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Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is the CHA2Ds2 VASc score?

A 
CHA2DS2 VASc score helps to determine whether or not to warfarinise a person in AF.
C- Congestive Heart Failure (1)
H- Hypertension/Treated HTN (1)
A2- Age >75 (2)
D- Diabetes
S- Prior Stroke or TIA (2)
V- Vascular disease (including ischeamic heart disease or vascular disease) (1)
A- age >65 (1)
S - female (1)
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2
Q

How do you interpret a CHA2DS2 VASc score?

A

0- No treatment is preffered to aspirin
1- oral anticoagulants is preferred to aspirin (dabigatran is an alternative)
2- Oral anticoagulants (dabigatran is an alternative.
Give warfarin with a target INR of 2-3

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3
Q

If a young patient presents with paroxysmal atrial fibrillation, how would you cardiovert them?

A

If patient with stable, Cardiovert using Amiodarone and Flecainide (Rhythm control rather than rate control). If they are unstable, use DC cardioversion.

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4
Q

What is stage 1 hypertension?

A

Clinical blood pressure reading >140/90 and subsequent Ambulatory Blood Pressure Monitoring average of >135-95.
Treat is over the age of 85 AND there is CVD, renal disease, diabetes, end organ damage, or a 10 yr cardiovascular risk of 20% or greater.

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5
Q

What is stage 2 hypertension?

A

Clinical blood pressure reading is >160/110 and subsequent ambulatory blood pressure monitoring of 150/90.
Offer drug treatment regardless of age.

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6
Q

What is stage 3 hypertension?

A

Clinical blood pressure reading is >180 or clinical diastolic reading is >110.
Treat immediately, AMBP not required.

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7
Q

What is the first line treatment of hypertension? What is the second line treatment?
What is third line treatment?

A

If 55 or of Afro-Carribean origin give dihydropyridine Calcium channel blocker (Amlopidine or Nifedipine).
In second line treatment, combine use of CCB and ACE Inhibitor.
Third line treatment add a thiazide like diuretic, like Indapamide. Fourth line: add spironolactone. Consider beta blocker if diuretics are contraindicated.

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8
Q

What drugs have been shown to improve mortality in heart failure?

A

ACE Inhibitors, Hydralazine, Beta Blockers, Spironalactone.

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9
Q

How do you treat heart failure?

A

First Line is ACE Inhibitor and a beta blocker.
Second line includes use of an aldosterone antagonist, Angiotensin II receptor blocker, or Hydralazine.
Give pneumococcus injection and annual influenza injection and nitrate. Give diuretics for fluid overload. May also consider treating with digoxin.

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10
Q

What are the signs of Aortic Stenosis?

A

Signs of aortic stenosis include:

  • Systolic Ejection Murmur
  • Quiet S2
  • Fourth Heart Sound
  • Narrow Pulse Pressure
  • Left ventricular hypertrophy
  • Left ventricular failure
  • Abnormal aortic valve gradient.
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11
Q

What are the causes of aortic stenosis?

A

Aortic stenosis is caused by:

  • Degenerative Calcification
  • Bicuspid aortic valve
  • HOCM
  • Post rheumatic heart disease
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12
Q

How do you manage aortic stenosis?

A

If the patient is asymptomatic and has an aortic valve gradient 50mmHg, or has left ventricular systolic dysfunction, then consider valvular replacement. Only consider balloon valvuloplasty for someone unfit for surgery.

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13
Q

What drug should not be prescribed with a beta blocker?

A

Verapramil should not be prescribed with a beta blocker.

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14
Q

What are the features of hypokalaemia on ECG?

A

In hypokalaemia, U have no pot(assium) and no T, but a long PR, and a long QT. Also ST elevation.
= U Waves (small, follow the T wave), absence of T waves, prolonged PR interval, long QT.

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15
Q

How does inspiration affect the heart?

A

Inspiration increases venous return, causing an increase in right cardiac output. The blood is sequestered in the lungs as it expands, hence left atrial filling is reduced and left heart output is reduced.

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16
Q

How does expiration affect the blood flow of the heart?

A

Upon expiration, left heart output increases and right heart output decreases (riles=right inspiratory, left expiratory)

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17
Q

What is pulses paradoxus? In what condition does it occur?

