Cardiology Flashcards
Essential hypertension
95% of HTN cases
A combination of environmental and genetic factors that result in a hypertensive phenotype
Secondary hypertension
Caused by an identifiable cause (usually endocrine), e.g. coarctation, Conn’s syndrome**, etc.
Clinical features of hypertension
Asymptomatic till end organ damage
Malignant hypertension
Uncontrolled HTN
Retinal changes
Progressive renal failure
Hypertension end-organ damage
CVD - Thrombotic and haemorrhagic stroke
Vascular disease
LVH - Compensatory response to chronically elevated BP
Renal failure - Renovascular damage/glomerular loss
What is isolated systolic HTN?
Common in the elderly (above 70 y.o)
Drugs of choice in isolated systolic HTN
Thiazides
Investigations in HTN
Repeated BP/Ambulatory BP
Assess for secondary cause (renal disease, Conn’s etc.)
Assess end-organ damage (echo, cardiac US, renal function)
Stages of HTN
Stage 1:
140/90 (135/90 now..)
Stage 2: 160/100 in clinic or 150/95 average
Severe:
BP >180/110
Management of severe HTN
If severe HTN:
Immediate management. Signs of papilloedema/retinal haemorrhages - same day assessment by specialist
Refer if phaeochromocytoma is suspected (labile/postural hypotension, headache, palpitations, pallor, diaphoresis)
Management of HTN <55 years or DM
ACE inhibitor or angiotension II receptor blocker
Ramipril
Management of HTN >55 years, no T2DM or afro-caribbean
Calcium channel blocker
Amlodipine
HTN if refractive after first line treatment
ACEi + Calc. channel blocker (ARB not ACE if Afro-caribbean)
OR
ACE inhibitor + Diuretic
HTN if refractive after second line treatment
A + C + D
HTN management if refractive after A+C+D
If potassium <4.5
Add low dose spironolactone
If potassium >4.5
Add alpha or beta blocker
Management of malignant HTN
Admit
Oral agents
Lower slowly (otherwise risk of stroke?)
Hyperlipidaemia
Elevated cholesterol + triglycerides
What transports cholesterol and triglycerides in the blood
Lipoproteins
What controls the signalling of lipid transport
Apoproteins (phospholipids and proteins)
Where is cholesterol metabolised
The liver
What is the balance between for blood cholesterol levels
Blood uptake
Cholesterol production
GI excretion (bile acids)
What secondary causes are there of hyperlipidaemia?
DM Hypothyroidism Renal failure Liver disease (esp. alcoholic) Biliary obstruction Steroids/oestrogens
Genetic causes of hyperlipidaemia
Familial hypercholesterolaemia
Apoprotein E genotype
Lipoprotein lipase deficiency
Lipids in atherosclosis (CAD)
> 6.5 doubles risk of lethal CAD
>7.8 gives 4 times the risk of lethal CAD
Which lipids are most important for indicating CAD
LDL cholesterol
HDL is protective
LDL:HDL ratio is a good indicator (>4 is high risk)
Lipid lowering
Diet:
Reduce fat intake (eggs, red meat, dairy products)
Reduce body weight
Lipid lowering drugs:
Statins are effective for lowering cholesterol (QRISK2)
How does hyperlipidaemia cause atherosclerosis?
Elevated cholesterol (especially oxidises LDL) damages the endothelium early in atherosclerosis and is taken up into the lipid core of established plaques by macrophages (foam cells)
Diagnosis of myocardial ischaemia
Tight retrosternal chest pain - radiation to the neck/down left arm
Pains occurring for >4 weeks, strong relation to exercise
How long can episodes of myocardial ischaemia be before infarction
If longer than 20-30 minutes, infarction has definitely occurred
When should you not do an x-ray in chest pain?
If patient has STEMI and needs to be treated with PCI and this would be delayed by x-ray
Do the x-ray immediately after
Markers of myocardial necrosis
Creatinine kinase
Aspartate aminotransferase
Lactate dehydrogenase
Troponin
Causes of raised troponin
Chronic/acute renal dysfunction Severe congestive heart failure HTN crisis Tachy/bradyarryhthmias PE Myocarditis Stroke etc.
Haemolgobin in myocardial ischaemia
Consider whether ischaemia could be a result of anaemia
Is the patient bleeding? Would antiplatelet therapy make this worse?
