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Ask Doctor Clarke 2018 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Three main causes of AF

A

Ischaemic Heart Disease Rheumatoid heart disease Thyrotoxicosis

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2
Q

What causes the 4th heart sound?

A

-atrial contraction on a non-compliant or hypertrophied ventricle -low pitched -always abnormal

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3
Q

4 conditions where a 4th heart sound may be present

A

Heart failure MI Cardiomyopathy Hypertension

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4
Q

Is the apex beat displaced in hypertension? Why?

A

Hypertension—> LV hypertrophy inwards —> apex beat isn’t moved, but is more powerful (Pressure overload)

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5
Q

By how much does CO decrease in AF?

A

25% as the atria contribute that amount to the LV volume

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6
Q

What is a third heart sound?

A

-normal in children and young adults <30 - a ventricular sound- blood rushing in during rapid filling phase of early diastole -stiff/ dilated ventricle suddenly reaches its elastic limit and decelerates the incoming rush of blood

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7
Q

4(+2) causes of a third heart sound

A

-heart failure -MI -Cardiomyopathy -hypertension -mitral and aortic regurgitation -constrictive pericarditis

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8
Q

Examination findings in IE

A

2 in hands- clubbing and splinters 1 in heart- changing murmur 2 in abdomen- splenomegaly, microscopic haematuria Rarer- osler, jeneway, Roth

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9
Q

4 stages of clubbing

A

Increased fluctuancy of nail bed Loss of angle (schamroth’s window test) Increased curvature of nail Expansion of the terminal phalanx

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10
Q

Two main causes for an irregularly irregular pulse?

A

AF and multiple ventricular ectopic- ectopics disappear on exercise as diastole shortens

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11
Q

How do you assess if AF is well controlled?

A

HR<80bpm

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12
Q

What is the goal INR in AF?

A

2-3

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13
Q

What’s the goal INR in mitral valve replacement? Aortic?

A

Mitral- 3-4 Aortic- 2-3

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14
Q

What are the criteria for rhythm control in AF?

A

-new onset within 48hrs -LVF - Reversible cause e.g. thyrotoxicosis - clinically indicated e.g. young - symptoms despite attempted rate control -acutely unwell

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15
Q

What is a pulse deficit in AF?

A
  • as rate increases diastolic filling time reduces -With fast ventricular response- impulses are fast and irregular -impulses close together -sometimes insufficient filling time to have a substantial output -enough blood to move the valves (can hear it) but not to feel a pulse (can’t feel it)
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16
Q

Features of aortic stenosis on examination

A

-slow rising pulse -low volume pulse, with low pulse pressure -JVP not elevated -apex beat forceful, but not displaced (pressure overload) Ejection systolic murmur

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17
Q

Causes of aortic stenosis

A

-degenerative calcification aortic stenosis -congenitally bicuspid valve with degenerative changes -rheumatic heart disease

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18
Q

Causes of LV pressure overload

A

Hypertension AS Coarctation of the aorta HYpertrophic Cardiomyopathy with LV outflow Tract Obstruction (subvalvar stenosis)

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19
Q

AS treatment

A

Symptoms are a good guide to severity- SAD- Syncope, Angina, Dyspnoea Valve replacement is definitive TAVI

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20
Q

Causes of MR

A

LAP Leaflet: congenital, endocarditis, degenerative Annular dilation: Cardiomyopathy, IHD with HF Papillary muscle and chordae: MV prolapse, ACS, Marfans

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21
Q

MR signs

A

Apex beat usually displaced Quiet first heart sound Pansystolic murmur radiates loudly to axilla Second heart sound not heard separately

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22
Q

MR treatment

A

Mild/moderate: ACEi, Diuretics (decrease afterload, decrease amount of regurge) +/- anticoagulants (if in AF, most will be) Severe: valve repair, not replacement

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23
Q

Aortic Sclerosis vs stenosis

A

Sclerosis—> thickening of leaflets Stenosis—>fusing and narrowing of leaflets Sclerosis: normal pulse, normal apex, ejection murmur in aortic area, no radiation. Stenosis: slow rising pulse, powerful non-displaced apex, ejection murmur at apex, radiates to carotid