A

Pulses paradoxus is an exaggeration of the effect for respiration on the cardiac output. There is a large drop in blood pressure upon expiration. It occurs in cardiac tamponade as the increased pressure in the chest cavity upon inspiration compresses the right heart and decreases VR to both sides of the heart.

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18
Q

What is BNP (brain natriuretic peptide)?

A

BNP (along with NT-proBNP) is secreted from the left ventricle of the heart. Elevated BNP is associated with left systolic dysfunction. It may aid therapy and response to diagnosis in patients with heart failure.

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19
Q

What are the types of cardiac troponins, when are they released? What conditions caused raised troponins?

A

Cardiac troponins are troponins I and T. They are released when there is myocyte damage or necrosis. They are particularly important for diagnosing an MI, but may also be caused by PE, septic shock, and acute pulmonary oedema.

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20
Q

What are the indications for echocardiography?

A

Indications include:valvular disease, endocarditis and rheumatic heart failure(possible identification of vegetations), intracardiac thrombus, infarcted tissue(measures left ventricular function), pericardial effusion, identification of structural heart disease.

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21
Q

What is a two dimensional echo used for?

A

A two dimensional echo is used to measure ejection fraction and ventricular thickness.

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22
Q

What is Doppler echocardiography used for?

A

A Doppler echocardiography is used to measure the speed and direction of the RBCs in the heart and great vessels of the heart in order to detect valvular regurgitation and stenosis of the blood vessels.

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23
Q

When would a transoesophageal echo (TOE) be used?

A

Toes are used if a patient is fat or has COPD. It is also better for congenital abnormalities, prosthetic valve dysfunction, aortic dissection, infective endocarditis, and systemic embolism.

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24
Q

What is a stress echo?

A

A stress echo is used in people who can’t do an exercise stress test (eg. have existing heart block, immobile). It uses a dose of intrope dobutamine that increases contractility and cardiac output.

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25
Q

When is CT used in cardiology?

A

Contrast CT is used for imaging aortic dissection or pulmonary embolism.

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26
Q

Describe the physiology of left heart failure, and list any other conditions that it can cause.

A

In left heart failure there is a decrease in left ventricular output, and an increase in left atrial pressure (same as pulmonary venous pressure). If it occurs acutely, it causes pulmonary congestion or pulmonary oedema. When it occurs gradually (eg mitral stenosis) there is reflex vasoconstriction causing pulmonary hypertension.

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27
Q

Describe the signs and symptoms of left sided heart failure.

A

Left heart failure presents with cardiomegaly, some pitting oedema, pleural effusion, pulmonary oedema, and a somewhat raised JVP. Possibly pulmonary hypertension.

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28
Q

Describe the physiology of right heart failure. What are the causes of right heart failure?

A

There is a reduction of right ventricular output for any given right atrial pressure. Causes of right heart failure are chronic lung disease (Cor pulmonale), multiple pulmonary emboli, and pulmonary (valvular ) stenosis.

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29
Q

What is the typical presentation of someone with right heart failure?

A

RHF presents with major oedema, a very raised JVP, an enlarged pulsatile liver, and ascities.

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30
Q

What is the difference between systolic and diastolic heart failure?

A

Systolic heart failure has impaired contraction, diastolic has impaired relaxation (poor ventricular filling or high filing pressures).

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31
Q

What are the causes of diastolic heart failure?

A

Volume overload (in valvular disease), uncontrolled hypertension, ischeamia, or cardiomyopathy.

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32
Q

How is systolic heart failure treated?

A

First Line is ACE Inhibitor and a beta blocker.
Second line includes use of an aldosterone antagonist, Angiotensin II receptor blocker, or Hydralazine.
Give pneumococcus injection and annual influenza injection and nitrate. Give diuretics for fluid overload. May also consider treating with digoxin.
Diastolic heart failure is more difficult to treat.

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33
Q

What are the causes of high output heart failure?

A

Shunt, beri beri, thyrotoxicosis, or severe aneamia

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34
Q

What is the typical clinical presentation of acute left heart failure?

