Miscellaneous Cardiology Flashcards
Right to left shunt
Blood flows from right side of heart (deoxygenated) into the left sided of the heart without passing through lungs to pick up oxygen (cyanosis).
Causes of a right to left shunt (cyanosis heart disease)
VSD
ASD
Patent ductus arteriosus
Transposition of the great arteries
Why are people with ASD VSD PDA usually not cyanotic?
Left sided heart pressure greater than right, so prevents the shunt
Eisenmenger syndrome
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
Complications of congenital heart disease
Heart failure
Arrhythmias
Endocarditis
Stroke
PE
Eisenmenger syndrome
Adult presentation of septal defects
Dyspnoea (pulmonary HTN, right sided heart failure)
Stroke (due to VTE)
AF
What is coarctation if aorta associated with
Turners syndrome
Conditions associated with VSD
Down’s syndrome
Turners syndrome
Adults signs of coarctation of the aorta
HTN
Murmur
Underdeveloped left arm
Underdeveloped left leg
Features of TOF
Cyanosis
Right to left shunt
Murmur
Right sided aortic arch
Boot shaped heart
Management of TOF
Surgical repair in 2 parts
Cyanotic episodes (Tet spells) helped by beta blockers
Most common cyanotic heart disease
At birth- transposition of the great arteries
Overall (1-2 months)- TOF
What is ebsteins anomaly
Low insertion of tricuspid valve- large atrium and small ventricle (atrialisation of the right ventricle)
Can be caused by lithium in utero
Associations of ebsteins anomaly
PFO or ASD
WPW syndrome
Clinical features of Ebsteins anomaly
Cyanosis
Prominent a wave in JVP
Hepatomegaly
Tricuspid regurgitation
RBBB
Pathophysiology of HOCM
Autosomal dominant
Defects in myosin genes
Diastolic dysfunction
Myofibrilar hypetrophy with chaotic myocytes (disarray) and fibrosis on biopsy
Features of HOCM
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)
HOCM associations
Friedrichs ataxia (neuro degenerative movement disorder)
WPW syndrome
HOCM Findings
Echo- LVH, MR
ECG- LVH, AF, deep Q waves, non specific ST segment and T wave abnormalities
What is Takotsubo cardiomyopathy
Non ischaemic cardiomyopathy associated with transient, apical ballooning of myocardium, associated with stress
Features of Takotsubo cardiomyopathy
Chest pain
Heart failure
ST elevation
Normal coronary angiogram
NB- treatment is supportive
Dilated cardiomyopathy
Most common type
Systolic dysfunction
Eccentric hypertrophy
Causes of dilated cardiomyopathy
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)
Features of dilated cardiomyopathy
Heart failure
Murmur
S3
Balloon appearance of heart on CXR
Restrictive cardiomyopathy
Amyloidosis
Post radiotherapy
Loefflers endocarditis
Beriberi
HOCM Management
ABCDE
Amiodarone
Beta blocker or verapamil for Sx
Cardiovertee defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis (not always)
Avoid- nitrates, ACE-I, inotropes
INR target range for mechanical valves
2.5-3.5
Complications of mechanical heart valves
Thrombus
Infective endocarditis (staphylococcus)
Haemolysis (anaemia)
Indications for a pacemaker
Symptomatic bradycardia
Mobitz type 2 AV block
Third degree heart block
Severe heart failure
HOCM (ICD)
ECG with a pacemaker
Sharp vertical line before all leads on the trace
Sing,e chamber
A line before either the P or the QRS complex
Dual chamber pacemaker
A line before either the P or the QRS
Target INR for AF
2-3
Reversing warfarin
Vitamin K and PCC
Reversing NOACs
Apixaban/rivaroxaban- andexanet alpha
Dabigatran- idarucizumab
Outcome of chadvasc score
0- no anticoagulation
1- consider anticoagulation
2- offer anticoagulation
Tests before starting amiodarone
TFT LFT UE CXR
Arrhythmogenic right ventricular cardiomyopathy
a form of inherited cardiovascular disease which may present with syncope or sudden cardiac death.
Investigations for ARVC
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
Management of ARVC
drugs: sotalol is the most widely used antiarrhythmic
catheter ablation to prevent ventricular tachycardia
implantable cardioverter-defibrillator
Amiodarone
Uses- ALS and VTach
MOA- blocking potassium channels
SE’s- hypo and hyperthyroid, fibrosis (lung and liver), neuropathy, grey skin, increased QT interval
Adenosine
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)
Atropine
Bradycardia
SE’s- anticholinergic
Causes of acyanotic heart disease
VSD (more common)
ASD (most common new diagnosis in adults- present later)
PDA
Coarctation of aorta
Aortic valve stenosis
Causes of cyanotic heart disease
Teratology of Fallot
Transposition of the great arteries (TGA)
Tricuspid atresia
Characteristics of Teratology of Fallot
VSD
RVH
RV outflow tract obstruction, pulmonary stenosis
Overriding aorta
Features of teratology of Fallot
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)
Causes of an S3 heart sound
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
Constrictive pericarditis
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
Constrictive pericarditis vs cardiac tamponade
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
ECG Normal Variants
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
Heart failure with preserved ejection fraction (HF-pEF)
No systolic (outflow) problem, but a diastolic (backlog) problem
Heart failure with reduced ejection fraction (HF-pEF)
Both diastolic and systolic dysfunction
Options for aortic valve replacement
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
fusion and capture beats
unsure
Miscellaneous cardiology
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
Digoxin
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
Digoxin Toxicity
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
AF and BBB
Atrial fibrillation with bundle branch block is the most likely cause of an irregular broad complex tachycardia in a stable patient
Potential risk of asystole
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
Shock
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
