Cardiology Flashcards
Define MI and the difference between STEMIs and NSTEMIs
MI occurs when cardiac myocytes die due to prolonged myocardial ischaemia. STEMIs show an ST elevation on ECG whereas NSTEMIs do not.
Causes of MI
ATHEROSCLEROSIS
Emboli, coronary spasm, vasculitis
MI risk factors
Age, males, FHx, smoking, HTN, obesity
Clinical manifestations of MI.
Crushing chest pain which may radiate to the arm/jaw.
Raised JVP, increased pulse and blood pressure changes, 4th heart sounds, signs of HF.
Anxiety, nausea, sweating, palpitatiions
First line investigations for MI
ECG - STEMI will show ST elevation and tall T waves
Troponin blood testing
Gold standard for investigating MI (often not needed)
Coronary angiography
Management of STEMI
Initially 300mg aspirin.
Hospital - aspirin +/- ticagrelor. Beta blcokers, CCBs
Other drugs used include GTN, antithrombins, statins, ACEi etc.
PRIMARY PCI IS THE TREATMENT OF CHOICE
Treatment of NSTEMI and unstable angina
Alleviate pain and secondary prevention (antiplatelets and antithrombotic)
Complications of MI
Cardiogenic shock, cardiac arrhythmias, pericarditis, emboli, aneurysms, ventricular rupture, papillary muscle rupture.
Can ACS occur without chest pain?
YES! This is called silent ACS and often occurs with elderly and diabetics.
Define angina
Chest pain caused by a mismatch between oxygen supply and demand by myocardial cells.
Main cause of stable angina
Atherosclerosis
Difference between stable and unstable angina.
Stable angina is a CCS induced by effort and relieved by rest. Unstable angina is an ACS which is not relieved by rest.
Investigations of angina
ECG, coronary angiography, perfusion MRI, bloods
Management of stable angina
Reassurance and lifestyle modifications
Medications
- Secondary prevention (aspirin, statins, ACEi)
- Anti-anginal drugs (beta blockers, CCBs)
- Exacerbations (GTN spray)
Revascularisation
Key presentations of stable angina
- Heavy central chest pain which may radiate to jaw/arms
- Pain occurs with exercise
- Pain eases with rest or GTN
(classical angina has 3/3, atypical angina has 2/3 and non-anginal chest pain has 1/3)
Define heart failure
An inability of the heart to deliver blood (and oxygen) at a rate enough to meet with the requirements of the metabolising tissues, despite normal or increased cardiac filling pressures.
Causes of heart failure
MYOCARDIAL DYSFUNCTION (usually from MI)
HTN, alcohol abuse, cardiomyopathy, valve disease, endocarditis, pericarditis
Different types of HF
HFREF (EF<40%) - commonly caused by IHD
HFPEF (EF>50%) - increased stiffness and decreased LV compliance leads to impaired diastolic filling
Key presentations of HF
Dyspnoea, fatigue, tachycardia, peripheral oedema
Signs of HF on examination
Displaced apex beat, tender hepatomegaly, cardiomegaly, pleural effusion, elevated JVP, 3rd an 4th heart sounds, ascites
1st line investigations for HF
ECG
NT-pro BNP blood test
Gold standard investigation for HF
Cardiac MRI
HF management
Prevention – lifestyle advice
Drug management – diuretics, ACEi, ARBs, beta blockers, aldosterone antagonists, vasodilators and nitrates
Revascularisation, myocardial stunning, transplantation
HF complications
AF, VF, kidney failure, anaemia, stroke
Define hypertension
An abnormally high blood pressure in the clinic (>140/90)
Causes of hypertension
Primary/Essential HTN = idiopathic
Secondary causes of HTN include pheochromocytoma, Conn’s and Cushing’s
Contributory lifestyle factors such as stress, smoking and obesity
1st line investigations for HTN
Clinical BP
Confirm with ambulatory or home BP
Other tests in patients with HTN
Bloods, urine dipstick, ECG, cholesterol, echo
HTN drug treatment for patients under 55
- ACEi (or ARB)
- ACEi + CCB
- ACEi + CCB + diuretic
- add beta blocker, alpha blocker or spironolactone
HTN drug treatment for patients over 55 or from an Afro-Caribbean background
- CCB
- CCB + ACEi
- CCB + ACEi + diuretic
- add beta blocker, alpha blocker or spironolactone
Thresholds for treatment of HTN
Low risk = 160/100
High risk = 140/90
BP targets for HTN
Routine = 140/90
Elderly = 150/90
PMH of stroke/CKD/diabetes = 130/80
Define atrial fibrillation and flutter
Tachyarrhythmia characterised by an irregularly irregular pulse, rapid HR and ECG changes. (Atrial flutter is chaotic beat but regularly irregular)
Causes of atrial fibrillation
IHD, HF, mitral valve disease, HTN, hyperthyroidism, alcohol induced
Pathophysiology of atrial fibrillation
Atrial ectopic beats (thought to originate in pulmonary veins) lead to dysfunction of the cardiac electrical signalling pathway. As a result, the atria no longer contract in a coordinated manner. Due to irregular contractions, the atria fail to empty properly. This may result in stagnant blood accumulating within the atrial appendage, increasing the risk of clot formation and embolic stroke.
