Cardiology Flashcards
1
Q
Essential hypertension
A
95% of HTN cases
A combination of environmental and genetic factors that result in a hypertensive phenotype
2
Q
Secondary hypertension
A
Caused by an identifiable cause (usually endocrine), e.g. coarctation, Conn’s syndrome**, etc.
3
Q
Clinical features of hypertension
A
Asymptomatic till end organ damage
4
Q
Malignant hypertension
A
Uncontrolled HTN
Retinal changes
Progressive renal failure
5
Q
Hypertension end-organ damage
A
CVD - Thrombotic and haemorrhagic stroke
Vascular disease
LVH - Compensatory response to chronically elevated BP
Renal failure - Renovascular damage/glomerular loss
6
Q
What is isolated systolic HTN?
A
Common in the elderly (above 70 y.o)
7
Q
Drugs of choice in isolated systolic HTN
A
Thiazides
8
Q
Investigations in HTN
A
Repeated BP/Ambulatory BP
Assess for secondary cause (renal disease, Conn’s etc.)
Assess end-organ damage (echo, cardiac US, renal function)
9
Q
Stages of HTN
A
Stage 1:
140/90 (135/90 now..)
Stage 2: 160/100 in clinic or 150/95 average
Severe:
BP >180/110
10
Q
Management of severe HTN
A
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)
11
Q
Management of HTN <55 years or DM
A
ACE inhibitor or angiotension II receptor blocker
Ramipril
12
Q
Management of HTN >55 years, no T2DM or afro-caribbean
A
Calcium channel blocker
Amlodipine
13
Q
HTN if refractive after first line treatment
A
ACEi + Calc. channel blocker (ARB not ACE if Afro-caribbean)
OR
ACE inhibitor + Diuretic
14
Q
HTN if refractive after second line treatment
A
A + C + D
15
Q
HTN management if refractive after A+C+D
A
If potassium <4.5
Add low dose spironolactone
If potassium >4.5
Add alpha or beta blocker
16
Q
Management of malignant HTN
A
Admit
Oral agents
Lower slowly (otherwise risk of stroke?)
17
Q
Hyperlipidaemia
A
Elevated cholesterol + triglycerides
18
Q
What transports cholesterol and triglycerides in the blood
A
Lipoproteins
19
Q
What controls the signalling of lipid transport
A
Apoproteins (phospholipids and proteins)
20
Q
Where is cholesterol metabolised
A
The liver
21
Q
What is the balance between for blood cholesterol levels
A
Blood uptake
Cholesterol production
GI excretion (bile acids)
22
Q
What secondary causes are there of hyperlipidaemia?
A
DM Hypothyroidism Renal failure Liver disease (esp. alcoholic) Biliary obstruction Steroids/oestrogens
23
Q
Genetic causes of hyperlipidaemia
A
Familial hypercholesterolaemia
Apoprotein E genotype
Lipoprotein lipase deficiency
24
Q
Lipids in atherosclosis (CAD)
A
> 6.5 doubles risk of lethal CAD
>7.8 gives 4 times the risk of lethal CAD
25
Which lipids are most important for indicating CAD
LDL cholesterol
HDL is protective
LDL:HDL ratio is a good indicator (>4 is high risk)
26
Lipid lowering
Diet:
Reduce fat intake (eggs, red meat, dairy products)
Reduce body weight
Lipid lowering drugs:
Statins are effective for lowering cholesterol (QRISK2)
27
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)
28
Diagnosis of myocardial ischaemia
Tight retrosternal chest pain - radiation to the neck/down left arm
Pains occurring for >4 weeks, strong relation to exercise
29
How long can episodes of myocardial ischaemia be before infarction
If longer than 20-30 minutes, infarction has definitely occurred
30
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
31
Markers of myocardial necrosis
Creatinine kinase
Aspartate aminotransferase
Lactate dehydrogenase
Troponin
32
Causes of raised troponin
```
Chronic/acute renal dysfunction
Severe congestive heart failure
HTN crisis
Tachy/bradyarryhthmias
PE
Myocarditis
Stroke etc.
