Cardiology Flashcards
1
Q
Myocardial infarction definition
A
Necrosis of the myocardium as a result of ischaemia
2
Q
MI/acute coronary syndrome classifications/DDx
A
Unstable angina - partial occlusion of a coronary artery. Troponin negative chest pain with normal/abnormal ECG
NSTEMI - severe but incomplete occlusion of a coronary artery. Troponin positive chest pain without ST elevation
STEMI - complete occlusion of coronary artery, ST elevation of 2mm in >=2 chest leads or 1mm in >=2 limb leads or left bundle branch block plus troponin positive chest pain
3
Q
Angina definition and types
A
Myocardial ischaemia that causes chest pain but does not lead to the death of myocardial tissue and does not lead to a troponin rise
stable = only during exertion, unstable = at rest
4
Q
Type 2 myocardial infarction definition
A
MI due to cardiac hypoperfusion for other reasons such as severe sepsis, hypotension, or coronary artery spasm
may not require conventional MI treatments
5
Q
Typical MI/ACS presentation
A
Chest pain
Can use SOCRATES mnemonic:
Site - central/left-sided
Onset - sudden
Character - crushing/someone sitting on your chest
Radiation - left arm, neck and jaw
Associated symptoms - nausea, sweating, clamminess, SoB, vomiting, syncope
Timing - constant
Exacerbating/relieving factors - worsened by exercise
Severity - often severe
6
Q
Atypical MI/ACS presentation
A
Epigastric pain
No pain (more commonly in elderly and diabetics)
Acute breathlessness
Palpitations
Syncope
Acute confusion
Diabetic hyperglycaemic crises
7
Q
MI/ACS investigations
A
ECG - look for ST elevation, left bundle branch block or other ST abnormalities (if shows STEMI then troponin is irrelevant -> it’s a STEMI)
Bloods:
Troponin - at least 3 hours after onset of pain, repeated after 6 hours
Renal function
HbA1c and lipid profile
FBC
CRP
D-dimer if needed to rule out PE
Chest X-ray
8
Q
NSTEMI/unstable angina ECG changes
A
ST depressions
T wave inversions
Pathological Q waves not typical
T wave inversions with ST changes = ongoing ischaemia
isolated T wave inversions = post-ischaemic
Do not necessarily represent the vessel location
9
Q
STEMI management
A
A-E for emergencies
- Targeted O2 therapy
- Loading dose of aspirin 300 mg
- GTN spray
- IV morphine/diamorphine
- Primary percutaneous coronary intervention for pts who present within 12hrs of onset of pain AND are <2hrs since first medical contact
10
Q
NSTEMI/unstable angina management
A
- Targeted O2 therapy
- Loading dose of aspirin 300 mg and fondaparinux
- GTN spray
- IV morphine/diamorphine
- Antithrombin therapy such as low mol weight heparin
- Pts with high 6 month mortality offered angiogram
11
Q
Post-MI management
A
- Aspirin 75mg + second anti-platelet (clopidogrel 75mg OD or ticagrelor 90mg OD)
- Beta blocker (normally bisoprolol)
- ACE-inhibitor (normally ramipril)
- High dose statin (e.g. Atorvastatin 80mg ON)
All patients should have an ECHO performed to assess systolic function and any evidence of heart failure should be treated
All patients should be referred to cardiac rehabilitation
Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia
12
Q
MI/ACS complications
A
Ventricular arrhythmia - usually self-resolve
Recurrent ischaemia/infarction/angina - inserted stends can thrombose, new infarcts can occur, and angina can continue for some time
Acute mitral regurgitation - due to papillary muscle rupture, presents with pansystolic murmur and severe & sudden heart failure
Congestive heart failure - due to impairment of heart muscle function secondary to the ischaemia
2nd, 3rd degree heart block
Cardiogenic shock
Cardiac tamponade
Ventricular septal defects
Left ventricular thrombus/aneurysm - post-anterior MI the myocardium can be susceptible to wall stress; can present as persisting ST elevation
Left/right ventricular free wall rupture - necrosis of the free walls of either ventricle can lead to rupture allowing blood into the pericardial space, causing a rapid tamponade
Dressler’s Syndrome - fever and pleuritic chest pain 2-3 weeks or up to a few weeks after an MI