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24
Q

Major criteria for rheumatic fever

A

JONES Joint involvement <3 myocarditis Nodules Erythema marginatum Sydenham chorea

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25
Q

Minor criteria for rheumatic fever

A

CAFE PAL CRP increase Arthralgia Fever ESR Elevated Prolonged PR interval An amnesia of Rheumatism Leukocytosis

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26
Q

Features of MS

A

Malar flush AF- all will be Anticoagulated JVP not raised until late Apex beat not displaced Apex beat tapping - feel valve snapping just before s1 CXR- prominent LA appendage- dilation of atrium due to pressure overload

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27
Q

MS treatment

A

Mild: medical (Anticoagulants, Diuretics, rate control in AF) Moderate: ?transseptal valvuloplasty/ replacement Severe (area from 5cm-1.5cm^2) with >5mm gradient- valve replacement

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28
Q

Signs of AR

A

Collapsing pulse (corrigan’s pulse) Collapsing pulse in neck (corrigans sign) JVP not raised Apex beat displaced Diastolic murmur follows second sound

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29
Q

Causes of AR

A

REALM Rheumatic heart disease Endocarditis Ankylosing spondylitis Luetic heart disease Marfans

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30
Q

AR management

A

Valve replacement if significant regurge

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31
Q

Three diagnostic features of ACS

A

Cardiac chest pain Tropoin positive ECG changes

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32
Q

ECG changes in ACS

A

T wave inversion ST depression ST elevation Q waves New LBBB

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33
Q

3 features of cardiac chest pain

A

-central, retrosternal, band-like constriction -non-pleuritic (not sharp or worse on breathing in) -radiation to neck/jaw/shoulder/arm

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34
Q

Suspect ACS if pain:

A

Last more than 15 mins Occurs at rest (unstable angina) Increasing in frequency (crescendo) Severe Associated with nausea, vomiting, sweating Non-resolving with nitrates

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35
Q

Independent risk factors for ACS

A

Smoking HTN Diabetes Hyperlipodaemia Family Hx CKD (HTN)

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36
Q

Investigations in ACS, and why?

A
  • FBC- Anaemia can cause Ischaemia -U&Es- impaired renal function can cause false positive elevation in creatinine, baseline required for ACEi -electrolytes- hypokalaemia and hyperkalaemia- arrhythmia -glucose- ?diabetes, aim for 4-11mmol -LFTs- baseline prior to statins, hepatic impairment is a relative contraindication to ticagrelor -lipids -serial troponins -ECG-duh
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37
Q

Medication to start after discharge for MI

A

ABCDE A-ACEi B- beta blocker C- cholesterol lowering - atorvostatin 80mg D- dual antiplatelet- aspirin and clopidogrel E- echo to assess LVF

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38
Q

Complications of MI

A

DARTH VADER Death Arrhythmia Rupture (free ventricular wall/ ventricular septum/ papillary muscles) Tamponade Heart failure (acute or chronic) Valve disease Aneurysm of ventricle Dressler’s syndrome thromboEmbolism (mural thrombus) Recurrence/ mitral Regurgitation

39
Q

6 qualities of pericardial pain

A

2 qualities like pleurisy: sharp, worse on inspiration 2 qualities like angina: retrosternal, radiates to left shoulder 2 qualities of its own: worse on lying flat, eased by sitting up

40
Q

Acute LVF on inspection

A

Patient looks acutely unwell- pale and grey Cold clammy peripheries ?cyanosis Frothy, blood stained sputum Orthopnoeic using accessory muscles May have a wheeze, cardiac asthma

41
Q

Acute LVF on examination

A
  • sinus tacky or AF -systolic hypotension- cardiogenic shock -signs or cardiomegaly (displaced apex beat, signs of valve disease) -third and fourth heart sounds -right sided or bilateral pleural Effusion
42
Q