```
33
Haemolgobin in myocardial ischaemia
Consider whether ischaemia could be a result of anaemia
Is the patient bleeding? Would antiplatelet therapy make this worse?
34
Infection and MI
Infection increases the risk of MI by up to 3 times - check the WCC and CRP
35
What should we check if you see a raised cholesterol
Thyroid levels
36
STEMI Pathology
Rupture or erosion of a coronary plaque leading to intracoronary thrombosis
37
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)
38
STEMI Ix features
Prolonged ST elevation
| Troponin elevated
39
'Threatened Q wave MI'
Where a STEMI, in the absence of treatment, progresses to Q wave or full thickness MI
40
What causes angina
Gradual narrowing of the coronary arteries due to the build up of fatty plaques within their walls
41
ECG leads anterior
V1-V4
42
ECG leads inferior
II, III, aVF
43
ECG leads lateral
I, V5-V6
44
Lateral infarct
Left circumflex
45
Inferior infarct
Right coronary
46
Anterior infarct
Left anterior descending
47
Management of ACS
MONA
Morphine
Oxygen
Nitrates
Aspirin
48
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)
49
Risk stratification in NSTEMI
GRACE
50
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
51
Secondary prevention of ACS
```
Aspirin
Second antiplatelet (e.g. clopidogrel)
Beta blocker
ACE inhibitor
Statin
```
52
When should we give O2 in STEMI?
<94%
53
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)
54
Ix findings NSTEMI
Raised troponin
| Non-raised ST segment
55
Ix findings unstable angina
ST depression/T wave inversion
| No rise in troponin
56
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
57
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
58
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)
59
Other causes of ST elevation
```
Old infarct
Pericarditis
Bundle branch block
Hyperkalaemia
Brugada syndrome
```
60
Left bundle branch block
If ST elevation and LBBB, still have very high suspicion of an MI
61
Thrombolysis in STEMI
Only if PCI unavailable for whatever reason.
| Use tPA tissue plasminogen activator
62
Immediate (<24 hours) complications of STEMI
Ventricular arrhythmias (VT, VF)
AF
Failed reperfusion
63
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
```
64
STEMI complications (weeks after)
Thromboembolism
Chronic heart failure
VT
Dressler's
65
What is Dressler's syndrome
Autoimmune pericarditis weeks after full thickness MI
66
How do we treat Dressler's syndrome
NSAIDs
Occasionally requires steroids
67
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
68
Nitrate side effects
Hypotension
Tachycardia
Headaches
Flushing
Nitrate tolerance - reduced efficacy after a while of using it
69
Aortic dissection
Sudden tear in the tunica intima of the aorta
70
Risk factors for aortic dissection
```
HTN
Trauma
Bicuspid aortic valve
Marfan's, Ehler's Danlos
Pregnancy
Syphilis
```
71
Heart failure
A syndrome in which inadequate cardiac output is compensated for by compensatory mechanisms (e.g. vent. dilation) which eventually become maladaptive
72
Three aspects of pathophysiology in heart failure
Neurohormonal activation
Cytokine activation
Ventricular dilation
73
Neurohormonal activation in HF
Increased vasoconstrictors (renin, angiotensin II, catecholamines etc.) provoke water and salt retention, increasing afterload
These decrease LV emptying further
74
B-type Natriuretic peptide (BNP)
Normal level excludes HF (it is a neurohormone activated in most HF in response to strain)
75
Cytokine activation in HF
IL-6 and TNF-alpha raised in HF
This pathology underlines the anaemia in chronic HF
76
Ventricular dilation in HF
Impaired systolic function (reduced ejection fraction) and fluid retention (dilation) increase the ventricular volume, making contraction less efficient
77
Law of Laplace
Describes the law in which a dilated heart is mechanically inefficient
78
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
79
De-novo acute HF
Usually a result of ischaemia
Can also be due to:
Viral myopathy
Toxins
Valve dysfunction
80
Decompensated acute heart failure
