Cardiology Flashcards
ECG leads and relevant blood supply
II, III, aVF - Right coronary artery
I, aVL, V5 + V6 - Left circumflex artery
V2-V4 - Left anterior descending artery
V2-V6 - Left main stem
V1, V2, V3 (posterior view) - RCA
How to calculate rate on an ecg
300 / number of large squares between two equivalent adjacent points
Rhythm in AF
No discernible P waves
Irregularly Irregular
Rhythm in Atrial flutter
Saw-toothed baseline
Rhythm in nodal/junctional rhythm
Regular QRS but no P waves
Normal axis deviation
Leads I and II +ve
Left axis deviation
Lead I +ve and lead II -ve (leaving)
Right axis deviation
Lead I -ve and lead II +ve (reaching)
Causes of right axis deviation
- Anterolateral MI
- RVH
- PE
- Left posterior hemiblock WPW
- Atrial Septal Defect secundum
Causes of left axis deviation
- Inferior MI
- LVH
- Left anterior hemiblock WPW
- Atrial septal defect primum
Causes of absent P waves
AF
Sinoatrial node block
Nodal rhythm
Cause of dissociated P waves
Complete heart block
P mitrale
bifid P waves = Left Atrial hypertrophy
HTN, AS, MR, MS
https://ecgwaves.com/the-ecg-in-left-and-right-atrial-enlargement-abnormality-p-pulmonale-p-mitrale/
P pulmonale
peaked p waves = Right Atrial hypertrophy
Pulmonary HTN, COPD
https://ecgwaves.com/the-ecg-in-left-and-right-atrial-enlargement-abnormality-p-pulmonale-p-mitrale/
Definition and causes of wide QRS
> 120ms (3 small squares)
Ventricular initiation
Conduction defect
WPW
Definition and cause of pathological Q wave
> 1mm wide and >2mm deep
Full thickness MI
Signs of RVH in the QRS complexes
Dominant r wave in V1 + deep S wave in V6
Signs of LVH in the QRS complexes
R wave in V6 >25mm
R wave in V5/V6 + S wave in V1 >35mm
Length of normal PR interval
120-200ms (3-5 small square)
Cause of long PR interval
Heart block
Causes of short PR interval
- Accessory conduction eg WPW
- Nodal rhythm
- Hypertrophic Cardiomyopathy
Cause of depressed PR segment
Pericarditis
Normal corrected QT interval (QTc)
380-420ms
Bazett’s formula
Used to calculate corrected QT interval
QTc = actual QT/√R-R
Causes of long QT interval (>420ms)
TIIMME
Toxins
- macrolides
- anti-arrhythmics: quinidine, amiodorone
- TCAs
- Histamine antagonists
Inherited eg Romano-Ward, Jervell Lange-Neilson syndrome
Ischaemia
Myocarditis
Mitral valve prolapse
Electrolytes
- ↓Mg, ↓K, ↓Ca, ↓ temp
Causes of short QT interval (<380ms)
Digoxin
Betablockers
Phenytoin
Causes of raised ST segment (>1mm in limbs; >2mm in chest)
Acute MI
Prinzmetal’s variant angina
Pericarditis - saddle-shaped
Aneurysm - ventricular
Causes of depressed ST segments (>0.5mm)
Ischaemia - flat
Digoxin - down-sloping
T waves are normally inverted in which leads
aVR and V1
Also V2-V3 less so and more commonly in Afro-Caribbeans
Leads in which inverted T waves is abnormal and causes
I, II and V4-6
- Strain
- Ischaemia
- Ventricular hypertrophy
- BBB
- Digoxin
Effect of hyperkalaemia and hypokalaemia on T waves
Hyperkalaemia - tented T waves
Hypokalaemia - flattened T waves
U waves on ECG
Occur after T waves
Seen in hypokalaemia
J waves / Osbourne waves on ECG
Occur between QRS and ST segment
Causes
- Hypothermia < 32
- Subarachnoid haemorrhage
- Hypercalcaemia
Causes of bradycardia
