clinic BP of 180/120 or higher w/ signs of retinal haemorrhages or papilledema
- Life threatening symptoms e.g. new onset confusion, chest pain, HF or AKI
Essential hypertension management
Give treatment to all pts w/ Stage 2 disease, and pts w/ Stage 1 disease who are <80 w/ end organ damage/QRISK >10%
Step 1:
- If T2DM or <55 = ACEi or ARB
- If >55 or of Black afro-caribbean origin = CCB
Step 2:
- Add the other drug from step 1 or a thiazide-like diuretic (e.g. indapamide)
Step 3:
- Use all 3 types of medication
Step 4 = resistant HTN:
- If blood potassium <4.5 then add spironolactone
- If >4.5 yhen increase thiazide-like diuretic dose or add an alpha blocker (doxazosin), beta blocker (atenolol) or refer to cardia
What are the blood pressure targets for pts w/ Essential hypertension?
- Age >80 ABPM target <145/85 (due to risk of postural drop)
- Age <80 ABPM target <135/85
- T1DM w/ end organ damage = <130/80
Define Pulmonary stenosis
Narrowing of the pulmonary valve, reducing the blood flow from the RV into the pulmonary bed - this results in a pressure gradient >10mmHg across the pulmonary valve during systole and reduced blood flow into the pulmonary circulation
Causes of Pulmonary stenosis
- Tetralogy of Fallot (valvular)
- Noonan syndrome (valvular)
- Williams syndrome (supravalvular)
- Congenital rubella
Very rarely due to carcinoid syndrome
Pulmonary stenosis features
Symptoms = causes RHF:
- Dyspnoea
- Fatigue
- Peripheral oedema
- Ascites
Signs:
- Raised JVP
- RV heave
- Ejection systolic murmur that radiates to the left shoulder and is best heard on expiration
- Widely split S2 w/ a delayed P2
Pulmonary stenosis investigations
- ECG = p pulmonale, RAD, LV hypertrophy
- CXR = prominant pulmonary arteries and post-stenotic dilation
- Echo = to look at the degree of stenosis and ventricular function
Pulmonary stenosis management
- Usually asymptomatic and doesn’t need treatment
- Valvuloplasty (valvular) or balloon angioplasty (supravalvular) in pts w/ a transvalvular pressure gradient of >50 mmHg
Define Rheumatic fever
An AI complication of Group A Strep infection (usually pharyngitis or scarlet fever) that occurs 2-4 weeks post infection
Abs formed as a result of the infection cross-react w/ the endocardial tissue, leading to valvular disease
Rheumatic fever features
Jones criteria say that diagnosis is likely if there is evidence of a recent strep infection plus either:
- 2 major criteria
- 1 major and 2 minor criteria
Major criteria:
- Arthritis = a migratory polyarthritis
- Pancarditis = inflammation of all layers of the myocardium - causes tachycardia, new murmur or a new conduction defect
- Sydenham’s chorea = abrupt, non-rhythmic involuntary movements along w/ muscle weakness and emotional disturbances
- Erythema marginatum = pink/red, non-pruritic rash on the trunk, thighs and arms - has raised, sharp outer edges ad a diffuse clear centre making a ring
- Subcut nodules = firm, mobile, painless lesions on extensor surfaces
Minor criteria:
- Fever
- Arthralgia
- Raised ESR and CRP
- Prolonged PR interval on ECG
Rheumatic fever management
- STAT dose of IV Benzylpenicillin followed by a 10 day course of phenoxymethylpenicillin to eradicate the Strep
- Aspirin/NSAIDs for arthritis
- Prednisolone +/- diuretics if the carditis is causing HF
- Haloperidol or Diazepam for Sydenham’s chorea
- Antihistamines for erythema marginatum
Causes of right heart strain
Anything which increases the pressure w/in the pulmonary circulation:
- PE
- Pulmonary HTN
- Chronic lung disease
- Pulmonary stenosis
- Pneumothorax
What are the characteristic ECG features of right heart strain?