Most common reason for AHF
```
Precipitating causes:
ACS
HTN crisis
Acute arrhythmia
Valvular disease
```
81
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
```
82
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
83
BP in AHF
Usually normal or slightly raised
84
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)
85
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)
86
Diagnosing chronic HF
BNP
If high (>400):
Transthoracic echo within 2 weeks
If raised (100-400):
Transthoracic echo within 6 weeks
87
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
88
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
89
Congestive heart failure
Biventricular failure
90
LHF to CHF
LHF results in secondary pulmonary HTN which results in RHF
91
LHF
Breathlessness, worse when lying down (orthopnoea)
Paroxysmal nocturnal dyspnoea
Gallop rhythm
Bibasilar crepitations
92
RHF
Fluid retention in the legs
Ascites (if severe)
Raised JVP
93
Pericardial constriction
Ascites more prominent than leg oedema, rare condition
94
CHF valves
Mitral/tricuspid regurgitation common
95
Common causes of HF
```
CAD
HTN
Age
Obesity
Alcohol related disease
Valvular heart disease
```
96
HF complications
```
VTE
AF
Pump failure
Ventricular arrhythmias
Sudden cardiac death
```
97
Causes of aortic stenosis
Congenital aortic stenosis
Premature calcification of a congenitally bicuspid aortic valve <65 y.o
Calcific aortic stenosis
98
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
99
Triad of symptoms with aortic stenosis
SAD
effort Syncope
effort Angina
effort Dyspnoea
All are exertional and all are progressive
100
Aortic stenosis rare symptom
Sudden cardiac death - becomes more likely as other symptoms develop
101
Murmur in aortic stenosis
Ejection systolic murmur
Harsh and loud
Soft/absent S2
Left sternal edge usually
102
Echo in aortic stenosis
Allows assessment of LV function and valve structure, as well as severity of stenosis
103
Features of aortic stenosis
```
Narrow pulse pressure
Slow rising pulse
Soft/absent S2
S4
Thrill
LVH or LVHF
```
104
Management of aortic stenosis
If asymptomatic - observation
Symptomatic - valve replacement
105
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)
106
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)
```
107
Symptoms in AR
If gradual onset, can be no symptoms
If the leak worsens:
LV decompensation
Exertional dyspnoea
108
Signs of AR
Collapsing pulse
| Hyperdynamic apex beat - due to volume overloaded left ventricle
109
Signs of wide pulse pressure (as seen in severe AR)
Corrigan's sign
De Musset's
Quinke's sign
Traube's phenomenon
110
Corrigan's sign
Visible carotid pulsations
111
De Mussett's sign
Head bobbing
112
Quinke's sign
Nail-bed pulsations
113
Traube's phenomenon
Also called pistol shot femorals:
| Auscultation of femoral arteries causing loud sounds during systole
114
Murmur in AR
Early diastolic murmur
Left sternal edge
Can accentuate by leaning forward and holding breath
115
Ix in AR
Echo/ECG:
LVH
Chest x-ray:
Enlarged heart
Aortic aneurysm potentially
Coronary angiography
116
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)
117
Aortic valve replacement
Open
| Percutaneous (place new over old, via femoral artery)
118
Mitral stenosis causes
```
Rheumatic fever (99% of cases)
SLE
```
119
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
120
Mitral stenosis signs
```
Mitral facies (malar flush)
Chronic HF signs (raised JVP, oedema)
AF
Right ventricular heave
Tapping apex beat
```
121
Murmur in mitral stenosis
Mid-diastolic murmur
Low-pitched
Rumbling
Opening snap precedes murmur
122
Ix in mitral stenosis
```
Echo:
Confirms diagnosis (usually shows rheumatic valve [thickened and distorted])
```
Chest x-ray:
Left atrial enlargement
Cardiomegaly
123
Mitral stenosis treatment
Medical:
Diuretics, digoxin and warfarin
Surgical:
Mitral valvotomy
Mitral valve replacement
124
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
125
Mitral valve prolapse features
Without mitral regurg. often does not cause any symptoms