Clinical manifestations of atrial fibrillation
Chest pain, dyspnoea, palpitations, fatigue, irregularly irregular pulse
1st line investigation
ECG
Tests other than ECG for atrial fibrillation
Blood tests, echo, TFTs, CXR
Differential diagnosis of atrial fibrillation
Tachycardias, ventricular atopic beats, Wolff-Parkinson-White
Management of atrial fibrillation
Beta blockers, rate-limiting CCBs, digoxin, amiodarone, anticoagulants
Complications of atrial fibrillation
STROKE, heart failure, sudden death
What is an electrical storm?
3 episodes of VF or VT during a 24-hour period
Arrhythmias other than atrial fibrillation
- Supraventricular tachycardia
- Ventricular tachycardia
- Sinus tachycardia
- AV blocks
- LBBB
- RBBB
- Ventricular ectopic
- Wolff-Parkinson-White
Define acute pericarditis
An inflammatory pericardiac syndrome with or without pericardial effusion
Causes of pericarditis
Viral, bacterial, autoimmune, neoplastic, metabolic, traumatic and iatrogenic, amyloidosis, aortic dissection
What is a pericardial effusion and what can it lead to?
A collection of fluid within the potential space of the pericardial sac - can lead to cardiac tamponade
Key presentations of pericardial effusion
Chest pain, pericardial chest rub, ECG abnormalities, pericardial effusion (2 of these required for diagnosis)
1st line diagnosis for pericarditis
Clinical diagnosis based on signs and symptoms
Other tests for pericarditis
ECG, CXR, echo, blood tests
Management of pericarditis
Sedentary activity, NSAIDs or aspirin, colchicine
Treatment of pericardial effusion
Pericardiocentesis
Complications of pericarditis
Cardiac tamponade
Constrictive pericarditis
Signs of cardiac tamponade
Pulsus paradoxus, muffled heart sounds, hypotension, increased JVP
Treatment of cardiac tamponade
Pericardiocentesis, pericardiectomy, thoracotomy
Define infective endocarditis
Infection of heart valves or other endocardial-lined structures within the heart.
Types of IE
Left-sided native IE
Left-sided prosthetic IE
Right-sided IE
Device related IE
Epidemiological changes in IE
Used to be a disease of the young affected by rheumatic heart disease. Now affects the elderly, drug abusers, those with congenital defects and prosthetic heart valves
Causes of IE
Bacteraemia arising from poor dental hygiene, IV drug abuse and soft tissue infections.
Pathophysiology of IE
Early microbial adherence is crucial. Bacterial adherence to a platelet-fibrin nidus. Hallmark of IE is vegetation.
Clinical manifestations of IE
Signs of systemic infection.
Heart murmurs, splinter haemorrhages, Osler’s nodes, Janeway lesions, Roth spots on fundoscopy, petechiae
1st line investigation for IE
Blood cultures - 3 samples from 3 peripheral sites
Other investigations for IE
TRANSTHORACIC ECHO, urinalysis, CXR
Management of IE
Antimicrobials
Treat complications
Surgery if antibiotics ineffective, complications occur or have a large vegetation needing removal
Complications of IE
HF, arrhythmias, abscess formation in cardiac muscle, emboli formation (stroke, vision loss)
Define aortic stenosis
Chronic progressive disease characterised by narrowing of the aortic valve area. Symptoms occur when the valve area is 1/4th of normal
Causes of aortic stenosis
Calcific aortic valvular disease - most common
Bicuspid aortic valve
Rheumatic heart disease
Pathophysiology of aortic stenosis
Narrowing of the aortic valve causes a pressure gradient to develop between LV and aorta (increased afterload)
LV function initially maintained by compensatory pressure hypertrophy. When these mechanisms are exhausted, LV function declines.
Key presentations of aortic stenosis
Exertion dyspnoea, exertion syncope, ejection systolic murmur, slow rising carotid pulse, soft or absent second heart sound
1st line investigations for aortic stenosis
Echocardiography
Doppler derived gradient and valve area
Other investigations for aortic stenosis
CXR, ECG, cardiac CT
Management of aortic stenosis
Surgical aortic valve replacement - definitive treatment
TAVI
Consider IE prophylaxis in dental procedures
Factors that decrease survival rates for aortic stenosis
Angina, syncope, HF
Define mitral regurgitation
Backflow of blood from the LV into the LA during systole due to abnormalities of the valves, chordae tendinea or papillary muscles
Causes of mitral regurgitation
Myxomatous degeneration Ischaemic MR Rheumatic heart disease IE Dilated and hypertrophic cardiomyopathy Collagen diseases
Pathophysiology of mitral regurgitation
Pure volume overload!