Acute pericarditis
13
Q
Stable angina definition/presentation
A
Troponin negative chest pain triggered by myocardial ischaemia
- Constriction/heavy discomfort to chest (may radiate to jaw/neck/arm)
- Brought on by exertion
- Alleviated by 5 mins rest or GTN spray
3/3 = typical angina
2/3 = atypical
0-1/3 = non-anginal
14
Q
Stable angina classes
A
Class I - no angina with normal physical activity, may be triggered by strenuous activity
Class II - angina pain causes slight limitation on normal physical activity
Class III: angina causes marked limitation on normal physical activity
Class IV: angina occurs with any physical activity and may occur at rest (unstable angina)
15
Q
Stable angina symptoms
A
Central, constricting chest pain that radiates to neck/jaw/arm
Exertional chest pain that is relieved on rest/GTN
Associated symptoms: nausea, vomiting, clamminess or sweating
Stable angina may have no clinical signs on examination at rest
16
Q
Stable angina investigations
A
ECG
Bloods - FBC and TFTs to exclude anaemia and hyperthyroidism which can exacerbate symptoms
CT coronary angiogram (indicated if typical/atypical angina pain or if ECG shows ischaemic changes in chest pain with <2 angina features)
If inconclusive, functional imaging to be used
17
Q
Stable angina management
A
optimise cardiovascular risk factors to reduce atherosclerotic processes
Secondary prevention: aspirin 75mg OD and statin 80mg ON
GTN spray for symptom relief: inform patient of side-effects (headache, flushing, dizziness) and to repeat dose if pain not stopped after 5 minutes
1st line = beta-blocker (bisoprolol) OR calcium channel blocker (verapamil or diltiazem). Do not combine due to risk of heart block
If neither can be tolerated to consider a long-acting nitrate (ISMN), ivabradine, nicorandil or ranolazine
2nd line = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker (amlodipine or nifedipine)
3rd line = beta-blocker (bisoprolol) AND long-acting dihydropyridine calcium channel blocker AND long-acting nitrate
18
Q
Scale on ECG paper
A
Small square = 0.04s
Large square = 0.2s
5 large squares = 1s
300 large squares = 1 min
19
Q
Limb electrodes colour/placement
A
(ride your green bike)
Red - right arm
Yellow - left arm
Green - left leg
Black - right leg
20
Q
Views of the heart by lead
A
V1-2 = septal
V3-4 = anterior
V5-6 = lateral
Lead I = lateral
Lead II = inferior
Lead III = inferior
aVR = lateral
aVL = lateral
aVF = inferior
21
Q
Normal cardiac axis ECG
A
Usually ~30 degrees
Leads I, II and III positive
Lead II most positive, then lead I, then lead III
aVR shows most negative deflection
22
Q
Right axis deviation ECG
A
Axis distorted to the right (90-180 degrees)
Lead III most positive, then lead II
Lead II deflected
Lead aVF more positive
23
Q
ECG leads angles
A
Lead I = 0 degrees
Lead II = 60 degrees
aVF = 90 degres
Lead III = 120 degrees
aVR = -150 degrees
aVL = -30 degrees
24
Q
Left axis deviation ECG
A
Depolarisation between -30 and -90
aVL then lead I most positive
Lead II negative
Lead III most negative
25
Atrial fibrillation ECG features
Lack of P wave
Narrow QRS complex
Fibrillating baseline
Irregularly irregular rhythm
26
Atrial fibrillation presentation
Palpitations
Chest pain
Shortness of breath
Lightheadedness
Syncope
On auscultation, variable intensity heart sound
Apical to radial pulse deficit
Irregularly irregular variable volume pulse
27
Distinguishing between a fib and atrial flutter
Afib shows no p waves
Atrial flutter has a characteristic sawtooth baseline
28
Afib investigations
ECG is definitive
Bloods to look for reversible causes such as infection, hyperthyroidism or alcohol use
Echocardiogram to look for cardiac causes
29
Acute afib management
A-E in emergency
1st line = synchronised DC cardioversion +/- amiodarone
If the patient is stable and onset of AF <48 hours:
Rate or rhythmn control
Rhythm control with DC cardioversion (+ sedation) or pharmacological anti-arrhythmics (fleicanide if no structural heart disease, amiodarone if history of structural heart disease).
