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Year 3 OSCE > Miscellaneous Cardiology > Flashcards

Miscellaneous Cardiology Flashcards

1
Q

Right to left shunt

A

Blood flows from right side of heart (deoxygenated) into the left sided of the heart without passing through lungs to pick up oxygen (cyanosis).

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2
Q

Causes of a right to left shunt (cyanosis heart disease)

A

VSD
ASD
Patent ductus arteriosus
Transposition of the great arteries

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3
Q

Why are people with ASD VSD PDA usually not cyanotic?

A

Left sided heart pressure greater than right, so prevents the shunt

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4
Q

Eisenmenger syndrome

A

When pulmonary pressure (hypertension) is greater than systemic pressure so blood flows from the right to left shunt causing cyanosis

NB- treated by heart-lung transplant

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5
Q

Complications of congenital heart disease

A

Heart failure
Arrhythmias
Endocarditis
Stroke
PE
Eisenmenger syndrome

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6
Q

Adult presentation of septal defects

A

Dyspnoea (pulmonary HTN, right sided heart failure)
Stroke (due to VTE)
AF

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7
Q

What is coarctation if aorta associated with

A

Turners syndrome

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8
Q

Conditions associated with VSD

A

Down’s syndrome
Turners syndrome

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9
Q

Adults signs of coarctation of the aorta

A

HTN
Murmur
Underdeveloped left arm
Underdeveloped left leg

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10
Q

Features of TOF

A

Cyanosis
Right to left shunt
Murmur
Right sided aortic arch
Boot shaped heart

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11
Q

Management of TOF

A

Surgical repair in 2 parts
Cyanotic episodes (Tet spells) helped by beta blockers

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12
Q

Most common cyanotic heart disease

A

At birth- transposition of the great arteries
Overall (1-2 months)- TOF

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13
Q

What is ebsteins anomaly

A

Low insertion of tricuspid valve- large atrium and small ventricle (atrialisation of the right ventricle)

Can be caused by lithium in utero

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14
Q

Associations of ebsteins anomaly

A

PFO or ASD
WPW syndrome

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15
Q

Clinical features of Ebsteins anomaly

A

Cyanosis
Prominent a wave in JVP
Hepatomegaly
Tricuspid regurgitation
RBBB

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16
Q

Pathophysiology of HOCM

A

Autosomal dominant
Defects in myosin genes
Diastolic dysfunction
Myofibrilar hypetrophy with chaotic myocytes (disarray) and fibrosis on biopsy

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17
Q

Features of HOCM

A

Often asymptomatic
Exertional dyspnoea
Syncope following exercise
Sudden death (ventricular arrhythmia)
Jerky pulse, large a waves
Systolic murmur
Bisferens pulse (2 S1 waves)

NB- can develop into Heart failure with preserved ejection fraction (HF-pEF)

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18
Q

HOCM associations

A

Friedrichs ataxia (neuro degenerative movement disorder)
WPW syndrome

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19
Q

HOCM Findings

A

Echo- LVH, MR

ECG- LVH, AF, deep Q waves, non specific ST segment and T wave abnormalities

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20
Q

What is Takotsubo cardiomyopathy

A

Non ischaemic cardiomyopathy associated with transient, apical ballooning of myocardium, associated with stress

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21
Q

Features of Takotsubo cardiomyopathy

A

Chest pain
Heart failure
ST elevation
Normal coronary angiogram

NB- treatment is supportive

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22
Q

Dilated cardiomyopathy

A

Most common type
Systolic dysfunction
Eccentric hypertrophy

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23
Q

Causes of dilated cardiomyopathy

A

Idiopathic (most common)
Myocarditis (cockasackiem Chaga)
IHD
Peripartum
HTN
Iatrogenic (doxorubicin)
Substance misuse eg. Alcohol and cocaine
Genetics eg. DMD
Infiltrative eg. Haemachromatosis or sarcoidosis
Wet beriberi (thiamine deficiency)

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24
Q

Features of dilated cardiomyopathy

A

Heart failure
Murmur
S3
Balloon appearance of heart on CXR

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25
Q

Restrictive cardiomyopathy

A

Amyloidosis
Post radiotherapy
Loefflers endocarditis
Beriberi

26
Q

HOCM Management

A

ABCDE
Amiodarone
Beta blocker or verapamil for Sx
Cardiovertee defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis (not always)

