CARDIO Flashcards
Aortic Dissection - Definition
A condition where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, and creating a false lumen. Type A (70%) = ascending aorta, Type B (30%) = descending aorta (distal to L subclavian artery) As the dissection extends, branches of the aorta occlude sequentially, may obstruct subclavian, carotid, coeliac and renal arteries Aortic valve incompetence, inferior MI and cardiac arrest may develop if dissection moves proximally
Aortic Dissection - Aetiology
Degenerative changes in the smooth muscle of the aortic media are the predisposing event.
Common causes and predisposing factors are:
. hypertension;
. aortic atherosclerosis;
. connective tissue disease (e.g. SLE, Marfans, Ehlers–Danlos);
. congenital cardiac abnormalities (e.g. aortic coarctation);
. aortitis (e.g. Takayasus aortitis, tertiary syphilis);
. iatrogenic (e.g. during angiography or angioplasty);
. trauma;
. crack cocaine.
Aortic Dissection - Epidemiology
Most common in males between 40 and 60 years.
EXTRA NOTES:
Pulsus paradoxus = abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is <10mmHg
All patients with Type A thoracic dissection should be considered for surgery
Management = crossmatch 10 units blood, hypotensives, labetolol
Aortic Dissection - History
Sudden central ‘tearing’ pain, may radiate to the back (may mimic an MI).
Aortic dissection can lead to occlusion of the aorta and its branches:
- Carotid obstruction = hemiparesis, dysphasia, blackout.
- Coronary artery obstruction = chest pain (angina or MI).
- Subclavian obstruction = Ataxia, loss of consciousness.
- Anterior spinal artery = paraplegia.
- Coeliac obstruction = severe abdominal pain (ischaemic bowel).
- Renal artery obstruction: Anuria, renal failure.
Aortic Dissection - Exam
Murmur on the back below left scapula, descending to abdomen.
Blood pressure (BP): Hypertension (BP discrepancy between arms of >20 mmHg), wide pulse pressure.
If hypotensive may signify tamponade, check for pulsus paradoxus.
Aortic insufficiency: Collapsing pulse, early diastolic murmur over aortic area.
Unequal arm pulses.
There may be a palpable abdominal mass.
Aortic Dissection- Investigation
Bloods: FBC, cross-match 10 units of blood, U&E (renal function), clotting.
CXR: Widened mediastinum, localized bulge in the aortic arch.
ECG: Often normal. Signs of left ventricular hypertrophy or inferior MI if dissection com-
promises the ostia of the right coronary artery.
CT-thorax: False lumen of dissection can be visualized.
Echocardiography: Transoesophageal is highly specific (TOE). Cardiac catheterization and aortography.
Aortic Regurgitation - Definition & Epidemiology
Reflux of blood from aorta into left ventricle (LV) during diastole. (AR) also called aortic insufficiency.
EPIDEMIOLOGY
Chronic AR often begins in the late 50s, documented most frequently in >80y/o
Aortic Regurgitation- Aetiology
- Aortic valve leaflet abnormalities or damage: Bicuspid aortic valve, infective endocarditis, rheumatic fever, trauma.
- Aortic root/ascending aorta dilation: Systemic hypertension, aortic dissection, aortitis (e.g. syphilis, Takayasus arteritis), arthritides (rheumatoid arthritis, seronegative arthrit- ides), Marfans syndrome, pseudoxanthoma elasticum, Ehlers–Danlos syndrome, osteogenesis imperfecta.
- Reflux of blood into the LV during diastole results in left ventricular dilation and high end-diastolic volume and high Stroke V. The combination of high SV and low end-diastolic pressure in the aorta may explain the collapsing pulse and the wide pulse pressure. In acute AR, the LV cannot adapt to the rapid increase in end-diastolic volume caused by regurgitant blood.
Aortic Regurgitation - History
Chronic AR: initially asymptomatic. Later, symptoms of heart failure: exertional dyspnoea, orthopnoea, fatigue. Occasionally angina.
Severe acute AR: sudden cardiovascular collapse.
Symptoms related to the aetiology, e.g. chest or back pain in patients with aortic dissection.
