Cardiology Flashcards
1
Q
Where do atherosclerotic plaques occur?
A
Peripheral and Coronary arteries.
2
Q
How are atherosclerotic plaques distributed?
A
Focally distributed - governed by haemodynamic factors (eg. changes in flow or turbulence)
3
Q
What is neointima?
A
Changes in blood flow altering the phenotype of endothelial cells.
Altered gene expression in endothelial cells, smooth muscle cells, macrophages, and fibroblasts.
4
Q
What makes up the structure of an atherosclerotic plaque?
A
- Lipid
- Necrotic core
- Connective tissue
- Fibrous cap
5
Q
Describe the progression of atherosclerosis.
A
- Fatty streak
- Intermediate lesions
- Fibrous plaques
- Plaque rupture
- Plaque erosion
6
Q
Describe the first stage of atherosclerosis - Fatty streak.
A
- Earliest lesion of atherosclerosis - <10 years
- Aggregations of lipid-laden macrophages and T lymphocytes within the tunica intima
- Scavenger receptors take up lipids
7
Q
Describe the second stage of atherosclerosis - Intermediate lesions.
A
- Lesion progresses to comprise layers of:
- Foam cells (Lipid-laden macrophages)
- Vascular smooth muscle cells
- T lymphocytes
- Adhesion and aggregation of platelets to vessel wall
- Isolated pools of extracellular lipid
8
Q
Describe the third stage of atherosclerosis - Fibrous plaques.
A
- Contains SMCs, macrophages, foam cells, and T-lymphocytes
- Covered by dense fibrous caps made of ECM proteins including collagen and elastin
- Impedes blood flow and prone to rupture
- Often calcified
9
Q
Describe the fourth stage of atherosclerosis - Plaque rupture.
A
- Plaque is constantly growing and receding
- In increased inflammatory conditions the fibrous cap becomes weak and plaque ruptures
- Exposure of basement membrane, collagen, necrotic tissue and haemorrhage of vessels causes thrombus formation
10
Q
What is atherosclerosis?
A
An inflammatory process characterised by hardened plaques within the intima of a vessel wall.
Eventually, plaque will either occlude the vessel lumen (restricting blood flow) or rupture (thrombus formation).
11
Q
Describe the fifth stage of atherosclerosis - Plaque erosion.
A
- Small early lesions
- Fibrous cap does not disrupt
- Luminal surface underneath the clot has less endothelium but more smooth muscle
- Prominent lipid core
12
Q
What is Percutaneous Coronary Intervention?
A
A non-surgical procedure that uses a catheter to place a stent into a narrowed blood vessel.
13
Q
What is Restenosis?
A
The recurrence of abnormal narrowing of an artery or valve after corrective therapy.
14
Q
What drugs are used to reduce restenosis in patients who have undergone corrective surgery?
A
Taxol and Sirolimus.
These work by reducing SMC proliferation after placement of stent.
15
Q
How does Aspirin help to treat CHD?
A
It’s an irreversible inhibitor of platelet cyclo-oxygenase.
16
Q
How does Clopidogrel/Ticagrelor help to treat CHD?
A
They are inhibitors of the stimulatory P2Y12 ADO receptor on platelets.
17
Q
How do Statins help to treat CHD?
A
Inhibit HMG CoA reductase - reduces cholesterol synthesis.
18
Q
What inflammation-causing cytokine is targeted using drugs alongside statin therapy?
A
IL-1
19
Q
What drug therapy is used as an alternative to statins if ineffective or not tolerated?
A
PCSK9 inhibitors.
20
Q
What are acute coronary syndromes?
A
A spectrum of acute cardiac conditions ranging from unstable angina to varying degrees of MI.
21
Q
What are the most common causes of Acute Coronary Syndromes?
A
Atherosclerotic rupture and consequential arterial thrombosis.
22
Q
Name some less common causes of Acute Coronary Syndromes?
A
- Coronary vasospasm without plaque rupture
- Drug abuse (amphetamines and cocaine)
- Spontaneous Coronary Artery Dissection
23
Q
What is Cardiac Troponin?
A
A protein complex functioning to regulate actin and myosin contraction.
24
Q
Why is Cardiac Troponin relevant in diagnosing Acute Coronary Syndromes?
A
- Highly sensitive marker for cardiac muscle injury
- Not specific for ACS (also increases in conditions that cause stress in myocardium such as PE, sepsis etc)
25
What is Primary Percutaneous Coronary Intervention (PPCI)?
- Reperfusion injury can occur as a result of opening up the blocked vessel
- Drug-eluting stent can reduce restenosis
26
What is the clinical classification of unstable angina?
- Cardiac chest pain at rest or during minimal exertion
- Severe and of new onset cardiac chest pain
- Cardiac chest pain with crescendo pattern
27
How is unstable angina diagnosed?
- History
- ECG (may present as ST-segment depression, transient ST-elevation, or T-wave inversion)
- No elevation in troponin = unstable angina not associated with damage to the heart
28
What are the characteristics of the chest pain associated with myocardial infarction?
- Occurs at rest
- Unremitting
- Usually severe, can be mild or absent (silent MI)
- Associated with autonomic symptoms eg. sweating, breathlessness, nausea and vomiting
29
What risk factors are associated with MI?
- Old age
- Diabetes
- Renal failure
- Left Ventricular Systolic Dysfunction (LVSD)
30
What is the process of initial management of MI by ambulance staff?
- If paramedics see presentation of ST-elevation, immediately sent for PPCI
- Aspirin (300mg) in the ambulance
- Morphine - reduces pain and myocardial oxygen demand
31
What is involved in hospital management of MI after diagnosis?
- Bed rest
- Oxygen therapy (if hypoxic)
- Pain relief
- Aspirin (+ P2Y12 inhibitor)
- Beta-blocker (antianginal therapy)
- Urgent Percutaneous Coronary Intervention
32
Name some of the functions of platelets during arterial thrombosis.
- Procoagulant activity (release of thrombin)
- Dense granule secretion (platelet activation)
- Alpha granule secretion (coagulation and inflammation)
- Platelet-fibrin clot
33
What is the process by which platelets prevent further rupture?
1. Shear flow
2. Initial adhesion GPIb/VWF
3. Rolling GPIb/VWF/α2β1/collagen
4. Stable adhesion activation/aggregation GPVI, GPIIb/IIIa
5. Platelets are activated by ADP, causing them to change shape, aggregate and seal off the endothelial breach
34
What combined therapy is used to manage ACS?
Asprin, P2Y12 inhibitors and GPIIb/IIIa antagonists.