DIVISIONS
- Drugs
- Ischaemia/infarction
- Vagal hypertonia
- Infection
- Sick sinus syndrome
- Infiltration
- HypO-thyroidism / kalaemia / thermia
- Neuro: ↑ ICP
- Septal defect: primum ASD
- Surgery or catherisation
Drugs which cause bradycardia
Antiarrythmics (type 1a, amiodarone)
Beta-blockers
Calcium channel blockers
Digoxin
Infections which cause bradycardia
Viral myocarditis
Rheumatic fever
Infective endocarditis
Infiltrative causes of bradycardia
Autoimmune Sarcoid Haemochromatosis Amyloid Muscular dystrophy
Definition of Narrow Complex Tachycardia
Rate >100bmp
QRS width <120ms
Management of SVT
see AS medicine notes, page 13
Definition of Broad Complex Tachycardias (VT)
Rate >100bmp
QRS width >120ms
Causes of VT
IM QVICK
- Infarction
- Myocarditis
- QT interval increase
- Valve abnormality - mitral prolapse, AS
- Iatrogenic - digoxin, antiarrythmics, catheter
- Cardiomegaly (esp. dilated)
- K↓, Mg↓, O2↓, acidosis
Management of VT
see AS medicine notes, page 14
Common causes of AF
IHD
Rheumatic heart disease
Thyrotoxicosis
Hypertension
Symptoms of AF
Asymptomatic Chest pain Palpitations Dyspnoea Faintness
Signs of AF
Irregualrly irregular pulse
Pulse deficit: difference between pulse and HS
Fast AF -> loss of diastolic filling -> no palpable pulse
Signs of LVF
CHA2-DS2-VAS Score components
- Congestive Heart Failure
- Hypertension
- Age≥75 (2 points)
- Diabetes
- Stroke or TIA (2 points)
- Vascular disease
- Age: 65-74yrs
- Sex: female
->Determines necessity of anticoagulation in AF
Score
0: aspirin 300mg
≥1: Warfarin
Management of Acute AF (≤48h)
Haemo unstable → emergency cardioversion
- electrical or pharmaceutical - 1st: Flecainide (if no structural heart disease) 2nd: Amiodarone
Control ventricular rate
- 1st line: diltiazem or verapamil or metoprolol
- 2nd line: digoxin or amiodarone
Start LMWH
Paroxysmal AF
- Self-limiting, <7d, recurs
- Anticoagulate: use CHADSVAS
- Rx “pill-in-pocket” : flecainide, propafenone
- Prevention: β-B, sotalol or amiodarone
Reasons to use rhythm control in persistent AF
- Symptomatic or CCF
- Younger (<65)
- Presenting first time with lone AF
- Secondary to treated precipitant
Rhythm control management in persistent AF
Echo first: structural abnormalities
- Anticoagulate with warfarin for ≥3wks or use echo to exclude intracardiac thrombus.
- Pre-Rx ≥4wks with sotalol or amiodarone if ↑ risk of failure
- Electrical or pharmacological cardioversion
- ≥ 4 wks anticoagulation afterwards (target INR 2.5)
Maintenance antiarrhythmic
- Not needed if successfully treated precipitant
- 1st: β-B (e.g. bisoprolol, metoprolol).
- 2nd: amiodarone
Rate control management in persistent AF
Target <90bpm at rest
- 1st line: β-B or rate-limiting CCB (NOT both!)
- 2nd line: add digoxin (don’t use as monotherapy)
- 3rd line: consider amiodarone
Management of permanent AF
RATE CONTROL
Possible reasons:
- Failed cardioversion / unlikely to succeed
- AF >1yr, valve disease, poor LV function
- Pt. doesn’t want cardioversion
Management of Atrial Flutter
Similar to AF, although normal drugs may not work
Try amiodarone to restore sinus and amiodarone or sotalol to maintain it
Cavotricuspid isthmus ablation (RA) is Rx of choice.