If DC cardioversion is delayed then heparin will be required to anticoagulate the patient
If the patient is stable and onset of AF >48 hours/unclear time of onset:
Rate control only
Rate control with beta-blockers or diltiazem
Need to anticoagulate for 3/52 prior to attempting cardioversion due to the risk of throwing off a clot
Also perform a TOE to exclude a mural thrombus
30
Afib complications
Heart failure
Systemic emboli leading to ischaemic stroke, mesenteric ischaemia or acute limb ischaemia
Bleeding
31
Management of chronic AF -rate control
Aims to reduce heart rate to reduce symptoms; first line approach
1st line = beta-blocker (bisoprolol; NOT sotalol) or rate-limiting calcium channel blocker (diltiazem; contraindicated in heart failure)
2nd line medications: dual therapy (under specialist guidance)
Digoxin monotherapy may be considered in those with non-paroxysmal AF who are sedentary
32
Management of chronic AF -rhythm control
The aims to revert a patient back into sinus rhythm
Should be offered to patients who have:
AF secondary to a reversible cause
Heart failure thought to be caused by AF
New-onset AF
Or those for whom a rhythm control strategy would be more suitable based on clinical judgement
Rhythm control can be achieved via two methods:
Electrical cardioversion
Pharmacological cardioversion: amiodarone (only for older, sedentary patients due to side effects), flecainide (can take PRN, preferred in young patients with normal hearts) or sotalol (for patients not meeting demographics for amiodarone and flecainide
Moment of return to sinus rhythm poses the highest stroke risk. Therefore, rhythm control should only be attempted if the onset of AF <48 hours, a patient has undergone 3/52 of anticoagulation or has had a TOE to exclude a mural thrombus
33
CHA2DS2VASc Score
C: 1 point for congestive cardiac failure
H: 1 point for hypertension
A2: 2 points if the patient is aged 75 or over
D: 1 point if the patient has diabetes mellitus
S2: 2 points if the patient has previously had a stroke or transient ischaemic attack (TIA)
V: 1 point if the patient has known vascular disease
A: 1 point if the patient is aged 65-74
Sc: 1 point if the patient is female
Males scoring 1 or more and females scoring 2 or more should be anti-coagulated
34
Anti-coagulation options in afib
Direct oral anticoagulants (DOACs):
Considered first line for anticoagulation in AF
Examples of DOACs are edoxaban, apixaban, rivaroxaban & dabigatran
Do not require monitoring
Generally associated with fewer bleeding risks compared to warfarin
Most have approximately 12 hour half-lives therefore if a patient misses a dose they are not covered
Warfarin:
Requires cover with LMWH for 5 days when initiating treatment (because warfarin is initially prothrombotic)
Requires regular INR monitoring
INR can be affected by a whole host of drugs and foods
Has 40 hour half-life therefore anticoagulant effect lasts days
Is the only oral anticoagulant licenced for valvular AF
Low Molecular Weight Heparin (LMWH):
eg enoxaparin
A rare option in patients who cannot tolerate oral treatment.
