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227 Cards in this Set
- Front
- Back
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Types of MIs:
1. ST elevation 2. ST depression |
1. Sub-endocardial
2. Transmural |
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Elevated cardiac biomarkers and no ST elevation?
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NSTEMI
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No elevated cardiac biomarkers and no ST elevation?
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Unstable angina
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Leads I, aVR and aVL
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Lateral
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Leads II, III and aVF
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Inferior
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Leads V1 and V2
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Septal
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Leads V3 and V4
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Anterior
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Leads V5 and V6
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Lateral
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Cardiac troponin I:
1. When rises 2. Peak levels 3. How many days 4. When do you check it |
1. At 4 hours
2. Peaks 1-2 days 3. Lasts for 7-10 days 4. At presentation and 8 hours later |
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CK-MM and CK-MB expression in skeletal muscle and myocardium
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CK-MM: 98%, 70%
CK-MB: 1%, 25-30% |
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What are BNP and NT-proBNP secreted in response to?
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Increased end-diastolic pressure and volume in the ventricles
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CKMB:CK activity ratio suggestive of myocardial source?
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> 2.5
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PCI anticoagulation regiment
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Before: apsirin 325mg and clopidogrel 300-600mg
During: unfractionated heparin, LMWH or bivalirudin (direct thrombin inhibitor) |
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First line drugs for NSTEMI/UA after initial treatment
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Beta-blockers
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What type of heart failure do you get with thiamine deficiency?
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High output failure with tachycardia and elevated biventricular filling pressures
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Signs and symptoms of thiamine deficiency heart failure
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Wide pulse pressure, tachycardia, 3rd HS, apical systolic murmur
ECG - decreased voltage, prolonged QT, and T wave abnormalities |
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What 3 vitamin deficiencies can lead to hyperhomocysteinaemia?
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Vitamin B6, B12 and folate
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Cardiac manifestations of hyperthyroidism
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Hypertension, sinus tachycardia, atrial fibrillation
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What is a Means-Lerman scratch?
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A systolic pleural friction rub heard in left 2nd intercostal space during expiration (due to hyperdynamic cardiac motion)
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Is hyperthryoid cardiomyopathy a high output state?
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No, systemic vascular resistance falls
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In acromegalic cardiomegaly what happens to the myocytes
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Increased size (hypertrophy) not number (hyperplasia)
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What causes Libman-Sachs endocarditis?
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SLE - verrucous valvular abnormalities almost entirely made of fibrin, usually left sided
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Which type of cardiomyopathy has the strongest genetic component?
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Hypertrophic at around 50%
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Four main causes of dilated cardiomyopathy
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1. Genetic
2. Alcohol 3. Autoimmune post viral 4. Drugs (chemo - anthracyclines) |
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Which cardiomyopathy most dramatically dilates the atria?
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Restricted
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Which investigation can differentiate between the cardiomyopathies?
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Echo
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Treatments for cardiomyopathies
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Dilated - beta-blockers and ARBs
Hypertrophic - beta-blockers and non-dihydro CCB Restrictive - diuretics |
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How does digoxin work?
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Prolongs the refractory period of the AV node and improves contractility by inhibiting the Na/K/ATPase pump
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What drugs does digoxin interact with?
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Diuretics (non K sparing), verapamil and amiodarone
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What are the 3 drugs that if used together will damage your kidneys?
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Diuretics, NSAID and ACEi
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Which drug has bad interactions with warfarin?
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Mifepristone
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Is LMWH renally excreted? Do you need to monitor with APTT?
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No and no
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What is LMWH mechanism in low doses?
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Inactivates factor Xa and inhibits conversion of prothrombin to thrombin
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What is LMWH mechanism in high doses?
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Inactivates factors IX, X, XI, XII thrombin and inhibits conversion of fibrinogen to fibrin
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Which drugs does LMWH interact with?
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Mifepristone and corticorelin
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How do ACEi work?
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Reduce angiotensin II levels, reduce vasoconstriction and aldosterone secretion, peripheral vasodilator, reduces afterload with little change in CO, HR or GFR
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How do ARBs work?
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Block angiotensin II AT1 receptors, causes vasodilation, reduces secretion of vasopressin and reduces production and secretion of aldosterone
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What are the two types of nitrates?
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1. Nitroglycerin (sublingual, transdermal or IV)
2. Isosorbide (oral) |
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What is the mechanism of nitrates?
