Cardiology Flashcards
1
Q
Three main causes of AF
A
Ischaemic Heart Disease Rheumatoid heart disease Thyrotoxicosis
2
Q
What causes the 4th heart sound?
A
-atrial contraction on a non-compliant or hypertrophied ventricle -low pitched -always abnormal
3
Q
4 conditions where a 4th heart sound may be present
A
Heart failure MI Cardiomyopathy Hypertension
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)
5
Q
By how much does CO decrease in AF?
A
25% as the atria contribute that amount to the LV volume
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
7
Q
4(+2) causes of a third heart sound
A
-heart failure -MI -Cardiomyopathy -hypertension -mitral and aortic regurgitation -constrictive pericarditis
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
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
10
Q
Two main causes for an irregularly irregular pulse?
A
AF and multiple ventricular ectopic- ectopics disappear on exercise as diastole shortens
11
Q
How do you assess if AF is well controlled?
A
HR<80bpm
12
Q
What is the goal INR in AF?
A
2-3
13
Q
What’s the goal INR in mitral valve replacement? Aortic?
A
Mitral- 3-4 Aortic- 2-3
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
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)
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
17
Q
Causes of aortic stenosis
A
-degenerative calcification aortic stenosis -congenitally bicuspid valve with degenerative changes -rheumatic heart disease
18
Q
Causes of LV pressure overload
A
Hypertension AS Coarctation of the aorta HYpertrophic Cardiomyopathy with LV outflow Tract Obstruction (subvalvar stenosis)
19
Q
AS treatment
A
Symptoms are a good guide to severity- SAD- Syncope, Angina, Dyspnoea Valve replacement is definitive TAVI
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
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
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
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
24
Q
Major criteria for rheumatic fever
A
JONES Joint involvement <3 myocarditis Nodules Erythema marginatum Sydenham chorea
25
Minor criteria for rheumatic fever
CAFE PAL CRP increase Arthralgia Fever ESR Elevated Prolonged PR interval An amnesia of Rheumatism Leukocytosis
26
Features of MS
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
27
MS treatment
Mild: medical (Anticoagulants, Diuretics, rate control in AF) Moderate: ?transseptal valvuloplasty/ replacement Severe (area from 5cm-1.5cm^2) with \>5mm gradient- valve replacement
28
Signs of AR
Collapsing pulse (corrigan’s pulse) Collapsing pulse in neck (corrigans sign) JVP not raised Apex beat displaced Diastolic murmur follows second sound
29
Causes of AR
REALM Rheumatic heart disease Endocarditis Ankylosing spondylitis Luetic heart disease Marfans
30
AR management
Valve replacement if significant regurge
31
Three diagnostic features of ACS
Cardiac chest pain Tropoin positive ECG changes
32
ECG changes in ACS
T wave inversion ST depression ST elevation Q waves New LBBB
33
3 features of cardiac chest pain
-central, retrosternal, band-like constriction -non-pleuritic (not sharp or worse on breathing in) -radiation to neck/jaw/shoulder/arm
34
Suspect ACS if pain:
Last more than 15 mins Occurs at rest (unstable angina) Increasing in frequency (crescendo) Severe Associated with nausea, vomiting, sweating Non-resolving with nitrates
35
Independent risk factors for ACS
Smoking HTN Diabetes Hyperlipodaemia Family Hx CKD (HTN)
36
Investigations in ACS, and why?
