Cardiology Flashcards
Pulmonary stenosis
Noonan’s syndrome, congenital rubella
Coarctation of aorta
Turner’s syndrome (bicuspid aortic valve)
Fallot’s teratology
Ventricular septal defect
Overlying aorta
Right ventricular outflow tract obstruction
Right ventricular hypertrophy
Cyanotic heart disease
Teratology of Fallots
Transposition of great arteries
Single ventricle
Tricuspid atresia
Heart failure in Infancy
Enlarged liver
Tachypnoea 60-100
Intercostal insuction
Early: feeding difficulty, failure to thrive, apnoea
Sympathetic innervation
Innervates: SA node (B1): increase heart rate Cardiac muscle (B1): increase contractility Blood vessels (B1 and B2): vasodilitation
Parasympathetic innervation
Basal vagal tone, slows heart rate and conduction in SA and AV nodes
Layers of blood vessel
Tunica adventitia: fibrous tissue
Tunica media: elastic membrane and smooth muscle layer
Tunica interna: internal elastic membrane, lamina propria
Basement membrane
Endothelium
Left axis deviation
Left ant hemiblock Inferior MI WPW RV pacing Normal variant Elevated diaphragm Lead misplacement Endocardial cushion defect
Right axis deviation
RVH Left post hemiblock PE COPD Lateral MI WPW Dextrocardia Septal defects
LBBB
QRS >120ms
Broad notched or slurred R waves in leads I, aVL and usually V5 and V6
Deep broad S waves in leads V1-2
Secondary ST-T changes
RBBB
QRS >120ms
Positive QRS in lead V1 (rSR’)
Broad S waves in leads I, V5-6
Usually secondary T wave inversion in leads V1-2
MI evolvement
Hyperacute T waves (first hour)
ST elevation (within 6 hours)
Inverted T waves (1-7days)
Hyperkalemia ECG
Tall peaked T waves
Flattened P waves
Widened QRS
Hypokalemia ECG
ST segmant depression
Prolonged QT interval
Low T waves
Prominent U waves
Hypercalcemia ECG
Shortened QT interval
Hypocalcemia ECG
Prolonged QT interval
Pericarditis ECG
Diffuse ST elevation + PR segment depression
Saddle ST segment
Digitalis effect
ST “scooping”
T wave depression or inversion
QT shortening +/- U waves
Side effects:
palpitations, fatigue, visual changes, decreased appetite, hallucinations, confusion and depression.
Massive PE
S1Q3T3 (S in I, Q and inverted T wave in III)
Sinus tachycardia and AF
RAD and RVH with strain
Troponin
Peak 1-2d, elevated up to 2 weeks.
Elevated with:
MI, CHF, acute PE, myocarditis, CRF, sepsis, hypovolaemia
CK-MB
Peak 1d, elevated up to 3d.
Elevated with: MI, myocarditis, pericarditis, muscular dystrophy, cardiac defibrillation
Transthoracic echo
Non-invasive, evaluation of RA, RV and LV
Transoesphageal echo
Down the esophagus, evaluation of LA, mitral and aortic valves, interatrial septum.
Stress echo
Demonstrates MI and assesses viability
Exercise testing
Demonstrates CAD in low risk patients. Positive shows ST elevation of >1mm.
CI: acute MI, aortic dissection, pericarditis, myocarditis, PE, severe AS, arterial HTN, inability to exercise adequately
Arrhythmias pathophysiology
Alterations in impulse formation
- Abnormal automacity
- Triggered activity due to afterdepolarisations
Alterations in impulse conduction
- Re-entry circuits
- Conduction block
- By-pass track
Arrhythmias approach
Bradyarrhythmia (100bpm)
[] Regular
\+ Narrow QRS (SVT)
- Sinus tachycardia
- Atrial tachycardia
- AVNRT
- AVRT
- Atrial flutter
\+ Wide QRS
- SVT with BBB
- Ventricular tachycardia
- AVRT
[] Irregular
\+ Narrow QRS (SVTs)
- Afib
- AF with variable block
- Multifocal atrial tachycardia
- Premature atrial contraction
\+ Wide QRS
- Afib with BBB
- AF with BBB and variable block
- Polymorphic VT
- Premature ventricular contractionBradyarrhythmias
Sinus bradycardia: increased vagal tone, sick sinus, increased ICP, hypothyroidism, hypothermia
Sinus block: sinus pacemaker fires but fails to depolarise atrial muscle, no initial P wave.