Infection and MI
Infection increases the risk of MI by up to 3 times - check the WCC and CRP
What should we check if you see a raised cholesterol
Thyroid levels
STEMI Pathology
Rupture or erosion of a coronary plaque leading to intracoronary thrombosis
Difference betwen STEMI and NSTEMI
STEMI - coronary artery has occluded entirely
NSTEMI - coronary artery either not entirely occluded or only transient in its occlusion (<20 minutes)
STEMI Ix features
Prolonged ST elevation
Troponin elevated
‘Threatened Q wave MI’
Where a STEMI, in the absence of treatment, progresses to Q wave or full thickness MI
What causes angina
Gradual narrowing of the coronary arteries due to the build up of fatty plaques within their walls
ECG leads anterior
V1-V4
ECG leads inferior
II, III, aVF
ECG leads lateral
I, V5-V6
Lateral infarct
Left circumflex
Inferior infarct
Right coronary
Anterior infarct
Left anterior descending
Management of ACS
MONA
Morphine
Oxygen
Nitrates
Aspirin
STEMI management
Revascularisation:
Give second antiplatelet drug in addition to the aspirin from MONA
Clopidogrel, prasugrel and ticgrelor are options
PCI - angioplasty with a stent (catheter via radial/femoral artery)
Risk stratification in NSTEMI
GRACE
NSTEMI and coronary angiography
Coronary angiography may be performed during the admission if the patient is considered high risk (using GRACE)
Otherwise will have coronary angiography as an outpatient
Secondary prevention of ACS
Aspirin Second antiplatelet (e.g. clopidogrel) Beta blocker ACE inhibitor Statin
When should we give O2 in STEMI?
<94%
Management of NSTEMI
MONA
Antithrombin - fondaparinux (if coronary angiography or high creatinine, give unfr. heparin instead)
Ticagrelor and prasugrel are now preferred to clopidogrel as the second antiplatelet
IV glycoprotein IIb and IIa receptor antagonists: eptifibatide or tirofiban (only if patient have a high risk of CVS events)
Ix findings NSTEMI
Raised troponin
Non-raised ST segment
Ix findings unstable angina
ST depression/T wave inversion
No rise in troponin
Angina pectoris presentation
Constricting discomfort in the front of chest, neck, shoulders, jaw or arms
Precipitated by physical exertion
Relieved by rest or GTN in <5 minutes
Typical angina has all 3. Atypical angina does not
Coronary angiography
Passing a catheter through radius or femoral into the ascending aorta and then into the coronary artery.
Radio-opaque dye is injected into the artery
X-ray is then taken
Management of angina pectoris
Aspirin + statin
Sublingual glyceryl trinitrate (for attacks)
Beta blocker/calcium channel blocker (depending on comorbidities etc.) (verapamil or diltiazem should be used as they have rate-limiting effects also)
Other causes of ST elevation
Old infarct Pericarditis Bundle branch block Hyperkalaemia Brugada syndrome
Left bundle branch block
If ST elevation and LBBB, still have very high suspicion of an MI
Thrombolysis in STEMI
Only if PCI unavailable for whatever reason.
Use tPA tissue plasminogen activator
Immediate (<24 hours) complications of STEMI
Ventricular arrhythmias (VT, VF)
AF
Failed reperfusion
STEMI complications (days after)
Cardiac rupture (into the pericardium) Re-infarction
HF
Cardiogenic shock (where the cardiac output can't maintain arterial BP): Severe impairment of LV function Infarction of the right ventricle Mechanical catastrophe - Vent. septal rupture, papillary muscle rupture
STEMI complications (weeks after)
Thromboembolism
Chronic heart failure
VT
Dressler’s
What is Dressler’s syndrome
Autoimmune pericarditis weeks after full thickness MI
How do we treat Dressler’s syndrome
NSAIDs
Occasionally requires steroids
Stratifying the risk of another MI
Lifestyle measures - stop smoking, alcohol, high intensity exercise, weight
LV function - usually measured by echo weeks after MI
Extent of coronary disease - angiography
Nitrate side effects
Hypotension
Tachycardia
Headaches
Flushing
Nitrate tolerance - reduced efficacy after a while of using it
Aortic dissection
Sudden tear in the tunica intima of the aorta
Risk factors for aortic dissection
HTN Trauma Bicuspid aortic valve Marfan's, Ehler's Danlos Pregnancy Syphilis
Heart failure
A syndrome in which inadequate cardiac output is compensated for by compensatory mechanisms (e.g. vent. dilation) which eventually become maladaptive
Three aspects of pathophysiology in heart failure