Aortic Regurgitation - Exam
- Collapsing ‘water-hammer’ pulse and wide pulse pressure
- Thrusting and heaving (volume-loaded) displaced apex beat (hyperdyamic)
- Early diastolic murmur at lower left sternal edge, better heard with patient sitting forward + expiration
- Ejection systolic murmur is often heard because of increased flow across the valve
- Austin-Flint mid-diastolic murmur (severe AR) = over the apex, from turbulent reflux hitting anterior cusp of the mitral valve and causing a physiological mitral stenosis
- Rare signs associated with a hyperdynamic pulse:
- Quincke’s sign = visible pulsations on nail bed
- de Musset’s sign = head nodding in time with pulse
- Becker’s sign = visible pulsations of the pupils and retinal arteries
- Müller’s sign = visible pulsations of the uvula
- Corrigan’s sign = visible pulsations in the neck
- Traube’s sign = Pistol-shot (systolic and diastolic) sounds heard on auscultation of the femoral arteris
Duroziezs sign: A systolic and diastolic bruit heard on partial compression of femoral artery
with a stethoscope.
Rosenbachs sign: Systolic pulsations of the liver.
Gerhards sign: Systolic pulsations of the spleen.
Hills sign: Popliteal cuff systolic pressure exceeding brachial pressure by >60 mmHg.
Aortic Regurgitation - Investigation
CXR: Cardiomegaly. Dilation of the ascending aorta. Signs of pulmonary oedema may be seen with left heart failure.
ECG: May show signs of left ventricular hypertrophy (deep S wave in V1–2, tall R wave in V5–6, inverted T waves in I, aVL, V5–6 and left-axis deviation).
Echocardiogram: 2D echo and M-mode may indicate the underlying cause (e.g. aortic root dilation, bicuspid aortic valve) or the effects of AR (left ventricular dilation/dysfunction and fluttering of the anterior mitral valve leaflet).
Doppler echocardiography for detecting AR and assessing severity.
Cardiac catheterization with angiography: If there is uncertainty about the functional state of the ventricle or the presence of coronary artery disease.
Aortic Stenosis - Definition
Narrowing of the left ventricular outflow at the level of the aortic valve.
Aortic Stenosis - Aetiology
- Stenosis secondary to rheumatic heart disease (commonest worldwide);
- calcification of a congenital bicuspid aortic valve, William’s syndrome
- calcification/degeneration of a tricuspid aortic valve in the elderly, (senile calcification)
Aortic Stenosis - History
Classic triad = angina, syncope and heart failure!
May be asymptomatic initially.
Angina (because of high O2 demand of the hypertrophied ventricles).
Syncope or dizziness on exercise.
Symptoms of heart failure (e.g. dyspnoea).
Aortic Stenosis - Examination
- BP: Narrow pulse pressure.
- Pulse: Slow-rising.
- Palpation: Thrill in the aortic area (if severe). Forceful sustained thrusting undisplaced apex
beat. - Auscultation: Harsh ejection systolic murmur at aortic area, radiating to the carotid artery
and apex. - Second heart sound (A2 component) may be softened or absent (because of
calcification). A bicuspid valve may produce an ejection click. May be an S4 (occurs more often with bicuspid valves)
Distinguish from aortic sclerosis and hypertrophic obstructive cardiomyopathy
(HOCM)
Aortic Stenosis -Investigations
- ECG: Signs of LV hypertrophy (deep S wave in V1–2, tall R wave in V5–6, inverted T waves in I, aVL, V5–6 and left-axis deviation), LBBB, LA enlargement.
- CXR: Post-stenotic enlargement of the ascending aorta, calcification of aortic valve.
- Echocardiogram: Visualizes structural changes of the valves and level of stenosis (valvar, supravalvar or subvalvar). Estimation of aortic valve area and pressure gradient across the
valve in systole and left ventricular function may be assessed. (DIAGNOSTIC)
-Doppler echo = can estimate gradient across valves, severe stenosis if peak gradient ≥ 50mmHg and valve area <1cm2
- Cardiac angiography: Allows differentiation from other causes of angina, and to assess for
concomitant coronary artery disease (50% of patients with severe aortic stenosis have significant coronary artery disease).