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They are pro-drugs that release NO, which activates soluble guanylate cyclase, increasing cGMP, activates protein kinase G, leads to dephosphorylation of myosin light chains and sequestration of intracellular caclium --> relaxation
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Describe tolerance in regards to nitrates
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Occurs with longer acting nitrates, IV and topical. Develops rapidly with continuous use, so 8 hours off a day
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Describe the types of beta-blockers
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Metoprolol, atenolol (B1)
Acebutolol (B1, ISA) Labetalol (A1, B1, B2) Carvedilol (A1, B1, B2, antioxidant) Sotalol (B1, B2, class III anti-arrhythmic) |
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What are some contraindications to beta-blockers?
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Bradycardia, high-degree heart block, asthmatics, claudication, Raynauds phenomenon, CHF
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Describe the types of CCBs
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Dihydropyridines: nifedipine, amlodipine, felodipine
Non-dihydro: diltiazem, verapamil (also a class IV anti-arrhythmic) |
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How do CCBs work?
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Inhibit calcium entry into cell via voltage-sensitive calcium channels, thus impair contraction and smooth muscle relaxation
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Which drugs have interactions with nitrates?
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Beta-blockers (increased risk of heart block and hypotension) and digoxin (reduced clearance)
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Which anti-epileptic is contraindicated with nifedipine?
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Phenytoin, it induced CYP3A4 and thus reduces the bioavailability of nifedipine
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Which drugs have interactions with verapamil?
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Oral hypertensives (vasodilators, ACEi, diuretics, beta-blockers), anti-arrhythmics, lithium, HIV drugs, erythromycin/clarithromycin
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What is aspirins mechanism of action?
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COX (cyclo-oxygenase) inhibitor, interferes with platelet aggregation by impairing production of thromboxane A2
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What is clopidogrels (Plavix) mechanism of action?
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Irreversibly inhibits a receptor called P2Y12, an adenosine disphosphate (ADP) chemoreceptor on platelet cell membranes
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How do statins work?
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They are HMG-CoA reductase inhibitors.
- inhibit cholesterol synthesis - increase LDL uptake - improve endothelial function - modulate inflammatory responses - maintain plaque stability - prevent thrombus formation |
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Which drugs will increase the likelihood of rhabdomyolysis with statins?
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Fibrates or niacin
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What is the most common cause of cor pulmonale?
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COPD
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What is the major mechanism by which cor pulmonale occurs?
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Pulmonary hypertension
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What are the two conditions that can cause acute cor pulmonale?
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PE and ARDS
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Does the RV better deal with pressure or volume overload?
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Handles volume overload better
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Changes in the RV that occur with cor pulmonale
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- fall in stroke volume
- dilatation and hypertrophy - becomes spherical in shape not crescent - increase myocardial O2 consumption with decreased perfusion - RV stiffness |
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What is a Graham Steel's murmur?
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Soft blowing decrescendo diastolic murmur in severe pulmonary artery hypertension
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Signs of PAH on x-ray
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Right descending pulmonary artery with a diameter > 16 mm
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What is the screening tool for PAH?
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Echo - may show flattening of leftward shift of the IV septum during systole suggests RV pressure overload, where as IV septal shift during diastole suggests volume overload
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What time defines an acute aortic dissection?
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< 14 days
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Which layer is torn in an aortic dissection?
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The intima, leading to degradation of the medial layer of the aortic wall
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Where is the most common site an intimal tear?
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Right lateral wall of ascending aorta
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What are type A and type B aortic dissection?
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Type A: involve ascending aorta
Type B: involve transverse and/or descending aorta NOT ascending |
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Where does the pain occur?
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Anterior chest pain - ascending aorta
Intrascapular pain - descending aorta |
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What is the outcome of occluding the following arteries:
- coronary - carotid - spinal - coeliac / sup mesenteric - renal - limb vessels |
- coronary: MI
- carotid: stroke - spinal: paraplegia - coeliac / sup mesenteric: acute abdomen - renal: renal failure - limb vessels: limb ischaemia |
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What sign is there of an aortic dissection on an x-ray?
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Broadening of the upper mediastinum and distortion of aortic 'knuckle'
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What is first line medical treatment for aortic dissection?
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Beta-blockers
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What is an aortic aneurysm?