35
What is the role of aspirin in treatment of ACS?
It prevents collagen-platelet binding through irreversible inactivation of cyclo-oxygenase-1.
36
What is the role of P2Y12 Inhibitors in the treatment of ACS?
They prevent P2Y12 receptor-mediated amplification of platelet activation (P2Y12 is the receptor for ADP).
37
Give 3 examples of P2Y12 Inhibitors.
1. Clopidogrel
2. Prasugrel
3. Ticagrelor
38
What is the major side effect of P2Y12 inhibitors?
Increases risk of bleeding - serious bleeding must subside before administration and risk of thrombosis vs risk of bleeding is monitored.
39
What is the role of GPIIb/IIIa Antagonists in the treatment of ACS?
They prevent amplification of platelet activation by binding to the GPIIb/IIIa complex (receptor for fibrinogen and vWF).
40
Give 3 examples of GPIIb/IIIa Antagonists.
- Abciximab
- Tirofiban
- Eptifibatide
41
What is the major side effect of GPIIb/IIIa Antagonists?
Increased risk of bleeding - used selectively and sparingly.
42
Why are GPIIb/IIIa Antagonists very useful in STEMI patients undergoing PCI?
Cover for delayed absorption of oral P2Y12 Inhibitors occurring due to opiates delaying gastric emptying.
43
What is the role of anticoagulants used in the treatment of ACS?
Targets formation and/or activity of thrombin - inhibiting both fibrin formation and platelet activation.
44
What anticoagulant is commonly used during Non-STEMI ACS?
Fondaparinux is used prior to coronary angiography (safer than heparins as it produces less bleeding).
45
What anticoagulants are used during PCI?
Full dose of anticoagluants, eg:
- Heparin
- Bivalirudin
46
What is angina?
Symptoms of chest pain and shortness of breath caused by the mismatch between oxygen supply and demand occurring as a consequence of restricted blood flow.
47
Give some causes of oxygen supply reduction associated with Ischaemic Heart Disease.
1. Common:
- Anaemia
- Hypoxaemia
2. Uncommon:
- Polycythemia
- Hypothermia
- Hypovolaemia
- Hypervolaemia
48
Give some causes of oxygen demand increase associated with Ischaemic Heart Disease.
1. Common:
- Hypertension
- Tachyarrhythmia
- Valvular heart disease
2. Uncommon:
- Hyperthyroidism
- Hypertrophic cardiomyopathy
49
What predisposing factors are associated with IHD?
- Age
- Smoking
- Family history
- Diabetes mellitus
- Hypertension
- Hyperlipidemia
- Physical inactivity
50
What environmental factors often highlight symptoms of Chronic Coronary Syndromes?
- Cold weather
- Heavy meals (post-prandial angina)
- Emotional stress
51
What are the three major physiological factors lending to oxygen mismatch?
- Impairment of blood flow by proximal arterial stenosis (eg. atherosclerosis)
- Increased distal resistance (eg. left ventricular hypertrophy)
- Reduced oxygen-carrying capacity of blood (eg.anaemia)
52
How does Ohm's Law relate to CCS?
F = ∆P/R
Flow = change in pressure gradient / resistance
53
How does Poisuille's Law relate to CCS?
F ∝ (ΔP x r^4) / ηL
Relationship between flow, pressure and resistance - radius has to fall below 75% before symptoms present.
54
What is Microvascular Angina?
Angina related to stenosis of cardiac microvasculature, not observed on a coronary angiogram.
(Most common in diabetes, LVH and older age)
55
What is Unstable Angina?
Recurrent episodes of angina at rest.
May be the initial presentation of IHD.
56
What is the most important information when taking a history of a patient with potential IHD?
- Personal details
- Presenting complaint (discuss pain)
- Risk factors
- Past medical history
- Drug history
- Family history (first degree relatives under 60)
- Social history (smoking)
57
What characteristics of chest pain suggest Ischaemic Cardiac pain?
- Heavy, tight pain
- Located centrally
- Provoked by cold weather, big meals or exertion
- Relieved by rest and GTN spray
- Associated with SOB
58
What are some differential diagnoses of chest pain?
- Pericarditis/myocarditis
- PE/chest infection
- Aortic dissection
- GORD
- Musculoskeletal
- Psychological
59
What are the NICE guidelines on diagnosis of CCS?
1. CT Coronary Angiogram (first-line diagnostic test)
2. Other non-invasive testing
3. Coronary angiography (when other testing is inconclusive)
60
What is exercise testing?
The patient undertakes mild exercise on a treadmill and an ECG is run simultaneously.
Any abnormalities - the patient is referred to catheterisation lab.
61
What is a Perfusion/Myoview scan?
An IV radio-labelled agent travels to the coronary arteries - areas of darkness signify and blockage.
62
What is a CT Coronary Angiography?
Non-invasive imaging of the coronary arteries used to identify poor blood flow and coronary calcification.
63
What is a Perfusion MRI?
MRI scan used to obtain perfusion maps with different parameters eg. blood volume, blood flow, mean transit time (MTT) and time to peak (TTP)
64
What is an Invasive Coronary Angiography?
Insertion of a catheter tube into a blood vessel (groin, upper thigh or neck) and up to coronary arteries. The catheter is injected with contrast dye to highlight blockages.
65
What effect do beta-blockers have on the heart?
Negative chronotropic (↓ HR) and ionotropic (↓ contractility) effect on the heart - reduces CO and O2 demand.
66
What are some common side effects of beta-blockers?
- Tiredness
- Bradycardia
- Erectile dysfunction
- Vasoconstriction in extremities
67
What is the major contraindication of beta-blockers?
Severe asthma.
68
What effect do Nitrates have on the heart?
Venous and arteriolar dilation - reduce the preload on the heart and dilate coronary arteries.
69
Name a common side effect of Nitrates.
Headaches.
70
What effect do Calcium Channel Blockers have on the heart?
- ↓ work - negative chronotropic (↓ HR) and ionotropic (↓ contractility) effects on the heart
- ↓ O2 demand
- ↓ afterload
71
What effect do statins have on the heart?
Reduction in LDL synthesis - reduced plaque formation in the coronary arteries.
72
Give an example of a statin.
HMG CoA Reductase Inhibitors.
73
What effect do ACE Inhibitors have on the heart?
Inhibits ACE - decreases BP
Vasodilatory effect due to decreased vasoconstrictor Angiotensin II
74
Give an example of an ACE Inhibitor.
Ramipril.
75
Define Diastolic Distensibility.
The pressure required to fill the ventricle to the same diastolic volume.