CXR features of Acute LVF

A

Cardiomegaly Upper lobe diversion Diffuse mottling of lung fields Prominent hilar shadows- bat wings Small pleural effusions Fluid in fissures

43
Q

Acute LVF investigations

A

FBC- exclude anaemia as contributory cause U&Es- monitor use of Diuretics Glucose- diabetes BNP- raise confirms diagnosis ABG- hypoxaemia and acute respiratory Acidosis Troponin- evidence of infarction ECG- arrhythmia, heart block, Ischaemia, ventricular hypertrophy Echo- within 48hrs for evidence of reduced LV ejection fraction and valvular Disease

44
Q

Causes of acute LVF

A

CHAMP Coronary syndrome Hypertensive emergency Arrhythmia Mechanical- acute valve leak, VSD, LV Aneurysm Pulmonary Embolism

45
Q

Acute LVF management

A

-sit up and give 15 l/minute O2 through non-rebreathe -IV Diuretics e.g. furosemide 40mg -IV vasodilators if systolic > 90mm (GTN/ isosorbide infusion) -consider inotropes e.g. donuts mine if systolic <90mm -Consider ITU if not improving or developing acute respiratory Acidosis -IV opiates if chest pain or distress

46
Q

ECG changes in hyperkalaemia

A

Low flat P waves Broad bizzare qrs Slurring into the ST Tall tented T waves

47
Q

Indications for a permanent pacemaker

A
  • sinoatrial Disease- sick sinus syndrome, tachybrady syndrome -AV nodal Disease- symptomatic 2 and 3 heart block -AF with a slow ventricular rate, or refractory fast AF treated with AV nodal ablation - cardiac resynchronisation therapy for heart failure
48
Q

Complications of pacemaker insertion

A
  • pulse generator- haematoma, infection, skin erosion, device failure -venous access- pneumothorax, air embolus - leads- lead displacement/fracture, venous thrombosis, endocarditis, cardiac perforation
49
Q

NYHA grading of heart failure

A

class I no limitation of physical activity ordinary physical activity does not cause fatigue, breathlessness or palpitation (includes asymptomatic left ventricular dysfunction) class II slight limitation of physical activity patients are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, breathlessness or angina pectoris (symptomatically ‘mild’ heart failure) class III marked limitation of physical activity although patients are comfortable at rest, less than ordinary activity will lead to symptoms (symptomatically ‘moderate’ heart failure) class IV inability to carry out any physical activity without discomfort symptoms of congestive cardiac failure are present even at rest. Increased discomfort with any physical activity (symptomatically ‘severe’ heart failure)

50
Q

Features of machanical valves

A

Noisy- can be heard from the end of the bed Ball and cage/ bi leaflet Require long term anticoagulation- avoid in women of childbearing age and elderly Early mortality- Aortic 5%, mitral 8%

51
Q

Features of bioprosthetic valves

A

Porcine valves are quiet, last 10-15 years Low rate of thromboembolism- no need for anticoagulation if in sinus If it fails, it fails suddenly with acute sever pulmonary oedema and cardiogenic shock Avoid anticoagulation- child bearing, elderly, peptic Ulcer

52
Q

Complications of valve replacement

A

POSH Valve Paravalvular leak- loosening of stent Obstruction-thrombus Subacute bacterial endocarditis Haemolysis due to turbulence Valve failure- rupturing com issuers with regurgitation, or calcification with stenosis

53
Q

Investigations in suspected infective endocarditis

A

FBC- raised WCC Raised ESR and CRP- acute phase response Urine dip and microscopy- microscopic haematuria 3 sets of blood cultures TTE +/- TOE

54
Q

IE management

A

-organism- strep viridans, staph, enterococci Strep- penicillin and gentamicin IV for >2weeks Oral antibiotics for a month Longer duration if non-strep, prosthetic valve or local complications (Abscess or fistula)

