Cardiology COPY Flashcards
1
Q
Describe the anatomy of the coronary arteries
A
- Left and right coronary arteries arise from the aorta (in the aortic sinuses, fill during diastole from back-flow in aorta to the aortic valve)
- Left coronary artery banches to left anterior descending (LAD), left marginal artery (LMA) and left circumflex artery (Cx)
- Right coronary artery branches to right marginal artery anteriorly, and posterior interventricular artery in 80-85% of individuals
2
Q
Describe the areas of the heart supplied by each coronary artery
A
- RCA - right side of heart
- Right atrium
- Right ventricle
- Inferior left ventricle
- Posterior septal area
- Circumflex artery - top, left and back of heart
- Left atrium
- Posterior aspect of left ventricle
- LAD - middle of heart
- Anterior aspect of left ventricle
- Anterior aspect of septum
3
Q
List the types of acute coronary sydrome
A
- Unstable angina - ischaemia without infarction
- No evident ECG changes (may have some transient changes)
- Negative troponin
- History suggestive of ACS
- 50% risk
- Unstable - onset of symptoms while resting or on very minor exertion, lasts longer than 5 minutes and does not cease with cessation of activity and/or use of GTN spray
- ST elevation MI
- ACS history
- Positive troponin
- Classical ECG changes - ST elevation or depression
- Non-ST elevation MI
- ACS history
- Positive troponin
- No ST elevation
4
Q
List the risk factors for ACS
A
Non-modifiable
- Age
- Gender - male
- FH of IHD - before age of 55
Modifiable
- Smoking
- Hypertension
- Diabetes
- Hyperlipidaemia
- Obesity
5
Q
Describe the pathophysiology of ACS
A
- Atherosclerosis - deposition of lipids in BV wall forming atherosclerotic plaque, causes narrowing of vessels
- Risk of rupture of plaque and embolus leading to ACS
- Atherosclerotic progression = Glagovian remodelling
- Initially with small plaque formation there is eccentric dilatation of coronary artery to compensate
- Increased myocardial oxygen demand e.g. exercise - not wide enough to supply blood to myocardium = angina/MI
- Full occluded coronary vessel = STEMI
- Partially occluded coronary vessel = NSTEMI or unstable angina
- Full thickness infarction of myocardial wall = Q wave infarction
- Partial thickness infarction of myocardial wall = non-Q wave infarction
- Q wave persists after MI - always seen on ECG
6
Q
List the symptoms associated with ACS
A
- Central constricting chest pain associated with
- Nausea and vomiting
- Sweating and clamminess
- Feeling of impending doom
- Shortness of breath
- Palpitations
- Pain radiation to jaw or arms
- Syncope - due to severe arrhythmia or hypotension
- Tachycardia
- Sinus bradycardia - excessive vagal stimulation, most common in inferior MI
- Sudden death - usually due to ventricular fibrillation or asystole
7
Q
Describe the signs/symptoms associated with an atypical presentation of an MI
A
- No chest pain - ‘silent MI’, common in women, diabetics, elderly
- Symptoms
- Shortness of breath – especially if on exertion
- Generalised weakness
- Dizziness
- Syncope
- Pulmonary oedema
- Epigastric pain
- Vomiting
- Acute confusional state
- Stroke
- Diabetic - hyperglycaemia
8
Q
List the signs which indicated impaired myocardial function
A
- Added heart sounds
- Pan-systolic murmur
- Pericardial rub
- Pulmonary oedema - crepitations
- Hypotension
- Quiet first heart sound
- Narrow pulse pressure - difference of <40mmHg
- Raised JVP
9
Q
What are the differential diagnoses for ACS?
A
- Cardiac
- Angina
- Pericarditis
- Myocarditis
- Aortic dissection
- Pulmonary
- PE
- Pneumothorax
- Anything that causes pleuritic chest pain e.g. pneumonia, lung cancer, RA/SLE, rib fracture etc.
- Oesophageal
- Oesophageal reflux
- Oesophageal spasm
- Tumour
- Oesophagitis
- MSK pain e.g. costochondritis
10
Q
How is potential ACS investigated?
A
Immediate
- ECG
- Bloods - FBC (anaemia, platelets), troponin, glucose, lipids, U&Es, ABG, LFTs, TFTs, HbA1c
- Assess oxygen saturation, BP, pulse, JVP, murmurs, signs of heart failure
Later (don’t delay treatment for)
- CXR - other causes of chest pain, pulmonary oedema
- Echocardiogram - functional damage
- CT coronary angiogram - coronary artery disease
11
Q
What can cause raised troponin?