Compensatory mechanisms - LA enlargement (leading to pulmonary HTN), LV hypertrophy and dilation, increased contractility
Key presentations of mitral regurgitation
Exertion dyspnoea, pansystolic murmur, displaced hyperdynamic apex beat, soft 1st heart sound, prominent 3rd heart sound, right heart failure
1st line investigations for mitral regurgitation
Echocardiogram
Other tests for mitral regurgitation
ECG, CXR, cardiac catheterisation
Management of mitral regurgitation
Vasodilators, rate control for AF, anticoagulants, diuretics
Serial echocardiography
IE prophylaxis
Surgery if symptomatic, EF <60% or new onset AF
Define aortic regurgitation
Leakage of blood into the LV from the aorta during diastole due to ineffective coaptation of aortic cusps
Causes of aortic regurgitation
Bicuspid aortic valve
Rheumatic heart disease
IE
Aortic dissection
Pathophysiology of aortic regurgitation
Combined pressure and volume overload
Compensatory mechanisms - LV dilation and hypertension - can lead to HF
Key presentations of aortic regurgitation
Hyperdynamic and displaced apical pulse, wide pulse pressure. Systolic ejection murmur, diastolic blowing murmur.
Significant symptoms occur late - angina, dyspnoea, LV failure, palpitations
How is aortic regurgitation diagnosed?
By physical exam. Then echocardiogram. Can also perform a CXR.
Aortic regurgitation management
IE prophylaxis
Serial echocardiograms
Vasodilators
Surgery - definitive treatment
Define mitral stenosis
Obstruction of LV inflow that prevents proper filling during diastole. Normal area is 4-6cm2 but symptoms arise at around <2cm2
Causes of mitral stenosis
Rheumatic carditis is predominant cause
IE
Mitral annular calcification
Pathophysiology of mitral stenosis
Progressive dyspnoea due to pulmonary congestion.
Increased trans-mitral pressure leads to LA dilation and AF
RHF due to pulmonary HTN
Haemoptysis
Key presentations of mitral stenosis
Mitral facies, small-volume pulse, a-wave jugular venous pulse, diastolic murmur, loud opening heart sound
1st line test for mitral stenosis
Echocardiogram
Other tests for mitral stenosis
CXR, ECG, cardiac catheterisation
Mitral stenosis management
IE prophylaxis
Serial echocardiogram
Diuretics, beta blockers/digoxin/CCBs
Percutaneous mitral balloon valvotomy
Mitral valve replacement in serious cases
Define shock
Acute circulatory failure resulting in inadequate organ perfusion. Systolic BP <90 or MAP <65
Types of shock
Anaphylactic shock (IgE mediated allergic reactions) Septic shock (uncontrolled infection) Hypovolaemic shock (bleeding, burns, fluid loss) Cardiogenic shock (arrhythmias, MI, PE, cardiac tamponade)
Other - tension pneumothorax, spinal cord injury, Addison’s, heat exhaustion
Investigation and management of shock
ABCDE
IV Fluids!
Depending on cause may need adrenaline, antibiotics, reperfusion therapy etc.
Definition of cardiomyopathy
A group of diseases of the myocardium that affect the mechanical or electrical function of the heart.
4 main groups of cardiomyopathy
Hypertrophic cardiomyopathy (HCM) Arrhythmogenic cardiomyopathy (ARVC) Dilated cardiomyopathy (DCM) Restrictive cardiomyopathy (RCM)
Causes of cardiomyopathy
GENETICS!!
HCM - sarcomeric protein gene mutations
DCM - cytoskeletal gene mutation
ARVC - desmosome gene mutations
Pathophysiology of HCM
Hyperdynamic contraction of the heart which impairs diastolic relaxion. Causes chaotic myofibrillar disarray with features of ischaemia causing arrhythmias.
Pathophysiology of DCM
Characterised by dilation of ventricles.
Pathophysiology of ARVC
RV becomes thin and the muscle is replaced by fat and fibrous tissue leading to dilation
Key presentation of cardiomyopathies
Arrhythmias!
Angina, SOB, palpitations, dizzy spells, syncope
Gold standard investigation for cardiomyopathy
Cardiac catheterisation
1st line tests for cardiomyopathy
ECG, echo, CMR
Important investigation to do for cardiomyopathy
GENETIC ANALYSIS!
And should try to test family members.
Management of cardiomyopathy
FAMILY EVALUATION
lifestyle modifications
Management of symptoms
HF management
Complications of cardiomyopathies
HF, blood clots, valvular issues, cardiac arrest, sudden death