55
Q

Modified duke criteria

A

Major criteria- 2 +ve blood cultures, +ve echo, new valve regurgitation Minor- predisposing factors, fever, vascular lesions, single blood culture, immunological manifestations (osler, Roth, Glomerulonephritis) Definite= 2 major + 1 minor/ 1 major + 3 minor

56
Q

Two approaches to angina management

A
  • increase blood flow acutely - GTN -decrease workload of the heart- beta blocker/ CCB
57
Q

Second line anti anginals

A

If beta blocker/ CCB not tolerated Long acting nitrate Nicorandil Ivanradine Ranolazine

58
Q

Recommended fasting TC and LDL ranges in secondary prevention

A

TC <4 mmol/L LDL <2 mmol/L

59
Q

Causes of gradually worsening dyspnoea

A

COPD fibrotic lung disease Cancer Pleural Effusion Multiple PE Anaemia

60
Q

Causes of heart failure

A

IHD HTN Cardiomyopathy Ess. Valvular heart disease High output- Anaemia, Pagets Arrhythmia

61
Q

NYHA classification of heart failure

A

1- normal 2- moderate exertion 3- minimal exertion 4- at rest

62
Q

Which drugs improve prognosis in HF

A

ACEi Beta blockers Aldosterone antagonist Diuretics and digoxin are symptomatic relief rather than prognosis

63
Q

HF first line management

A

ACEi beta blocker

64
Q

Second line HF management

A

ARB Aldosterone antagonist Hydralazine, nitrate Diuretics for congestion and fluid retention at any stage

65
Q

Criteria for cardiac resynchronisation therapy

A

NYHA III-IV, symptoms on optimal medical management, EF<35%, QRS>150ms

66
Q

Hypertension stages

A

Normal <120/80 Pre-HTN 120-139/80-89 Stage 1 clinic >140/90 HBPM >135/85 Stage 2 clinic >160/100 HBPM >150/95 Stage 3 clinic >180/110

67
Q

Criteria for LVH on ECG

A

Tall R waves in V5-6 (>25mm/ combined S+R>35mm), deep S wave in V1-2 May also get t wave inversion in lateral leads Left axis deviation

68
Q

What’s the significance of LVH in HTN?

A

Indicates end-organ damage, indication for antihypertensive therapy, even in phase 1 HTN

69
Q

Grading of Hypertensive retinopathy

A

I- tortuous retinal arteries, with thick shiny walls II- AV nipping III- flame haemorrhages and cotton wool spots IV- papilloedema

70
Q

Causes of secondary HTN

A

Renal/ renovascular disease- Renal artery stenosis, glomerulonephritis Endocrine- Cushing’s, conns, phaeochromocytoma, acromegaly Medications- COP, steroids Coarctation of the aorta Pregnancy

71
Q

Electrolyte Abnormalities caused by thiazides

A

Hyponatraemia Hypokalaemia Hyperuracemia Hypercalcaemia- decreased urinary calcium excretion Hyperglycaemia

72
Q

Complications of HTN

A

Stroke CVD HF PVD Renal failure Retinopathy

73
Q

Rate control of AF

A

Beta blockers Calcium channel blockers - verapamil Digoxin

74
Q

Types of AF

A

Paroxysmal- rhythm control Permanent- rate control Persistent- management varies

75
Q

Rhythm control in AF

A

Beta blockers Class 1 anti arrhythmics Class 3 anti arrhythmics

76
Q

Causes of AF

A

Cardiac Heart failure Heart ischaemia (MI) Hypertension (Mitral) valve disease Congenital heart disease (rare) Pulmonary PE Pneumonia Bronchocarcinoma Other Hyperthyroidism (fast AF) – Sometimes hypothyroidism can also cause slow AF Alcohol Post-operatively Sepsis High caffeine intake Antiarrhythmic drugs! ↓K+ ↑Mg2+

77
Q

Management of acute AF

A

This is AF <48h hours duration. patients will usually be younger and are more likely to have an identifiable cause. Treat the underlying condition (e.g. MI, pneumonia). Control the ventricular rate (see below) Initiate anticoagulation – with heparin (5000-10000U IV). This prevents thrombus formation – and thrombi are a contraindication for cardioversion. If anticoagulants are contra-indicated, then do a TOE (trans-oesophageal ultrasound) before mechanical cardioversion to rule out the presence of a thrombus. Consider DC or drug cardioversion (see below) Acutely ill patient – DC cardioversion – Don’t delay treatment to give anticoagulants! Cardioversion should be performed in an ITU setting, with sedation. The patient should be shocked at 200J initially. if this is unsuccessful, try two further attempts at 360J.