With mitral regurg., 'click' mid-systole
Predisposes to bacterial endocarditis
126
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)
127
Symptoms of mitral regurgitation
Heart failure symptoms:
Breathlessness
Effort intolerance
Fatigue
128
Mitral regurgitation murmur
Loud pansystolic murmur at the apex
129
Treatment of mitral regurgitation
Medical:
Diuretics
Angiotensin converting enzyme inhibitors
If intrinsic valve disease, can perform surgery to repair/replace
130
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
131
Cardiomyopathy
Primary heart muscle diseases that are classified according to the echo findings
132
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
133
Causes of dilated cardiomyopathy
```
Idiopathic
Hypothyroid, thyrotoxicosis
Coxsackie B, HIV, diphtheria
Alcohol
Haemochromatosis
Sarcoid
Familial DCM or Duchenne's muscular dystrophy
```
134
Hypertrophic cardiomyopathy
Genetic condition characterised by asymmetrical hypertrophy of the LV, especially the septum
Causes an outflow tract obstruction and diastolic dysfunction
Secondary MR
135
Symptoms of hypertrophic cardiomyopathy
Breathlessness
Dizziness
Chest pain
Sudden death (due to vent. arrhythmias)
136
How do we treat hypertrophic cardiomyopathy
Exertional symptoms:
Beta blockers
Calcium channel antagonists
High risk of vent. tachy:
Amiodarone
Genetics/family screening + counselling
137
Restrictive cardiomyopathy
Causes cong. HF
Due to infiltration of the myocardium (e.g. by amyloid)
Treat with diuretics (though is usually refractive)
138
Acute pericarditis features
Pleuritic chest pain
Often positional (relieved by sitting forward)
Cough, dyspnoea, tachycardia, tachypnoea
Pericardial rub may be heard
139
Acute pericarditis ECG features
Saddle shaped ST elevation, widespread
| PR depression
140
Ix in pericarditis
ECG
| Transthoracic echo
141
Causes of pericarditis
```
Viral infections (coxsackie)
TB
Uraemia
Trauma
Dressler's syndrome
Hypothyroid
Malignancy
Connective tissue disease
```
142
Treatment of pericarditis
Treat underlying cause
NSAIDs
Colchicine
143
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
144
What is cardiac tamponade
Accumulation of pericardial effusion to the point where there is impaired heart function/filling
145
Features of cardiac tamponade
Beck's triad:
Hypotension
Raised JVP
Muffled heart sounds
Dyspnoea
Tachycardia
Pulsus paradoxus
Kussmaul's sign
146
What is pulsus paradoxus
An abnormally large drop in BP during inspiration
147
What is Kussmaul's sign
Paradoxical rise in JVP on inspiration - indicative of limited right vent. filling
148
Treatment of cardiac tamponade
Urgent pericardiocentesis
149
Constrictive pericarditis features
Progressive exertional dyspnoea
Peripheral oedema
Ascites
150
Constrictive pericarditis
Recurrent pericarditis can cause pericardial fibrosis sufficient enough to constrict the heart and impede cardiac filling/emptying
151
Treatment of constructive pericarditis
Diuretics or surgery
152
Causes of a pericardial effusion
Exudates:
Metastatic malignancy
Acute pericarditis
Haemopericardium:
Aortic dissection
Trauma
Transudates:
Heart/liver failure
Nephrotic syndrome
Myxoedema
153
Infective endocarditis
An infection of the lining of the heart, usually the valves
154
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)
155
Sources of infective endocarditis infections
Dental procedures/abscesses
Skin infections
GI infections
IVDU
156
Risk factors for infective endocarditis
Prosthetic valves
Rheumatic valve disease
Cong. heart defects
157
Causative organisms in IE
```
Staph aureus (skin infection)
Staph epidermidis (following surgery)
Strep viridans (dental)
```
158
Modified Duke's criteria
IE if:
2 major criteria
1 major, 3 minor
5 minor
159
Major criteria in Duke's
Positive blood cultures
| Evidence of endocardial involvement (echocardiogram or new valvular regurgitation)
160
Minor criteria in Duke's
```
Predisposing heart condition
Fever >38
Vascular phenomena (signs peripherally)
Predisposing heart condition
IVDU
Glomerulonephritis etc.