Neurohormonal activation
Cytokine activation
Ventricular dilation
Neurohormonal activation in HF
Increased vasoconstrictors (renin, angiotensin II, catecholamines etc.) provoke water and salt retention, increasing afterload
These decrease LV emptying further
B-type Natriuretic peptide (BNP)
Normal level excludes HF (it is a neurohormone activated in most HF in response to strain)
Cytokine activation in HF
IL-6 and TNF-alpha raised in HF
This pathology underlines the anaemia in chronic HF
Ventricular dilation in HF
Impaired systolic function (reduced ejection fraction) and fluid retention (dilation) increase the ventricular volume, making contraction less efficient
Law of Laplace
Describes the law in which a dilated heart is mechanically inefficient
Acute heart failure
Life-threatening emergency as a result of sudden onset or worsening of heart failure symptoms
Can happen in existing or non-existing HF, is usually the result of a functional/structural abnormality
De-novo acute HF
Usually a result of ischaemia
Can also be due to:
Viral myopathy
Toxins
Valve dysfunction
Decompensated acute heart failure
Most common reason for AHF
Precipitating causes: ACS HTN crisis Acute arrhythmia Valvular disease
Clinical features of AHF
Symptoms: Breathlessness Reduced exercise tolerance Oedema Fatigue
Signs: Cyanosis Tachycardia Elevated JVP Displaced apex beat S3 Heart sound Bibasal crackle or wheeze
Diagnostic work up for AHF
Blood tests - underlying abnormality (e.g. infection, anaemia, abnormal electrolytes)
CXR - Pulmonary venous congestion, interstitial oedema, cardiomegaly
Echo - pericardial effusion, tamponade
BNP - >100mg/litre
BP in AHF
Usually normal or slightly raised
Management of AHF
POD MAN
Position (sit up)
Oxygen
Diuretic (furosemide) fluid restriction
Morphine
Anti-emetic
Nitrates (GTN infusion is SBP >110, 2 puffs GTN spray if >90)
How do we classify HF
New York Heart Association (NYHA) classification
Class I: No symptoms
Class II: mild symptoms (ordinary activity results in fatigue, palpitations, dyspnoea)
Class III: moderate symptoms (less than ordinary activity results in symptoms)
Class IV: severe symptoms (unable to carry out activity without discomfort)
Diagnosing chronic HF
BNP
If high (>400):
Transthoracic echo within 2 weeks
If raised (100-400):
Transthoracic echo within 6 weeks
Chronic HF clinical features
Dyspnoea Cough (pink/frothy sputum) Orthopnoea Paroxysmal nocturnal dyspnoea Wheeze Weight loss Bibasal crackles on examination
RHF signs:
Raised JVP
Ankle oedema
Hepatomegaly
Management of CHF
First line:
ACEi + beta blocker (start one at a time)
+ furosemide if oedema as well
Second line: Aldosterone antagonist (spironolactone, eplerenone), angiotensin II receptor blocker or hydralazine with nitrate
Third line:
Digoxin
Congestive heart failure
Biventricular failure
LHF to CHF
LHF results in secondary pulmonary HTN which results in RHF
LHF
Breathlessness, worse when lying down (orthopnoea)
Paroxysmal nocturnal dyspnoea
Gallop rhythm
Bibasilar crepitations
RHF
Fluid retention in the legs
Ascites (if severe)
Raised JVP
Pericardial constriction
Ascites more prominent than leg oedema, rare condition
CHF valves
Mitral/tricuspid regurgitation common
Common causes of HF
CAD HTN Age Obesity Alcohol related disease Valvular heart disease
HF complications
VTE AF Pump failure Ventricular arrhythmias Sudden cardiac death
Causes of aortic stenosis
Congenital aortic stenosis
Premature calcification of a congenitally bicuspid aortic valve <65 y.o
Calcific aortic stenosis
Calcific aortic stenosis
Common
>65 y.o
At age 80 about 10% of the population have this
Renal failure/hypercholesterolaemia can make this occur earlier
Triad of symptoms with aortic stenosis
SAD
effort Syncope
effort Angina
effort Dyspnoea
All are exertional and all are progressive
Aortic stenosis rare symptom
Sudden cardiac death - becomes more likely as other symptoms develop
Murmur in aortic stenosis
Ejection systolic murmur
Harsh and loud
Soft/absent S2
Left sternal edge usually
Echo in aortic stenosis
Allows assessment of LV function and valve structure, as well as severity of stenosis
Features of aortic stenosis
Narrow pulse pressure Slow rising pulse Soft/absent S2 S4 Thrill LVH or LVHF
Management of aortic stenosis
If asymptomatic - observation
Symptomatic - valve replacement
What comorbidities should you assess for in aortic stenosis?