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A permanent pathological dilation of the aorta with a diameter > 1.5 time expected
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What is the difference between a true and false aneurysm?
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True - involves all layers
False - does not involve all layers |
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What risk factor has the strongest association with aortic aneurysm?
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Smoking
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What percentage of aneurysms originate below the renal arteries?
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90%
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What are the 3 classifications of aneurysms?
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Congenital
Infectious Inflammatory |
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Where does pain occur in aneurysms?
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Abdominal, back and groin pain
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What is the classical triad of symptoms for a ruptured aneurysm?
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Abdo/back pain, pulsatile abdo mass and hypotension
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What are the indications for an aneurysm repair?
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1. > 5.5cm
2. all symptomatic AAAs 3. distal embolisation |
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Open AAA repair 30 day mortalities?
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5-8% elective asymptomatic
10-20% emergency symptomatic 50% ruptured |
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What is the female to male ratio for aortitis?
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9:1
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What is Takayasu arteritis?
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Chronic vasculitis of aorta and branches, 80-90% are women, "pulseless" disease as carotid and limb pulses are diminished or absent in nearly 85%, has focal skip lesions rather than diffuse involvement
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What are the 3 phases of aortitis?
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1. The prepulseless inflammatory period characterised by non-specific symptoms (fever, fatigue, arthralgia, weight loss)
2. Vascular inflammation with pain and tenderness over arteries 3. Fibrotic stage with predominant ischaemic symptoms |
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What is first line medical treatment for aortitis?
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Prednisone (corticosteroids)
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What happens in normal sinus arrhythmia?
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Inspiration accelerates HR and expiration slows HR
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What will be the heart rate with escape beats arising from:
1. atria 2. AV node 3. ventricles |
1. 60-80
2. 40-60 with P waves absent 3. 20-40 with abnormal QRS |
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What is a first degree SA block?
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Where there is a lag between SA node firing and depolarisation, not shown on ECG
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What is a type I second degree SA block?
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Wenckebach block - rhythm is irregular, RR interval gets progressively smaller until a QRS segment is dropped
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What is a type II second degree SA block?
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Sinus exit block - regular rhythm (normal or slow), followed by a pause that is a multiple of the RR interval
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What is a third degree SA block?
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Similar to sinus arrest - caused by failure to conduct impulses, rhythm is irregular (normal or slow) followed by a long pause that is not a multiple of the RR interval, ends with a P wave.
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What is chronotropic incompetence?
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Failure to increase HR with exercise (failure to reach 85% of predicted max or failure to achieve > 100 bpm)
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What is the atrial rate?
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300 bpm
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How do you reveal flutter waves if difficult to interpret?
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Apply carotid sinus pressure or IV adenosine (induces a temporary AV block)
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Treatment for atrial flutter?
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Digoxin, beta-blockers and verapamil to control ventricular rate.
Restore sinus rhythm by DC cardioversion of IV amiodarone. |
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What is the prevalence of atrial fibrillation?
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0.5%
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What is the common clinical presentation for AF?
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Palpitations, SOB, fatigue
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What are the 3 classifications for AF?
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1. Paroxysmal (intermittent, self-terminating)
2. Persistent (prolonged episodes terminated by cardioversion) 3. Permanent (cardioversion fails) |
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First line treatment for AF?
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Paroxysmal - beta-blockers
Persistent/permanent - digoxin |
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What is the CHADS score?
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Assesses the risk of thromboembolism in AF
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When do you start anticoagulation based on the CHADS score?
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0 - aspirin only
1 - warfarin or asirin 2 + warfarin |
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What is included in the CHADS score?
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Congestive HF (1 pt)
HTN (1 pt) Age > 74 yrs (1 pt) DM (1 pt) Stroke/TIA (2 pts) |
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What is the stroke risk per year in regards to the CHADS score?
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0 - 1.9%
1 - 2.8% 2 - 4.0% 3 - 5.9% 4 - 8.5% 5 - 12.% 6 - 18.2% |
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What is first degree AV block?
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Prolongation of the PR interval on ECG (>200ms)
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What is Mobitz I second degree AV block?
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Wenckebach block - progressive prolongation of PR interval, followed by a pause (non conducted P wave)
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What is Mobitz II second degree AV block?
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Constant PR interval followed by sudden failure of P wave to be conducted, happen in a regular pattern (3:1, 2:1, etc)
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What is high-grade second degree AV block?