ST depression and T wave inversion in right ventricle (V1-V3) and inferior leads (II, III and aVF)
Define Secondary hypertension
A persistent high BP due to an identifiable cause
Should suspect in younger pts
Causes of Secondary hypertension
Primary intrinsic renal diseases (most common):
- CKD
- Glomerulonephritis
- Diabetic nephropathy
- Polycystic kidney disease
- Chronic pyelonephritis
Vascular disease:
- Renal artery stenosis = atherosclerosis in older pts, fibromuscular hyperplasia in younger pts
- Aortic coarctation = narrowing of the aortic arch forces the LV to pump harder leading to HTN
- Vasculitis’s
Endocrine:
- Conn’s disease = hypokalaemia and hypernatraemia
- Cushing’s disease = excess cortisol leads to increased absorption of sodium and increased vascular sensitivity to catecholamines and angiotensin II driving HTN
- Pheochromocytoma = triad of sweating, headaches and tachycardia
Drugs:
- NSAIDs
- Corticosteroids (Cushing’s syndrome)
- Mineralocorticoids
- Clozapine/olanzapine
- Cocaine/amphetamines
When do you suspect secondary hypertension?
- Pts <40 w/ few comorbidities
- Severe HTN/ treatment resistant
- New HTN in pts w/ previously low readings
- HTN associated w/ symptoms of electrolyte disturbances
Define Sick sinus syndrome
The clinical manifestations of intrinsic SAN dysfunction
Sick sinus syndrome features
Symptoms:
- Dizzy spells
- Syncope
- Chest pain
- Palpitations
- Angina
- Low-output heart failure
Signs:
- Sinus bradycardia
- Sinoatrial block
- Periods of sinus arrest
- Abnormally long pause after a premature beat
Sick sinus syndrome management
Atrial or dual-chamber pacemaker - but only if there are significant symptoms
Define Stable angina
Typical chest pain triggered by a mismatch of myocardial O2 supply and demand resulting in myocardial ischaemia - usually due to coronary artery disease
Typical chest pain is defined by:
1) Constriction/heavy discomfort to the chest that may radiate to the jaw/neck/arm
2) Brought on by exertion
3) Alleviated by rest (<5 min) or GTN spray
- 3/3 = typical angina pain
- 2/3 = atypical angina pain
- 0-1/3 = non-anginal pain
Stable angina classification
Classed by its limitations on day-to-day activity:
- Class I = non angina w/ normal activity, only strenuous
- Class II = angina pain causes slight limitation on normal physical activity
- Class III = angina pain causes marked limitation on normal physical activity
- Class IV = angina occurs w/ any physical activity and may become unstable
Stable angina investigations
- ECG to rule out MI
- 1st line = CTCA =-if typical/atypical anginal pain or ECG shows ischaemic changes
- 2nd line = if CTCA inconclusive - stress echo, myocardial perfusion SPECT, cardiac MRI
- 3rd line = invasive coronary angiography
Stable angina management
Conservative:
- Smocking cessation
- Glycaemic control
- HTN control
- Hyperlipidaemia control
- WL
- Reduce alcohol intake
Medical:
- Secondary prevention =Aspirin 75 OD and statin 80mg ON
- GTN spray for symptom relief
Emergency management (pain not subsiding after 2 GTN sprays):
- 1st line = bisoprolol or verapamil/diltiazem
- 2nd line = bisoprolol and amlodipine/nifedipine
- 3rd line = bisoprolol and amlodipine/nifedipine and long-acting nitrate (ivabradine/nicorandil/ranolazine)
CABG/PCI in pts with uncontrolled symptoms or complex 3 vessel disease
Define Cardiac syncope
Transient loss of consciousness as a result of inadequate CO leading to cerebral hypoperfusion
Causes of Cardiac syncope
Structural:
- Aortic stenosis
- Ischaemic cardiomyopathy
- HOCM
- Cardiac tamponade
Electrical:
- Tachyarrhythmias = SVT or VT/VF
- Bradyarrhythmia’s = sick sinus syndrome or AVN block
- Brugada syndrome
What is the target INR for pt w/ atrial fibrillation?
2-3
What is the target INR for pt w/ metallic valve replacement?
Aortic = 2-3
Mitral = 2.5-3.5
What is the target INR for pt following VTE?