Avoid- nitrates, ACE-I, inotropes

27
Q

INR target range for mechanical valves

A

2.5-3.5

28
Q

Complications of mechanical heart valves

A

Thrombus
Infective endocarditis (staphylococcus)
Haemolysis (anaemia)

29
Q

Indications for a pacemaker

A

Symptomatic bradycardia
Mobitz type 2 AV block
Third degree heart block
Severe heart failure
HOCM (ICD)

30
Q

ECG with a pacemaker

A

Sharp vertical line before all leads on the trace

31
Q

Sing,e chamber

A

A line before either the P or the QRS complex

32
Q

Dual chamber pacemaker

A

A line before either the P or the QRS

33
Q

Target INR for AF

A

2-3

34
Q

Reversing warfarin

A

Vitamin K and PCC

35
Q

Reversing NOACs

A

Apixaban/rivaroxaban- andexanet alpha
Dabigatran- idarucizumab

36
Q

Outcome of chadvasc score

A

0- no anticoagulation
1- consider anticoagulation
2- offer anticoagulation

37
Q

Tests before starting amiodarone

A

TFT LFT UE CXR

38
Q

Arrhythmogenic right ventricular cardiomyopathy

A

a form of inherited cardiovascular disease which may present with syncope or sudden cardiac death.

39
Q

Investigations for ARVC

A

ECG abnormalities in V1-3, typically T wave inversion. An epsilon wave is found in about 50% of those with ARV - this is best described as a terminal notch in the QRS complex
echo changes are often subtle in the early stages but may show an enlarged, hypokinetic right ventricle with a thin free wall
magnetic resonance imaging is useful to show fibrofatty tissue

40
Q

Management of ARVC

A

drugs: sotalol is the most widely used antiarrhythmic
catheter ablation to prevent ventricular tachycardia
implantable cardioverter-defibrillator

41
Q

Amiodarone

A

Uses- ALS and VTach

MOA- blocking potassium channels

SE’s- hypo and hyperthyroid, fibrosis (lung and liver), neuropathy, grey skin, increased QT interval

42
Q

Adenosine

A

Uses- SVT

MOA- causes transient heart block in the AV node, and is an agonist of the A1 receptor in the atrioventricular node

SE’s- avoid in asthmatics, chest pain, bronchospasm
transient flushing (sense of heart stop & impending doom), can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

43
Q

Atropine

A

Bradycardia

SE’s- anticholinergic

44
Q

Causes of acyanotic heart disease

A

VSD (more common)
ASD (most common new diagnosis in adults- present later)
PDA
Coarctation of aorta
Aortic valve stenosis

45
Q

Causes of cyanotic heart disease

A

Teratology of Fallot
Transposition of the great arteries (TGA)
Tricuspid atresia

46
Q

Characteristics of Teratology of Fallot

A

VSD
RVH
RV outflow tract obstruction, pulmonary stenosis
Overriding aorta

47
Q

Features of teratology of Fallot

A

Most common cause of congenital cyanotic heart disease, although as it presents at 1-2 months, TGA is more common at birth

Cyanosis
Right to left shunt
Systolic murmur
Right sided aortic arch (25% patients)
Boot shaped heart X ray, ECG- RVH

Surgical repair (2 parts, beta blockers)

48
Q

Causes of an S3 heart sound

A

caused by diastolic filling of the ventricle
considered normal if < 30 years old (may persist in women up to 50 years old)
heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

49
Q

Constrictive pericarditis

A

Causes- recent cardiac surgery, any cause of pericarditis, particularly TB

Features;

dyspnoea
right heart failure: elevated JVP, ascites, oedema, hepatomegaly
JVP shows prominent x and y descent
pericardial knock - loud S3
Kussmaul’s sign is positive (a paradoxical rise in JVP during inspiration)

NB- pericardial calcification on CXR

50
Q

Constrictive pericarditis vs cardiac tamponade

A

JVP: tamponade, only X (tamponade tampaX), pericarditis, X & Y

Pulsus parodoxus (fall in BP >10 during inspiration): tamponade, present, pericarditis, absent