A
- Acutely
- MI
- Acute heart failure
- Tachyarrhythmias
- Pulmonary embolism
- Sepsis
- Apical ballooning syndrome (Takosubo cardiomyopathy)
- Chronic
- Renal failure - kidneys clear troponin from blood
- Chronic heart failure
- Infiltrative cardiomyopathies e.g. amyloidosis, haemochromatosis, sarcoidosis
12
Q
Which ECG changes indicate a STEMI?
A
- Early - within hours
- ST elevation (or reciprocal ST depression)
- Left bundle branch block - WiLLiaM, W in V1, M in V6
- Hyperacute tented T waves
- Within 24 hours
- Inverted T waves - may or may not persist
- ST segment usually returns to normal
- Within days
- Pathological Q waves (>25% of the height of the R wave and/or greater than 0.04s width and/or greater than 2mm height) - may be permanent so can indicate previous MI
13
Q
How can the location of a STEMI be determined?
A
- Each lead represents a specific area of the heart - changes in that lead can indicate STEMI in that area
- Anterior - V2-4
- Inferior - II, III, aVF
- Septal - V1, V2
- Lateral - V5, V6
- High lateral - I, aVL
14
Q
What ECG changes indicate an NSTEMI?
A
- No ST elevation
- ECG may be normal
- ST depression
- Hyperacute T waves - early sign
- T-wave inversion - late sign, can indicate previous MI
- Pathological Q waves
15
Q
Which coronary arteries supply each area of the heart?
A
- Left coronary artery - anterolateral
- Left anterior descending - anterior
- Circumflex - lateral
- Right coronary artery - inferior
16
Q
How are STEMIs, NSTEMIs and unstable angina distinguished diagnostically?
A
- STEMI - suggestive history, positive troponin, ST elevation on ECG
- NSTEMI - suggestive history, elevated troponin levels, absence of ST elevation but may have other ECG changes
- Unstable angina - suggestive history, negative troponin, absence of ST elevation but may have other ECG changes
17
Q
Describe the initial management of a STEMI presenting to A&E
A
- Oxygen and monitor ECG
- Call 999 and ask for emergency PCI transfer - some patients with multiple comorbidities not suitable for PCI or may be logistical reasons why not possible, may need thrombolytic therapy
- Morphine 5-10mg by slow IV injection
- Metoclopramide IV 10mg
- Aspirin oral 300mg (if patient already taking aspirin already give 75mg)
- Ticagrelor oral 180mg stat
- Heparin IV 5000 units (unless patient has already recieved treatment dose of fondaparinux or enoxaparin)
18
Q
How is thrombolysis for STEMI given?
A
- Tenecteplase + normal medical management (morphine, metoclopramide, aspirin, heparin)
- Don’t give stat ticagrelor dose, prescribe 90mg oral twice daily starting 24 hours after thrombolysis
- Weight based dose of ticagrelor
19
Q
Why is PPCI preferred to thrombolysis for acute STEMI treatment?
A
- Improves survival
- Reduces strokes
- Reduces the chance of further MI
- Reduces the chance of further angina
- Speeds up recovery
- Shortens the time spent in hospital
20
Q
How are STEMIs managed following initial treatment?
A
- Monitor in coronary care unit for complications of MI
- Drugs for secondary prevention
- ACE inhibitors
- Ramipril 1.25mg-2.5mg twice daily initially depending on BP, then increase to 5mg
- Beta blockers
- Atenolol 25-50mg twice daily or if evidence of HF bisoprolol 1.25-10mg daily or carvedilol 3.125mg-25mg twice daily
- Statin - atorvastatin 40-80mg daily
- Eplerenone - only for diabetes and LVSD or clinical HF
- Calcium channel blockers considered for anginal symptoms (amplodipine)
- Nitrates considered for anginal symptoms (isosorbide mononitrate)
- ACE inhibitors
- Echo - LV function and cardiac structure
- Cardiac rehabilitation
- If LVSD at >9 months consider primary prevention ICD
21
Q
How are NSTEMIs managed?
A
- Acute management same - oxygen, aspirin 300mg orally, morphine, metoclopramide, heparin, ticagrelor
- Assess need for PCI (thrombolysis not indicated) - use GRACE score, if medium or high risk considered for early PCI (within 4 days of admission)
- Monitor in coronary care unit for complications
- Secondary prevention - B-blocker (atenolol), ACE inhibitor, statin (atorvastatin), aspirin
22
Q
Describe the GRACE score for ACS
A
- Age
- HR
- SBP
- Creatinine
- HF
- Cardiac arrest at admission?