76
What are some consequences of hypertension?
- Stroke (Ischaemic and haemorrhage)
- MI
- Heart failure
- Chronic Renal Disease
- Cognitive decline
- Premature death
- Increases risk of AF
77
What can be offered to confirm a diagnosis of hypertension?
Ambulatory Blood Pressure Monitoring (ABPM) over 24 hours.
78
Define Stage 1 Hypertension.
Clinical = 140/90
Ambulatory = 135/85
79
Define Stage 2 Hypertension.
Clinical = 160/100
Ambulatory = 150/95
80
Define severe hypertension.
Clinical = 180/110
81
How is Primary Hypertension treated?
Lifestyle modification and antihypertensive drug therapy.
82
Who should be offered antihypertensive drug treatment for hypertension?
1. Individuals aged 80 or younger
2. Individuals with one or more of the following:
- Target organ damage
- Established CVD
- Renal Disease
- Diabetes
- 10 year CVD risk of >20%
83
Describe the mechanisms of BP control.
(Targets for therapy)
- Cardiac output and peripheral resistance
- RAAS and Noradrenaline (Sympathetic NS)
- Local vascular vasoconstrictor and vasodilator mediators
84
Describe the renin-angiotensin-aldosterone system (RAAS).
1. Kidney receptors detect low BP, renin is released from juxtaglomerular cells
2. Renin converts angiotensinogen to angiotensin I
3. ACE from the lungs converts angiotensin I to angiotensin II
4. Angiotensin II stimulates aldosterone release resulting in increased Na+ and water reabsorption 5. Increased blood volume = Increased BP
85
Describe how Noradrenaline (sympathetic NS) increases BP.
1. A drop in BP results in the release of noradrenaline, leading to vasoconstriction and increased contractility
2. Increased peripheral resistance and cardiac output increases BP
3. Induces renin release (augments RAAS)
86
Give 4 examples of ACE inhibitors.
- Ramipril
- Enalapril
- Perindopril
- Trandolapril
87
What are the indications for ACE inhibitors?
- Hypertension
- Heart failure
- Diabetic neuropathy
88
What are the ADRs associated with ACE inhibitors - related to reduced angiotensin II formation?
- Hypotension
- Acute renal failure (increased renin release)
- Hyperkalaemia
- Teratogenic in pregnancy
89
What are the ADRs associated with ACE inhibitors - related to increased kinins?
- Chronic dry cough
- Rash
- Anaphylactoid reaction
90
Give examples of Angiotensin II Receptor Blockers (ARBs).
- Candesartan
- Losartan
- Valsartan
- Telmisartan
91
What are the indications of ARBs?
- Hypertension (when ACEi is contradicted)
- Diabetic neuropathy
- Heart failure
92
What ADRs are associated with ARBs?
- Symptomatic hypotension
- Hyperkalaemia
- Potential renal dysfunction
- Rash
- Angiooedema
- Teratogenic in pregnancy
93
What are the indications of Calcium Channel Blockers (CCBs)?
- Hypertension
- Ischaemic heart disease
- Arrhythmia
94
Give examples of Calcium Channel Blockers.
- Dihydropyridines (eg. amlodipine)
- Phenylalkylamines (eg. verapamil)
- Benzothiozepines (eg. diltiazem)
95
What are the actions of Dihydropyridines?
Affect vascular smooth muscle - peripheral arterial vasodilators.
96
What are the actions of Phenylalkylamines?
1. Directly affects the heart
- Reduces HR (negatively chronotropic) and force of contraction (negatively inotropic).
97
What are the actions of Benzothiozepines?
Intermediate heart and peripheral vascular effects.
98
What ADRs are associated with CCBs - due to peripheral vasodilation? (Mainly Dihydropyridines)
- Flushing
- Headache
- Peripheral oedema
- Palpitations
99
What ADRs are associated with CCBs - due to negative chronotropic effect? (Phenylalkylamines and Benzothiozepines)
- Bradycardia
- Atrioventricular block
- Postural hypotension
100
What ADRs are associated with CCBs - due to negative inotropic effect? (Benzothiozepines)
- Worsening of HF
- Constipation (Verapamil)
101
Give examples of beta-blockers.
- Bisoprolol
- Propanolol
- Atenolol
- Carvedilol
102
What are the indications for beta-blockers?
- IHD (angina)
- Heart failure
- Arrhythmia
- Hypertension
103
Which beta-blockers are B1 sensitive?
Metoprolol and Bisoprolol.
104
Which beta-blockers are non-selective?
- Propanolol
- Nadolol
- Carvedilol
105
What are the ADRs associated with beta-blockers?
- Fatigue
- Headache
- Sleep disturbance
- Bradycardia
- Hypotension
- Cold peripheries
- Erectile dysfunction
106
How do Diuretics reduce blood pressure?
Increased excretion of water, salt and metabolites in urine.
107
What are the indications for Diuretics?
- Hypertension
- Heart failure
108
What are the different classes of Diuretics?
- Thiazide diuretics (act on distal tubule)
- Loop diuretics (act on ascending loop of henle)
- Potassium-sparing diuretics (aldosterone antagonists)
109
Give examples of Diuretics.
- Thiazide diuretics (bendroflumethiazide, hydrochlorothiazide)
- Loop diuretics (furosemide, bumetanide)
- Potassium-sparing diuretics (spironolactone, eplerenone)
110
What are the ADRs associated with Diuretics?
- Hypovolaemia (mainly loop)
- Hypotension (mainly loop)
- Hypokalaemia
- Hyponatraemia
- Hypomagnesaemia
- Hypocalcium
- Hyperuricaemia (gout)
- Erectile dysfunction (thiazides)
- Impaired glucose tolerance (thiazides)
111
What other antihypertensives exist?
1. α1-adrenoceptor blocker (doxazosin)
2. Centrally acting antihypertensives (moxonidine, methyldopa - can be used in pregnancy)
3. Direct renin inhibitor: aliskiren
112
Define Heart Failure.
A complex clinical syndrome of signs and symptoms that suggest the efficiency of the heart is impaired.
113
What are the different types of HF?
- Left ventricular Systolic Dysfunction (most common)
- Heart Failure with Preserved Ejection Fraction (diastolic failure)
- Acute/chronic Heart Failure
114
What is the underlying principle of treatment?
Vasodilator therapy via neurohumoral blockade (RAAS-SNS).
115
What is the symptomatic treatment of congestion?
Diuretics (usually loop).
116
What is the first line treatment involved in disease-influencing neurohumoral blockade therapy?
ACE inhibitors and beta-blockers (low dose and slow up-titration).