```
161
Ix in IE
```
Blood culture (>12 hours apart 3 times)
Blood tests
Urine dipstick (haematuria)
Echocardiogram
Transoesophogeal echo
```
162
Management of IE
Amoxicillin initially
Vancomycin (if prosthetic valve)
Flucloxacillin (if staph)
Benzylpenicillin (if strep. e.g. strep viridans)
Occasionally surgery
163
Prophylaxis of IE
If you have valvular problems and are undergoing a procedure with a high risk of bacteraemia, give prophylactic abx
164
Myocarditis
Inflammation of the heart muscle caused by:
Viral infections - coxsackie
Bact. infections
Radiation exposure.
165
Myocarditis features
Acute HF
Tachycardia out of proportion to the severity of HF
Sudden cardiac death
166
Treatment of myocarditis
No specific treatment
| HF therapies
167
Supraventricular arrhythmias
Originate in the atria or around the AV node
168
Ventricular arrhythmias
Originate in the ventricles
169
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
170
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
171
Wolff-Parkinson White
A congenital accessory conducting pathway
Get a 'delta' wave before the QRS complex
Can get axis deviation (left or right)
172
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
173
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
174
AF pathology
Atria depolarise spontaneously in a rapid uncoordinated fashion, bombarding the AV node with signals
175
Causes of AF
Cardiac - Ischaemic heart disease, hypertensive heart disease, mitral valve disease, pericarditis
Metabolic - Thyrotoxicosis, alcohol
Pulmonary - PE, pneumonia, COPD, cor pulmonale
Idiopathic
176
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
177
When to rate, when to rhythm control in AF
Rate:
>65 y.o
Hx of IHD
```
Rhythm:
<65
Symptomatic
First presentation
Cong. heart failure
```
178
Anticoagulation in AF
CHA2DS2VASc score
```
0 = no treatment
1 = consider anticoagulation
2 = offer anticoagulation
```
179
Atrial flutter
Atria depolarise in a rapid coordinated fashion as a result of macro re-entry circuits
180
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
181
Treatment of atrial flutter
Cardioversion
| Radiofrequency ablation
182
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
183
Pulseless VT management
DC cardiovert
| Immediate anaesthesia
184
Haemodynamically stable VT management
IV lidocaine (one drug only - don't combine)
Amiodarone (one drug only)
DC cardioversion
185
Two types of VT
Monomorphic - most commonly caused by MI
Polymorphic - caused by prolonged QT interval
186
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
```
187
Polymorphic VT management
DC cardiovert
IV magnesium
Correction of metabolic cause
188
Long-term management of VT
Beta blockers, amiodarone, sprinolactone etc.
Revascularisation (if coronary artery disease)
ICD
189
Ventricular fibrillation
```
Caused by:
IHD
Cardiomyopathies
Channelopathies (Brugada's etc.)
WPW etc.
```
190
Which are the shockable rhythms
VT
| VF
191
Stokes-Adams attack
Sudden onset syncope
Lasts <60 seconds
Pale and still as if dead
Recovery back to normal rapidly
Classical syncope in bradyarrhythmias
192
Aetiology of bradyarrhythmias
Sinoatrial node disease
Atrioventricular block
193
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
194
Treatment of AV block
Mobitz type 2 + complete heart block:
| Pacemaker