Sick sinus: sinus node dysfunction
AV conduction blocks
First degree: prolonged PR interval >200ms
Second degree: described by ratio of P waves to QRS
- Type 1 (Mobitz I): gradual prolongation of PR interval
- Type 2 (Mobitz II): abrupt failure of conduction of P wave, increased risk of 3rd degree AV block (permanent pacing)
Third degree: complete AV block, escape pacemaker rhythm distal to the block, no relationship between P and QRS.
Supraventricular tachyarrhythmias
Originate from atria or AV node, have narrow QRS. Include: Sinus tachycardia Premature ectopics Atrial flutter Multifocal atrial tachcardia Atrial fibrillation AV nodal re-entrant tachycardia
CHADS2-VASc score
Congestive heart failure Hypertension Age >75 (2) Diabetes Stroke/TIA (2) Vascular disease Age 65-75 Sex category (female)
Scores >2 should start on oral anticoagulants
HAS-BLED score
Hypertension Abnormal renal or liver function Stroke Bleeding Labile INRs (in TI < 65%) Elderly >65 Drugs (alcohol, or antiplatelets)
AF management
Rate control
- B blocker, diltiazem, verapamil, (digoxin, amiodarone)
Anticoagulation
- Warfarin
Cardioversion (electrical)
- if 48hrs: anticoagulate for 3wks prior and 4 weeks post cardioversion
Etiology
- HTN, CAD, valvular disease, pericarditis, cardiomyopathy, myocarditis, ASD, post-operative, PE, COPD, thyrotoxicosis, sick sinus, “holiday heart”
Premature ectopics
Premature atrial contraction (different P wave morphology) or junctional premature beat (near AV node, P wave not seen)
Atrial flutter
Rapid regular atrial depolarisation from a macro-re-entry circuit within the atrium (~300bpm). Diagnosis by carotid sinus massage, Valsalva maneuver, adenosine (decrease AV conduction)
Multifocal atrial tachycardia
Irregular rhythm caused by presence of 3 or more atrial foci, >3 distinct P wave morphology. Treat with CCB
Atrial fibrillation
Single circuit re-entry/ectopic foci, tachycardia causes remodelling that further promotes AF resulting in suboptimal CO, increases risk of thrombus.
AV nodal re-entrant tachycardia
Re-entrant circuit with fast and slow conducting pathways around the AV node. Accounts for 60-70% of paroxysmal SVTs.
Acute management: Valsalva or carotid massage, adenosine first line and then metoprolol, digoxin.
Long term management: B-blocker, diltiazem, digoxin, antiarrhythmics, catheter ablation.
Pre-excitation syndromes
Subset of SVTs mediated by accessory pathway which can lead to ventricular excitation.
- Wolff-Parkinson-White
Wolff-Parkinson-White syndrome
Congenital defect of the conduction pathway. An accessory conduction tract allows early electrical activation of part of one ventricle and bypasses AV node. Shows as:
Slurring of QRS (delta wave),
PR interval
Ventricular tachyarrhythmias
Premature ventricular contraction Accelerated idioventricular rhythm Ventricular tachycardia Torsades de pointes Ventricular fibrillation
Premature ventricular contraction
QRS >120ms with no preceding P wave. Usually benign.
Accelerated idioventricular rhythm
Ectopic ventricular rhythm with rate 50-100bpm. Frequently occurs in patients with acute MI or other types of heart disease
Ventricular tachycardia
> 3 consecutive ectopic ventricular complexes. Rate >100bpm.