Aortic Stenosis- Extra notes
Pulse pressure = difference between systolic and diastolic pressure
Aortic sclerosis = senile degeneration with no left ventricular outflow tract degeneration. The pulse character is normal, a thrill is not palpable and ejection systolic murmur radiates only faintly. S2 normal.
Signs of LVH = deep S wave in V1-2, tall R wave in V5-6, inverted T wave in I, aVL and V5-6, LAD
William’s syndrome = rare neurodevelopmental disorder characterized by a distinctive ‘elfin’ facial appearance, along with a low nasal bridge, unusually cheerful demeanour and ease with strangers, developmental delay coupled with language deficiencies, profound visuo-spatial impairments, supravalvular aortic stenosis and transient high calcium
Atrial Fibrillation - definition
Rapid, chaotic and ineffective atrial electrical conduction. Often subdivided into: ‘permanent’, ‘persistent’ (>7 days and responsive to cardioversion), and ‘paroxysmal’.
EPIDEMIOLOGY
Very common in the elderly, may be paroxysmal
Atrial Fibrillation- Aetiology
There may be no identifiable cause (‘lone’ atrial fibrillation (AF)).
Secondary causes lead to abnormal atrial electrical pathways that result in AF.
Systemic causes: Thyrotoxicosis, hypertension, pneumonia, alcohol.
Heart: Mitral valve disease, ischaemic heart disease, rheumatic heart disease, cardiomyopathy, pericarditis, sick sinus syndrome, atrial myxoma.
Lung: Bronchial carcinoma, pulmonary embolism.
Atrial Fibrillation- Symptoms
Often asymptomatic. Some patients experience palpitations or syncope. Symptoms of the cause of the AF.
Atrial Fibrillation- Examination
Irregularly irregular pulse, difference in apical beat and radial pulse.
Look for thyroid disease and valvular heart disease.
Atrial Fibrillation-Investigations
- ECG: Uneven baseline (fibrillations) with absent P waves, irregular QRS complexes. If there is a saw-tooth baseline, consider if there is atrial flutter.
- Blood: Cardiacenzymes, TFT, lipidprofile, U&E, Mg2, Ca2, (risk of digoxin toxicity high with hypokalaemia, hypomagnesaemia or hypercalcaemia).
- Echocardiogram: To assess for mitral valve disease, left atrial dilation, left ventricular dysfunction or structural abnormalities.
Atrial Fibrillation- Management
Treat any reversible cause (e.g. thyrotoxicosis, chest infection). Specific treatment strategy focuses on:
(1) Rhythm control:
If the AF is >48h from onset, anticoagulate (at least 3–4 weeks) before attempting cardioversion.
- DC cardioversion: Synchronized DC shock (2x 100 J, 1 x 200 J).
- Chemical cardioversion: Flecainide (contraindicated if there is history of ischaemic heart disease) or amiodarone.
- Prophylaxis against AF: Sotalol, amiodarone or flecainide. Also consider providing ‘pill-in-
the-pocket’ strategy for suitable patients.
(2) Rate control = Chronic ‘permanent’ AF: Ventricular rate control with digoxin, verapamil and/or b- blockers. Aim for rate of 90/min..
(3) Stroke risk stratification:
Low-risk patients can be managed with aspirin, and high-risk patients require anticoagulation with warfarin
Risk factors indicating high risk are previous thromboembolic event, age 75 years with hypertension, diabetes or vascular disease, and/or clinical evidence of valve disease, heart failure or impaired left ventricular function.
COMPLICATIONS Thromboembolism, increased with LA enlargement/ LV dysfunction. Heart failure (or worsens existing heart failure), Dilated cardiomyopathy, Angina.
PROGNOSIS
Chronic AF in a diseased heart does not usually return to sinus rhythm.
EXTRA
Atrial myxoma = benign tumour of the heart, found on interatrial septum (left more common than right)
Fleicanide = VG Na+ channel blocker, slowing the upstroke of the cardiac action potential
Amiodarone = K+ channel blocker (main), β-blocker, Ca2+/Na+ channel blocker
Verapamil = VG Ca2+ channel blocker
CHA2DS2VASC = Congestive heart failure, Hypertension (>140/90), Age≥75, Diabetes, Prior stroke/TIA/thromboembolism, vascular disease (PVD, MI), Age 64-75 years, Sex (female)
Cardioversion more likely if: AF recent, <65y/o, underlying cause has been successfully treated
Cardiac Arrest - definition
Acute cessation of cardiac function.