A

Acute dyspnoea, rapidly progressing to acute respiratory distress and orthopnoea. Rapid pulse, patient is cool, pale, and clammy. BP may be high due to sympathetic activation or low due to cardiogenic shock. Elevated JVP, triple heart sound, crepitations in the lung base due to pulmonary oedema.

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35
Q

What is the typical clinical presentation of chronic heart failure?

A

Chronic heart failure px with lethargy, listlessness, and fatigue, poor exercise tolerance, low BP, cold peripheries, oligouria and ureamia, due to poor renal perfusion,possible weightloss, skeletal atrophy. If left heart:pulmonary congestion with bibasal all creps, cardiomegaly, and some peripheral oedema and raised JVP Right heart failure :elevated JVP, liver congestion, and oedema.

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36
Q

What types of arrhythmias cause the feel irregular heart beats?

A

Ectopic beats, atrial fibrillation.

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37
Q

What type of arrhythmias cause irregular discrete attacks of palpitations?

A

SVT, VT.

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38
Q

What type of arrhythmias cause continuous irregular palpitation?

A

Sinus tachycardia, high stroke volume (aneamia, tachycardia, valve disease).

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39
Q

What are the causes of cardiac arrest?

A

Coronary artery disease (85%), structural heart disease (aortic stenosis, hypertrophic or dilated cardiomyopathy,arrythmogenic right ventricular dysplasia, congenital heart disease) and 5% from other (Wolff Parkinson’s White, Brugada, Long QT syndrome and adverse drug reactions such as tornadoes du point, and severe electrolyte abnormalities).

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40
Q

When does VT cause cardiac arrest?

A

Ventricular tachycardia causes cardiac arrest when it’s pulses are so fast as to prevent cardiac filling. VT also has a habit of progressing into ventricular fibrillation.

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41
Q

What are the reversible causes of asystole?

A

Tension Pneumothorax, Thrombosis, Tamponade, and Toxins.

Hypoxia, Hypovoleamia, Hypothermia, and Hypokaleamia.

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42
Q

What are the causes of pulse less electrical activity?

A

Hypovoleamia, cardiac tamponade, tension pneumothorax.

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43
Q

What drugs may be given during cardiac arrest?

A

Adrenaline 1mg IV every 3-5mins. Consideration should be given to the use of amiodarone, particularly if VT or V fun re establishes itself after defibrillation. May also consider magnesium.

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44
Q

When might you hear a third heart sound?

A

Pregnancy, young person, or heart failure.

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45
Q

Which murmur radiates from the apex to the axilla?

A

Mitral Regurgitation

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46
Q

Which murmur radiates to the base of the neck?

A

Aortic stenosis

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47
Q

What are the causes of an ejection systolic murmur?

A

Aortic stenosis, pulmonary stenosis, aortic or pulmonary flow murmurs.

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48
Q

What causes a pan systolic murmur?

A

Mitral regurgitation, tricuspid regurgitation, VSD.

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49
Q

What causes a late systolic murmur?

A

Mitral valve prolapse

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50
Q

What causes an early diastolic murmur?

A

Mitral stenosis, tricuspid stenosis, mitral flow murmurs, tricuspid flow murmurs

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51
Q

What causes the first heart sound?

A

The closure of the mitral and tricuspid valves.

52
Q

What causes the second heart sound?

A

The closure of the aortic and pulmonary valves.

53
Q

What causes the third heart sound?

A

The third heart sound is caused by the ventricular wall due to an abrupt cessation of rapid filling.

54
Q

What drugs should be avoided in congestive heart failure?

A

Verpamil, NSAIDS, and corticosteroids.

55
Q

What is enoxaparin?

A

Enoxaparin is a heparin marketed for the prevention of VTE in bedridden patients. Reserve for patients at high risk of clot and low risk of bleeding.

56
Q

How do ace inhibitors work?

A

Ave inhibitors prevent the conversion of angiotensin 1 to angiotensin 2 and thereby decrease the effects of angiotensin 2 induced vasoconstriction, sodium retention, and aldosterone release. It is used for hypetertension, all left sided heart failure (reduces mortality by 10%) , post mi with patients with left ventricular dysfunction, diabetic nephropathy, or to prevent renal failure in patients with persistent proteinuria

57
Q

What actions do you need to take when starting a patient on ACE Inhibitors?