Wide QRS >140ms
AV disociation
Can be monomorphic or polymorphic.
Rx: sustained VT requires electrical cardioversion.
Torsades de Pointes
Predisposition:
- Congenital long QT syndromes
- Drugs quinidine, phenothiazines, erythromycin, quinolones
- Electrolytes hypokalemia, hypomagnesia
Rx: IV magnesium, temporary pacing, electrical cardioversion if hemodynamically unstable
Ventricular fibrillation
Requires prompt ventilation and cardiac support
Electrical pacing
Indications: symptomatic bradycardia, hemodynamic instability, Mobitz II, complete heart block
Pacing techniques:
Temporary: transvenous or external
Permanent: into RA or apex RV
Implantable cardioverter defibrillators
For spontaneous VT or VF
Catheter ablation
Indications:
- Paroxysmal SVT (most AVNRT)
- Atrial flutter
- Afib pulmonary vein ablation
- VT arises in RV outflow tract
Stable angina
Rx:
- Lifestyle modification, diet, exercise, statins
- Antiplatelet therapy: aspirin, clopidogrel
- Beta-blockers: increase coronary perfusion, decrease demand, decrease afterload (BP)
- Nitrates: symptomatic control, decrase preload and afterload, maintain nitrate free intervals to prevent tolerance
- CCB: second-line to increase coronary perfusion
- ACE inhibitors:for hypertension
- Revascularisation
NSTEMI
Incomplete or transient vessel occlusion.
Criteria:
- symptoms of angina
- rise and fall of serum markers of myocardial necrosis
- evolution of ischemic ECG changes without ST elevation
Rx:
- Clopidogrel 300mg
- Aspirin 150mg
- Ticagrelor 180mg
- Enoxaparin infusion
- Beta blockers
- Statins
- ACEi
STEMI
Total coronary occlusion resulting in MI.
Criteria:
- ST elevation in 2 leads or new BBB
- elevated cardiac enzymes. PCI within 90mins.
Rx
- < 90mins PCI
- > 90mins fibrinolysis: tenectaplase bolus, aspirin, clopidogrel, enoxaparin, beta-blocker
Long term management of ACS
1) Education, risk factor modification
2) Antiplatelet and anticoagulation: aspirin, clopidogrel, warfarin if high risk
3) Beta blockers
4) Nitrates
5) CCB
6) ACEi
7) Spironolactone if signs of heart failure
8) Statins
CABG
Indications:
- > 50% of LMCA
- > 70% of LAD, LCx or RCA
Grafts - Saphenous vein - Left internal thoracic artery Right internal thoracic artery - Radial artery
Congestive heart failure
Left heart failure
Low cardiac output: fatigue, syncope, systemic hypotension, cool extremities, slow cap refill, peripheral cyanosis, pulsus alternans, mitral regurge, S3
Venous congestion: dyspnea, orthopnea, PND, cough, crackles
Right sided heart failure:
Low cardiac output: left sided symptoms due to underfilling, tricuspid regurgitation, S3
Venous congestion: peripheral edema, elevated JVP, Kussmal’s sign, hepatosplenomegaly, pulsatile liver
Most common causes of CHF:
- CAD
- HTN
- Idiopathic/dilated cardiomyopathy
- Valvular
- Alcohol
Precipitants of existing CHF:
- Hypertension
- Endocarditis
- Anemia
- Rheumatic heart disease and valvular disease
- Thyrotoxicosis
- Failure to take meds
- Arrhythmia
- Infection
- Lung problems
- Endocrine
- Dietarty indiscretions
CHF management
Lifestyle measures: alcohol consumption, smoking, diet exercise, fluid restriction Medications: - ACEi/ARBs - Beta-blockers - Furosemide - Spironolactone (mortality benefit) - Digoxin (additional symptom control) - Antiarrhythmic (for those with AF) - Anticoagulants (if needed)
Pulmonary edema - acute management
Furosemide Morphine (decrease anxiety and pre-load) Nitroglycerin Oxygen Positive airway pressure CPAP
Myocarditis
Inflammatory process, important cause of dilated cardiomyopathy.