78
Q

Control of chronic AF

A

Control the ventricular rate Rate control is as good as rhythm control in chronic AF – i.e. generally you don’t need to cardiovert – as the outcomes are the same as if the rate only is well controlled. Exceptions include:Young patients, 1st episode of AF 1st line – β-blocker OR Ca2+ blocker using both together is contraindicated as it can cause heart block 2nd line – same as above, but add digoxin, or amiodarone. Digoxin as the sole treatment for AF is not widely acceptable – may be suitable for some very sedentary elderly patients. Don’t give β-blockers with verapamil or diltiazem (L- type calcium channel blockers) as there is a risk of bradycardia Anticoagulate – with warfarin (INR 2-3) – long term therapy Aspirin is an inferior alternative, but may be acceptable in low risk patients (See CHADS2 score below). Usually only used if warfarin is contraindicated, or in very low risk patients (CHADS ≤1) Check platelets and blood count, and be wary in patients with past bleeds, low Hb, high risk of falls, and on NSAID therapy.

79
Q

Management for paroxysmal AF

A

This is a condition where short spells of AF come and go, and upon investigation, the patient may often be in sinus rhythm. Use the ‘pill in the pocket’ treatment – i.e. flecainide or sotalol PRN – these drugs control the rhythm. Only suitable if systolic BP >100, and no underlying LV dysfunction 1st line – Sotolol / bisoprolol (β-blockers) Young patients – flecainide / verapamil – 1st line in younger patients, but avoided in older ones, as they are negatively ionotropic – i.e. they cause vasodilation. 2nd line – amiodarone – tends to be used in those with some LV dysfunction 3rd line – digoxin – has a weak effect, and takes several weeks to become effective, but useful in those with severe LV dysfunction, as it is positively ionotropic. Anticoagulate (as for chronic AF)

80
Q

Chronic AF Cardioversion

A

Patient has had >3 weeks of anticoagulant therapy TOE has proven no thrombus Unlikely if AF has been apparent for >12 months, although if it is a first attempt at cardioversion, many consultants may still ‘give it a go’ LV dilation is a good predictor of outcome. Those with a LV of diameter >5.5cm are unlikely to have a successful cardioversion – although, again, some consultants may still try. If the patient is on digoxin, make sure you stop the digoxin a few days before the treatment.

81
Q

DC Cardioversion in AF

A

Should be done in an ITU or CCU setting Give O2 Give sedation Give monophasic DC cardioversion, increasing the voltage if normal rhythm is not obtained: 100J (not commonly used, only effective in 20% of patients) 200J 360J (two attempts) DC cardioversion has a success rate of about 70% The procedure The defibrillator needs to be in ‘sync mode’ as the shock has to be delivered at a certain point in the cycle – the R wave. If you give the shock at the T wave, you risk causing VF. Thus, in practice, make sure you hold down the shock button until the shock is delivered. Perform a full 12-lead ECG afterwards to check whether the procedure was successful. After cardioversion continue with all the pre-cardioversion medications. Review at 3 months. Most patients who relapse do so within the first month. If still in sinus rhythm at 3 months, then you can begin to think about stopping some of the drug treatments.

82
Q

Drug Cardioversion in AF

A

Amiodarone is usually the drug of choice. Can be given: IV – 5mg/Kg in 1 hr, then a further 900mg up to 1.2g in a 24hr period PO –200mg/8hr for 1 week, then 200mg/12hr for 1 week, then 200mg/day maintenance. Flecainide may also used, but it is negatively ionotropic (reduces the strength of contractions). Used in patients with no known IHD or WPW syndrome.