Involves daily treatment dose injections
35
Heart failure definition
Failure of the heart to generate sufficient cardiac output to meet the metabolic demands of the body
36
Low-output heart failure definition and causes
When cardiac output is reduced due to a primary problem with the heart and the heart is unable to meet the body's needs
AAPPTT
Anaemia
Arteriovenous malformation
Paget's disease
Pregnancy
Thyrotoxicosis
Thiamine deficiency (wet Beri-Beri)
37
High-output HF definition
a heart that has a normal cardiac output, but there is an increase in peripheral metabolic demands that the heart is unable to meet
38
Systolic vs diastolic heart failure definition
Systolic dysfunction = an impairment of ventricular contraction despite adequate ventricular filling e.g. ischaemic heart disease, dilated cardiomyopathy, myocarditis
Diastolic dysfunction =the inability of the ventricles to relax and fill normally; the heart is still able to pump well but pumps out less blood per contraction due to reduced diastolic filling e.g. uncontrolled chronic hypertension (significant left ventricular hypertrophy reduces filling of the left ventricle), hypetrophic cardiomyopathy, cardiac tamponade, constrictive pericarditis
39
Acute vs chronic heart failure definition
Acute HF = new-onset of HF symptoms (acute mitral regurgitation following an MI) or an acute deterioration in a patient with known chronic HF
Chronic HF progresses more slowly and may take many years to develop
40
Presentation of left heart failure
Causes pulmonary congestion
Shortness of breath on exertion
Orthopnoea
Paroxysmal nocturnal dyspnoea
Nocturnal cough (± pink frothy sputum)
fatigue
Tachypnoea
Bibasal fine crackles on auscultation of the lungs
Cyanosis
Prolonged capillary refill time
Hypotension
Less common signs: pulsus alternans (alternating strong and weak pulse), S3 gallop rhythm (produced by large amounts of blood striking compliant left ventricle), features of functional mitral regurgitation
41
Presentation of right heart failure
Causes venous congestion
Ankle swelling
Weight gain
Abdominal swelling and discomfort
Anorexia and nausea
Raised JVP
Pitting peripheral oedema (ankle to thighs to sacrum)
Tender smooth hepatomegaly
Ascites
Transudative pleural effusions (typically bilaterally)
42
Heart failure investigations
For stable patient in GP
1. NT-pro-BNP level (released by centricles in response to myocardial stretch), high negative predicted value (2000ng/L (236pmol/L): refer urgently for specialist assessment and TTE <2 weeks; 400-2000ng/L (47-236pmol/L): refer for specialist assessment and TTE <6 weeks)
2. 12-lead ECG
3. Transthoracic echo, look at ejection fraction (if <40% = HFrEF, systolic dysfunction; >40% with raised BNP HFpEF, diastolic dysfunction)
4. Bloods (U&E), LFTs, FTF, glucose, lipid profile
5. CXR - ABCDE signs
A: Alveolar oedema (with 'batwing' perihilar shadowing)
B: Kerley B lines (caused by interstitial oedema)
C: Cardiomegaly (cardiothoracic ratio >0.5)
D: upper lobe blood diversion
E: Pleural effusions (typically bilateral transudates)
F: Fluid in the horizontal fissure
43
Heart failure conservative management
Weight loss if BMI >30
Smoking cessation
Salt and fluid restriction - improves mortality
Supervised exercise-based group rehabilitation programme for people with heart failure
44
Heart failure medical management
Symptomatic relief for fluid overload = loop diuretics
1st line = ACE-I and beta blocker
ARB if ACE-I intolerant, hydralazine if ARB and ACE-I intolerant
2nd line = aldosterone antagonist (spironolactone or eplerenone)
If symptoms persist consider:
Hydralazine and a nitrate for Afro-Caribbean patients
Ivabradine if in sinus rhythm and impaired EF
Digoxin = useful in those with AF. This worsens mortality but improves morbidity
Also SGLT2 if needed as add on
(BASH for systolic - beta blocker, ACE-I, spironolactone, hydralazine)
45
Heart sounds
S1- tricuspid valve closure
S2 - aortic + pulmonary valve closure
S3 - ventricular filling aka diastole - this would correspond to the T wave
S4 - atria contract against a stiff ventricle - this would correspond to the p wave
46
Atrial flutter symptoms
asymptomatic
palpitations
lightheadedness
syncope
chest pain
47
Atrial flutter ECG features
Regular rhythm
Saw-tooth baseline with repetition at 300bpm (these are atrial flutter waves)
Narrow QRS complexes
Ventricular rate which depends on the level of AV block:
150bpm if 2:1
100bpm if 3:1
75bpm if 4:1
60bpm if 5:1
48
Atrial flutter management - hemodynamically unstable patients
Signs of haemodynamic instability:
Shock: suggests end-organ hypoperfusion.