Etiology:
- Idiopathic
- Infectious (coxsackie B, poliovirus, HIV, mumps)
- Toxic
- Hypersensitivity
- Systemic diseases (SLE, RA, sarcoidosis, autoimmune)
Diagnosis: increased cardiac enzymes, echo shows dilated, hypokinetic chanmbers, segmental wall motion abnormalities, myocardial biopsy
Management: supportive, usually self limited but may progress to dilated cardiomyopathy.
Dilated cardiomyopathy
Unexplained dilation and impaired systolic function of one or both ventricles.
May present as: CHF, systemic or pulmonary emboli, arrhythmias, sudden death
Hypertrophic cardiomyopathy
Unexplained ventricular hypertrophy.
Can be due to genetic defect of cardiomyocyte protein, results in myocyte hypertrophy and disarray. May cause obstruction of LV outflow tract
Restrictive cardiomyopathy
Impaired ventricular filling with preserved systolic function in non-dilated, non-hypertrophied ventricle. Caused by fibrosis/infiltration
Infective endocarditis
Duke’s criteria
Rheumatic fever
Complications
Acute: myocarditis, conduction abnormalities, valvulitis, acute pericarditis
Chronic: rheumatic valvular disease, adhesion, calcification of valves
Aortic stenosis
Etiology: congenital, calcification, rheumatic disease
Signs + symptoms
- exertional angina, syncope, dyspnea, PND orthopnea, peripheral edema
- narrow pulse pressure, brachial radial delay
- ejection systolic murmur radiating to clavicle
- LVH and strain, CHF
Aortic regurge
Etiology: Marfan’s, atherosclerosis and dissecting aneurysm, congenital, IE
Signs + symptoms:
- LVF, dyspnea, orthopnea, PND
- waterhammer pulse, bisferiens pulse, wide pulse pressure, hyperdynamic apex
- Early diastolic murmur at LLSB best heard sittin g forward, full expiration
Mitral stenosis
Etiology: rheumatic disease, congenital
Signs + symptoms:
- SOB on exertion, orthopnea, fatigue, palpitations, peripheral edema, malar flush
- afib, left parasternal heave, iastolic thrill at apex
- mid-diastolic rumble at apex radiates to axilla
Mitral regurgitation
Etiology: mitral valve prolapse, congenital, LV dilatation, IE abcess, papillary muscle rupture
Signs + symptoms
- dyspnea, orthopnea, palpitations, peripheral edema
- displaced hyperdynamic apex, left parasternal heave, apical thrill
- holosytolic murmur at apex, radiating to axilla
Tricuspid stenosis
Etiology: rheumatic disease, congenital, carcinoid syndrome
Symptoms + Signs:
- peripheral edema, fatige, palpitations
- prominent a waves in JVP, Kussmaul’s sign
- diastolic rumble in LLSB
Tricuspid regurgitation
Etiology: RV dilatation, IE, rheumatic disease, congenital, carcinoid
Signs + symptoms:
- peripheral edema, fatigue palpitations
- cv waves, Kussmaul’s signs,
- holosystolic murmur at LLSB accentutated by inspiration
Pulmonary stenosis
Etiology: congenital
Signs + symptoms:
- chest pain, syncope, fatigue, peripheral edema
- systolic murmur at LUSB accentuated by inspiration, pulmonary ejection click
Acute pericarditis
Most commonly viral (Coxsackie B), can be secondary to MI or Dressler’s syndrome
Pericardial effuction
Transudative: CHF, hypoalbuminemia,/hypoproteinemia, hypothyroidism
Exudative: similar causes to acute pericarditis
Cardiac tamponade
Features: tachypnea, dyspnea, shock, pulsus paradoxus
Treatment: pericardiocentesis, pericardiotomy
Constrictive pericarditis
Chronic pericarditis resulting in fibrosed, thickened, adherent, calcified pericardium.