Kussmaul’s sign: tamponade, rare, pericarditis, present

CXR calcification- constrictive pericarditis

51
Q

ECG Normal Variants

A

Normal variants on the ECG:
-Sinus arrhythmia
-Right axis deviation (tall and thin individuals)
-Left axis deviation (short, obese individuals)
-Partial right bundle branch block

Athletes often have a high vagal tone which results in additional normal variants:
-Sinus bradycardia
-1st degree atrioventricular block
-Wenckebach phenomenon (2nd degree atrioventricular block Mobitz type 1)
-Junctional escape rhythm

NB- LBBB is never a normal variant

52
Q

Heart failure with preserved ejection fraction (HF-pEF)

A

No systolic (outflow) problem, but a diastolic (backlog) problem

53
Q

Heart failure with reduced ejection fraction (HF-pEF)

A

Both diastolic and systolic dysfunction

54
Q

Options for aortic valve replacement

A

surgical AVR is the treatment of choice for young, low/medium operative risk patients. Cardiovascular disease may coexist. For this reason, an angiogram is often done prior to surgery so that the procedures can be combined

transcatheter AVR (TAVR) is used for patients with a high operative risk

balloon valvuloplasty
may be used in children with no aortic valve calcification
in adults limited to patients with critical aortic stenosis who are not fit for valve replacement

55
Q

fusion and capture beats

A

unsure

56
Q

Miscellaneous cardiology

A

Cardiogenic Shock:
e.g. MI, valve abnormality

increased SVR (vasoconstriction in response to low BP)
increased HR (sympathetic response)
decreased cardiac output
decreased blood pressure

Hypovolaemic shock:
blood volume depletion
e.g. haemorrhage, vomiting, diarrhoea, dehydration, third-space losses during major operations

increased SVR
increased HR
decreased cardiac output
decreased blood pressure

Septic shock:
occurs when the peripheral vascular dilatation causes a fall in SVR
similar response may occur in anaphylactic shock, neurogenic shock

reduced SVR
increased HR
normal/increased cardiac output
decreased blood pressure

57
Q

Digoxin

A

used for rate control in the management of atrial fibrillation. As it has positive inotropic properties it is sometimes used for improving symptoms (but not mortality) in patients with heart failure

MOA;
decreases conduction through the atrioventricular node which slows the ventricular rate in atrial fibrillation and flutter
increases the force of cardiac muscle contraction due to inhibition of the Na+/K+ ATPase pump. Also stimulates vagus nerve

Monitoring;
digoxin level is not monitored routinely, except in suspected toxicity
if toxicity is suspected, digoxin concentrations should be measured within 8 to 12 hours of the last dose

58
Q

Digoxin Toxicity

A

Toxicity;
Toxicity may occur even when the concentration is within the therapeutic range.

Features;
generally unwell, lethargy, nausea & vomiting, anorexia, confusion, yellow-green vision
arrhythmias (e.g. AV block, bradycardia)
gynaecomastia

Precipitating factors
classically: hypokalaemia
digoxin normally binds to the ATPase pump on the same site as potassium. Hypokalaemia → digoxin more easily bind to the ATPase pump → increased inhibitory effects
increasing age
renal failure
myocardial ischaemia
hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
hypoalbuminaemia
hypothermia
hypothyroidism
drugs: amiodarone, quinidine, verapamil, diltiazem, spironolactone (competes for secretion in distal convoluted tubule therefore reduce excretion), ciclosporin. Also drugs which cause hypokalaemia e.g. thiazides and loop diuretics

Management;
Digibind
correct arrhythmias
monitor potassium

59
Q

AF and BBB

A

Atrial fibrillation with bundle branch block is the most likely cause of an irregular broad complex tachycardia in a stable patient

60
Q

Potential risk of asystole

A

The following are risk factors for asystole. Even if there is a satisfactory response to atropine specialist help is indicated to consider the need for transvenous pacing:

complete heart block with broad complex QRS
recent asystole
Mobitz type II AV block
ventricular pause > 3 seconds

61
Q

Shock

A

5 types

Cardiogenic
Hypovolaemic
Neurogenic
Anaphylactic
Septic

All cause hypotension and tachycardia, except neurogenic which causes hypotension and bradycardia

C/H shock cause increased SR

A/S shock cause decreased SR

Year 3 OSCE (61 decks)

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