Cardiology Flashcards
Describe the principles of thromboembolism prevention in Atrial Fibrillation
Risk of stroke and systemic embolism should be assessed using the CHA2DS2-VASc Score
Men with a score of 1 or more and women with a score of 2 or more are more likely to benefit from oral anticoagulation
OACs prevent the majority of ischaemic strokes in AF and can prolong in life, a net clinical benefit is almost universal
Vitamin K Antagonists (e.g Warfarin) - Only treatment to be used in patients with mitral stenosis or mechanical valve prosthesis
DOACs (e.g. Dabigatran, Apixaban, Rivaroxaban) - Predictable onset and offset without need for regular monitoring
Non-pharmacological approaches include transcatheter occlusion of the left atrial appendage, where it is endothelialised by the cardiac tissue (it has been shown to be non-inferior to VKAs for stroke prevention in non-valvular AF)
Describe the microbiology of organisms associated with infective endocarditis
- In descending order of frequency
- Staph. Aureus
- Associated with IVDU
- Staph Epidermis
- Device/Line Related IE or Early PVE
- Strep Viridans (oral Streptococci)
- NVE
- Strep Gallolyticus (non-oral Streptococci)
- Enterococci
The above account for more than 85% of all cases of IE
Most commonly S. Aureus (26.6%)
The remainder below account for a small minority
- HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella Corrodens, Kingella)
- Candida Species
- Other/Polymicrobial
Describe the non-pharmacological management of hypertension
Exercise
Weight Loss
Reduction in Na Intake
Reduction in Alcohol Intake
Smoking Cessation
Describe the pathophysiology and treatment of Transposition of the Great Arteries
Pulmonary Artery and Aorta are switched
LV –> Pulmonary A.
RV –> Aorta
Treated by prostaglandins to keep the ductus arteriosus patent followed by an arterial switch operation
Describe the pathophysiology of heart failure
Dysfunction of the ventricles begins with myocardial damage which may be due to infection or ischaemia
This results in a perceived reduction in the circulating volume and pressure
Compensatory mechanisms are initiated to correct this, including increase in sympathetic tone, RAS activation, adrenaline and natriuretic peptide release
Angiotensin II is produced, which increased sodium and water retention which initially helps to increase the blood volume and pressure to maintain cardiac output
However, in the long term these mechanisms perpetuate the disease
Increased HR = Increased Oxygen Demand
Increased Total Peripheral Resistance = Increased Workload - Contributes to Underperfusion and Ischaemia of the heart
Increased Stretching of Ventricular Wall = Reduced Contractility - Leads to fluid transudation into interstitial tissue causing peripheral and pulmonary oedema
Describe the diagnosis of infective endocarditis and its diagnostic criteria
3 Sets of Blood Cultures
Echocardiography (TTE as first line)
Elevated WCC/CRP
ECG
Haematuria or Pyuria on Urinalysis
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Modified Duke Criteria states a diagnosis of IE is definite in the presence of 2 major criteria, 1 major and 3 minor criteria or 5 minor criteria
Major Criteria: Blood Cultures +ve for IE and Evidence of Endocardial Involvement
Minor Criteria: Predisposition, Fever, Vascular Phenomena, Immunological Phenomena, Microbiological Evidence
Describe the pathophysiology and treatment of Coarctation of the Aorta
‘a narrowing in the aorta, most commonly at the site of insertion of the ductus arteriosus, just distal to the left subclavian artery’
Acyanotic defect with a left to right shunt
Typically presents at Day 3, when ductus arteriosus closes
Upper body hypertension and lower body hypotension
May require surgical balloon opening and stenting
Describe the pathophysiology of acute coronary syndromes
ACS is a spectrum of disease from Unstable Angina on one end to STEMI at the other, with NSTEMI in the middle
The typically arise on a background of atherosclerosis and coronary artery disease
When a plaque in the coronary arteries ruptures and disrupts blood flow, heart muscle supplied by that vessel will become ischaemic and soon will infarct and necrose
These are typically Type 1 MIs
Type 2 MIs are due to an increased oxygen demand or decreased oxygen supply (e.g. due to heart failure, sepsis etc.)