Cardiac Arrest - Aetiology
Classical reversible causes of cardiac arrest are the four Hs and four Ts: Hypoxia Hypothermia Hypovolaemia Hypo- or hyperkalaemia Tamponade Tension pneumothorax Thromboembolism Toxins and other metabolic disorders (drugs, therapeutic agents, sepsis)
Cardiac Arrest- Examination (History too)
Hx - Doesn’t apply
Exam - Unconscious, patient is not breathing, absent carotid pulses.
Cardiac Arrest- Investigations
Cardiac monitor: Classification of the rhythm directs management (see below). Bloods: ABG, U&E, FBC, cross-match, clotting, toxicology screen, glucose.
Cardiac Arrest- Management
Safety: Approach any arrest scene with caution as the cause of the arrest may still pose a threat. Defibrillators and oxygen are hazards. Help should be summoned as soon as possible.
Basic life support: DR ABC
1. If the arrest is witnessed and monitored, consider giving a precordial thump if no
defibrillator immediately available.
2. Clear and maintain airway with head tilt (if no spinal injury), jaw thrust and chin lift.
3. Assess breathing by look, listen and feel.
If not breathing, give two effective breaths immediately.
4. Assess circulation at carotid pulse for 10 s.
If absent, give 30 chest compressions at rate of 100min 1. Continue cycles of 30 compressions for every two breaths.
5. Proceed to advanced life support as soon as possible.
Advanced life support:
1. Attach cardiac monitor and defibrillator.
2. Assess the rhythm:
(A) If pulseless ventricular tachycardia (VT)2 or ventricular fibrillation (VF)3 (‘shockable rhythm’):
- Defibrillate once: 150–360 J biphasic, 360 J monophasic. (Ensure no one is touching
patient or bed when defibrillating.)
- Resume CPR immediately for 2 min, and then return to 2.
- Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
- If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus
(or lidocaine).
(B) If pulseless electrical activity (PEA) or asystole:
- CPR for 2 min, and then return to 2.
- Administer adrenaline (1 mg IV) every 3–5 min.
- Atropine (3 mg IV, once only) if asystole or PEA with rate <60 min 1.
(C) During CPR:
- Check electrodes, paddle positions and contacts.
- Secure airway (e.g. attempt endotracheal intubation, high-flow oxygen). Once airway
secure, give continuous compressions and breaths.
- Consider magnesium, bicarbonate, external pacing.
- Stop CPR and check pulse only if change in rhythm or signs of life.
Treatment of reversible causes:
Hypothermia: Warm slowly.
Hypo- or hyperkalaemia: Correction of electrolytes.
Hypovolaemia: IV colloids, crystalloids or blood products.
Tamponade: Pericardiocentesis under xiphisternum up and leftwards.
Tension pneumothorax: Needle into second intercostal space, mid-clavicular line. Thromboembolism: (see Pulmonary embolism, Myocardial infarction).
Toxins: (see drug formulary for antidotes).
COMPLICATIONS Irreversible hypoxic brain damage, death.
P R O G N O S I S Resuscitation is less successful in the arrests that occur outside hospital. Duration of inadequate effective cardiac output is associated with poor prognosis.
Cardiac Failure - Definition
Inability of the cardiac output to meet the bodys demands despite normal venous pressures.
Cardiac Failure - Aetiology
Low output ( low cardiac output):
Left heart failure: Ischaemic heart disease, hypertension, cardiomyopathy, aortic valve
disease, mitral regurgitation.
Right heart failure: Secondary to left heart failure, infarction, cardiomyopathy, pulmonary
hypertension/embolus/valve disease, chronic lung disease, tricuspid regurgitation, con-
strictive pericarditis/pericardial tamponade.
Biventricular failure: Arrhythmia, cardiomyopathy (dilated or restrictive), myocarditis, drug
toxicity.
High output (high demand): Anaemia, beriberi, pregnancy, Pagets disease, hyperthyroidism,
arteriovenous malformation.
Cardiac Failure - Epidemiology
Left: Tachycardia, tachypnoea, displaced apex beat, bilateral basal crackles, third heart sound
(gallop rhythm: rapid ventricular filling), pansystolic murmur (functional mitral
regurgitation).