- ST-segment deviation?
- Elevated cardiac enzyme/markers?
- Gives probability of death/death or MI in-hospital and after 6 months
- GRACE >140 in NSTEMI - urgent inpatient angiogram, may benefit from PPCI
23
Q
How is unstable angina managed acutely?
A
- Suggestive history but normal investigations
- Use risk score e.g. GRACE score to determine whether to discharge home or admit
- Secondary prevention?
24
Q
List the potential complications of an MI
A
- Arrhythmias
- VT/VF - DC cardioversion
- AF (heart failure/LVSD or other structural complication)
- Heart failure
- Diuretics, inotropes, vasodilators
- Cardiogenic shock
- IABP (intra-aortic balloon pump, ventricular assist device)
- Myocardial rupture
- Septum - VSD (surgery)
- Papillary muscle - mitral regurgitation (surgery)
- Free wall - tamponade, usually fatal)
- Pericarditis e.g. Dressler’s syndrome (global ST elevation)
- Psychological
- Anxiety/depression
- Cardiac rehabilitation
25
Q
Define Dressler’s syndrome
A
- Post-MI syndrome, usually 2-3 weeks after
- Caused by localised autoimmune response, pericarditis
- Presentation
- Fever
- Pleuritic chest pain
- Pericardial effusions
- Anaemia
- Raised ESR
- Cardiomegaly on CXR
- Pericardial rub on auscultation
- ECG - global ST elevation and T wave inversion
- Management - NSAIDs, steroids, pericardiocentesis? Usually self limiting
26
Q
List the lifestyle measures taken for secondary prevention of MI
A
- Stop smoking
- Reduce alcohol consumption
- Mediterranean diet
- Cardiac rehabilitation (a specific exercise regime for patients post MI)
- Optimise treatment of other medical conditions (e.g. diabetes and hypertension)
27
Q
Describe type 1-4 MI
A
Type 1: Traditional MI due to an acute coronary event
Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with PCI / coronary stunting / CABG
28
Q
Define stable angina
A
- Manifestation of coronary artery disease (ischaemic heart disease)
- Symptoms of insufficient blood supply to myocardium (ischaemia without infarct), brought on by exertion and relieved by GTN spray + rest
- Differentiated from unstable angina - comes on at rest, not relieved by GTN/time
29
Q
Describe the typical presentation of stable angina
A
- Central or left sided chest discomfort - may radiate to jaw, arm
- Can very from mild –> severe
- Tight/crushing nature
- Dyspnoea
- Usually brought on by exertion, relieved by rest
- Duration - several minutes
30
Q
What causes stable angina?
A
- Same causes as ACS
- Atheroma of coronary arteries
- Aortic valve disease
- Hypertrophic cardiomyopathy
31
Q
How is stable angina investigated?
A
- Physical examination - heart sounds, signs of HF
- Bloods
- ECG - rule out ACS, may have changes e.g. Q waves, ST depression, LBBB, T-wave flattening/inversion
- FBC - anaemia
- U&Es - prior to contrast in CT coronary angiography and other medications
- LFTs
- Lipid profile
- TFTs
- HbA1c and fasting glucose
- Confirm diagnosis with imaging
- CT coronary angiogram - gold-standard investigation
- CXR - other causes of chest pain, signs of heart failure
- Echo - left ventricular function + heart anatomy
32
Q
How is stable angina managed?
A
- Refer to cardiology - urgently if unstable
- Advise patient about diagnosis and when to call ambulance
- Medical management
- Immediate symptomatic relief - GTN
- Long term symptomatic relief - beta-blocker or calcium channel blocker
- Secondary prevention - aspirin (75mg once daily), statin (atorvastatin 80mg once daily), ACE inhibitor, beta-blocker (already on for symptomatic relief)
- Procedural/surgical interventions
- PCA with coronary angioplasty - offered to patients with proximal or extensive disease on CT coronary angiography
- Coronary artery bypass graft (CABG) offered to patients with severe stenosis (midline sternotomy, associated with greater complications)
33
Q
Define heart failure
A
Clinical syndrome in which the heart is unable to pump adequate amounts of blood to meet the body’s metabolic demand.