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Multiple P waves in a row that should conduct but do not, ratio can be 3:1 or higher, PR interval is constant
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What is third grade AV block?
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No supraventricular impulses, P waves reflect a sinus node rhythm independent from QRS rhythm, which represent escape rhythms
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What vessels supply the AV node?
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90% right circumferential artery
10% circumflex artery |
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What are Morgagni-Adams-Stokes episodes?
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Syncopal episodes due to slow HR with 3rd degree AV blocks
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What are the ECG signs of ventricular tachyarrhythmias?
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Wide QRS (greater than 0.12 sec), followed by prolonged compensatory pause, no P waves
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Where does ventricular tachycardia originate?
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Bundle of His
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What does sustained ventricular tachycardia mean?
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> 30s, medical emergency
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What two electrolyte abnormalities predispose for VT?
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Hypokalaemia and hypomagnesia
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What is a fusion beat?
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Mixed morphology due to AV node/His-Purkinje occurring at same time as ventricular depolarisation
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What is a capture beat?
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Occurs when atrial impulse arrives at the AV node at a fortuitous time - normal P wave and QRS complex
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Acute treatment for VT
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- ALS and DC cardioversion 100-200 J
- IV access, adrenalin 2mg, repeat at 5' intervals - Lidocaine or amiodarone - Intubation and PPV |
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Chronic treatment for VT
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Anti-arrhythmic drugs
Pacemaker, ICD Diet, smoking cessation |
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What is torsades de pointes?
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Polymorphic VT in the setting of a prolonged QT interval
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Acquired vs congenital torsades de pointes?
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Acquired - K channel blocking medications (quinidine, erythromycin, haloperidol)
Congenital - genetic disorders involving abnormal cardiac ion channels |
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Treatment for torsades de pointes
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1. Temporary transvenous pacing (90-100 bpm)
2. Magnesium sulphate 50%, 4 mL IV 3. Isoprenaline 20 mcg IV 4. Lignocaine 75-100mg IV |
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What is Brugada syndrome?
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A channelopathy characterised by polymoprhic VT and VF --> cardiac arrest --> sudden death
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ECG findings in Brugada syndrome?
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Incomplete RBBB and ST elevation (three types - J point, saddleback, and ?)
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Treatment for Brugada syndrome
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ICD (implantable cardiac defibrillator)
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What is Wolff-Parkinson-White syndrome?
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Is a pre-excitation syndrome where there is a conducting fibre connecting the atrium and ventricle, causing early excitation of the ventricle
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ECG findings in WPW syndrome
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Slurred upstroke of QRS known as a delta wave
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Treatment for WPW syndrome
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Monitor every 2 years.
Catheter ablation Vagal maneouvres Propranolol 80mg and Diltiazem 120mg PRN |
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What is ventricular fibrillation?
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Simultaneous presence of multiple activation wavefronts within the ventricle, no cardiac output
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What ECG signs are there for VF?
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No true QRS complex, chaotic wide tachyarrhythmia
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What is the risk of sudden death in VF?
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75%
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What is the cardiac arrest score (Thompson and McCullogh)?
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SBP greater or less than 90 mmHg
Time to ROSC more or less than 25 mins Neurological responsiveness |
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Treatment for VF
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Defibrillation
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What is asystole?
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Cardiac standstill, no cardiac output, not ventricular depolarisaiton
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How do you diagnose asystole?
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Flat line rhythm in 2 perpendicular leads, ruling out VF or ECG malfunction
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What are the 5 steps to work-up asystole?
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1. 12 lead ECG
2. Pulse oximetry 3. ABG 4. K levels 5. Echo |
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Treatment for asystole
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1. CPR and IV adrenalin
2. Endotracheal intubation and positive pressure ventilation 100% oxygen DO NOT defib unless a shockable rhythm is diagnosed |
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Causes of asystole
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Primary - intrinsic factors in hearts conduction system (SA nod block, complete heart block or both)
Secondary - extrinsic factors, usually hypoxia and metabolic acidosis |
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What is systolic HF?
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Depressed ejection fraction (<40-50%)
(e.g. CAD, hypertension, volume overload) |
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What is diastolic HF?
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Preserved ejection fraction
(e.g. storage disorders, fibrosis, restrictive cardiomyopathy) |
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What are some high output disorders?
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Thyrotoxicosis, beri beri, chronic anaemia
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What does heart failure mean?