Describe complications of an acute myocardial infarction
Arrhythmias (AF, VT, VF)
Heart Failure
Cardiogenic Shock
Myocardial Rupture
Psychological Effects (Anxiety and Depression)
Describe and diagnose this ECG
Regular, Sinus Rhythm
150bpm
P Waves followed by QRS Complex (1:1)
Narrow QRS
= Sinus Tachycardia
Describe the management of common valvular heart disorders
Symptomatic medical management of heart failure symptoms, AF, oedema etc with Beta Blockers, ACE Inhibitors, Digoxin, Diuretics, Nitrates
Surgical valve replacement is an option for some, with either a tissue or mechanical valve (the latter requires life-long anticoagulation but generally lasts longer)
Procedural options include TAVI (transcatheter aortic valve implantation), MitraClip (transcatheter mitral valve repair) or valvuloplasty (widening of a stenotic aortic valve using a balloon catheter)
State which lead in a standard 12 lead ECG represents each position in the heart (i.e. Anterior, Lateral, Inferior, Septal)
Describe and diagnose this ECG
Regular Rhythym
Rate - 83bpm
ST elevation in V1-4
Reciprocal ST depression in III
Hyperacute peaked T waves in V2-4
= (Anterior) STEMI
Describe the clinical features of infective endocarditis
May be acute or sub-acute onset
Fever
Breathlessness
Night Sweats
Fatigue
Anorexia
Dyspnea
Weight Loss
New Heart Murmur
Symptoms of Heart Failure
Embolic Phenomena (Stroke, Pleuritic Chest Pain, Abdominal Pain, Back Pain)
Splinter Haemorrhages
Janeway Lesions
Petechial Rash
Osler’s Nodes
Roth Spots (Retina)
Describe the pathophysiology and treatment of Tetralogy of Fallot
Ventricular Septal Defect + Overriding Aorta + RV Outflow Obstruction (Pulmonary Stenosis) + RV Hypertrophy
Cyanotic defect with right to left shunt
Curative open heart surgery to repair various defects
Management of acute ‘tet spells’ with beta-blockers and oxygen
Discuss strategies for prevention and treatment of peripheral vascular disease
Smoking Cessation
Control of Hypertension
Statins (should be prescribed to all patients with symptomatic coronary artery disease, regardless of cholesterol levels)
Improve Glycaemic Control
Weight Management
Describe the basic physics underlying an ECG
ECG records the electrical activity of the heart from the skin
This is usually done by a 12-Lead ECG, where a lead is an electrical vector
Unipolar Leads measure the potential variation at a single point (Limb Leads aVR, aVL and aVF and Chest Leads V1-V6)
Bipolar Leads measure the potential difference between two points (Leads I, II and III)
State causes/precipitants of Atrial Fibrillation
Coronary Artery Disease, Structural Heart Disease, Heart Failure, Valvular Disease, Hypertension
Thyroid Dysfunction, COPD, Diabetes, Obesity, Electrolyte Disturbance, Pulmonary Emboli
Infection, Smoking, Caffeine, Alcohol Excess
Describe the common bradyarrhythmias
- Sinus Bradycardia
- Rate <60bpm
- Regular, Narrow QRS
- P Waves Present
- P:QRS - 1:1
- Junctional Bradycardia
- Rate <60bpm
- Regular, Narrow QRS
- No P Waves
- Second Degree AV Block
- Slowest Rate (<60bpm)
- Irregular, Narrow QRS
- P:QRS is not 1:1
- Complete AV Block
- Rate <60bpm
- Regular, Broad QRS
- No Relation Between P and QRS
Describe the pathophysiology and treatment of an Atrial Septal Defect
Acyanotic defect with a left to right shunt
Most common defect is a Secundum ASD (basically a patent foramen ovale) followed by a Primum ASD (basically a partial AVSD)
Can result in arrhythmias, heart failure, wheeze, split-second heart sound and an ejection systolic murmur
Percutaneous catheterisation is most often used for secundum defects with surgical closure reserved for more complex defects
State a systematic approach to interpreting an ECG
- Consider clinical context
- Check date, time and patient details