34
Q
List the types of heart failure
A
- Systolic HF - inability of the heart to contract efficiently to eject adequate volumes of blood to meet the bodies metabolic demand, most common
- Diastolic HF - reduction in heart compliance resulting in compromised ventricular filling and therefore ejection
- Left HF - inability of left ventricle to pump adequate amount of blood leading to pulmonary circulation congestion and pulmonary oedema
- Ejection fraction of <40%
- Right HF - inability of right ventricle to pump adequate amount of blood leading to systemic venous congstion, therefore peripheral oedema and hepatic congestion
- Most commonly due to respiratory disease e.g. COPD
- Raised JVP and peripheral oedema indicate right HF
- Congestive HF - failure of both right and left ventricles, common
- Acute HF - acute onset of symptoms usually due to an acute event e.g. MI, ventricular aneurysm
- Chronic HGF - slow symptom presentation usually due to slow progressive underlying disease
- Acute-on-chronic - acute deterioration of a chronic condition usually following an acute event (infections, MI)
35
Q
What causes heart failure?
A
- Ischaemic heart disease - causes impaired ventricular function, reduced contractility
- Myocardial ischaemia
- Myocardial infarction
- Hypertension - increases strain on heart, leads to hypertrophy which has risk of arrhythmia, heart gets too big for coronary system to perfuse
- Valvular disease
- Mitral/tricuspid regurgitation - volume overload
- Aortic stenosis - pressure overload
- Pericardial disease - pericarditis, pericardial effusion
- Drugs
- Beta-blocks, calcium channel blockers, anti-arrhythmics
- Alcohol - AF, dilated cardiomyopathy
- Cocaine
- Arrhythmias
- Bradycardia
- Tachycardia - reduced ventricular filling, increased heart oxygen demand
- AF - less ventricular filling
- Cardiomyopathies
- Congestive - weakening and dilation of ventricular wall leading to overstretching and reduced contractile efficiency
- Hypertrophic - thickening of heart muscle wall leading to reduced compliance and reduced cardiac output
- Restrictive - sarcoidosis, amyloidosis, haemochromatosis
- Severe anaemia
- Pulmonary hypertension - pulmonary pathologies e.g. COPD
36
Q
List risk factors for heart failure
A
- Age
- Family history and genetics
- Lifestyle - diet, smoking, cocaine use, alcohol, lack of physical activity
- Serious lung disease
- Obesity
- HTN
- Diabetes
- CKD
- Anaemia
- Race/ethnicity - Afrocaribbean people more at risk
- Sex - men develop at a younger age, more likely to have reduced ejection fraction (women have preserved ejection fraction more commonly, more symptomatic)
37
Q
Describe the pathophysiology of symptoms in decompensated heart failure
A
- Drop in cardiac output - reduced sensed volume
- Increased vagal and sympathetic tone to increase heart contractility and rate therefore output
- Vasoconstriction of veins and arteries
- Release of adrenaline
- Low kidney perfusion (due to reduced CO) stimulates RAS, angiotensin II causes vasoconstriction, aldosterone release and ADH causing sodium and waer retention by kidneys
- These mechanisms are initially beneficial to increase blood volume, therefore venous return and CO, but chronically worsen the situation by increasing the workload and strain on the heart, increased oxygen demand on the heart and fluid retention
- Fluid retention –> movement of fluid into interstitial tissue causing peripheral and pulmonary oedema
38
Q
Describe the symptoms associated with heart failure
A
- Dyspnoea - especially on exertion, due to pulmonary oedema and respiratory muscle weakness
- Orthopnoea - breathlessness on lying flat
- Paroxysmal nocturnal duspnoea - occurs lying down/sleeping causing sudden awakening
- Fatigue, lethargy and exercise intolerance
- Inability of heart to raise CO during exercise
- Tissue hypoperfusion e.g. muscle
- Peripheral oedema - swollen ankles
- Weight loss
- Wheeze
- Cough - often worse at night, classic sign is pink frothy sputum
39
Q
Which signs on clinical examination are suggestive of heart failure?
A
- Fluid overload
- Peripheral oedema - ankles +/- sacrum, pitting oedema
- Ascites
- Elevated JVP
- Hypotension
- Tachycardia
- Cardiac heave
- Displaced apex beat - sign of cardiomegaly
- Bilateral crepitations +/- wheeze
- Cachexia
- Hepatic tenderness/hepatomegaly
40
Q
How is heart failure diagnosed?