A

Stop potassium supplements and potassium soaring diuretics, stop other diuretics for 24 hours, start with a low dose, check renal function and electrolytes before starting and then review 2 weeks later and remember that the onset of ace inhibitor induced angioedema may not occur for several years. Ace inhibitors may cause cough. They have a low incidence of side effects if dosed appropriately.

58
Q

How do beta blockers work?

A

Beta blockers competitively block beta receptors in the heart, peripheral vasculature, bronchi, pancreas, uterus, kidney, brain, and liver. They reduce blood pressure by reducing cardiac output, effect the CNS, and reduce renin output. Their anti angina effect comes from causing a decrease in work by decreasing heart rate and contractility. Anti-arrhythmic properties due to antisympathetic effect that decreases the heart rate and dulls electrical activity. Hence beta blockers are used to teat HTN, angina, arrhythmias, MI, heart failure, and glaucoma.

59
Q

What are beta1 selective beta blockers?

A

Beta 1 selective beta blockers are cardioselective and have a high affinity for beta1 receptors in the heart with less effect on beta2receptors in the bro chi and peripheral vasculature. Beta1 selectivity diminishes with higher doses.

60
Q

What is atrioventricular nodal re entrant tachycardia?

A

AVNRT comes from a recently circuit caused by the AV node. It occurs in healthy individuals and can cause an increased heart rate for an hour or so. The ECG shows tachycardia with a normal QRS complex. AVNT may be terminated with carotid sinus pressure or a valsa lava manoeuvre. It can also be treated using IV verapamil or adenosine.

61
Q

What is Wolf Parkinson white syndrome?

A

In Atrioventricular nodal rentrant tachycardia there is an extra band of conducting tissue (similar to the purkinje fibre tract) that connects atria and the ventricles. It is known as the accessory pathway tract. Half of these cases only conduct to the atria in a retrograde fashion, and do not alter the appearance of the ECG. The other half of cases will conduct the other way. The conduction of each beat takes place partly n the AV node and partly in the accessory tissue. This produces a decreased PR interval and a ‘slurrring’ of the QRS interval, known as the delta wave. When there is a delta wave and a reduced PR interval on the ECG, the patient is diagnosed with Manifest Accessory Pathway. If the AV node and Accessory pathway have different conduction speeds, then a recently loop develops causing tachycardia. This is referred to as Wolf Parkinson White Syndrome.

62
Q

What do ventricular ectopics look like on ECG?

A

Ventricular ectopics are wide uncoordinated QRS complexes on ECG. They may occur singularly, in couplets or in triplets. If there is an alternating sinus and ectopic ventricular contractions it is termed ‘bigeminy’. Ventricular ectopics are generally benign but may be an indication of underlying heart disease, or of digoxin toxicity.

63
Q

What are the common causes of ventricular tachycardia?

A

The common causes of ventricular tachycardia are MI, cardiomyopathy, and chronic ischeamia heart disease. It is extremely serious as it causes heamodynamically compromise and can turn into VF.

64
Q

What does an ECG for VT show?

A

The ECG for VT shows broad QRS complexes at a heart rate greater then 120bpm. VT can occasionally occur in normal healthy hearts.

65
Q

What is the management for VT?

A

Prompt action is required for VT. you need to restore sinus rhythm, and then follow with prophylactic therapy. If the BP is 90bpm, IV amiodarone may be given as a bonus, followed by a continuous infuse. Beta blockers are useful at preventing VT by reducing automaticity, and inducing AV block. Additional amiodarone may help.

66
Q

What is torsades de pointes?

A

Torsades de pointes is a complication of prolonged ventricular repolarisation (prolonged QT syndrome). The ECG shows rapid irregular complexes that oscillate from being upright to inverted and seem to twist around the baseline. The arrhythmia is non sustained, but repetitive, and it may degenerate into VF. During periods of sinus rhythm, the ECG will show a long QT interval.

67
Q

How is torsades de pointes treated?