Causes: idiopathic, post-infectious, radiation, post-cardiac surgery, uremia, MI
Features: similar to CHF with pericardial knock, increased JVP, Kussmaul’s sign
Acute arterial occlusion
Embolic or thombotic, aortic dissection, trauma. Increase risk with hypercoagulable states
Acute limb ischemia: Pain Pallor Pulselessness Paresthesia Paralysis Perishingly cold
Investigations
- ABI
- ECG
- FBC
- PT/INR
Treatment:
- Heparin bolus and continuous infusion
Complications:
- Compartment syndrome
- Renal failure from toxic metabolites
Chronic arterial occlusion
Atherosclerosis of lower extremities. Risks same as CAD.
Features:
- claudication
- critical limb ischemia: night pain, tissue loss
- signs of poor perfusion
Investigations
- ABI
- Arterial duplex
- CTA/MRA
- Arteriography
Treatment:
- Conservative: lifestyle changes, exercise, foot care
- Pharmacotherapy: aspirin
- Surgical: stenting, angioplasty, bypass grafting
Carotid artery disease
Atherosclerosis of carotid artery, commonly near carotid bifurication.
Features: TIA, reversible ischemic neurologic deficit, stroke, retinal insufficiency, amaurosis fugax, MCA occlusive symptoms
Investigations:
- FBC, PT/INR
- Fundoscopy
- Carotid bruits
- Carotid duplex
- Angiogram
Aortic dissection
Tear in aorta intima allowing blood to disect into media.
Causes:
- HTN
- Connective tissue disease (Marfan’s, Ehlers-Danlos), cystic medial necrosis, atherosclerosis
Features: sudden onset tearing chest pain radiating to back, HTN, asymmetric BP and pulses between arms, ischemic syndromes due to occlusion of branches, unseating of aortic valve cusps, syncope.
Investigations: CXR - widened mediastinum, left pleural effusion TEE ECG CT
Treatment
- Beta-blocker, then nitroprusside, aim BP of 110mmHg
- Surgical resection with intimal tear
Aortic aneurysm
Localised dilatation of an artery 1.5x the normal diameter.
Etiology: degenerative, traumatic, etc
75% asymptomatic. Common presentation: syncope, pain, hypotension, palpable pulsatile mass above umbilicus.
Investigations:
- Abdominal US
- CT/MRI
- Doppler/duplex
Treatment
- Conservative: CV risk factor reduction, watchful waiting US every 6/12
- Surgical: >5.5cm or >0.4cm/yr, requires elective AAA repair
Superficial venous thrombosis
Erythema, induration and tenderness along superficial vein.
Features: most common in greater saphenous vein, pain and cord-like swelling along the vein, induration, erythema and tenderness correspond to dilated and often thrombosed superficial veins
Conservative: compression bandages, NSAID, aspirin, surgical excision
Varicose veins
Distention of tortuous superficial veins from incompetent valves in the saphenous.
Features: diffuse aching, fullness/tightness, nocturnal cramping, aggravated by prolonged standing, visible long tortuous behaviour, ulceration, hyperpigmentation and induration.
Complications:
- recurrent superficial thrombophlebitis
- hemorrhage
- ulceration, eczema, lipodermatosclerosis and hyperpigmentation
Treatment
- Elevation and compression stockings
- Surgical ligation and stripping
Chronic venous insufficiency
Due to muscle pump dysfunction and valvular incompetence from phlebitis, varicosities or DVT
Investigations:
Compression stockings, leg elevation.
Lymphedema
Obstruction of lymphatic drainage resulting in edema with high protein content.
Classically non-pitting edema.
Treatment:
- Skin hygiene
- Compression bandages, lymphedema sleeve
- Exercise, massage and manual lymph drainage therapy.