A
- Clinical presentation
- Bloods - FBC (anaemia), U&Es (hyponatraemia due to dilution), LFTs (extent of liver congestion/damage), BNP (NT-proBNP), TFTs (rule out thyrotoxicosis), HbA1c (diabetes)
- Echocardiogram
- Reduced ejection fraction, structural/functional abnormalities of heart
- ECG - may indicate cause of HF
- MI
- BBB
- Ventricular hypertrophy
- Pericardial disease
- Arrhythmias
- CXR - signs of pulmonary congestion
- Angiography - assess extent of IHD
41
Q
Describe the CXR signs seen in heart failure
A
- Cardiomegaly - heart size >1/2 thoracic cavity (cardiothoracic ratio >0.5)
- Must be PA X-ray to assess heart size
- Kerley B lines - interstitial oedema
- Pleural effusions
- Upper zone vessel enlargement
- Alveolar oedema (bat-wing opacities)
42
Q
How is heart failure classified?
A
- New York Heart Association Classification (1 year mortality)
- Grade I (5%) - no limitation on function
- Grade II (10%) - slight limitation, moderate exertion causes symptoms, no symptoms at rest
- Grade III (20%) - marked limitation, mild exertion causes symptoms, no marked symptoms at rest
- Grade IV (50%) - severe limitation, any exertion causes symptoms, may also have symptoms at rest
43
Q
What complications are associated with heart failure?
A
- Muscle underperfusion - muscle weakness and atrophy causing fatigue, exercise intolerance and dyspnoea
- Increased risk of thromboembolism and strokes due to blood stasis, arrhythmias and atheromas
- Arrhythmias e.g. ventricular tachycardia in advanced HF –> ventricular arrhythmias and cardiac arrest
- Increased infection risk - can initiate acute on chronic event
- Depression and impaired quality of life
- Sudden cardiac death
- Poor prognosis - 50% mortality within 5 years of diagnosis
44
Q
How is heart failure managed?
A
- Refer to specialist (urgent if NT-proBNP >2,000ng/L)
- Heart failure specialist nurse input
- Lifestyle measures
- Stop smoking
- Exercise if tolerated
- Reduce salt
- Fluid restriction
- Reduce alcohol intake
- Flu vaccination yearly
- Medical management
- ACE inhibitor e.g. ramipril titrated as tolerated up to 10mg once daily
- Beta blocker e.g. bisoprolol titrated as tolerated up to 10mg once daily
- Aldosterone antagonist when symptoms not controlled by ACEI/B-blocker (spironolactone or eplerenone)
- Loop diuretics improves symptoms in acute fluid overload e.g. furosemide 40mg once daily
- Other drugs used with specialist input e.g. digoxin, calcium channel blocker, (amlodipine) ivabridine, angiotensin receptor neprilysin inhibitor (ARNI)
- Surgical intervention
- Revascularisation in IHD - CABG or angioplasty
- Valvular replacement
- Implanted automatic cardiodefibrillator or pacemkaer
- Heart transplant considered in end stages
45
Q
How is acute decompensated heart failure managed?
A
- Usually presents with dyspnoea, anxiety and tachycardia
- Sit upright, 100% oxygen flow
- Do an ECG, FBC, U&Es, cardiac enzymes, ABG, CXR
- Sublingual 2 puffs nitrates or oral to enhance myocardial perfusion
- IV opiates to reduce anxiety and preload
- IV furosemide 40-80mg to reduce fluid retention
- If systolic >90 give IV isosorbide dinitrate 2-10mg/h, if systolic <90 treat as cardiogenic shock
46
Q
What is the rationale behind medical management of heart failure?
A
- Improve prognosis
- ACEi
- B1 beta blockers e.g. bisoprolol, atenolol, carvedilol
- Angiotensin-II receptor antagonists
- Spironolactone
- Improve symptoms
- Loop diuretics
- Digoxin
- Vasodilators e.g. nitrates, hydralazine
47
Q
How should patients be monitored on heart failure management?
A
- Diuretics - renal function monitored
- ACE inhibitors - U&Es before treatment then after 1-2 weeks of treatment
- Beta-blockers - monitor heart rate and BP when adjusting dose
- ARBs - must have normal serum potassium and adequate renal function to commence
48
Q
Define infective endocarditis
A
Infection of the endocardium by bacteria, or rarely fungi. Most commonly affects heart valves (natural or prosthetic), but can occur anywhere along the lining of the heart or blood vessels. Formation of vegetation, resulting in damage to endocardium.
49
Q
Which heart valves are most commonly affected by infective endocarditis?