A

Treatment for torsades should be directed at the underlying cause (eg hypokaleamia, hypo,amnesia, or hypocalceamia). IV magnesium should be given in all cases.
Only use DC cardioversion if absolutely needed.

68
Q

What is brugada syndrome?

A

Brugada syndrome is a related genetic disorder that may present with polymorphic VT or sudden death. It is characterised by a sodium channel defect and abnormal ECG.

69
Q

What is sick sinus syndrome?

A

Sick sinus syndrome is also known as sinoatrial disease. It occurs when there is fibrosis, degenerative changes, or ischemia of the SA node. The condition causes a variety of arrhythmias (sinus bradycardia, sinus arrest, atrial fibrillation, atrial ectopics, and junctional beats). Consequently, the patient can present with dizziness, fainting, tachycardia, bradycardia, palpitations, or pauses with no ventricular or atrial contractility. A pacemaker can help symptoms, but not prognosis. Consequently there is very little point in using a pacemaker in asymptomatic patients.

70
Q

What is first degree heart block?

A

First degree heart block occurs when there is a prolonged PR interval, but each beat makes it through. PR interval must be greater than 0.02 seconds. It rarely causes symptoms.

71
Q

What is second degree heart block?

A

Second degree heart block is divided into mobitz type one (wenkebach) and mobitz type two.

72
Q

What is Mobitz type one?

A

Mobitz type one heart block is also known as Wenkebach. It is where there is successive prolongation of the PR interval until eventually a beat is dropped and the pattern is reset. This is a fairly benign condition, and is sometimes observed at rest or in the sleep of young adults with high vagal tone.

73
Q

What is Mobitz type two?

A

Mobitz type two is a type of second degree heart block. It occurs when the PR intervals remain the same, but some of the p waves are not conducted. This is bad and carries a risk of asystole. It is usually associated with damage to the his-purkinje system.

74
Q

What is third degree heart block?

A

Third degree heart block occurs when atrial and ventricular depolarisations are completely unrelated to each other. If there are narrow QRS complexes, then the ventricular system is maintained by an escape rhythm, from the AV node, or by the bundle of his. If there are broad QRS complexes, the ventricles are being depolarised by the distal purkinje tissues. This produces a slow regular pulse that does not vary with exercise.

75
Q

What type of arrhythmias cause stokes Adams attacks?

A

Stokes Adams attacks occur with third degree heart block or with mobitz type two second degree heart block 2:1.

76
Q

Heart block and right ventricular dysfunction are associated with what preceding event?

A

Heart block and right ventricular dysfunction are associated with inferior MI (the right coronary artery supplies the AV node).

77
Q

What are the causes of right bundle branch block?

A

The causes of right bundle branch block are: Coronary artery disease, pulmonary disease (eg. PE), congenital heart disease, normal.

78
Q

What are the causes of left bundle branch block?

A

The causes of left bundle branch block include coronary artery disease, hypertension, cardiomyopathy, aortic alive disease.

79
Q

What sort of condition is seen in anterior hemi-block (left fascicle) and in posterior hemi-block (left fasicle also)?

A

Anterior hemiblock produces left axis deviation, posterior hemiblock produces right axis deviation.

80
Q

Describe the pathological process of atherosclerosis.

A

Fatty streaks occur at the sites of shear stress, such as bifurcations and are associated with abnormal endothelial dysfunction. The endothelial cells express receptors that allow monocytes to bind them. These monocytes migrate into the intima and take up oxidised low density lipoproteins (LDL). They they become lipid laden macrophages or foam cells. When these foam cells die, they release their contents, causing extra cellular lipid pools to form in the wall.

81
Q

How do you investigate someone presenting with stable angina?

A

If someone presents with stable angina, they should be tested with an exercise stress test. If the stress test is equivocal, then they should consider having a myocardial perfusion scan. This involves taking myocardial perfusion scan when a patient is at rest or during stress (exercise or pharmacological with a controlled dose of dobutamine). This is done after administration of an IV radioactive intravenous isotope, such as technetium tetrofosmin. Transthoracic echocardiography can also be used. Alternatively there is coronary arteriography. Coronary arteriography provides a detailed and anatomical view of coronary artery disease.

82
Q

How should stable angina be medically managed?