- Assess technical quality (artefaxct, paper speed (normal is 25mm/s) and gain (normal is 10mV/mm)
- Identify P wave, QRS complex and T wave
- Measure HR
- Check intervals
- Look at P/QRS/T morphology
N.B - Do not rely on automatic interpretation and look at old ECGs if possible
Describe the non-pharmacological management of Atrial Fibrillation
- Acute Rhythm Control
- Synchronised Direct Current Cardioversion
- 3 weeks of anticoagulation prior to DCCV followed by 4 further weeks of anticoagulation
- Transcatheter Therapy
- Isolation of pulmonary veins by Radio Frequency Ablation or Cryoballoon
- Surgical Therapy
- Maze procedure (channelled impulse propagation)
- Synchronised Direct Current Cardioversion
- Rate Control
- Transcatheter Therapy
- Ablation of AV node/His bundle, resulting in iatrogenic 3rd-degree heart block
- Controls ventricular rate in AF, however, renders patient Pt pacemaker dependent for life
- Transcatheter Therapy
Describe and diagnose this ECG
Regular, Sinus Rhythm
Rate = 56bpm
P:QRS is 1:1
Sinus Bradycardia
Describe the pharmacological management of hypertension
- ACE Inhibitor
- e.g. Lisonipril
- Angiotensin II Receptro Blocker
- e.g. Candesartan
- Ca Channel Blocker
- e.g. Amlodipine
- Thiazid-Like Diuretics
- e.g. Bendroflumothiazide
- Beta-Blocker
- e.g. Atenolol
Describe the complications of hypertension
Stroke, MI, Heart Failure, Renal Failure
HTN doubles cardiovascular disease risk for every 20mmHg increase in systolic pressure
Describe the investigation and treatment of acute limb ischaemia
Investigations: MRI, CT Angiography or Invasive Arteriogram
Management: Angioplasty, Bypass Surgery, Thrombolysis or Embolectomy
Describe and diagnose this ECG
Irregular Rhythym
Narrow QRS
No discernible P waves
= Atrial Fibrillation
Describe the pharmacological management of Atrial Fibrillation
Strategies include Rate versus Rhythm control
NICE recommends rate control as the first line strategy in most patients
- Rate Control
- Class IV: Calcium Channel Blockers (e.g. Verapamil or Diltiazem)
- Class II: Beta Blockers (e.g. Carvedilol or Bisoprolol)
- Class V: Other (e.g. Digoxin)
- Rhythm Control
- Class I: Na Channel Blockers (e.g. Flecainide)
- Class III: K Channel Blockers (e.g. Amiodarone)
Describe the main imaging techniques used in cardiology and their indications
- ECG
- Representation of electrical activity of the heart, showing abnormalities of rhythm, conduction or repolarisation
- Used in myocardial infarction, AF
- CXR
- Can give information on the cardiac silhouette, pulmonary vasculature and great vessels
- Can be used to detect pulmonary oedema and pleural effusions
- Echocardiography
- Transthoracic or Transoesophageal
- Gives information on blood flow through the heart (function), valves and chambers (structure)
- Can be used in conjunction with doppler
- Indications include valve assessment, pericardial assessment and assessment of inducable ischaemia
- Nuclear Perfusion Imaging
- Used to assess ischaemia and ejection fraction
- Cardiac CT
- Used to assess coronary artery or great vessel anatomy
- Requires low heart rate and radiation dose
- Angiography
- Both diagnostic and therapeutic
- Used to assess ischaemia, valves, ventricular pressure or in Primary PCI
- Risks include CVA, MI or death
- Cardiac MRI
- Indications include assessment of structure and function, great vessel assessment and tissue characterisation (e.g. infiltrative cardiomyopathies or previous infarction)
Describe the management options for acute myocardial infarction
Oxygen and ECG
Aspirin 300mg PO
Morphine 5-10mg IV
Metoclopramide 10mg IV (Anti-Emetic)
Ticagrelor 180mg PO
Heparin 5000U IV
Activate Primary PCI Team and Arrange Immediate Transfer to GJNH
If not suitable for PPCI, thrombolysis should be given with Tenecteplase (and Clopidogrel in place of Ticagrelor)