Acute LVF: Tachypnoea, cyanosis, tachycardia, peripheral shutdown, pulsus alternans, gallop
rhythm, wheeze cardiac asthma, fine crackles throughout the lung.
Right: “ JVP, hepatomegaly, ascites, ankle/sacral pitting, oedema, signs of functional
tricuspid regurgitation (see Tricuspid regurgitation).
Cardiac Failure - History
Left (symptoms caused by pulmonary congestion): Dyspnoea (New York Heart Association classification):
1. no dyspnoea;
2. dyspnoea on ordinary activities;
3. dyspnoea on less than ordinary activities;
4. dyspnoea at rest.
Orthopnoea, paroxysmal nocturnal dyspnoea, fatigue.
Acute LVF: Dyspnoea, wheeze, cough and pink frothy sputum.
Right: Swollen ankles, fatigue, “ weight (resulting from oedema), # exercise tolerance,
anorexia, nausea.
Cardiac Failure -Investigations
Blood: FBC, U&Es, LFTs, CRP, glucose, lipids, TFTs.
In acute LVF: ABG, troponin, brain natriuretic peptide (BNP). “ Plasma BNP suggests the
diagnosis of cardiac failure. A low plasma BNP rules out cardiac failure (90% sensitivity). CXR (in acute LVF): Cardiomegaly (heart >50 % of thoracic width), prominent upper lobe vessels, pleural effusion, interstitial oedema (‘Kerley B lines’), perihilar shadowing (‘bats
wings’), fluid in the fissures.
ECG: May be normal. May have ischaemic changes, arrhythmia, left ventricular hypertrophy
(seen in hypertension).
Echocardiogram: To assess ventricular contraction. If left ventricular ejection fraction (LVEF)
<40%: systolic dysfunction. Diastolic dysfunction: # compliance leading to a restrictive
filling defect.
Swan–Ganz catheter: Allows measurements of right atrial, right ventricular, pulmonary
artery, pulmonary wedge and left ventricular end-diastolic pressures.
Cardiac Failure - Management
Acute LVF: Cardiogenic shock: Severe cardiac failure with low BP requires the use of inotropes (e.g. dopamine, dobutamine) and should be managed in ITU
Pulmonary oedema: Sit up patient, 60–100% O2 and consider CPAP. Other first-line therapies are diamorphine (venodilator and anxiolytic effect), GTN infusion ( decrease preload), IV furo- semide if fluid overloaded (venodilator and later diuretic effect). Monitor BP, respiratory rate, sat. O2, urine output, ECG. Treat the cause, e.g. myocardial infarction, arrhythmia.Chronic LVF: Treat the cause, e.g. hypertension. Treat exacerbating factors, e.g. anaemia. The following drug therapies are evidence-based.1
ACE-inhibitors (e.g. enalapril, perindopril, ramipril): Inhibit intracardiac renin-angiotensin
system which may contribute to myocardial hypertrophy and remodelling. ACE inhibitors
slow progression of the heart failure and improve survival.
b-Blockers (bisprolol or carvedilol): Block the effects of chronically activated sympathetic
system, slow progression of the heart failure and improve survival. The benefits of ACE
inhibitors and b-blockers are additive.
Loop diuretics (e.g. furosemide) and dietary salt restriction to correct fluid overload. Aldosterone antagonists (spironolactone or, if not tolerated, eplerenone) improve survival in
patients with NYHA class III/IV symptoms and on standard therapy. Monitor Kþ (may cause hyperkalaemia). May be used to assist in the management of diuretic-induced hypokalaemia.
Angiotensin receptor blockers (ARB) (e.g. candesartan): May be added in patients with persistent symptoms despite ACE inhibitors and b-blockers. Monitor Kþ (may cause hyperkalaemia).
Hydralazine and a nitrate: May be added in patients (particularly in Afro-Caribbeans) with persistent symptoms despite therapy with an ACE inhibitor and b-blocker.