- 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
37
Medication to start after discharge for MI
ABCDE A-ACEi B- beta blocker C- cholesterol lowering - atorvostatin 80mg D- dual antiplatelet- aspirin and clopidogrel E- echo to assess LVF
38
Complications of MI
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
6 qualities of pericardial pain
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
Acute LVF on inspection
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
Acute LVF on examination
- 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
CXR features of Acute LVF
Cardiomegaly Upper lobe diversion Diffuse mottling of lung fields Prominent hilar shadows- bat wings Small pleural effusions Fluid in fissures
43
Acute LVF investigations
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
Causes of acute LVF
CHAMP Coronary syndrome Hypertensive emergency Arrhythmia Mechanical- acute valve leak, VSD, LV Aneurysm Pulmonary Embolism
45
Acute LVF management
-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
ECG changes in hyperkalaemia
Low flat P waves Broad bizzare qrs Slurring into the ST Tall tented T waves
47
Indications for a permanent pacemaker
- 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
Complications of pacemaker insertion
- pulse generator- haematoma, infection, skin erosion, device failure -venous access- pneumothorax, air embolus - leads- lead displacement/fracture, venous thrombosis, endocarditis, cardiac perforation
49
NYHA grading of heart failure
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
Features of machanical valves
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
Features of bioprosthetic valves
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
Complications of valve replacement
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
Investigations in suspected infective endocarditis
FBC- raised WCC Raised ESR and CRP- acute phase response Urine dip and microscopy- microscopic haematuria 3 sets of blood cultures TTE +/- TOE
54
IE management
-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
Modified duke criteria
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
Two approaches to angina management
- increase blood flow acutely - GTN -decrease workload of the heart- beta blocker/ CCB
57
Second line anti anginals
If beta blocker/ CCB not tolerated Long acting nitrate Nicorandil Ivanradine Ranolazine
58
Recommended fasting TC and LDL ranges in secondary prevention
TC \<4 mmol/L LDL \<2 mmol/L
59
Causes of gradually worsening dyspnoea
COPD fibrotic lung disease Cancer Pleural Effusion Multiple PE Anaemia
60
Causes of heart failure
IHD HTN Cardiomyopathy Ess. Valvular heart disease High output- Anaemia, Pagets Arrhythmia
61
NYHA classification of heart failure
1- normal 2- moderate exertion 3- minimal exertion 4- at rest
62
Which drugs improve prognosis in HF
ACEi Beta blockers Aldosterone antagonist Diuretics and digoxin are symptomatic relief rather than prognosis
63
HF first line management
ACEi beta blocker
64
Second line HF management
ARB Aldosterone antagonist Hydralazine, nitrate Diuretics for congestion and fluid retention at any stage
65
Criteria for cardiac resynchronisation therapy
NYHA III-IV, symptoms on optimal medical management, EF\<35%, QRS\>150ms
66
Hypertension stages
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
Criteria for LVH on ECG
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
What’s the significance of LVH in HTN?
Indicates end-organ damage, indication for antihypertensive therapy, even in phase 1 HTN
69
Grading of Hypertensive retinopathy
I- tortuous retinal arteries, with thick shiny walls II- AV nipping III- flame haemorrhages and cotton wool spots IV- papilloedema
70
Causes of secondary HTN
Renal/ renovascular disease- Renal artery stenosis, glomerulonephritis Endocrine- Cushing’s, conns, phaeochromocytoma, acromegaly Medications- COP, steroids Coarctation of the aorta Pregnancy
71
Electrolyte Abnormalities caused by thiazides
Hyponatraemia Hypokalaemia Hyperuracemia Hypercalcaemia- decreased urinary calcium excretion Hyperglycaemia
72
Complications of HTN
Stroke CVD HF PVD Renal failure Retinopathy
73
Rate control of AF
Beta blockers Calcium channel blockers - verapamil Digoxin
74
Types of AF
Paroxysmal- rhythm control Permanent- rate control Persistent- management varies
75
Rhythm control in AF
Beta blockers Class 1 anti arrhythmics Class 3 anti arrhythmics
76
Causes of AF
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
Management of acute AF
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
Control of chronic AF
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
Management for paroxysmal AF
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
Chronic AF Cardioversion
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
DC Cardioversion in AF
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
Drug Cardioversion in AF
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
What’s the risk stratification score used in AF?
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
When discontinue Anticoagulants in AF?
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
HAS-BLED score
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
Differentials in acute chest pain
MI/ACS Angina PE Aortic dissection GORD Pericarditis MSK
87
Post MI ECG changes
T-wave inversion - 24hrs Pathological Q waves- within days. Don’t occur with subendocardial MI
88
Indications for Thrombosis is in MI
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
Contraindications to Thrombolysis is in MI
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
Reversible causes of cardiac arrest
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
Hypersensitivity reactions
ACID Allergic- anaphylaxis cytotoxic - goodpastures Immune complex deposition - PAN Delayed- Steven johnson’s
92
Rheumatic fever criteria
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
Radiation of murmurs
AS- carotid AR- lean forward held breath MS- LL apex bell MR- axilla sat normally diaphragm
94
Pathological q wave criteria
\>1 ss wide \>1/3 of the r wave