Describe investigations used in the diagnosis of Atrial Fibrillation
ECG: Irregularly Irregular Rhythm, No Discernible P Waves, Absence of Isoelectric Baseline, Fibrillatory Waves
TFTs, Echocardiogram, LFTs, U&Es, CRP, Blood Cultures
Describe the clinical manifestations and natural history of peripheral vascular disease
PVD is associated with atherosclerosis and arterial narrowing in the periphery, resulting in reduced blood and oxygen supply to muscles and other tissues
Intermittent Claudication is a muscle pain (ache, cramp or fatigue) on mild exertion, usually in the calf, that is relieved by rest
Chronic Limb Ischaemia (i.e. Stable Angina) may present with dry skin, diminished or absent pulse, ulceration or peripheral discolouration
Acute Limb Ischaemia is an acute thrombotic occlusion of a pre-existing stenotic arterial segment or by an embolus
Describe options for non-pharmacological management of heart failure
Lifestyle Modification
Implantable Cardioverter Defibrillator
Cardiac Resynchronisation Therapy
CABG
Ventricular Assist Device
Transplant
Describe the mechanism of action of drugs used to manage heart failure
- ACE Inhibitors or Angiotensin II Receptor Blocks
- e.g. Enalapril or Valsartan
- Reduce activity of AngII to reduce afterload and fluid retention to slow progression of LV dysfunction
- Beta Blockers
- e.g. Carvedilol
- Reduces afterload and HR to reduce work on the heart
- Mineralocorticoid Receptor Antagonist
- e.g. Spironolactone
- Inhibits sodium resorption to reduce retention of sodium and water
- Ivabradine
- Acts on the ‘funny channel’ to reduce HR
- Digoxin
- Increases force of contraction while reducing rate of conduction through the AV node
Describe the pathogenesis of and pathological changes seen in mitral regurgitation
May be due to endocarditis, rheumatic valve disease, Marfan’s syndrome, cardiomyopathy or Ehlers-Danlos syndrome
Causes pressure overload in both the LA and LV, causing LA and LV dilation
Can lead to pulmonary hypertension, secondary right heart dilation and atrial fibrillation
Symptoms include SOB, palpitations, RH failure symptoms
Signs include a pan-systolic murmur, heave, displaced apex
Describe the pathogenesis of and pathological changes seen in aortic stenosis
Stenosis arises from thickening and calcification of the valve leaflets
Stenosis results in a pressure overload in the LV leading to LV hypertrophy
May arise congenitally, or due to rheumatic valve disease
Symptoms include SOB, (pre)syncope, chest pain and reduced exercise capacity
Signs include an ejection systolic murmur and slow rising pulse
Describe the pathogenesis of and pathological changes seen in aortic regurgitation
Can arise due to a variety of reasons, including degeneration, rheumatic valve disease, aortic root dilation, Marfan’s. SLE or endocarditis
Backflow of blood into the LV causes a volume overload and LV dilation
Symptoms include SOB and reduced exercise tolerance
Signs include a diastolic crescendo murmur
Describe the causes of hypertension
Primary HTN is by definition idiopathic (risk factors include age, gender, ethnicity, diet, physical activity, obesity, alcohol excess and stress)
Secondary HTN accounts for 5-10% of cases and causes include hyperaldosteronism, thyroid disorders, phaeochromocytoma, renal artery stenosis, NSAIDs and cocaine use
Describe and diagnose this ECG
Regular Rhythym
No Relation Between P and QRS
HR <60bpm
Complete Heart Block
Describe features of a normal ECG
Sinus Rhythym (each P wave is followed by a QRS complex)
Normal HR
PR interval <1 large square (<200ms)
QR interval <3 small squares (<120ms)
QT interval <11 small squares (<440ms)
Positive QRS complex in leads I and II
P wave upright in inferior leads
ST segment flat
T wave has same polarity as QRS complex
Describe and diagnose this ECG
Irregular Rhythm
Saw Tooth Pattern