Digoxin: Positive inotrope, # hospitalization, but does not improve survival.
n-3 polyunsaturated fatty acids: Provide a small beneficial advantage in terms of mortality. Cardiac resynchronization therapy (CRT): Biventricular pacing improves symptoms and
survival in patients with LVEF 35%, cardiac dyssynchrony (QRS>120msec) and moderate to severe symptoms despite optimal medical therapy. Most patients who meet these criteria are also candidates for an implantable cardiac defibrillator (ICD) and receive a combined device.
Avoid drugs that can adversely affect patients with heart failure due to systolic dysfunction, e.g. NSAIDs, non-dihydropyridine calcium channel blockers (i.e. diltiazem and verapamil).
C O M P L I C A T I O N S Respiratory failure, cardiogenic shock, death.
P R O G N O S I S Fifty per cent of patients with severe heart failure die within 2 years.
Cardiomyopathy - definition
Primary disease of the myocardium. Cardiomyopathy may be dilated, hy- pertrophic or restrictive.
Cardiomyopathy - Aetiology
The majority are idiopathic.
Dilated: Post-viral myocarditis, alcohol, drugs (e.g. doxorubicin, cocaine), familial ( 25% of
idiopathic cases, usually autosomal dominant), thyrotoxicosis, haemochromatosis,
peripartum.
Hypertrophic: Up to 50% of cases are genetic (autosomal dominant) with mutations in
b-myosin, troponin T or a-tropomyosin (components of the contractile apparatus). Restrictive: Amyloidosis, sarcoidosis, haemochromatosis.
Cardiomyopathy - History
Dilated: Symptoms of heart failure, arrhythmias, thromboembolism, family history of sudden death.
Hypertrophic: Usually none. Syncope, angina, arrhythmias, family history of sudden death. Restrictive: Dyspnoea, fatigue, arrhythmias, ankle or abdominal swelling.
Enquire about family history of sudden death.
Cardiomyopathy - Examination
Dilated: “ JVP, displaced apex beat, functional mitral and tricuspid regurgitations, third heart sound.
Hypertrophic: Jerky carotid pulse, double apex beat, ejection systolic murmur. Restrictive: “ JVP (Kussmauls sign: further “ on inspiration), palpable apex beat, third heart
sound, ascites, ankle oedema, hepatomegaly.
Cardiomyopathy - Investigations
CXR: May show cardiomegaly, and signs of heart failure.
ECG:
All types: Non-specific ST changes, conduction defects, arrhythmias
Hypertrophic: Left-axis deviation, signs of left ventricular hypertrophy (see Aortic stenosis), Q
waves in inferior and lateral leads.
Restrictive: Low voltage complexes.
Echocardiography:
Dilated: Dilated ventricles with ‘global’ hypokinesia.
Hypertrophic: Ventricular hypertrophy (disproportionate septal involvement)
Restrictive: Non-dilated non-hypertrophied ventricles. Atrial enlargement, preserved systolic
function, diastolic dysfunction, granular or ‘sparkling’ appearance of myocardium in
amyloidosis.
Cardiac catheterization: May be necessary for measurement of pressures. Endomyocardial biopsy: May be helpful in restrictive cardiomyopathy. Pedigree or genetic analysis: Rarely necessary.
Cardiomyopathy - Management
Dilated: Treat heart failure and arrhythmias. Consider implantable cardiac defibrillators (ICD) for recurrent VTs.
Hypertrophic: Treat arrhythmias with drugs, ICD for survivors of sudden death, reduce outflow tract gradients, pacemaker, surgery (e.g. septal myomectomy, septal ablation with ethanol). Screen family members with ECG or echocardiography.
Restrictive: No specific treatment. Manage the underlying cause.
Cardiac transplantation: May be considered in end-stage heart failure in all cardiomyop-
athy types.
C O M P L I C A T I O N S Heart failure, arrhythmias (atrial and ventricular). Dilated and hypertrophic cardiomyopathy: Sudden death and embolism. Hypertrophic: Infective endocarditis.
PROGNOSIS
Dilated: Depends on the aetiology, New York Heart Association functional class and ejection fraction.
Hypertrophic: Ventricular tachyarrhythmias are the major cause of sudden death. Restrictive: Poor prognosis, many die within the first year after diagnosis.
Heart Block - definition
Impairment of the atrioventricular (AV) node impulse conduction, as repre- sented by the interval between P wave and QRS complex.