117
What are the stages after first-line neurohumoral blockade therapy?
1. Aldosterone antagonists
2. Aldosterone Receptor antagonist and Neprilysin Inhibitor (ARNIs)
3. SGLT2 inhibitor
If ACEi intolerant - ARBs
118
Give some examples of Nitrates.
- Isosorbide mononitrate (tablet)
- GTN spray
- GTN infusion (acute/severe angina)
119
What effect do Nitrates have on the heart?
- Arterial and venous dilators
- Reduce preload and afterload
- Lower BP
120
What effect do Nitrates have on the heart?
- Arterial and venous dilators
- Reduce preload and afterload
- Lower BP
121
What are the indications for Nitrates?
- IHD (angina)
- Heart failure
122
What are the ADRs associated with Nitrates?
- Headache
- GTN spray syncope
- Potential tolerance to the drug
123
What are the different types of Cardiac Natriuretic Peptides (CNPs)?
- Atrial natriuretic peptide (ANP) - atria
- Brain natriuretic peptide (BNP) - ventricles (found in the brain and heart
124
What causes the physiological release of CNPs?
- Stretching of atrial and ventricular muscle cells
- Raised atrial or ventricular pressure
- Volume overload
125
What effect do CNPs have on renal excretion?
Increases renal excretion of sodium (natriuresis) and water (diuresis).
126
What effect do CNPs have on vascular smooth muscle?
Relax vascular smooth muscle of renal glomeruli to preserve filtration pressure in the kidney while still removing Na+.
127
What effect do CNPs have on the release of other chemical mediators?
Reduces aldosterone, angiotensin II, endothelin and ADH release.
128
What are CNPs a counter-regulatory system to?
The renin-angiotensin-aldosterone system (RAAS).
129
What are Natriuretic Peptides metabolised by?
Neutral Endopeptidase (NEP or neprilysin).
130
How can the inhibition of NP metabolism be used in the treatment of heart failure?
NEP inhibition increases levels of NPs.
131
Give examples of NEP inhibitors.
- Sacubitril (neprilysin inhibitor)
- Valsartan (ARB)
- Entresto (combination of the above) - very effective in heart failure
132
What are the symptoms of Chronic Stable Angina?
- Chest pain (predictable, infrequent and stable)
- Radiating pain to neck, teeth, jaw and arms
- Breathlessness
- Relived by rest or GTN spray
133
What are the symptoms of Unstable Angina (NSTEMI) chest pain?
- Unpredictable (at rest)
- Frequent and unstable
134
What is the nature of STEMI chest pain?
- Unpredictable
- Pain at rest
- Persistant
135
How are patients with chronic stable angina generally treated?
1. Antiplatelet therapy (aspirin, ticagrelor, clopidogrel)
2. Lipid-lowering therapy (statins)
3. Short-acting nitrate (GTN spray)
136
How is frequent angina treated?
1. First line:
- Beta-blockers or CCBs
2. Second line:
- Long-acting nitrates
137
What are the Class I Anti-arrhythmics?
Sodium Channel Blockers:
- 1A: quinidine
- 1B: lidocaine
- 1C: flecainide
138
What are the Class II Anti-arrhythmics?
Beta-blockers:
- Non-selective (eg. propanolol)
- Beta-1 selective (eg. bisoprolol, metoprolol)
139
What are the Class III Anti-arrhythmics?
Prolongs action potential (eg. amiodarone and sotalol)
140
What are the Class IV Anti-arrhythmics?
Calcium Channel Blockers (only phenylalkylamines and benzothiozepines).
141
Which Anti-arrhythmics involve rate control and which involve rhythm control?
Rhythm control = Class I and III
Rate control = Class II and IV
142
What ADRs are associated with Amiodarone?
- Bradycardia
- Interstitial Lung Disease
- Hyper- and Hypothyroidism
- Hepatic dysfunction
- Photosensitivity
- Drug interactions
143
What type of drug is Digoxin?
Cardiac glycoside.
144
What is the mechanism of action of Digoxin?
It inhibits the Na/K pup, causing an increase in Ca2+ inside the cells of the heart.
145
What affect does digoxin have on the heart?
- Bradycardia
- Slows AV condunction
- Increased ectopic activity
- increased force of contraction
146
What are the indications for Digoxin?
- Atrial Fibrillation (reduces ventricular rate response)
- Severe heart failure (+ve inotropic effect)
147
What ADRs are associated with Digoxin?
- Narrow therapeutic range
- Nausea
- Vomiting
- Diarrhoea
- Confusion
148
What are the 4 aspects of Tetralogy of Fallot?
1. Ventricular Septal Defect
2. Pulmonary Stenosis
3. Hypertrophy of right ventricle
4. Overriding aorta
149
What is the key issue with Tetralogy of Fallot?
Anterior dislocation of the septum below the pulmonary outflow which causes the other issues.
150
What are Fallot spells?
A drop in the blood oxygen levels and deep cyanosis.
151
How many babies are born with Tetralogy of Fallot?
1 in 1000
10% of all birth defects.
152
What is the treatment for Tetralogy of Fallot?
Surgical repair
(Blalock-Thomas-Taussig Shunt or complete repair)
153
What is a Ventricular Septal Defect (VSD)?
An abnormal connection between the two ventricles.
154
How common are Ventricular Septal Defects?
Most common congenital heart defect (~20%).
Most close spontaneously during childhood.
155
What is the physiology of VSD?
High pressure in LV, low pressure in RV - blood flows from left to right.
156
What are the clinical signs of Large VSD?
- Small, breathless, skinny baby
- Increased resp rate
- Tachycardia
- Big heart
- Murmur
157
What are the clinical signs of Small VSD?
- Loud systolic murmur
- Thrill (buzzing sensation)
- Well grown
- Normal heart size
158
What is Eisenmenger's Syndrome?
- High pressure pulmonary blood flow
- Damage to the delicate pulmonary vasculature
- RV pressure increases, blood moves into LV
- Patient becomes cyanotic
159
What are Atrial Septal Defects (ASD)?
An abnormal connection between the two atria.
Often presents in adulthood (common).
160
What is the physiology of ASD?
- Slightly higher pressure in the LA than RA
- Shunt is left to right
- Increased flow into right heart and lungs
161
What are the clinical signs of ASD?
- Pulmonary Flow murmur
- Fixed split-second heart sound
- Large heart and pulmonary arteries
162
What are Atrio-Ventricular Septal Defects (AVSD)?
Hole in the centre of the heart, involves the ventricular and atrial septum, mitral and tricuspid valves. Can be complete or partial (often associated with Trisomy 21).