Syncope: cerebral hypoperfusion.
Chest pain: myocardial ischaemia.
Pulmonary oedema: evidence of heart failure.
If signs of haemodynamic instability:
1st line = direct current synchronised cardioversion +/- amiodarone
49
Atrial flutter management - hemodynamically stable patients
Treat reversible causes: fluid rehydration (in septic/dehydrated patients) can revert atrial flutter into sinus rhythm.
Rate and rhythmn control
1st line = beta-blocker (bisoprolol) OR calcium channel blocker (diltiazem, verapamil)
2nd line = if rate control fails to control flutter than consider cardioversion.
3rd line = recurrent or refractory flutter managed with ablation of arrhythmogenic foci at cavotricuspid isthmus. Success rate high at 90%.
Suitable for those symptomatic despite rate control and those in which cardioversion has failed
50
Ventricular fibrillation definition
Irregular broad complex tachycardia
Always a pulseless rhythm
Polymorphic and irregular QRS complexes
51
Ventricular fibrillation management
Follow ALS algorithm
VF is a shockable rhythm so a 200J bi-phasice unsynchronised shock should be administered
IV adrenaline (1mg of 10ml 1:10,000 solution) and IV amiodarone (300mg) should be administered after delivery of the 3rd shock
Adrenaline should be administered every 3-5 minutes thereafter
52
Heart block definition
Obstruction in electrical conduction system of the heart
Can occur anywhere from the SA node, to the AV node to the bundle of His or bundle branches themselves
53
First degree heart block definition/causes/management
Prolonged conduction of electrical activity via AV node
PR interval >200ms on ECG
Causes
High vagal tone: e.g. athletes
Acute inferior MI
Electrolyte abnormalities: e.g. hyperkalaemia
Drugs: e.g. NHP-CCBs, beta-blockers, digoxin, cholinesterase inhibitors
Management
First degree heart block itself is benign and does not need treating. However, any pathological underlying cause should be reversed
54
Second degree heart block Mobitz type I/Wenkebach definition/causes/management
second degree heart block that is usually due to reversible conduction block at the AV node. It is characterised by progressive lengthening of the PR interval which results in a P wave that fails to conduct a QRS
Causes
MI (mainly inferior)
Drugs such as beta/calcium channel blockers, digoxin
Professional athletes due to high vagal tone
Myocarditis
Cardiac surgery
Management
It is generally asymptomatic and does not require any specific management as the risk of high AV block/complete heart block is low. If symptoms do arise, ECG monitoring may be required, precipitating drugs must be stopped and if they are bradycardic with adverse features they should be treated with atropine
55
Second degree heart block Mobitz type II definition
second degree AV block where there are intermittent non-conducted P waves. The PR interval is constant (may be normal or prolonged) and there may no pattern or fixed ratios such as 2:1 or 3:1 block. It is usually caused by conduction system failure, especially at the His-Purkinje system.
In most cases there is a broad QRS indicating a distal block in the His-Purkinje system and many patients have pre-existing left bundle branch block/bifascicular block
56
Second degree heart block Mobitz type II causes
Infarction: particularly anterior MI which damages the bundle branches
Surgery: mitral valve repair or septal ablation
Inflammatory/autoimmune: rheumatic heart disease, SLE, systemic sclerosis, myocarditis
Fibrosis: Lenegre's disease
Infiltration: sarcoidosis, haemochromatosis, amyloidosis
Medication: beta-blockers, calcium channel blockers, Digoxin, amiodarone
57
Second degree heart block Mobitz type II management
Definitive management is with a permanent pacemaker as these patients are at risk of complete heart block and at risk of becoming haemodynamically unstable
58
Third degree heart block definition
atrial impulses fail to be conducted to the ventricles. Sufficient cardiac output may be secondary to a ventricular or junctional escape rhythm.