No discernible P waves
= Atrial Flutter
Describe the radiological signs of heart failure
Pleural Effusions
Cardiomegaly
Kerley B Lines (horizontal lines of the periphery of the lower posterior lung fields)
Upper Lobe Pulmonary Venous Congestion
Interstitial Oedema
Describe features of critical ischaemia in the imminently non-viable limb
‘limb pain that occurs at rest, or impending limb loss that is caused by severe compromise of blood flow to the affected extremity’
Clinically presents with 6 Ps:
Pain
Pallor
Paraesthesia
Paralysis
Pulseless
Perishing Cold
Describe long term management following an acute myocardial infarction
Monitor in Coronary Care Unit
Secondary prevention pharmacotherapy (ACEi, Beta Blockers, Statins, Nitrates, Aspirin
Echocardiogram for assessment of LV function
Cardiac Rehabilitation
Describe the diagnosis of an acute myocardial infarction
Clinical history consistent with ACS
ECG changes (ST elevation/depression in 2 contiguous leads)
Raised troponin
HEART score >5
Describe the narrow complex tachyarrhythmias
- Sinus Tachycardia
- Rate >100bpm
- Regular, Narrow QRS
- P Waves Present
- P:QRS is 1:1
- Atrial Fibrillation
- Variable Rate (Fast)
- Irregular, Narrow QRS
- No P Waves
- Atrial Flutter
- Rate approx. 300bpm
- Regular, Narrow QRS
- May Get Variable AV Block
- Sawtooth Atrial Activity
- Supraventricular Tachycardia
- Rate >150bpm
- Regular, Narrow QRS
- P:QRS is 1:1
- P Waves May be Present
Describe the clinical presentation of heart failure
Symptoms: Dyspnea, Orthopnoea, PND, Fatigue, Exercise Intolerance, Cough, Ankle Swelling
Signs: Peripheral Oedema, Elevated JVP, 3rd Heart Sound, Displaced Apex (Cardiomegaly), Lung Crackles (Pulmonary Oedema), Pleural Effusion
Describe the investigations used in the diagnosis of hypertension
Office BP Measurement
24 Hour Ambulatory BP Monitoring (BP taken every 20-30mins throughout the day)
Home BP Monitoring (2 readings, twice a day, taken over 4-7 days)
Other tests include U&Es, Glucose, Lipid Profile, TFTs, LFTs, Urinalysis, ECG, Echo, Renal Ultrasound, Renin, Aldosterone
Assess CV risk, presence of secondary HTN or end organ damage
Describe the clinical presentation of coronary artery disease
Chest, Back or Jaw Pain (typically crushing)
Sweatiness, Clamminess
SOB
Tachycardia
Distress
Crackles
Elevated JVP
Shock
Arrhythmia
Describe the pathogenesis of and pathological changes seen in mitral stenosis
Almost always caused by rheumatic valve disease
Obstruction of the mitral valve leads to pressure overload in the left atrium and pulmonary circulation which can result in atrial/pulmonary hypertension, AF and secondary right heart failure
Symptoms include SOB, palpitations, chest pain, syncope, RH failure symptoms and haemoptysis
Signs include a loud S1 and an opening snap close to S2
Describe the management of infective endocarditis
Empirical antibiotics should be given as soon as blood cultures are obtained
NVE: Amoxicillin + Flucloxacillin + Gentamicin
PVE: Vancomycin + Gentamicin + Rifampicin
IV treatment give for at least 4-6 weeks
40-50% of patients undergo cardiac surgery due to valve dysfunction leading to heart failure, uncontrolled infection or to prevent embolism
Describe the pathophysiology of Tricuspid Atresia and its surgical management
Malformation of the tricuspid valve, resulting in an inability of blood flow from the right atrium to the right ventricle
Therefore, it requires both an atrial and ventricular septal defect so blood can pass from the right atrium to the pulmonary arteries
Managed surgically by the Fontan or TCPC procedure
In Fontan circulation, the single ventricle supports systemic circulation while systemic venous return is directed to pulmonary arteries (bypassing the ventricular mass)
The ASD is closed and the pulmonary aa. grafted to the RA, bypassing the RV