Acute coronary syndrome definition
ACS = unstable angina + evolving MI
Divided into:
- ST elevation or new onset LBBB
- NSTEMI
Modifiable risk factors for ACS
- Hypertension
- Diabetes
- Smoking
- ↑cholesterol
- Obesity
Non-modifiable risk factors for ACS
- Age
- Male
- Family history of MI < 55yrs
Typical ACS symptoms
Acute central/left chest pain >20min Radiates to left jaw or arm Nausea Sweating Dyspnoea Palpitations
Symptoms of silent MI
Syncope
Delirium
Post-op oliguria / hypotension
More common in elderly and diabetics
Clinical signs of ACS
Anxiety
Pallor Sweating
Pulse ↑/↓
BP ↑/↓
4th heart sound
Signs of LVF (basal creps, ↑ JVP, 3rd HS)
PSM: papillary muscle dysfunction / rupture
ECG changes in STEMI
- Normal
- ST elevation + hyperacute (tall) T waves
- Q waves: full-thickness infarct
- Normalisation of ST segments
- T wave inversion
- (New onset LBBB also = STEMI)
ECG changes in NSTEMI
- ST depression
- T wave inversion
No Q waves = subendocardial infarct
Diagnosis of NSTEMI, STEMI and UA
STEMI / LBBB: Typical symptoms + ST elevation (/LBBB)
NSTEMI: Typical symptoms + no ST elevation + +ve trop
UA: Typical symptoms + no ST elevation + -ve trop
MI complications
Death Passing PRAAED st
Death
Pump failure
Pericarditis Rupture - myomalacia cordis Arrhythmias Aneurysms - ventricular Embolism Dressler’s Syndrome - pleuro-pericarditis
Presentation of pericarditis post MI
Occurs early after MI
- Mild fever
- Central chest pain / change in pain
- Relieved by sitting forward
- Pericardial friction rub
Saddle-shaped ST elevation ± PR depression on ECG
Presentation of Dressler’s syndrome post MI
2-6 weeks after
- Recurrent pericarditis
- Pleural effusions
- Fever
- Anaemia
- ↑ESR
Due to auto-antibodies vs. myocyte sarcolemma
STEMI management
10 steps
1) 12 lead ECG
2) 2-4L oxygen (aim sats 92-98)
3) Iv access, FBC, U+E, glucose, lipids
4) Brief Hx and Exam (CV risk factors, Thrombolysis Contraindications)
5) Antiplatelets - Aspirin/Clopidogrel both 300mg PO (then 75mg/d; asp = indefinite, clop = 1month)
6) Analgesia - Morphine 5-10mg IV; Metoclopramide 10mg IV
7) Anti-ischaemia - GTN 2 puffs or 1 tablet; β-B atenolol 5mg IV (CI: asthma, LVF)
8) LMWH: e.g. enoxaparin IV then SC
9) Admit to CCU for monitoring - Arrhythmias, Continue meds except CCBs
10) Primary PCI or Thrombolysis
ECG criteria for thrombolysis treatment of MI
- ST elevation > 1mm in 2+ limbs or > 2mm in 2+ chest leads.
- New LBBB
- Posterior: Deep ST “depression” and tall “R” waves in V1-V3
Contraindications to thrombolysis after MI
AGAINST
Aortic dissection GI bleeding Allergic reaction previously Iatrogenic - recent surgery Neuro - cerebral neoplasm or CVA history Severe HTN >200/120 Trauma - including CPR
Also contraindicated beyond 24hrs from onset of pain
Everyday drug regime post MI
- ACEi: start w/i 24hrs of MI (e.g. lisinopril 2.5mg)
- β-blocker: e.g. bisoprolol 10mg OD (or, CCB)
- Cardiac rehabilitation (group exercise and info) / Heart Manual
- DVT prophylaxis until fully mobile -> Continue for 3mo if large anterior MI
- Statin: regardless of basal lipids (e.g. atorvastatin 80mg)
Lifestyle advice after MI
Stop smoking Diet: oily fish, fruit, veg, ↓ sat fats Exercise: 30min OD Work: return in 2 months Sex: avoid for 1 month Driving :avoid for 1 month
CV risk scoring systems
GRACE or TIMI
Angina classification
-Stable: induced by effort
-Unstable: occurs at rest / minimal exertion
-Decubitus: induced by lying down
-Prinzmetal’s / variant: occurs during rest -> Due to coronary spasm; ST elevation during attack: resolves as pain
subsides.