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Refers to structural or functional abnormalities of the heart causing a constellation of symptoms
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How does LV dysfunction get compensated?
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Renin-angiotensin-aldosterone system - water and salt retention
Increased myocardial contractility Vasodilation - ANP, BNP prostaglandins, NO |
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What are the best biomarkers for HF?
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BNP and N-terminal pro-BNP, with a depressed ejection fraction
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How do you treat CCF?
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Assess fluid status, add diuretics, ACEi and beta-blockers, then ARB then aldosterone antagonist/digoxin
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What is the M:F ratio for infective carditis?
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2.5 to 1
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What is the most common aetiological agent
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Strep viridans
Staph aureus in acute |
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What are some risk factors for IE?
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PHx of IE, artificial heart valves, congenital heart disease, post-heart transplant
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Differentiate between acute and sub-acute IE
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Acute - days to weeks, fevers, tachycardia and fatigue
Sub-acute - weeks to months, vague constitutional symptoms |
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Uncommon findings on examination in IE?
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Janeway lesions, Osler nodes, Roth spots, splinter haemorrahges, palatal petechiae
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What investigation must be performed in all cases of IE?
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Blood cultures and Echo
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What is the Dukes criteria?
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Need 2 major, 1 maj and 3 minor, or 5 minor
- MAJOR: 2 separate +ve cultures, evidence of endocardial involvement - MINOR: heart condition, IVDU, fever, vascular phenomenon, immunological phenomenon, microbiological evidence, echo |
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Treatment for acutely ill IE?
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ABC, blood cultures, echo, broad spectrum ABs (vanc, gent, cefepime)
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Treatment for sub-acute IE?
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Blood cultures, empirical ABs (ceftriaxone, gentamicin)
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Treatment for native valve IE?
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Gentamicin and beta lactam
HACEK - 3rd/4th gen ceph |
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What is myocarditis?
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Inflammation of the myocardium due to infection or circulating toxins, in the absence of CAD
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Most common cause of myocarditis?
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Developed - Coxsackie (35 in 1000), Influenza A/B (25 in 1000)
Worldwide - Trypanosoma cruzi (Chagas' disease) |
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What are the inflammatory cytokines?
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IL1, IL2, IFNy, TNFa
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What are the 4 classifications of myocarditis?
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1. Fulminant - acute illness following viral syndrome, either resolves spontaneously or death
2. Acute - insidious onset, progress to dilated cardiomyopathy 3. Chronic active - insidious onset, LV dysfunction 4. Chronic persistent - insidious onset, no LV dysfunction |
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Common signs of myocarditis on examination?
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Elevated neck veins, S3 gallop (Ken-tuc-ky), sinus tachycardia, atrial and ventricular arrhythmias
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What labs do you do in myocarditis?
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Troponins and CK (elevated proportional to extent of damage)
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What is the treatment of Chagas' disease?
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Benznidazole and nifurtimox
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Treatment for myocarditis?
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Unless specific organism isolated, supportive.
LV dysfunction - ACEi or ARB Haem unstable - vasodilator, inotropes End stage failure - transplant, LV assist device + anticoag |
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Prognosis of myocarditis?
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Mostly excellent, except for fulminant
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What is the function of the pericardium
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Limit distension of the heart, contribute to haemodynamic interdependence of ventricles, barrier to infection
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What is cardiac tamponade?
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Acute heart failure due to a large or rapidly developing pericardial effusion
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What is Becks triad?
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Classic cardiac tamponade features - hypotension, soft or absent heart sounds, jugular venous dystension
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What is pulsus paradoxus?
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A greater than normal (10mmHg) inspiratory decline in systolic arterial pressure
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What are the 4 clinical classifications of pericarditis?
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- Acute: <6w
- Sub-acute: 6w-6m - Chronic: >6m - Recurrent |
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Describe innervation to the pericardium
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Fibrous and parietal serous - phrenic
Visceral serous - vagus + sympathetic |
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List the 4 diagnostic features of pericarditis
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1. Chest pain - retrosternal, shoulders and neck, aggravated by movement
2. Pericardiac friction rub - heard in systole, present in 85%, high pitched scratching sound 3. Pleural effusion - seen on echo 4. ECG - PR interval depression (sensitive indicator of acute pericarditis), also ST elevation |
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Treatment for pericarditis
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Analgesia - aspirin, indomethacin
Corticosteroids Antimicrobial therapy if bacterial Percardectomy for constrictive |
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Demand or supply led? Stable and unstable angina.