163
What is the physiology of AVSD?
Instead of two separate AV valves there is one malformed one - usually leaks to some degree.
164
What is Patent Ductus Arteriosus?
A continuous "machinery" murmur with a large heart, causes Eisenmenger's syndrome.
165
How is Patent Ductus Arteriosus treated?
Surgical or Percutanous closure.
166
What is Coarctation of the Aorta?
Narrowing of the aorta at the site of insertion of the ductus arteriosus.
167
What are the clinical signs of Coarctation of the Aorta?
- Right arm hypertension
- Bruits over the scapulae and back
- Murmur
168
What long term problems may be caused by Coarctation of the Aorta?
- Hypertension
- CAD
- Subarachnoid haemorrhage
- Re-coarctation
- Aneurysm at repair site
169
How is Coarctation of the aorta treated?
Surgical or percutaneous repair.
170
What is Bicuspid Aortic Valve (BAV)?
- Normal AV has three cusps
- Bicuspid AVs are common (1-2% of the population)
171
What is the issue with BAV?
- Can be severely stenotic in infancy/childhood
- Degenerate/ become regurgitant quicker than normal
- Less efficient
172
What is Pulmonary Stenosis?
- Narrowing of the outflow of the right ventricle
- Can be valvar, sub-valvar, supra-valvar or branch
- 8-12% of all congenital heart defects
173
How is Pulmonary Stenosis treated?
- Balloon valvuloplasty
- Open valvotomy
- Open trans-annular patch
- Shunt
174
What are the two layers the pericardium?
- Serous pericardium
- Fibrous pericardium
175
Describe the Serous Pericardium.
- Enclosed by fibrous pericardium
- Divided into two layers (each made up of a single sheet of epithelial cells) - Outer Parietal layer and Internal Visceral layer
176
Describe the Fibrous Pericardium?
- Continuous with the central tendon of the diaphragm
- 2mm thick layer made of tough connective tissue
177
What is found between the parietal and visceral pericardium?
The pericardial cavity - contains 50ml of serous fluid (to minimise friction generated by the heart during contraction)
178
What vessels are contained within the pericardium?
Roots of the great vessels:
- Aorta
- Pulmonary artery
- Pulmonary veins
- SVC
- IVC
179
What are the functions of the pericardium?
- Fixes the heart in the mediastinum and limits motion
- Prevents overfilling of the heart
- Lubrication
- Protection from infection (physical barrier)§
180
What is the relevance of the small reserve volume associated with the pericardial sac?
The volume of pericardial fluid changes based on the physiological state.
181
What is Cardiac Tamponade?
If the volume of serous fluid is exceeded, the pressure is transferred to the cardiac chambers.
The increase in pericardial fluid pressure can prevent the heart from expanding and ventricles from filling sufficiently.
182
What clinical signs are associated with Cardiac Tamponade?
- Reduced intrathoracic pressure during inspiration
- Increased venous return to the RA (suction due to compression)
- Increased RA compliance, reducing RA filling
- Decrease in systolic blood pressure by >10mmHg
183
What is Chronic Pericardial Effusion?
- Chronic accumulation of fluid allowing the adaption of the parietal pericardium
- Increased compliance reduced the effect on diastolic filling of the chambers
184
Define Acute Pericarditis.
An inflammatory pericardial syndrome with or without pericardial effusion.
185
Define Pericardial Effusion.
An accumulation of excess fluid in the pericardial cavity.
Pericardial fluid contains blood components such as fibrin, RBCs and WBCs.
186
How is Pericarditis diagnosed?
1. Clinical diagnosis made with two of the following:
- Chest pain (85-90%)
- Friction rub (33%)
- ECG changes (60%)
- Pericardial effusion (60%)
187
What are the infectious causes of Pericarditis?
1. Viral (most common)
- Enteroviruses
- Herpesviruses
- Adenoviruses
- Parvovirus B19
2. Bacterial (rare)
- Mycobacterium TB
188
What are the non-infectious causes of Pericarditis?
- Autoimmune (most common)
- Neoplastic
- Metabolic
- Traumatic and Iatrogenic
189
Give examples of autoimmune causes of pericarditis.
1. Sjorgen's syndrome
2. Rheumatoid arthritis
3. Scleroderma
4. Systemic vasculitides
190
Give examples of neoplastic causes of pericarditis.
Secondary metastatic tumours - mostly lung and breast cancer and lymphoma.
191
Give examples of metabolic causes of pericarditis.
Uraemia and Myxoedema.
192
Give examples of traumatic and iatrogenic caused of pericarditis.
1. Early onset:
- Direct injury (eg. penetrating thoracic injury)
- Indirect injury (eg. radiation injury)
2. Delayed onset:
- Pericardial injury syndromes (eg. Post-MI)
- Iatrogenic trauma (eg. Pacemaker lead insertion or PCI)
193
Give examples of other causes of pericarditis.
- Amyloidosis
- Aortic dissection
- Pulmonary arterial hypertension
- Chronic heart failure
194
What is the nature of chest pain associated with pericarditis?
- Severe, sharp and pleuritic
- No constricting crushing pain (Ischaemic pain)
- Rapid onset
- Radiating to arm
- Relieved by sitting forward
- Exacerbated by lying down
195
What other clinical presentations are associated with pericarditis?
- Dyspnoea
- Cough
- Systemic disturbance (eg. viral symptoms, rash, joint pain)
196
What is a pericardial rub?
- Extra heart sound heard upon auscultation
- Three components (one systolic, two diastolic)
- Sound resembles scratching/crushing of snow
- Audible friction of walls rubbing against each other
197
What are the signs of effusion associated with pericarditis?
Pulses Paradoxus - large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration
198
What is Beck's Triad?
Three clinical signs associated with Pericardial Tamponade:
- Hypotension
- Muffled heart sounds
- Raised jugular venous pressure
199
What characteristics of an ECG can be associated with Pericarditis?
- Diffuse ST elevation
- Concave ST segment
- Saddle shaped
- PR depression
200
What blood tests are used to investigate Pericarditis?
- FBC (increased White Cell Count)
- Erythrocyte Sedimentation Rate (ESR)
- Troponin
201
Give examples of differential diagnoses related to chest pain.
- Pneumonia
- PE
- GORD
- MI/ischaemia
- Aortic dissection
- Pancreatitis
- Pneumothorax
- Pneumonia
- Peritonitis
- HSV (shingles)
202
How is Pericarditis managed?