-Syndrome X: angina pain + ST elevation on exercise
test but no evidence of coronary atherosclerosis -> Probably represents small vessel disease
Treatment of angina
1) Lifestyle changes
2) CV prophylaxis - low dose Aspirin, ACEi. Statins, Antihypertensives
3) GTN + either B-blocker or CCB
4) PCI
5) CABG
Definition of heart failure
CO is inadequate for the body’s requirements despite adequate filling pressures
Steps in compensatory phase of Heart failure
Reduced CO initially → compensation
- Starling effect dilates heart to enhance contractility
- Remodelling → hypertrophy
- RAS and ANP/BNP release
- Sympathetic activation
Steps in the decompensatory phase of heart failure
-Progressive dilatation → impaired contractility +
functional valve regurgitation
- Hypertrophy → relative myocardial ischaemia
- RAS activation → Na+
and fluid retention → ↑ venous pressure → oedema
- Sympathetic excess → ↑ afterload → ↓ CO
Causes of pump failure leading to low output HF
1) systolic failure (impaired contraction)
- Ischaemia/MI
- Dilated cardiomyopathy
- HTN
- Myocarditis
2) Diastolic failure (impaired filling)
- Pericardial effusion/tamponade/constriction
- Restrictive/hypertrophic cardiomyopathy
3) Arrhythmias
- Bradycaria/ Heart Block
- Tachycardias
- Anti-arrythmics (eg B-b, verapamil)
Causes of low output HF other than pump failure
Excessive pre-load
- AR, MR
- Fluid overload
Excessive afterload
- AS
- HTN
- HOCM
Causes of high output HF
Due to increased needs
- Anaemia, AVM
- Thyrotoxicosis, Thiamine deficiency (beri beri)
- Pregnancy, Paget’s
Causes of RVF
- Secondary to LVF
- Cor pulmonale
- Tricuspid and pulmonary valve disease
Symptoms of RVF
Anorexia and nausea
Signs of RVF
Raised JVP
Tender smooth hepatomegaly
Pitting oedema
Ascites
Causes of LVF
1) IHD
2) idiopathic dilated cardiomyopathy
3) systemic HTN
4) Mitral and aortic valve disease
can also be caused by specific cardiomyopathies
Symptoms of LVF
Fatigue Exertional dyspnoea Orthopnoea and PND Nocturnal cough (+/- pink frothy sputum) S3 + tachycardia (gallop) Wheeze Bibasal creps
Acute vs Chronic HF
Acute
- New onset or decompensation of chronic
- peripheral / pulmonary oedema
- +/- peripheral hypoperfusion
Chronic
- Develops / progresses slowly
- Venous congestion common
- Arterial pressure maintained until very late
Criteria for defining Chronic heart failure
Framingham Criteria
2 major criteria or 1 major and two minor
Major criteria of the Framingham Criteria for CCF
- PND
- +ve abdominojugular reflux
- Neck vein distension
- S3
- Basal creps
- Cardiomegaly
- Acute pulmonary oedema
- ↑ CVP (>16cmH2O)
- Wt. loss >4.5kg in 5d secondary to Rx
Minor criteria of the Framingham Criteria for CCF
- Bilateral ankle oedema
- SOBOE
- ↑HR >120
- Nocturnal cough
- Hepatomegaly
- Pleural effusion
- 30% ↓ vital capacity
Signs of CCF on CXR
ABCDE
- Alveolar shadowing
- Kerley B lines
- Cardiomegaly
(cardiothoracic ratio >50%) - Upper lobe Diversion
- Effusions
- Fluid in the fissures
Signs of CCF on Echo
key investigation
- Global systolic and diastolic function -> Ejection fraction normally ~60%
- Focal / global hypokinesia
- Hypertrophy
- Valve lesions
- Intracardiac shunts
BNP is secreted from ventricles in response to…
- Increased pressure -> stretch
- Tachycardia
- Glucocorticoids
- Thyroid hormones
Actions of BNP
- ↑ GFR and ↓ renal Na reabsorption
- ↓ preload by relaxing smooth muscle
Level of BNP to diagnose heart failure
> 100
- BNP correlates c¯ LV dysfunction -> i.e. ↑ most in decompensated heart failure
- ↑ BNP = ↑ mortality
- BNP also ↑ in RHF: cor pulmonale, PE
New York Hear Association Classification
- No limitation of activity
- Comfortable @ rest, dyspnoea on ordinary activity
- Marked limitation of ordinary activity
- Dyspnoea @ rest, all activity → discomfort
Treatable precipitants / causes of chronic heart disease
Underlying cause
- Valve disease
- Arrhythmias
- Ischaemia
Exacerbating factors
- Anaemia
- Infection
- ↑BP
1st line treatment for chronic heart failure
ACEi/ARB + β-B + loop diuretic