A
- Mitral valve
- Aortic valve
- Tricuspid valve - most common site in IVDU
- Pulmonary valve (rare)
50
Q
List the risk factors for infective endocarditis
A
- Underlying valve abnormalities in 55-75%
- Aortic stenosis
- Mitral valve prolapse
- Previous rheumatic heart disease
- Age related valvular degeneration
- Prosthetic valve - both mechanical and bioprostheses
- IVDU - often tricuspid valve and right side of heart, can be multiple organisms, often more sub-acute insidious onset
- No identifiable risk factors in 30%
51
Q
Describe the pathophysiology of infective endocarditis
A
- Endocardial damage occurs at areas of high haemodynamic pressure (higher shearing forces on endocardium)
- Heart valves
- Mostly left side (higher pressure blood flow) except IVDU
- Thrombi form at damaged site, mainly made of platelets and fibrin, initially sterile (‘sterile vegetations’)
- At times of transient bacteraemia (e.g. from poor oral hygiene, UTIs, other GU infections, IV drug injection, soft tissue infection, cannulae, cardiac surgery) bacteria can colonise the thrombi –> vegetation
- Vegetations can break off to form emboli and cause an obstruction, commonly affect CNS, lungs, spleen, kidneys, liver
- Vegetation forms biofilm (especially on prosthetic valves) - difficult for antibiotics to penetrate and treat
52
Q
Which organisms most commonly cause infective endocarditis?
A
- Native valve infection
- Strep species - Strep viridans
- Enterococci
- IVDU
- Staph. aureus
- Higher incidence of gram negative organisms (HACEK, enterobacteriacaea, psuedomonas auerginosa) and fungal organisms
- Prosthetic valve infections
- Coagulative negative staphylococci - good at forming biofilm
- Gram negative and fungal infection more common
Streptococcal endocarditis, especially caused by viridans present more indolently - subacute endocarditis
Staph. aureus, gram negative and fungal endocarditis present acutely, causing rapid valve destruction
53
Q
Describe the pathophysiology of rheumatic heart disease
A
- Streptococcus pyogenes infection (e.g. strep throat)
- Infection partially/not treated
- Liberation of Streptolysin ‘O’ exotoxin
- Anti-Streptolysin O antibodies produced against Streptolysin
- Cross-reactivity of antibodies - cardiac valves have similar antigenic structure so antibodies attack valves
- Stenosis or regurgitation of valves
54
Q
Describe the pathophysiology of endocarditis in IVDU
A
- Classed as separate entity due to tendency to involve right-sided valves
- Right sided due to:
- Particulate induced endothelial damage to right-sided valves
- Increased bacterial loads in these patients
- Direct physiologic effects of injected drugs
- Deficient immune response caused by IVDU
- Tricuspid valve endocarditis more common than aortic or mitral (do occasionally occur)
- Underlying valve normal in 75-93%, repeated bouts of IE in an IVDU will lead to gradual increase in structural abnormalities of the valve
55
Q
Describe the presentation of infective endocarditis
A
- Acute - valve destruction and systemic infection developing over days to weeks
- Subacute - presentation over weeks to months, rarely leads to systemic infection
- Early manifestations of infection
- Fever and new mumur - IE until proven otherwise
- Fatigue and malaise
- Embolic events
- Can take days-weeks to occur
- Seen earlier in acute endocarditis
- Small emboli
- Petechiae
- Splinter haemorrhages
- Janeway lesions - non-tender, small erythematous or haemorrhagic or nodular lesions on palm or sole due to septic emboli
- Haematuria
- Large emboli
- CVA
- Renal infarction
- Right sided endocarditis - tricuspid valve involvement
- Septic pulmonary emboli - pleuritic chest pain and classical CXR appearance
- Long-term effects
- Immunological reaction
- Splenomegaly
- Nephritis
- Vasculitic lesions of skin and eye
- Osler’s nodes - painful palpable lesions on hands and feet
- Clubbing
- Tissue damage (seen more in acute endocarditis)
- Valve destruction
- Valve abscess - aortic root abscess, high mortality, need surgical intervention
56
Q
What causes petechiae?
A
- Local trauma
- Crying - petechiae around eyes
- Vasculitis e.g. IE
- Thrombocytopaenia
- Malignancy
- Viral infection - particularly in children
- Leukaemia
- Typhus
57
Q
What criteria is used in the diagnosis of infective endocarditis?
A
Duke Criteria
Major criteria
- Positive blood culture for infective organism (on 2 separate tests if >12 hours apart, or on 3/3 or 3/4 tests >1 hour apart)
- Evidence of IE from other tests
- Echocardiogram shows - strictures, unusual blood flow, implanted/unusual material, abscesses
- New valve regurgitation
Minor criteria
- Fever >38 degrees
- Risk factor for IE e.g. IVDU, congenital heart condition, prosthetic valve
- Usual echo, but not findings stated above
- Immunological factors present - Roth spots, Osler’s nodes, glomerulonephritis, rheumatoid factor
- Blood cultures positive but major criteria not satisfied
- Vascular abnormalities, embolism, aneurysm, infarcts, conjunctival haemorrhage, intracranial haemorrhage etc.