2-3
Define Torsades des pointes
A specific form of polymorphic VT that occurs in the context of QT prolongation
Has a characteristic ECG morphology where the QRS complex twists around the isoelectric line
Torsades des pointes management
TdP often self-reverts back into sinus rhythm, but due to the risk of degeneration into VF or cardiac arrest sustain TdP needs to be terminated
- If haemodynamically unstable = DC cardioversion
- If stable = 2mg IV magnesium sulfate over 1-2 mins
Define Tricuspid regurgitation
When the tricuspid valve fails to prevent blood leaking back into the R atrium during systole - this causes an increase in the pressure inside the RA and forces the RV to pump harder
Severe tricuspid regurgitation can lead to RHF over time
Causes of Tricuspid regurgitation
- Infective endocarditis
- Rheumatic heart disease
- Chronic lung disease
- PE
- Secondary to pulmonary stenosis
Tricuspid regurgitation features
- Tends to be asymptomatic even when severe, but can cause symptoms of RHF
- Pansystolic murmur, loudest in the left parasternal area and on inspiration
Tricuspid regurgitation management
Conservative = if asymptomatic, monitor with echos
Medical:
- Traet underlying cause
- Treat RHF and loop duiretics for fluid overload
Surgical - if severe, symptomatic and refractory:
- Ring annuloplasty
- Valve replacement
Which congenital heart defects occur in Turner’s syndrome?
Bicuspid aortic valve (most common)
Coarctation of the aorta
Define Ventricular septal defects
A cardiac defect where there is a hole in the septum allowing blood to flow from the LV to the RV (due to the larger pressure of the LV) - either congenital (most common) or acquired post-MI
This leads to increased load to the LV (as blood passes through the lungs twice) and increases the pressure in the right side of the heart
In severe cases, the pressure in the RV exceeds that of the LV, leading to a reversal of the shunt (right to left) and deoxygenated blood entering systemic circulation = Eisenmenger’s syndrome
Ventricular septal defects features
Symptoms:
- Small = asymptomatic
- Large = childhood SOB, faltering growth and fatigue
- Undetected = decompensated HF or Eisenmenger’s (cyanosis)
Signs:
- Loud, harsh panstolic murmur at the left lower sternal edge
- Signs of HF
- Eisenmenger’s = cyanosis, clubbing
Ventricular septal defects management
- Majority will self resolve by 6 years old
- Closure via catheter insertion if doesn’t close by itself
Define Wellen’s syndrome
An ECG pattern caused by severe proximal LAD stenosis
It poses a major risk of a major anterior MI
Wellen’s syndrome features
ECG:
- Biphasic, inverted T waves in leads V2 and V3
- Can have an absence of Q waves and minimal ST elevation
Commonly have a Hx of resolved chest pain or unstable angina
Wellen’s syndrome management
PCI in the LAD coronary artery
Define Wolff-Parkinson-White syndrome
The presence of a congenital accessory electrical pathway between the atria and the ventricles
Predisposes pts to supraventricular tachycardia, esp AVRT
Wolff-Parkinson-White syndrome classification
Type A = accessory pathway between LA and LV
Type B = accessory pathway between RA and RV
Wolff-Parkinson-White syndrome features
ECG:
- Delta wave (slurred upstroke in the QRS)
- Short PR interval <120ms
- Broadened QRS
- Narrow complex tachycardia
Symptoms:
- Mostly asymptomatic
- Symptoms of supraventricular tachycardia
Wolff-Parkinson-White syndrome management
Long-term:
- Monitored w/ ECGs if asymptomatic
- Amiodarone/sotalol if paroxysmal SVT
- Radiofrequency ablation of the accessory pathway is definitive
Emergency:
- Adverse signs = DC cardioversion
- Stable NCT = vagal manouvers then IV adenosine
- Stable BCT = Flecainide then DC cadioversion
What drugs are contraindicated in Wolff-Parkinson-White syndrome?
AVN blockers as this causes more electrical activity to be conducted down the accessory pathway, increasing risk of arrhythmias
- Digoxin
- Adenosine
- Verapamil or diltiazem