A

Treat stable angina with low dose aspirin, a statin, sublingual GTN, and a beta blocker. Add a calcium channel antagonist or a long acting nitrate later if needed.

83
Q

When does CABG improve survival?

A

CABG improves survival in patients with left main vessels disease, or three vessel coronary disease.

84
Q

What conditions make up acute coronary syndrome?

A

Acute coronary syndrome consists of either unstable angina, or an MI that is either a STEMI, or a non-STEMI.

85
Q

What is the typical presentation for a person with acute coronary syndrome?

A

Chest pain (dull, crushing), sob, vomiting, pale diaphoretic, tachycardia or bradycardia. May have loc, may be febrile, may show signs of decreased perfusion. Painless, or ‘silent’ MI is more common in diabetics and older patients.

86
Q

What findings may be found on investigation of acute coronary syndrome?

A

An ECG may show ST segment elevation or a new bundle branch block. The T wave subsequently becomes inverted because of a change in ventricular repolarisation. This change will persist after the MI. A non ST segment elevation means that there is a partial occlusion of a major vessel, or an occlusion of a minor artery.

87
Q

What leads can an anteroseptal infarction be seen in?

A

An anteroseptal infarction can be seen in leads V1 to V4.

88
Q

In what ECG leads can you see an anterolateral infarction?

A

An anterolateral MI can be seen in V4 to V6, lead I and aVL

89
Q

What are the markers used to show infarction of the cardiac tissue? What are the other signs or results upon investigation that may be seen?

A

Troponins and CKMB. They raise 4-6 hours after an MI. the CKMB is more sensitive and specific. Troponins remind raised for two weeks, where as CKMB remains elevated for 24 hours. Other investigations might show a leucocytosis, an elevated ESR and CRP, and pulmonary oedema on CXR. An echo is important for showing left and right cardiac function, as well as detecting important complications such as mural thrombus, cardiac rupture, ventricular septal defect, mitral regurgitation, and pericardial effusion.

90
Q

How do you manage someone who presents with presumed cardiac chest pain?

A

Order serial ECGs and cardiac markers. Give then oxygen, nitrates, and morphine. Also given them aspirin with clopidegrel or with ticagrelor.

91
Q

How do you manage someone who has confirmed unstable angina?

A

Unstable angina has been confirmed once the ECG has shown no ST elevation and the cardiac markers are not elevated. They should be put on a permanent prescription of aspirin. If they cannot use aspirin then they should permanently be on clopidegrel. They should also be put on a statin ( eg simvastatin) irrespective of their cholesterol levels. If they have reduced left ventricular dysfunction they should be put on a beta blocker ( eg. Propranolol) unless contraindicated. If they have a LV ejection fraction <40, renal disease, HTN, or diabetes they should be on an ACE inhibitor (eg. Captopril). They should also undergo lifestyle changes.

92
Q

How do you treat a confirmed STEMI who is heamodynamically unstable?

A

Treat with emergency revascularisation (within 48 hours) if revascularisation fails an urgent coronary artery bypass is recommended. Patients suffering from cardiogenic shock may benefit from a dobutamine infusion. An intranet is balloon pump may be indicated if pharmacological measures do not quickly improve the shocked state. `

93
Q

How do you treat someone who has presented with a STEMI who is heamodynamically stable?

A

If the patient can access percutaneous cardiac intervention (revascularisation) for stent placement within 90 minutes of first presenting then this route should be taken. If they cannot, but they are within 12 hours of the first onset of symptoms onset then they should undertake thrombolysis (eg. reteplase, alteplase, tenectaplase), and then receive PCI within 6 hours. They should also be given anticoagulation consisting of a GPIIB/IIIa inhibitor (abciximab, eptifibatide, tirofiban) and a heparin (enoxaparin, heparin). They should also receive aspirin and clopidegrel, beta blocker, statin, morphine, GTN, oxygen, and glucose control. Longterm they should be on clopidegrel and aspirin, an ace inhibitor, a beta blocker, and a statin.

94
Q

What are the symptoms of an abdominal aortic aneurysm?

A

Abdominal, back or groin pain with a pulsatile mass and hypotension. Able to be viewed on ultrasound.

