• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

Card Range To Study



Play button


Play button




Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

227 Cards in this Set

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