IE definitely present
- 2 major criteria present OR
- 1 major, 3 minor criteria OR
- 5 minor criteria
IE possibly present
- 1-4 minor criteria AND
- No other more likely diagnosis
58
Q
How is infective endocarditis investigated?
A
- Blood cultures
- Constant bacteraemia so no need to wait for fever
- 3 sets of blood cultures required - if organism only found in one could be due to contamination
- Volume most important factor in organism detection - 10mls/bottle required
- Before antibiotics
- Aseptic technique - reduce risk of contamination and risk of needle stick injury
- Echocardiogram
- Transthoracic - non-invasive, 50% sensitivity
- Transoesophageal - invasive, 85-100% sensitivity
- Transthoracic performed first, if negative and high clinical suspicious remains, transoesophageal indicated
- Duke criteria
- Other bloods
- FBC - might have anaemia of chronic disease, raised WCC, thrombocytopaenia or thrombocytosis
- U&Es - renal dysfunction common due to emboli
- LFTs - ALP raied
- Inflammatory markers - CRP and ESR likely raised
- Urine - haematuria, proteinuria common
- ECG - new AV block suggestive of abscess formation
- CXR - evidence of heart failure, cardiomegaly, pulmonary emboli and/or abcesses (right sided)
59
Q
How is infective endocarditis managed?
A
- Medical - antimicrobial therapy
- Surgical - valve replacement, partial valve repair
60
Q
What are the indications for surgery in infective endocarditis?
A
- Heart failure
- Uncontrollable infection
- Abscess, false aneurysm, enlarging vegetation (urgent)
- Persisting fever and positive blood cultures >7 days
- Infection caused by multi-drug resistant organisms
- Prevention of embolism
- Large vegetations (>10mm) and embolic episode
61
Q
Describe antimicrobial therapy in infective endocarditis
A
- High dose antibiotics
- Treatment tailored to organism susceptibility
- Duration of therapy
- Native valves - 4 weeks
- Prosthetic valves - 6 weeks
- IV therapy for duration in most cases - oral may not penetrate vegetations
- Empirical therapy
- Native - IV amoxicillin + IV flucloxicillin + IV gentamicin (vancomycin + gentamicin in penicillin/beta-lactam allergy)
- Prosthetic - IV vancomycin + IV gentamicin
62
Q
Which antibiotics should be used for treatment of infective endocarditis caused by:
- Streptococcal species
- Enterococcal species
- S. aureus (MSSA)
- S. aureus (MRSA)
- CoNS
And describe the rationale behind antimicrobial choices for these infections.
A
- Benzylpenicillin +/- gentamicin
- Amoxicillin or vancomycin +/- gentamicin
- Flucloxacillin +/- gentamicin
- Vancomycin +/- gentamicin
- Vancomycin +/- gentamicin +/- rifampicin
Organisms often intrinsically resistant to gentamicin, but pencillin/vancomycin act by destroying the bacterial cell wall, which allows the gentamicin to exert its effect –> synergy
63
Q
Define hypertension and describe classifications of hypertension
A
High BP
BP >140/90 in clinic or >135/85 with ambulatory or home readings
Mild (Grade 1) - SBP 140-159 or DBP 90-99
Moderate (Grade 2) - SBP 160-179 or DBP 100-109
Severe (Grade 3) - SBP >180 or DBP >110
64
Q
Describe the pathophysiology of hypertension
A
- Majority of cases have no identifiable cause = essential/primary hypertension
- Genetic influences + environmental factors
- Defects in renal sodium haemostasis - inadequate sodium excretion –> salt and water retention –> increased plasma and extracellular fluid volume –> increased cardiac output
- Functional vasoconstriction + increased natriuretic hormone –> increased vascular reactivity –> increased total peripheral resistance
- Defects in vascular smooth muscle growth and structure –> increased vascular wall thickness –> increased total peripheral resistance
- Environmental factors
- Obesity
- Sleep apnoea
- Alcohol intake
- Sodium intake
- Stress
- Insulin intolerance
- Due to identifiable disease process = secondary hypertension
- Renal disease
- Endocrine disease - Cushing’s syndrome, Conn’s syndrome, adrenal hyperplasia, phaeochromocytoma, acromegaly
- Congenital disease - coarctation of the aorta
- Neurological disease - raised intracranial pressure, brainstem lesions
- Pregnancy - pre-eclampsia
- Drugs - OCP, steroids, NSAIDs, EPO
65
Q
What are the pathological consequences of hypertension?