ECG shows severe bradycardia and complete dissociation between the P waves and the QRS complexes. patients are at high risk of asystole, ventricular tachycardia and cardiac arrest
59
Third degree heart block causes
Myocardial infarction: especially inferior
Drugs acting at the AVN: beta blockers, dihydropyridine calcium channel blockers, or adenosine
Idiopathic fibrosis
60
Third degree heart block management
Permanent pacemaker requires insertion due to the risk of sudden death
61
Primary hypertension definition
primary hypertension is characterised by persistently elevated blood pressure due to age-related pathophysiological changes
accounts for approximately 90-95% of cases of hypertension
62
Hypertension definition
a 24h ambulatory blood pressure average reading (ABPM) that is more than or equal to 135/85mmHg
63
Hypertension classification
Stage 1: Clinic => 140/90mmHg; ABPM => 135/85mmHg
Stage 2: Clinic => 160/100mmHg; ABPM =>150/95mmHg
Stage 3: Clinic systolic BP (SBP) => 180 or diastolic BP (DBP) =>120mmHg
64
Hypertension investigations
ABPM or home blood pressure monitoring if ABPM is not tolerated or declined
Alongside ABPM: assessment for end-organ damage and assessment of cardiovascular risk (QRISK2 scores)
Urine dip and albumin:creatinine level
Blood glucose, lipids and renal function
Fundoscopy for evidence of hypertensive retinopathy
ECG: look for evidence of LV hypertrophy
Referral for same-day specialist assessment should be arranged for people with:
Clinic blood pressure of 180/120mmHg and higher with signs of retinal haemorrhage or papilloedema (accelerated hypertension) or life-threatening symptoms (e.g. new onset confusion, chest pain, heart failure signs or AKI)
65
Hypertension medical management - when to start treatment
Stage 1 hypertensive patients who are <80 years old with end organ damage, CVS disease, renal disease, diabetes or 10-year CVS risk >10% OR
Anyone with stage 2 hypertension
66
Hypertension treatment NICE guidelines
Step 1:
ACE-inhibitor (e.g. Ramipril) if <=55 years old or has T2D
DHP-Calcium Channel Blocker (e.g. Amlodipine) if >55 years old OR African or Caribbean ethnicity
If unable to tolerate ACE-inhibitor then switch to Angiotensin Receptor Blocker (e.g. Candesartan)
Step 2:
(If maximal dose of Step 1 has failed or not tolerated)
Combine CCB and ACE-I/ARB
Step 3:
(If maximal doses of Step 2 has failed or not tolerated)
Add thiazide-like diuretic (e.g. Indapamide)
Step 4: Resistant Hypertension
If blood potassium <4.5mmol/L then add spironolactone
If >4.5mmol/L increase thiazide-like diuretic dose
Other options at this point if the potassium is >4.5mmol/L include:
Alpha blocker (e.g. Doxazosin)
Beta blocker (e.g. Atenolol)
Referral to cardiology for further advice
67
Hypertension ABPM targets
Age <80 ABPM target <135/85
Age >80 ABPM target <145/85 (due to risk of postural drop and falls)
T1DM with end-organ damage <130/80
68
ACEI side effects
persistent dry cough
headaches
dizziness
rash
hyperkalaemia
69
Asbestosis definition
chronic lung condition characterized by diffuse interstitial fibrosis
It occurs in patients who have a history of exposure to asbestos and have developed pleural plaque disease
typically manifests ≥10 years following exposure
70
Asbestosis signs/symptoms
Dyspnoea
Chronic cough
Crepitations on auscultation
Finger clubbing
Cyanosis
Reduced chest expansion
71
Asbestosis investigations
Detailed patient history focusing on occupational asbestos exposure
Chest x-ray: May reveal linear interstitial fibrosis, pleural plaques, pleural thickening, or atelectasis
Pulmonary function tests: May be normal or show a restrictive pattern (reduced FVC and TLC with a normal FEV1/FVC ratio) or obstructive pattern (reduced FEV1)
High resolution CT: May demonstrate pleural thickening and pleural plaques