Renal failure
DM
Cholesterol +/- angiogram - CAD
FBC to check for iron (vWD can be a result of AS)
Aortic regurgitation causes
Disease affecting the valve: Rheumatic heart disease Endocarditis SLE Aortic stenosis
Disease resulting in aortic root dilation (and thus the aortic valve ring): HTN Marfan's Ankylosing spondylitis Syphilis Aortic dissection (acutely)
Symptoms in AR
If gradual onset, can be no symptoms
If the leak worsens:
LV decompensation
Exertional dyspnoea
Signs of AR
Collapsing pulse
Hyperdynamic apex beat - due to volume overloaded left ventricle
Signs of wide pulse pressure (as seen in severe AR)
Corrigan’s sign
De Musset’s
Quinke’s sign
Traube’s phenomenon
Corrigan’s sign
Visible carotid pulsations
De Mussett’s sign
Head bobbing
Quinke’s sign
Nail-bed pulsations
Traube’s phenomenon
Also called pistol shot femorals:
Auscultation of femoral arteries causing loud sounds during systole
Murmur in AR
Early diastolic murmur
Left sternal edge
Can accentuate by leaning forward and holding breath
Ix in AR
Echo/ECG:
LVH
Chest x-ray:
Enlarged heart
Aortic aneurysm potentially
Coronary angiography
Treatment of AR
For LVH function:
ACEi
Diuretics
Aortic valve replacement (though can’t do this if AR is the result of root dilation of course)
Aortic valve replacement
Open
Percutaneous (place new over old, via femoral artery)
Mitral stenosis causes
Rheumatic fever (99% of cases) SLE
Symptoms of mitral stenosis
Progressive exertional dyspnoea (as a result of HF)
Sudden symptoms usually a result of concurrent AF leading to high risk of thromboemboli
Mitral stenosis signs
Mitral facies (malar flush) Chronic HF signs (raised JVP, oedema) AF Right ventricular heave Tapping apex beat
Murmur in mitral stenosis
Mid-diastolic murmur
Low-pitched
Rumbling
Opening snap precedes murmur
Ix in mitral stenosis
Echo: Confirms diagnosis (usually shows rheumatic valve [thickened and distorted])
Chest x-ray:
Left atrial enlargement
Cardiomegaly
Mitral stenosis treatment
Medical:
Diuretics, digoxin and warfarin
Surgical:
Mitral valvotomy
Mitral valve replacement
Mitral valve prolapse (Barlow’s syndrome)
Mitral valve is larger than usual/chordae are too long
Mitral valve prolapses back into atria during systole as a result
Mitral valve prolapse features
Without mitral regurg. often does not cause any symptoms
With mitral regurg., ‘click’ mid-systole
Predisposes to bacterial endocarditis
Mitral regurgitation causes
Extremely common condition with two pathologies:
Intrinsic valve disease:
Myxomatous degeneration
Rheumatic heart disease
Infective endocarditis
Secondary (functional):
Stretching of the valve ring when dilated (usually from LHF)
Symptoms of mitral regurgitation
Heart failure symptoms:
Breathlessness
Effort intolerance
Fatigue
Mitral regurgitation murmur
Loud pansystolic murmur at the apex
Treatment of mitral regurgitation
Medical:
Diuretics
Angiotensin converting enzyme inhibitors
If intrinsic valve disease, can perform surgery to repair/replace
Dilated cardiomyopathy
Most common form of cardiomyopathy, accounting for 90% of cases
Dilated heart leading to predominately systolic dysfunction
All 4 chambers are dilated (L>R)
Eccentric hypertrophy
Mitral regurgitation + AF are common
Cardiomyopathy
Primary heart muscle diseases that are classified according to the echo findings
Treatment of dilated cardiomyopathy
As per heart failure:
First line:
ACEi + beta blocker (start one at a time)
+ furosemide if oedema as well
Second line: Aldosterone antagonist (spironolactone, eplerenone), angiotensin II receptor blocker or hydralazine with nitrate
Third line:
Digoxin
If patient is young, consider heart transplant
Causes of dilated cardiomyopathy
Idiopathic Hypothyroid, thyrotoxicosis Coxsackie B, HIV, diphtheria Alcohol Haemochromatosis Sarcoid Familial DCM or Duchenne's muscular dystrophy
Hypertrophic cardiomyopathy