eg lisinopril or candesartan ; carvedilol or bisprolol ; frusemide or butmetanide
for β-B’s, ‘start low and go slow’
E.g. carvedilol 3.125mg/12h → 25-50mg/24h
- Wait ≥2wks between increments
Treatment of severe pulmonary oedema - 10 steps
1 - sit patient up
2 - 15L O2, target 94-98
3 - Iv access + monitor ECG (treat arrhythmias)
4 - Diamorphine 2.5-5mg IV + Metoclopramide 10 mg IV
5 - Frusemide 40-80 mg IV
6 - GTN 2 puffs
7 - CXR, ECG, ?echo
8 - if SBP >100, start nitrate IV
9 - if worsening, consider CPAP, more frusemide or ↑ nitrate infusion
10 - if SBP <100, treat as cardiogenic shock ie consider inotropes
Causes of severe pulmonary oedema
Cardiogenic
- MI
- Arrythmia
- Fluid overload: renal, iatrogenic
Non-cardiogenic
- ARDS: sepsis, post-op, trauma
- upper airway obstruction
- Neurogenic: head injury
signs of left sided or congestive heart failure
- narrow pulse pressure
- raised jvp
- displaced thrusting apex with systolic thrill
- left parasternal heave
- S3 present
- Mid-diastolic flow murmur
- Bibasal crackles
- Peripheral oedema
Causes of mitral regurgitation
Rheumatic heart disease Ischaemic Heart disease Endocarditis Mitral valve disease Papillary muscle dysfunction (due to IHD or endocarditis) Connective tissue diseases Congenital (ASD etc) Collagen disorders Hypertrophic cardiomyopathy
Signs of mitral stenosis
Malar flush
Opening snap
Giant V waves
Graham Steel murmur (high pitched brief early diastolic murmur due to secondary pulmonary regurgitation)
Symptoms of mitral stenosis
Dyspnoea, reduced exercise tolerance
Orthopnoea and PND
Palpitations
Dysphagia (oesophagus compressed by left atrium)
Haemoptysis secondary to pulmonary hypertension)
Causes of mitral stenosis
SYMPTOMS MAY BE PRECIPITATED BY CHANGES SUCH AS AF OR PREGNANCY
Rheumatic heart disease Congenital Carcinoid syndrome (increased serotonin causes increased collagen production in heart) SLE Mucopolysccharidoses
Causes of aortic regurgitation
Rheumatic heart disease
Bicuspid aortic valve
Infective endocarditis
Aortic root dilatation (eg in collagen disorders)
Inflammatory (eg RA, Reiter’s syndrome, ank spond, syphilis)
Quincke’s sign
capillary nail bed pulsations
Corrigan’s sign
visible carotid pulsations
De Musset’s sign
head nodding with each heartbeat
Muller’s sign
pulsation of the uvula
Duroziez’s sign
diastolic femoral bruit when compressed distally
Traube’s sign
pistol shot femorals
Austin Flint murmur
mid-diastolic murmur heart at the apex.
thought to be caused by a regurgitant jet interfering with the opening of the anterior mitral valve leaflet ie mimics mitral stenosis
Rosenburg’s sign
pulsatile liver
Gerhadt’s sign
enlarged spleen
Symptoms of aortic stenosis
Chest pain
SOB
Syncope
In absence of other disease, onset of symptoms in AS is a sign of severity and requires consideration of surgery
Causes of aortic stenosis
Bicuspid valve
Rheumatic heart disease
Calcific
Congenital
Symptoms of tricuspid regurgitation
Fatigue
Abdo pain
Ankle swelling
Anorexia
Causes of tricuspid regurgitation
Secondary (most common):
- chronic left heart failure
- Primary pulmonary hyper tension
- cor pulmonale due to chronic cardiorespiratory disease and hypoxia
- right venticular infarction
- Eisenmenger’s syndrome (pulmonary hypertension, resulting in reversal of a congenital shunt eg VSD)
Primary:
- Congenital eg Ebsten’s anomaly
- Rheumatic heart disease
- right-sided endocarditis
- carcinoid syndrome
- blunt trauma
Long term complications of prosthetic valves
Thromboembolic disease Infective endocarditis Valve failure Valve dehiscence Haemolysis Anticoagulation complications: GI haemorrhage
Small VSD
Haemodynamically insignificant
Harsh pansystolic murmur heard at left lower sternal edge (smaller the hole the larger the murmur)
Large VSD
Presents with cardiac failure in first few months of life
narrow pulse pressure and mid-diastolic murmur (high flow through mitral valve)
May lead to RHF and Eisenmenger’s syndrome (pulmonary hypertension, resulting in reversal of a congenital shunt eg VSD)