- No physical activity until resolution of inflammatory symptoms
- NSAIDs (ibuprofen or aspirin)
- Colchicine
203
What pericarditis complications are associated with high risk patients?
- Higher fever
- Subacute onset
- Large pericardial onset
- Cardiac tamponade
- Lack of response to pain relief
204
What pericarditis complications are associated with low risk patients?
- Myopericarditis
- Immunosuppression
- Trauma
205
What is the rate of Acute Pericarditis recurrence?
15-30% (Colchicine reduces rate by 50%)
206
What are the different types of Cardiomyopathy?
- Hypertrophic
- Dilated
- Arrhythmogenic Right/Left Ventricular
207
What is the usual inheritance pattern for Cardiomyopathy?
Autosomal dominant - offspring have a 50% chance of being affected.
208
What is Naxo's disease?
A Recessive condition with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C).
209
What are the histological features of Cardiomyopathy?
- Chaotic arrangement of cells and myofibrils
- Thicker artery walls
210
What type of mutation causes Hypertrophic Cardiomyopathy?
Sarcomeric gene mutations.
211
Describe the pathophysiology of Hypertrophic Cardiomyopathy.
Systole is normal but diastole is affected - the heart is unable to relax properly due to thickening of the ventricular walls.
212
What are the symptoms of Hypertrophic Cardiomyopathy?
- Angina
- Dyspnoea
- Syncope
213
What ECG abnormalities are associated with Hypertrophic Cardiomyopathy?
- Deep Q waves
- Large inverted T waves
- Non-sustained ventricular tachycardia (NSVT)
214
What type of mutation causes Arrhythmogenic Cardiomyopathy?
Desmosome gene mutations.
215
What does Arrhythmogenic Cardiomyopathy often present with?
Atrial Fibrillation.
216
Describe the pathophysiology of Arrhythmogenic Cardiomyopathy.
Desmosome mutations lead to myocytes being pulled apart and ventricular tissue is replaced with fatty fibrous tissue.
217
What is the major clinical sign associated with Arrhythmogenic Cardiomyopathy?
Ventricular tachycardia.
218
What ECG abnormalities are associated with Arrhythmogenic Cardiomyopathy?
- Epsilon waves (specifically ARVC)
- T wave inversion
219
What type of mutation causes Dilated Cardiomyopathy?
Cytoskeletal gene mutations.
220
Describe the pathophysiology of Dilated Cardiomyopathy?
Ventricular dilation and dysfunction causes poor contractility.
221
What are the symptoms of Dilated Cardiomyopathy?
- Breathlessness
- Tiredness
- Oedema
222
What ECG abnormalities are associated with Dilated Cardiomyopathy?
Non-specific T wave changes.
223
What are channelopathies?
Mutations in genes coding for ion channels.
224
Name the four main channelopathies.
- Long QT syndrome
- Short QT syndrome
- Brugada
- Catecholaminergic polymorphic ventricular tachycardia (CPVT)
225
What is the commonest symptom of channelopathies?
Recurrent syncope episodes.
226
What is Brugada Syndrome?
A channelopathy caused by a mutation in the cardiac sodium channel gene.
227
What are the symptoms of Brugada Syndrome?
Mostly asymptomatic but can cause syncope or sudden cardiac death.
228
What are the common rhythmic abnormalities associated with Brugada Syndrome?
Ventricular fibrillation or polymorphic ventricular tachycardia.
229
What ECG abnormalities are associated with Brugada Syndrome?
Characteristic ST elevation in chest leads.
230
What is Aortic Stenosis?
Narrowing of the aortic valve (normal area = 3-4cm^2)
231
When do symptoms of aortic stenosis present?
Valve area 1/4 of normal.
232
What are the 3 types of aortic stenosis?
- Supravalvular
- Subvalvular
- Valvular
233
What are the congenital causes of aortic stenosis?
- Congenital aortic stenosis
- Congenital bicuspid valve
234
What are the acquired causes of aortic stenosis?
- Degenerative calcification
- Rheumatic heart disease
- Rare causes
235
When are symptoms first noticed for congenital vs acquired aortic stenosis?
Congenital: 30 - 50 years old
Acquired: 70 - 80 years old
236
Describe the pathophysiology of aortic stenosis.
Pressure gradient develops between left ventricle and the aorta (increased afterload)
237
What are the compensatory mechanisms in aortic stenosis?
LV function initially maintained by compensatory pressure hypertrophy.
If this fails LV function declines.
238
What are the clinical presentations of aortic stenosis?
- Syncope on exertion (15%)
- Angina (35%)
- Dyspnoea (50%)
- Sudden death (rare)
239
What are the physical signs associated with aortic stenosis?
- Pulsus tardus (slow rising carotid pulse)
- Pulsus parvus (decreased pulse amplitude)
- Heart sounds (soft/absent 2nd heart sound)
- Ejection systolic murmur
240
What is the prognosis of aortic stenosis?
If with angina: 50% survive for 5 years
If with syncope: 50% survive for 3 years
If with heart failure: mean survival under 2 years
241
How is aortic stenosis graded?
Mild - area >1.5cm^2
Moderate - area 1.0-1.5cm^2
Severe - area <1.0cm^2
242
What investigation can assess the severity of aortic stenosis?
Echocardiogram:
- LV size and function
- Doppler-derived gradient and valve area
243
What is the general care in the management of aortic stenosis?
- Fastidious dental hygiene
- Consider infective endocarditis prophylaxis in dental procedures
244
What is the surgical management of aortic stenosis?
Valve replacement or definitive treatment.
245
What is the medical management of aortic stenosis?
Mechanical problem (a limited role for medication).
Contraindication for vasodilators.
246
What is TAVI?
Transcatheter Aortic Valve Implantation.
247
What are the indications for intervention in aortic stenosis?
- Any symptomatic patient with severe aortic stenosis
- Any patient with decreasing ejection fraction
- Any patient undergoing CABG with moderate or severe aortic stenosis
248
What is Mitral Regurgitation?
The mitral valve does not close properly, allowing for blood to flow backwards from LV to LA.
249
What are the causes of chronic mitral regurgitation?
- Myxomatus degeneration
- Ischaemic mitral regurgitation
- Rheumatic heart disease
- Infective endocarditis
250
What is the pathophysiology of mitral regurgitation?
Pure volume overload.
251
What are the compensatory mechanisms in mitral regurgitation?
- Left atrial enlargement
- Left ventricular hypertrophy
- Increased contractility
252
WHat are the clinical presentations of mitral regurgitation?
- Pansystolic murmur at apex, radiating to the axilla
- Exertion dyspnoea
- Heart failure
253
What are the clinical presentations of mitral regurgitation?