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Stable angina - demand led
Unstable - supply led |
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What are the pressures in idiopathic pulmonary artery hypertension?
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Mean pulmonary artery pressure >25
Pulmonary capillary wedge pressure <15 |
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What genetic mutation is associated with IPAH?
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Bone morphogenetic protein receptor type 2 (BMPR2) - member of TFGb superfamily
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What happens to levels of prostacycline, thromboxane A2, endothelin 1 and NO in IPAH?
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Prostacyclin and NO - decrease
Thromboxane A2 and Endothelin 1 - increase |
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What is the cause of death in IPAH?
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Increased pulmonary vascular resistances -> RV overload -> RV failure -> death
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How do you classify IPAH?
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Functional classes
1. No limitation of physical activity 2. Mild limitation of physical activity 3, Marked limitation of activity 4. Unable to perform any activity, signs of RV failure at rest |
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What is a good biomarker of pulmonary artery pressure in IPAH?
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BNP - elevated, correlated to pulmonary artery pressures
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Treatment of IPAH
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Lifestyle, CCBs (amlod, nifed), prostacycline, phosphodiesterase 5 inhibitors
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What is Eisenmenger syndrome?
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Any anomalous circulatory communications to leads to obliterative pulmonary vascular disease
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What is essential vs secondary hypertension?
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Essential - no underlying cause, 90%
Secondary - due to precipitating factor which is identifiable (renovascular, endocrine, drugs) |
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How do you defined grade 1, 2 and 3 hypertension?
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Grade 1 - 140-159, 90-99
Grade 2 - 160-179, 100-109 Grade 3 - >180, >110 |
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What are some environmental risk factors for hypertension?
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Age, increased salt intake, obesity, sedentary lifestyle, excess alcohol intake, diabetes, dyslipidaemia, smoking
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What signs of hypertension might you see on fundoscopy?
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AV nicking, copper wiring, hard exudates, haemorrhages, papilloedema
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Treatment of hypertension
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Lifestyle
Thiazide diuretic ACEi, ARB, b-blocker, CCB |
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What is the most common cause of mitral stenosis?
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Rheumatic fever (95%)
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How do you grade mitral stenosis?
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Mild - gradient <5mmHg, valve area >1.5cm2
Moderate - gradient 5-10mmHg, valve area 1-1.5cm2 Severe - gradient >10mmHg, valve area <1cm2 |
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What is a common complication of mitral stenosis?
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AF (<20% stay in sinus rhythm)
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What might you hear on auscultation in mitral stenosis?
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Loud first heart sound, opening snap, mid-diastolic murmur
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What ECG findings might you see in mitral stenosis?
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Bifid P waves = P mitrale
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What definitive treatment is there for mitral stenosis?
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Balloon valvuloplasty, mitral valvotomy, mitral valve replacement
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How do chronic and acute mitral regurgitation differ in presentation?
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Chronic - like mitral stenosis
Acute - acute pulmonary oedema |
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Signs of mitral regurg on examination
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AF, cardiomegaly, displaced apex beat, apical pansystolic murmur, soft s2, apical s3
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How do you differentiate between medical and surgical treatment in mitral regurg?
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LV EF > 60%, LV end-systolic diameter <45mm = medical
LV EF < 60%, LV end-systolic diameter >45mm = surgical |
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Causes of aortic stenosis?
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Congenital, bicuspsid valve calcification, senile degenerative, rheumatic aortic stenosis
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What percentage of symptomatic patients are male in aortic stenosis?
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80%
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What is the natural progression of aortic stenosis?
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CO is maintained by increasing LV pressure, eventually failure -> pulmonary oedema.
Remain asymptomatic for years but deteriorate quickly (die 3-5 years after onset of Sx) |
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Signs of aortic stenosis on examination
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Ejection systolic murmur, slow rising carotid pulse (carotid pulsus parvus et tardus), narrow pulse pressure
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What is the Gallavardin phenomenon?
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Dissociation between noisy and musical components of systolic murmur heard in aortic stenosis
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Treatment for aortic stenosis
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Asymptomatic - watch and wait, Doppler every 1-2 years
Symptoomatic - aortic valve replacement, can use aortic balloon valvuloplasty on young congenital stenosis |
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Causes of acquired aortic regurgitation?