Genetic condition characterised by asymmetrical hypertrophy of the LV, especially the septum
Causes an outflow tract obstruction and diastolic dysfunction
Secondary MR
Symptoms of hypertrophic cardiomyopathy
Breathlessness
Dizziness
Chest pain
Sudden death (due to vent. arrhythmias)
How do we treat hypertrophic cardiomyopathy
Exertional symptoms:
Beta blockers
Calcium channel antagonists
High risk of vent. tachy:
Amiodarone
Genetics/family screening + counselling
Restrictive cardiomyopathy
Causes cong. HF
Due to infiltration of the myocardium (e.g. by amyloid)
Treat with diuretics (though is usually refractive)
Acute pericarditis features
Pleuritic chest pain
Often positional (relieved by sitting forward)
Cough, dyspnoea, tachycardia, tachypnoea
Pericardial rub may be heard
Acute pericarditis ECG features
Saddle shaped ST elevation, widespread
PR depression
Ix in pericarditis
ECG
Transthoracic echo
Causes of pericarditis
Viral infections (coxsackie) TB Uraemia Trauma Dressler's syndrome Hypothyroid Malignancy Connective tissue disease
Treatment of pericarditis
Treat underlying cause
NSAIDs
Colchicine
When do we use CABG
We can use this in CAD to reduce angina symptoms as well as reduce risk of an MI
Involves using the saphenous vein
What is cardiac tamponade
Accumulation of pericardial effusion to the point where there is impaired heart function/filling
Features of cardiac tamponade
Beck’s triad:
Hypotension
Raised JVP
Muffled heart sounds
Dyspnoea
Tachycardia
Pulsus paradoxus
Kussmaul’s sign
What is pulsus paradoxus
An abnormally large drop in BP during inspiration
What is Kussmaul’s sign
Paradoxical rise in JVP on inspiration - indicative of limited right vent. filling
Treatment of cardiac tamponade
Urgent pericardiocentesis
Constrictive pericarditis features
Progressive exertional dyspnoea
Peripheral oedema
Ascites
Constrictive pericarditis
Recurrent pericarditis can cause pericardial fibrosis sufficient enough to constrict the heart and impede cardiac filling/emptying
Treatment of constructive pericarditis
Diuretics or surgery
Causes of a pericardial effusion
Exudates:
Metastatic malignancy
Acute pericarditis
Haemopericardium:
Aortic dissection
Trauma
Transudates:
Heart/liver failure
Nephrotic syndrome
Myxoedema
Infective endocarditis
An infection of the lining of the heart, usually the valves
Pathology of infective endocarditis
Blood-borne organisms settle on a heart valve causing fibrin deposits to accumulate there alongside microorganisms and form vegetations
You get symptoms due to:
Valve damage (causing heart failure)
Embolisation of infected material (abscesses, vital organ infarctions)
Immune response to chronic infection (renal failure)
Sources of infective endocarditis infections
Dental procedures/abscesses
Skin infections
GI infections
IVDU
Risk factors for infective endocarditis
Prosthetic valves
Rheumatic valve disease
Cong. heart defects
Causative organisms in IE
Staph aureus (skin infection) Staph epidermidis (following surgery) Strep viridans (dental)
Modified Duke’s criteria
IE if:
2 major criteria
1 major, 3 minor
5 minor
Major criteria in Duke’s
Positive blood cultures
Evidence of endocardial involvement (echocardiogram or new valvular regurgitation)
Minor criteria in Duke’s
Predisposing heart condition Fever >38 Vascular phenomena (signs peripherally) Predisposing heart condition IVDU Glomerulonephritis etc.
Ix in IE
Blood culture (>12 hours apart 3 times) Blood tests Urine dipstick (haematuria) Echocardiogram Transoesophogeal echo
Management of IE
Amoxicillin initially
Vancomycin (if prosthetic valve)
Flucloxacillin (if staph)
Benzylpenicillin (if strep. e.g. strep viridans)
Occasionally surgery
Prophylaxis of IE
If you have valvular problems and are undergoing a procedure with a high risk of bacteraemia, give prophylactic abx
Myocarditis
Inflammation of the heart muscle caused by:
Viral infections - coxsackie
Bact. infections
Radiation exposure.