95
Q

What factors predispose to an aortic dissection?

A

HTN, aortic atherosclerosis, aortic aneurysm, aortic coarctation, Marfans.

96
Q

What are the principle causes of valvular regurgitation?

A

Valvular regurgitation can be caused by congenital causes, endocarditis, chronic/acute rheumatic carditis, valve ring dilatation from dilated cardiomyopathy, syphilitic aortitis, traumatic valve rupture, senile degeneration, myocardial infarction causing damage to the chorded and papillary muscles.

97
Q

What are the causes of valvular stenosis?

A

Congenital, rheumatic carditis, and senile degeneration.

98
Q

Acute rheumatic fever is an autoimmune reaction to what disease?

A

Acute rheumatic fever is an autoimmune reaction to Group A streptococcal infections.

99
Q

What are the clinical features of rheumatic fever?

A

Sydnams chorea, Prior sore throat, dyspnoea, syncope, pericarditis, aortic or mitral regurg, heart block, subcutaneous nodules over bones or tendons, oedema, polyartheritis plus arthralgia (acute painful asymmetric migratory arthritis affecting the knees ankles elbows and wrists), fever, erythema marginatum.

100
Q

What investigation results are found for acute rheumatic fever?

A

There is an increased ESR, an increased CRP, leucocytosis, throat swab culture (positive for group A b-haemolytic streptococci) ASO (anti streptomycin O antibodies), CXR may show pulmonary congestion or cardiomegaly. ECG, echocardiography may show cardiac dilatation and valve abnormalities.

101
Q

How do you treat acute rheumatic fever?

A

Acute rheumatic fever is treated with benzoyl penicillin or phenoxymethylpenicillin. If there is penicillin allergy, give arythromycin or cephalosporins. Aspirin to reduce joint pain.

102
Q

What valves does rheumatic heart disease affect, in order of most common to least common?

A

Mitral valve, aortic valve, tricuspid, then pulmonary. 40% of people have aortic stenosis and mitral regurgitation, whereas only 25% have just mitral regurgitation.

103
Q

What are the causes of mitral stenosis?

A

Mitral stenosis mainly occurs due to rheumatic heart disease. However it does occur due to calcification in the elderly, or in rare congenital defects.

104
Q

What happens in mitral stenosis?

A

There is a reduction in blood that travels from the LA to the LV. This causes a build-up causing pulmonary congestion. The patient experiences dyspnoea, and there is dilatation and hypertrophy of the left atrium. Because the cardiac output becomes dependent on the atrial contractions, atrial fibrillation can be very dangerous.

105
Q

What are the causes of mitral valve regurgitation?

A

Mitral regurgitation can be caused by rheumatic heart disease, infarction of the papillary muscles, dilatation of the left ventricle and the mitral valve ring, mitral valve prolapse, and endocarditis. Mitral valve prolapse is having a floppy mitral valve that goes backwards. It’s one of the more common causes of mitral regurgitation and is caused by Marfan’s disease and congenital abnormalities.

106
Q

What are the causes of aortic stenosis?

A

Rheumatic fever, senile calcification, and bicuspid aortic disease.

107
Q

What are the symptoms of aortic stenosis?

A

Aortic stenosis causes exercise intolerance, syncope, dyspnoea, lethargy, angina, sudden death, and acute pulmonary oedema.

108
Q

What are the signs of aortic stenosis?

A

Signs of aortic stenosis include an ejection systolic murmur that radiates to the neck. A slow rising pulse. Left ventricular pressure overload causing a thrusting apex beat, and signs of pulmonary congestion.

109
Q

What are the causes of aortic regurgitation?

A

Aortic regurgitation is caused by rheumatic heart fever, bicuspid aortic valve, left ventricular hypertrophy, aortic dissection, aneurysm, Marfan’s dilatation, syphilis or ankylosing spondylitis.

110
Q

What are the signs and symptoms of aortic regurgitation?

A

Aortic regurgitation presents with a early diastolic murmur, collapsing pulse, head bobbing (de Musset’s sign), awareness of own heartbeat, palpations worse when lying on the left side, capillary pulsations in the nail bed (Quincke’s sign)

111
Q

What is bacterial endocarditis?