Bronchoscopy + biopsy: Has limited use as it normally cannot sample enough tissue for a diagnosis
Open lung biopsy: May be considered for a definitive diagnosis if cancer is suspected
72
Asbestosis management
Smoking cessation: Essential to slow down disease progression
Pulmonary rehabilitation: Helps to improve lung function and quality of life
Oxygen therapy: Recommended if SpO2 ≤89%
Lung transplant: May be considered in severe cases
Reporting to coroner: Deaths due to asbestosis must be reported
73
Jobs with high risk of asbestos exposure
Construction Workers
Shipbuilders and Navy Personnel
Power Plant Workers
Automobile Mechanics
Railroad Workers
Electricians
Plumbers and Pipefitters
HVAC Workers
Demolition Workers
Firefighters
Textile Workers
Miners
74
Sarcoidosis definition
multi-system disease that is characterised by the formation of granulomas, leading to widespread inflammatory changes and complications across multiple body systems
(Granulomas are small, organized collections of immune cells that form in response to chronic inflammation or the presence of foreign substances in the body. typically composed of macrophages)
75
Acute sarcoidosis presentation
aka Löfgren syndrome
Fever
Polyarthralgia (painful joints)
Erythema nodosum (skin inflammation)
Bilateral hilar lymphadenopathy (bilateral enlargement of the lymph nodes of pulmonary hila)
76
Chronic sarcoidosis presentation
Pulmonary: Dry cough, dyspnoea, reduced exercise tolerance, and crepitations on examination
Constitutional: Fatigue, weight loss, arthralgia, low-grade fever, lymphadenopathy, and enlarged parotid glands
Neurological: Meningitis, peripheral neuropathy, bilateral Bell's palsy
Ocular: Uveitis, keratoconjunctivitis sicca
Cardiac: Arrhythmias, restrictive cardiomyopathy
Abdominal: Hepatomegaly, splenomegaly, renal stones
Dermatological: Erythema nodosum, lupus pernio
77
Sarcoidosis investigations
definitive diagnosis of sarcoidosis is made through tissue biopsy (e.g., lung, lymph nodes), which typically reveals non-caseating granulomas
other investigations can also suggest a diagnosis of sarcoidosis:
Blood tests: May show raised ESR, ACE (not specific or diagnostic), and calcium levels; lymphocytes may be reduced
Chest x-ray or CT: May reveal stages of disease progression
Stage 1 - Bilateral hilar lymphadenopathy (BHL)
Stage 2 - BHL with peripheral infiltrates
Stage 3 - Peripheral infiltrates alone
Stage 4 - Pulmonary fibrosis
78
Sarcoidosis management
Bilateral hilar lymphadenopathy alone: Usually self-limiting and often does not require treatment
Acute sarcoidosis: Bed rest and NSAIDs for symptom control
Steroid treatment: Oral or intravenous, depending on the severity of the disease
Immunosuppressants: Used in severe disease
79
Measuring rate on an ECG
Count the number of QRSs on one line of the ECG (usually lead II – running along the bottom) and multiply by six
OR
Count the number of large squares between R waves and divide 300 by this number (if the patient is in atrial fibrillation report a rate range rather than a single value)
80
Assessing axis deflection on ECG
As a general rule if the net deflections in leads I and aVF are positive then the axis is normal
If lead I has a net negative deflection whilst aVF is positive then there is right axis deviation
If lead I has a positive deflection and aVF has a negative deflection then there is left axis deviation
81
Causes of left axis deviation
Can be normal if the diaphragms are raised e.g. Ascites, pregnancy
Left ventricular hypertrophy (LVH)
Left anterior hemiblock (see notes on heart block)
Inferior myocardial infaction
Hyperkalaemia
Vertricular tachycardia (VT)
Paced rhythm
82
Causes of right axis deviation
Normal in children or young thin adults
Right ventricular hypertrophy (RVH)
Often due to respiratory disease
Pulmonary embolism (PE)
Anterolateral myocardial infarction