- Pansystolic murmur at apex, radiating to the axilla
- Exertion dyspnoea
- Heart failure
254
How long is the compensatory phase of mitral regurgitation?
10 to 15 years
255
What caused mortality to increase in patients with mitral regurgitation?
- Symptoms develop
- Ejection fraction falls to below 60%
256
What is the cause of mortality in patients with mitral regurgitation?
Progressive dyspnoea and heart failure.
257
What ECG abnormalities are associated with mitral regurgitation?
- LA enlargement
- AF
- LV hypertrophy
258
What do chest X-rays show in mitral regurgitation?
- LA enlargement
- Central pulmonary artery enlargement
259
What does an echocardiogram show in mitral regurgitation?
- Estimation of LA and LV size and function
- Valve structure
(Transoesophageal echocardiogram (TOE) most useful)
260
What monitoring is done in mitral regurgitation?
Echocardiogram:
- Mild: 2-3 years
- Moderate: 1-2 years
- Severe: 6-12 months
261
What medications can be given in the management of mitral regurgitaiton?
- Vasodilators (eg. ACEi)
- Rate control for AF (eg. beta-blockers, CCBs)
- Anticoagulation in AF and flutter
- Diuretics for fluid overload
262
When is infective endocarditis prophylaxis given in mitral regurgitation?
- Prosthetic valves
- History of infective endocarditis for dental procedures
263
When is surgery indicated for mitral regurgitation?
1. Any symptoms at rest or exercise
2. If asymptomatic:
- Ejection fraction <60%
- LV end-systolic diameter >45mm
264
What is aortic regurgitation?
Leakage of blood into the LV during diastole due to ineffective coaptation of the aortic cusps.
265
What are the causes of aortic regurgitation?
- Bicuspid aortic valve
- Rheumatic heart disease
- Infective endocarditis
266
What is the pathophysiology of aortic regurgitation?
Combined pressure and volume overload.
267
What are the compensatory mechanisms of aortic regurgitation?
LV dilation and hypertrophy.
268
Why can aortic regurgitation lead to heart failure?
Progressive LV dilation.
269
What are the clinical presentations of aortic regurgitation?
- Wide pulse pressure
- Hyperdynamic and displaced apical pulse
270
What can be found on auscultation of aortic regurgitation?
- Diastolic blowing murmur at the left sternal border
- Austin flint murmur (systolic ejection murmur) at the apex
271
What are the progressive symptoms of aortic regurgitation and when do they present?
- 40 to 50 years
- Dyspnoea on exertion
- Palpitations
272
How is a chest X-ray used to evaluate aortic regurgitation?
- Enlarged cardiac silhouette
- Aortic root enlargement
273
How is an echocardiogram used to evaluate aortic regurgitation?
- AV and aortic root evaluation
- LV dimensions and function
274
What are the general considerations of aortic regurgitation management?
Infective endocarditis prophylaxis.
275
What is the medical management of aortic regurgitation?
Vasodilators (ACEi improve stroke volume and reduce regurgitation only if patient is asymptomatic or hypertensive).
276
What is the definitive treatment of aortic regurgitation?
Surgical intervention - valve replacement
277
When is atrial regurgitation indicated for surgery?
- Any symptoms at rest or exercise
- Treat asymptomatic patients if ejection fraction <50% or LV dilated
278
What is mitral stenosis?
Obstruction of LV inflow that prevents proper filling in diastole.
279
What is the normal mitral valve area?
4-6cm^2
280
What are the causes of mitral stenosis?
- Rheumatic heart disease
- Infective endocarditis
- Mitral annular calcification
281
What is the pathophysiology of mitral stenosis?
- Progressive dyspnoea
- Increased transmitral pressures - LA enlargement and AF
- RH failure symptoms
- Haemoptysis
282
What are the clinical presentations of mitral stenosis?
- Prominent 'a' wave in jugular venous pulsations
- Signs of right heart failure (advanced disease)
- Mitral facies (pink-blue patches on cheeks)
- Heart sounds
283
What are the heart sounds in mitral stenosis?
- Low-pitched diastolic rumble most prominent at apex
- Loud opening S1 snap
(Best heard when patient is laying on LHS in expiration)
284
Which heart sounds indicate severe mitral stenosis?
Shorter S2 to opening snap interval.
285
What causes mortality in mitral stenosis?
- Progressive pulmonary oedema
- Infection
- Thromboembolism
286
How can ECGs evaluate the severity of mitral stenosis?
AF and LA enlargement.
287
How can chest X-rays evaluate the severity of mitral stenosis?
- LA enlargement
- Pulmonary oedema
- Calcific mitral valve (rare)
288
How can echocardiograms evaluate the severity of mitral stenosis?
- Gold standard diagnostic tool
- Assess mitral valve mobility, pressure gradient, and mitral valve area
289
How is the mitral stenosis monitored?
Serial echocardiography:
- Mild - 3-5 years
- Moderate 1-2 years
- Severe - yearly
290
How can medications be used to manage mitral stenosis?
- Mechanical problem (medication does not prevent progression)
- Beta-blockers
- CCBs
- Digoxin
- Diuretics
291
What general care should be taken in the management of mitral stenosis?
Infective endocarditis prophylaxis for patients with prosthetic valves, or a history of infective endocarditis for dental procedures.
292
What is the best management for mitral stenosis?
- Percutaneous mitral balloon valvotomy
- Diagnose patients early
293
What is Infective Endocarditis?
Infection of the heart valves or other endocardial lined structures within the heart (eg. septal defects, pacemaker leads).
294
What are the different types of Infective Endocarditis?
- Left-sided Native (mitral or aortic)
- Left-sided Prosthetic (early - within a year, late - after a year)
- Right-sided IE (rarely prosthetic).
- Device related (e.g. pacemakers, defibrillators)
295
How does the nature of Infective Endocarditis affect the outcome?
Left-sided: More likely to cause thrombo-emboli systematically
Right-sided: More likely to spread to cause a pulmonary embolism
296
What are the risk factors for Infective Endocarditis?
- Having a regurgitant or prosthetic valve
- If infectious material is introduced into the bloodstream during surgery
- Individuals who have had IE previously
297
What groups are at increased risk of Infective Endocarditis?
- Elderly
- IV drug users
- Individuals with artificial valves
- Young people with congenital heart diseases
298
What three bacteria are most likely to cause Infective Endocarditis?
- Streptococcus viridans (Group B haemolytic optochin resistant)
- Staphylococcus aureus
- Staphylococcus epidermis (coagulase -ve staph)
299
What are the two main sites vegetation adheres to in Infective Endocarditis?