A
- Increased peripheral vascular resistance
- Atherosclerosis - endothelial damage
- Microaneurysms in the brain (Charcot-Bouchard aneurysms) –> haemorrhagic stroke
- Cardiovascular events
- Atherosclerosis
- Aortic aneurysm
- Cardiac failure
- Atrial fibrillation
- Cerebrovascular events i.e. haemorrhage or clot
- Renal effects - renal failure and other renal problems
- Eye effects
- Visual disturbance due to papilloedema and retinal haemorrhages
66
Q
List the risk factor associated with primary hypertension
A
- Non-modifiable
- Age
- Gender
- Ethnicity
- Genetic factors
- Modifiable
- Diet
- Physical activity
- Obesity
- Alcohol in excess
- Stress
67
Q
Describe the clinical presentation of hypertension
A
- Usually asymptomatic and discovered incidentally
- May have headaches
- Epistaxis (nosebleeds) but very uncommon and only if BP is very high
- Signs
- Coarctation of aorta can cause radio-femoral delay
- Renal artery bruits
68
Q
How is hypertension diagnosed?
A
- BP should be measured every 5 years to screen for hypertension, more in patients on the borderline for diagnosis (>135/85 - annual review) and every year for patients with type 2 diabetes
- Patients with clinical blood pressure between 140/90 and 180/20 should have 24 hour ambulatory blood pressure or home readings to confirm the diagnosis
- Also should measure in both arms, if difference is more than 15mmHg use the reading from the arm with the higher pressure
- Should be investigated for evidence of target organ damage
- Bloods - HbA1c, U&Es, cholesterol
- Urinalysis - haematuria, proteinuria
- ECG - left ventricular hypertrophy
- Check fundi for evidence of retinopathy
- CXR if evidence of coarctation
- Aldosterone for primary aldosteronism
69
Q
How is hypertension management stratified?
A
Aim to get BP to less than 140/90, in high risk populations may benefit from lower (120/80) to reduce CV risk
- If ambulatory or home BP >135/85 and not high risk - lifestyle intervention and annual review
- Ambulatory or home BP >135/85 and high risk or 10 year CV risk >20% - initiate drug treatment and lifestyle intervention
- SBP 160-179 and/or DBP 100-109 (and unchanged on ambulatory or home monitoring) - initiate drug treatment and lifestyle intervention
- Clinic SBP >180 or DBP >110 and no evidence of papilloedema or retinal exudates or haemorrhages - initiate drug treatment and lifestyle intervention
- Clinic SBP >180 or DBP >110 and evidence of papilloedema or retinal exudates or haemorrhages - refer urgently
70
Q
List the high risk patients in hypertension management
A
- Target organ damage
- Known cardiovascular disease
- Previous stroke or TIA
- Renal disease
- Diabetes mellitus
71
Q
Which lifestyle interventions are used in hypertension management?
A
- Aim for healthy BMI
- Exercise
- Healthy diet
- Reduce alcohol intake
- Reduce salt intake
- Stop smoking
- Reduce caffeine intake
72
Q
Describe medical management of hypertension
A
- <55 years
- Step 1 - ACE inhibitor (or ARB if intolerant to ACE inhibitor - usually dry cough)
- Step 2 - ACEi (or ARB) + calcium channel blocker
- Step 3 - ACEi (or ARB) + calcium channel blocker + thiazide-type diuretic
- Add - further diuretic therapy (spironolactone 25 mg daily if K+ <4.5mmol/L) or beta blocker
- >55 years or black patients (African or Carribbean) of any age
- Step 1 - calcium channel blocker
- Step 2 - ACEi (or ARB) + calcium channel blocker
- Step 3 - ACEi (or ARB) + calcium channel blocker + thiazide type diuretic
- Add - further diuretic therapy (spironolactone 25 mg daily if K+ <4.5mmol/L) or beta blocker
ACEi e.g. ramipril 1.25-10mg once daily
ARB e.g. candesartan 8mg-32mg once daily
Calcium channel blocker e.g. amlodipine 5-10mg once daily
Thiazide diuretic e.g. indapamide 2.5mg once daily
Beta blocker e.g. bisoprolol 5-20mg once daily