Left posterior hemiblock (rare)
Septal defect
83
Features of PR interval on ECG
Prolonged in first degree heart block
Shortened in rapid conduction via accessory pathway eg WPW
Depression in pericarditis
84
Features of P wave on ECG
Absent in afib
Dissociated from QRS in heart block
Notched (p mitrale) in left atrial hypertrophy
Peaked p waves (p pulmonale) in right atrial hypertrophy and hypokalaemia
85
Normal Q wave leads
initial downward deflection in the QRS complex
normal in left sided leads (V5, V6, lead I, aVL)
if >1 small square long and >2mm deep or in other leads = pathological
86
Wide QRS complex
>3 small squares/0.12 seconds
Bundle branch blocks (LBBB or RBBB)
Hyperkalaemia
Paced rhythm
Ventricular pre-excitation (e.g. Wolf Parkinson White)
Ventricular rhythm
Tricyclic antidepressant (TCA) poisoning
87
Small QRS complex
pericardial effusion
high BMI
emphysema, cardiomyopathy
88
Tall QRS complex
left ventricular hypertrophy
young, tall, thin people
89
Hyperkalaemia ECG
Small p-wave
Tall, tented (peaked) t-wave
Wide QRS
90
Infective endocarditis in intravenous drug users most commonly affects the _________ valve
tricuspid
91
Beta-blockers should be stopped in acute heart failure if...
patient has heart rate < 50/min, second or third degree AV block, or shock
92
STEMI management for patient receiving PCI
prasugrel is given in addition to aspirin. If patient is on an anticoagulant then clopidogrel used instead
93
NSTEMI/unstable angina management
Aspirin 300 mg
Fondaparinux if no immediate PCI planned
If GRACE <3, give ticagrelor unless on oral anticoagulants, in which case give clopodigrel
If GRACE >3, offer PCI within 72 hours unless unstable, give unfractionated heparin and prasugrel/ticagrelor (swap for clopodigrel if on oral anticoagulants)
94
Interpreting NT-proBNP results
if levels are >400 pg/ml arrange specialist assessment (including transthoracic echocardiography) within 2 weeks
if levels are 100-400 pg/ml arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks
95
myocarditis vs endocarditis vs pericarditis definition
endocarditis = inflammation of lining in the heart chambers and the valves
Myocarditis = inflammation of the muscle
Pericarditis = inflammation of pericardium (sac around heart)
96
Infective endocarditis - staph aureus
now the most common cause of infective endocarditis
particularly common in acute presentation and IVDUs
97
Infective endocarditis - strep viridans
historically Streptococcus viridans was the most common cause of infective endocarditis. This is no longer the case, except in developing countries
technically
Streptococcus viridans refers to viridans streptococci, rather than a particular organism. The two most notable viridans streptococci are Streptococcus mitis and Streptococcus sanguinis
they are both commonly found in the mouth and in particular dental plaque so endocarditis caused by these organisms is linked with poor dental hygiene or following a dental procedure
98
Infective endocarditis - coagulase-negative Staphylococci
eg Staphylococcus epidermidis
commonly colonize indwelling lines and are the most common cause of endocarditis in patients following prosthetic valve surgery, usually the result of perioperative contamination
after 2 months the spectrum of organisms which cause endocarditis return to normal (i.e. Staphylococcus aureus is the most common cause)
99
Infective endocarditis - streptococcus bovis
associated with colorectal cancer
the subtype Streptococcus gallolyticus is most linked with colorectal cancer
100
Managing STEMI/NSTEMI if patient is hypotensive...
be careful with nitrates
101
Drugs causing long QT syndrome
amiodarone, sotalol, class 1a antiarrhythmic drugs
tricyclic antidepressants, selective serotonin reuptake inhibitors (especially citalopram)
methadone
chloroquine
terfenadine**
erythromycin
haloperidol
ondanestron