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Rheumatic disease, IE, trauma, aortic dilatation (Marfans, aneurysm, dissection, connective tissue disease)
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Signs on examination of aortic regurgitation
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Collapsing pulse (water hammer or Corrigan's pulse), boudnign peripheral pulses, Quincke's sign (capillary pulsation in nail beds), Duroziez's sign (femoral bruit, "pistol shot"), de Musset's sign (head nodding with pulse)
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Mumurs found in aortic regurgitation
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Early diastolic mumur
Austin-Flint murmur (soft mid diastolic) |
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What end-systolic LV diameter indicates surgical intervention?
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>55mm
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What is the most common cause of tricuspid stenosis?
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Rheumatic disease, usually occurs with mitral stenosis
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What level of diastolic pressure across the tricuspid valve can cause systemic venous congestion?
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4+ mmHg
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What are the hallmark signs of tricuspid stenosis?
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Hepatic congestion = cirrhosis, jaundice, malnutrition, anasarca, ascites, splenomegaly, jugular veins distended
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ECG features of tricuspid stenosis
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Tall peaked P waves in lead II (RA enlargement)
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Are mechanical or bioprostethic valves preferred in triscupid valve replacement?
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Bioprosthetic, mechanical valves in the tricuspid position are more prone to thromboembolic complications
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What is tricuspid regurgitation usually caused by?
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Secondary to RV enlargement due to pulmonary artery hypertension
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What is Ebstein's malformation?
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Congenital abnormality where the tricuspid valve is displaced towards the right ventricular apex, with enlargement of right atrium
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How do patients with tricuspid regurgitation present?
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Ascites from advances liver disease from chronic congestion or fibrosis, also gut congestion with symptoms of dyspepsia or indigestion, also fluid retention and leg oedema
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How do you treat pulmonary stenosis?
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Usually don't, but if gradient >50mmHg then balloon valvuloplasty
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What is a Graham Steel murmur?
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A high-pitched, descrescendo, diastolic blowing murmur along the left sternal border - seen in pulmonary regurgitation
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How does removal or destruction of the pulmonary valve affect the heart?
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It usually doesn't, unless there is significant pulmonary artery hypertension as well
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When is acute rheumatic fever most common?
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5-15 years
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What triggers ARF?
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An immune mediated delayed response to infection with group A strep
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What is the pathophysiology of ARF involving the heart?
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Antigens cross react with cardiac myosin and sarcolemmal membrane proteins
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What percentage of patients with ARF will develop rheumatic heart disease?
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60%
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Risk factors for ARF
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ATSI (5 in 1000), poverty, overcrowded living conditions, HLA D8/17
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What are the classic cardiac manifestations of RHD?
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Mitral regurgitation and/or mitral stensosi sometimes with aortic regurgitation
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What are Aschoff nodules?
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Pathopneumonic of RHD and only occur in the heart, composed on multinucleated giant cells surrounded by macrophages and T cells
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When do carditis and arthritis occur in ARF?
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Carditis - younger patients, pancarditis
Arthritis - high strep titres (painful, asymmetric, migratory of large joints) |
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What is erythema marginatum?
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Lesions start as red macules which fade in the centre, mainly on trunk and proximal extremities. Occur in ARF
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What is Sydenham's chorea?
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St Vitus dance - occurs 3 months after ARF, more common in females, purposeless involuntary movement of hands feet or face, resolves in a few months
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How often does Sydenham's chorea occur in ARF?
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Up to 1/3
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How common is polyarthritis in ARF?
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75%
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What is a Carey Coombs murmur?
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Soft mid-diastolic murmur due to valvulitis
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What percentage of throat swabs will be positive for strep A at time of ARF diagnosis?
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25%
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What are the Jones criteria?
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Need 2 major or, 2 major and 2 minor, plus evidence of infection
- MAJOR: carditis, polyarthritis, chorea, erythema marginatum, subcut nodules - MINOR: fever, arthralgia, raised eSR/CRP, 1st degree AV block - EVIDENCE: scarlet fever, raised ASO, positive throat culture |
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How is Sydenham's chorea treated?
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Carbamazepine or sodium valproate
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How is ARF treated?
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Single dose of 11/2 million units IM benzathine penicillin G, OR
Oral penicillin 500 mg PO twice daily for 10 days |