Myocarditis features
Acute HF
Tachycardia out of proportion to the severity of HF
Sudden cardiac death
Treatment of myocarditis
No specific treatment
HF therapies
Supraventricular arrhythmias
Originate in the atria or around the AV node
Ventricular arrhythmias
Originate in the ventricles
AV-reciprocating tachycardias (paroxysmal SVT)
A re-entrant circuit set up by an accessory pathway. Can be between:
Atria and the ventricles
(AV re-entrant tachycardia)
Between the atrium and AV node (AV nodal re-entrant tachycardia) - most common type
SVT ECG diagnosis
Regular narrow QRS tachycardia
Can have abnormal P waves that are activated retrogradely
If AVNRT - can be upside down and following the QRS complex
Wolff-Parkinson White
A congenital accessory conducting pathway
Get a ‘delta’ wave before the QRS complex
Can get axis deviation (left or right)
Treatment of SVT
Vasovagal maneuvres:
Valsalva maneuvre - blow out through nose with eyes shut and holding nose
Carotid sinus massage
Swallow a cold drink
Drugs: IV adenosine (6mg > 12mg > 12mg) Beta blockers (verapamil, flecanide)
Radiofrequency ablation
Atrial fibrillation different types
Paroxysmal AF - Where attacks terminate spotaneously
Persistent AF - where attacks do not terminate without medical intervention
Permanent AF - AF considered to be permanent with/without intervention
AF pathology
Atria depolarise spontaneously in a rapid uncoordinated fashion, bombarding the AV node with signals
Causes of AF
Cardiac - Ischaemic heart disease, hypertensive heart disease, mitral valve disease, pericarditis
Metabolic - Thyrotoxicosis, alcohol
Pulmonary - PE, pneumonia, COPD, cor pulmonale
Idiopathic
Treatment of AF
Rate control - beta blockers, calcium channel blockers, digoxin
Rhythm control - Sotalol, amiodarone, flecainide
Cardioversion:
Electrical cardioversion if haemodynamically unstable
Amiodarone or flecainide
When to rate, when to rhythm control in AF
Rate:
>65 y.o
Hx of IHD
Rhythm: <65 Symptomatic First presentation Cong. heart failure
Anticoagulation in AF
CHA2DS2VASc score
0 = no treatment 1 = consider anticoagulation 2 = offer anticoagulation
Atrial flutter
Atria depolarise in a rapid coordinated fashion as a result of macro re-entry circuits
Atrial flutter ECG
Sawtooth appearance
Atrial rate may be 300, though depending on degree of AV block you may see a ventricular rate of half that
Treatment of atrial flutter
Cardioversion
Radiofrequency ablation
Ventricular tachycardia
Broad QRS with abnormal shape
Suspect when there is heart disease (e.g. heart failure damage)
Can be pulseless or haemodynamically stable VT
Pulseless VT management
DC cardiovert
Immediate anaesthesia
Haemodynamically stable VT management
IV lidocaine (one drug only - don’t combine)
Amiodarone (one drug only)
DC cardioversion
Two types of VT
Monomorphic - most commonly caused by MI
Polymorphic - caused by prolonged QT interval
Causes of a prolonged QT interval
Drugs: Amiodarone Antiarrhythmic drugs Tricyclic antidepressants Fluoxetine Chloroquine Erythromycin
Other: Bradycardia Congenital Hypocalcaemia Hypokalaemia Hypomagnesaemia MI Myocarditis Hypothermia Subarachnoid haemorrhage
Polymorphic VT management
DC cardiovert
IV magnesium
Correction of metabolic cause
Long-term management of VT
Beta blockers, amiodarone, sprinolactone etc.
Revascularisation (if coronary artery disease)
ICD
Ventricular fibrillation
Caused by: IHD Cardiomyopathies Channelopathies (Brugada's etc.) WPW etc.
Which are the shockable rhythms
VT
VF
Stokes-Adams attack
Sudden onset syncope
Lasts <60 seconds
Pale and still as if dead
Recovery back to normal rapidly
Classical syncope in bradyarrhythmias
Aetiology of bradyarrhythmias
Sinoatrial node disease
Atrioventricular block
AV block types
Impaired electrical conduction between atria and ventricles
First degree:
PR interval >0.2 seconds
Asymptomatic
Second degree:
Mobitz type 1 (Wenckeback) - progression prolongation of PR interval till dropped beat
Mobitz type 2 - PR interval constant but P wave not always followed by a QRS complex
Third degree:
No association between P waves and QRS
Treatment of AV block
Mobitz type 2 + complete heart block:
Pacemaker