83
Q

What’s the risk stratification score used in AF?

A

the risk of thrombo-embolic stroke, and thus the degree of anticoagulant therapy required in atrial fibrillation can be assessed using the CHA2DS2-VASc score. Any score above 2 requires anticoagulation: Description Score C Congestive heart failure / LV dysfunction 1 H Hypertension 1 A2 Age ≥75 2 D Diabetes 1 S2 Stroke (previous stroke, TIA or thromboembolic disease) 2 V Vascular disease (e.g. peripheral vascular disease, ischaemic heart disease, previous MI) 1 A Age 65-74 1 Sc Sex (female) 1 Results: Score <2 – low risk – no specific anticoagulation Score ≥ 2 – high risk warfarin (target INR 2-3)

84
Q

When discontinue Anticoagulants in AF?

A

Sinus rhythm No RF’s for emboli (CHADS = 0) AF recurrence unlikely (e.g. no previous failed cardioversions, no structural heart disease, AF duration <12 months)

85
Q

HAS-BLED score

A

Hypertension (Systolic >= 160mmHg) 1 Abnormal renal function 1 Abnormal liver function 1 Age >= 65 years 1 Stroke in past 1 Bleeding 1 Labile INRs 1 Taking other drugs as well 1 Alcohol intake at same time 1 score of 3 or more indicates increased one year bleed risk on anticoagulation sufficient to justify caution or more regular review

86
Q

Differentials in acute chest pain

A

MI/ACS Angina PE Aortic dissection GORD Pericarditis MSK

87
Q

Post MI ECG changes

A

T-wave inversion - 24hrs Pathological Q waves- within days. Don’t occur with subendocardial MI

88
Q

Indications for Thrombosis is in MI

A

definite clinical diagnosis of acute myocardial infarction short interval since the onset of symptoms: normally 12 hr treat up to 24 hr if ST elevation is persisting and the infarct is large ECG signs: regional ST elevation of >2 mm in chest leads and >1 mm in limb leads regional ST depression in cases of posterior infarction left bundle branch block no contraindications to thrombolysis present

89
Q

Contraindications to Thrombolysis is in MI

A

Prior intracranial hemorrhage (ICH) Known structural cerebral vascular lesion Known malignant intracranial neoplasm Ischemic stroke within 3 months Suspected aortic dissection Active bleeding or bleeding diathesis (excluding menses) Significant closed head trauma or facial trauma within 3 months Intracranial or intraspinal surgery within 2 months Severe uncontrolled hypertension (unresponsive to emergency therapy) For streptokinase, prior treatment within the previous 6 months

90
Q

Reversible causes of cardiac arrest

A

4Hs and 4Ts: hypoxia hypovolaemia hyperkalaemia, hypokalaemia, other electrolyte disturbances hypothermia tension pneumothorax cardiac tamponade drug toxicity and therapeutics thromboembolism and other outflow obstructions

91
Q

Hypersensitivity reactions

A

ACID Allergic- anaphylaxis cytotoxic - goodpastures Immune complex deposition - PAN Delayed- Steven johnson’s

92
Q

Rheumatic fever criteria

A

J – Joint involvement which is usually migratory and inflammatory joint involvement that starts in the lower joints and ascends to upper joints O – (“O” Looks like heart shape) – indicating that patients can develop myocarditis or inflammation of the heart N – Nodules that are subcutaneous E – Erythema marginatum which is a rash of ring-like lesions that can start in the trunk or arms. When joined with other rings, it can create a snake-like appearance S – Sydenham chorea is a late feature which is characterized by jerky, uncontrollable, and purposeless movements resembling twitches

93
Q

Radiation of murmurs

A

AS- carotid AR- lean forward held breath MS- LL apex bell MR- axilla sat normally diaphragm

94
Q

Pathological q wave criteria

A

>1 ss wide >1/3 of the r wave

Ask Doctor Clarke 2018 (12 decks)

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