A

Bacterial endocarditis is infection of the lining of a heart vessel, blood vessel, or septal defect. It is normally caused by bacteria, but can also be caused by rickettsia, chlamydia, or a fungus.

112
Q

What infective agent is the most common cause of infective endocarditis?

A

The most common cause of infective endocarditis is staph aureus.

113
Q

What is a patent ductus arteriosus?

A

A patent ductus arteriosus allows blood to pass from the aorta to the pulmonary artery. As much as 50% of the cardiac output is recirculated through the lungs increasing cardiac work. The ECG is usually normal. If pulmonary vascular resistance increases, there can be a reversing of the shunt, causing Eisenmengers syndrome. A PDA can be closed during catherisation with an implantable occlusive device.

114
Q

What is coarctation of the aorta?

A

Coarctation of the aorta is more common in males, and is associated with beri cerebral aneurysms and bicuspid aortic valves. The blood pressure is raised in the upper body, but is normal or low in the legs. Death may occur from left ventricular failure, aortic dissection, or cerebral haemorrhage.

115
Q

What are the features of tetralogy of fallot?

A

The features of tetralogy of fallot include right ventricular hypertrophy, VSD, pulmonary stenosis, and overarching aorta.

116
Q

How does tetralogy of fallot present?

A

Tetralogy of fallot presents in neonate a with cyanosis, and in older children with growth retardation, clubbing, cyanosis, and polycythemia.

117
Q

What is myocarditis?

A

Myocarditis is inflammation of the myocardium, and may be due to autoimmune process, infection, or circulating toxins.

118
Q

What is the most common cause of myocarditis?

A

Viral infections are the most common cause of myocarditis, such as the coxsackie virus, influenzae A and B. other causes include immunosuppressive, corticosteroid treatment, immunosuppressants, radiation, previous myocardial damage, and exercise. Toxic causes include lithium, cocaine, and anti cancer drugs such as doxorubicin. It can also be caused by lupus and rheumatoid arthritis.

119
Q

What is the prognosis for myocarditis?

A

The disease is usually self limiting and the prognosis is good. However, death may occur due to ventricular arrhythmia or rapidly progressive heart failure.

120
Q

What is cardiomyopathy?

A

Cardiomyopathy is the measurable deterioration of the function of the myocardium for any reason. The term is usually reserved for ‘severe myocardial disease leading to heart failure’. Types of cardiomyopathies include dilated cardiomyopathy, hypertrophic cardiomyopathy, arrythmogenic right ventricular cardiomyopathy, obliterative cardiomyopathy, and restrictive cardiomyopathy

121
Q

What are the signs of cardiac tamponade?

A

Cardiac tamponade presents with a raised JVP, tachycardia, hypotension, distant heart sounds, pulses paradoxus >10mmHg.

122
Q

What would you use to treat someone with AF with rate control?

A

First line: Beta blocker or non dihydropyradine beta blocker (eg. diltiazem or verapamil)
If patient has coexisting heart failure choose digoxin.

123
Q

How would you a treat a patient with a history of atrial fibrillation in order to maintain sinus rhythm?

A

Sotolol, amiodarone, flecainide.

124
Q

What are the factors that favour rate control of AF?

A

More likely to use rate control is age >65 years, or has a history of ischeamic heart disease.

125
Q

What are the factors that would make you favour rhythm control of AF?

A 
Younger than 65 years
Asymptomatic
First presentation
First time onset AF or AF secondary to a corrected precipitant.
Congestive Heart failure.
126
Q

What is HCM?

A

Hypertrophic cardiomyopathy is the most common cardiomyopathy and is the most common cause of sudden cardiac death in young people. Presentation varies from asymptomatic to symptoms of heart failure. Physical examination may be normal at rest. Family history may be present, echo should be used to screen family members. Medical therapy is used for symptomatic patients. A subset of patients with increased risk of sudden cardiac death should undergo defibrillator implantation.

127
Q

What are the causes of a fourth heart sound?

A

A fourth heart sound may be heard in aortic stenosis, HOCM, and hypertension. It is caused by atrial contraction against a stiff ventricle.

Medicine (16 decks)

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