- Atrial surface of AV valves
- Ventricular surface of SL valves
300
What are the main clinical presentations of Infective Endocarditis?
- Signs of systemic infection (eg. fever and sweats)
- Embolisation (eg. stroke, PE, MI)
- Valve dysfunction
301
What are the five main signs associated with Infective Endocarditis?
- Splinter haemorrhages (small blood spots underneath the nail)
- Osler's nodes (painful, red, raised lesions found on the hands and feet)
- Janeway lesions
- Roth spots (small retinal haemorrhage)
- Heart murmurs
302
What investigations might be done if Infective Endocarditis is expected?
- Blood cultures
- Echocardiogram (shows endocardial involvement)
- Blood samples (raised ESR/CRP)
- ECG
303
What are the advantages and disadvantages of Trans-Thoracic Echocardiogram?
1. Advantages:
- Safe
- Non-invasive
- No discomfort
2. Disadvantages
- Lower quality imaging
304
What are the advantages and disadvantages of Trans-Oesophageal Echocardiography?
1. Advantages:
- Excellent imaging
2. Disadvantages:
- Discomfort
- Small risk of perforation or aspiration
305
What is the criteria for diagnosis of Infective Endocarditis?
Duke's Criteria: Acombination of major and minor symptoms associated with IE.
1. Definite:
- Two major
- One major and three minor
- Five minor
2. Possible:
- One major and one minor
- Three minor
306
What are the major and minor signs of Infective Endocarditis according to Duke's Criteria?
Major:
- Positive blood culture
- Echocardiography showing endocardial involvement
Minor:
- Fever
- Pre-disposing factor
- Vascular phenomena
- Immunological problems
- Microbiological evidence
307
How is Infective Endocarditis treated?
- Antimicrobials based on culture
- Treat complications (eg. arrhythmia, HF etc)
- Surgery
308
What are the indications for surgery in Infective Endocarditis?
- Antibiotics not working
- Complications (e.g. aortic root abscess, severe valve damage)
- Removal of infected devices
- Valve replacement
- Removal of large vegetation before they embolise
309
Why is it important to remove large vegetations?
To prevent them embolising and causing a stroke, MI etc.
310
What are the normal interval times for each wave on an ECG? (in Milliseconds)
PR - 120-200
ST - 270-330
QT - 350-420
QRS - 80-110
311
What do low amplitude P waves suggest?
- AF
- Obesity
- Hyeprkalaemia
312
What do high amplitude P waves suggest?
Right atrial enlargement.
313
What do broad-notched P waves suggest?
Left atrial enlargement.
314
What does a short PR interval suggest?
- Younger patients
- Pre-excitation eg. Wolf-Parkinson-White syndrome
315
What does a long PR interval suggest?
Disorders of the AV node and specialised conducting tissue.
316
What does a broad QRS interval suggest?
- Ventricular conduction delay
- Pre-excitation
317
What does a small QRS interval suggest?
- Obese patient
- Pericardial effusion
- Infiltrative cardiac disease
318
What does a tall QRS interval suggest?
- Left ventricular hypertrophy
- Thin patient
319
What do "Long QT" or "Short QT" syndromes suggest?
Excessively rapid or slow repolarisation - can be arrhythmogenic. (Congenital, drugs or electrolyte disturbances)
320
What does an elevated ST segment suggest?
- Early repolarisation
- Myocardial infarction
- Pericarditis/myocarditis
321
What does T wave inversion suggest?
- Ischaemia/infarction
- Myocardial strain (hypertrophy)
- Myocardial disease (cardiomyopathy)
322
What are the 5 types of Tachycardia?
- Atrial Fibrillation
- Atrial Flutter
- Supraventricular Tachycardia (SVT)
- Ventricular Tachycardia
- Ventricular Fibrillation
323
What are the common causes of Bradycardia?
- Conduction tissue fibrosis
- Ischaemia
- Inflammation/infiltrative disease
- Drugs
324
How do Ischaemia and Infarction present on an ECG?
- T wave flattening inversion
- ST segment depression
- ST segment elevation
- Q waves - old infarction
325
What are Ectopic beats?
- Very common
- Non-sustained beats arising from ectopic regions of atria or ventricles
- Generally benign
326
What is Atrial Fibrillation?
- Commonest sustained arrhythmia
- Paroxysmal or persistant
- Rapid chaotic firing caused loss of mechanical contraction and irregular ventricular response
327
What is the medical treatment for AF?
- Treat underlying cause
- Rate control (eg. beta-blockers, CCBs)
- Restore sinus rhythm (eg. cardioversion)
- Maintain sinus rhythm (eg. amiodarone, flecainide)
328
What is the surgical intervention for AF?
Catheter ablation
329
What is a major risk of AF?
Stroke due to thrombus formation.
(Risk is calculated with CHA2DS2-VASc score)
330
How is SVT treated?
- Valsalva manouvres
- Beta-blockers or CCBs
- Catheter ablation
331
What are Accessory Pathways?
Congenital remnant muscle strands between the atrium and ventricle.
Can manifest as pre-excitation or be concealed (normal ECG)
332
What is an "electrical storm"?
- 3 or more sustained episodes of VT or VF
- High risk/poor prognosis
- Manage on CCU/ITU
333
How is an electrical storm treated?
- Correct any provoking factors
- Beta-blockers
- Sedation
- Amiodarone
- Overdrive pacing
- Catheter ablation
334
What is Heart Failure?
An inability of the heart to deliver blood at a rate commensurate with the requirement of the metabolising tissues, despite normal or increased cardiac filling rates.
335
What are the causes of Heart Failure?
- Myocardial dysfunction as a result of IHD (commonest)
- Hypertension
- Alcohol excess
- Cardiomyopathy
- Valvular
- Endocardial/Pericardial
336
What are the main phenotypes of Heart Failure?
- HF with reduced ejection fraction (HFrEF)
- HF with preserved ejection fraction (HRpEF)
337
What are the symptoms of HF?
- Breathlessness
- Tiredness
- Cold peripheries
- Leg swelling
- Increased weight
338
What are the clinical signs of HF?
- Tachycardia
- Displaced apex beat
- Added heart sounds and murmurs
- Hepatomegaly
- Peripheral and sacral oedema
- Ascites
339
What is the New York Heart Association (NYHA) classification?
Class I: No limitation (asymptomatic)
Class II: Slight limitation
Class III: Marked limitation
Class IV: Inability to carry out any physical activity without discomfort
340
What is the treatment of HF-PEF?
- Spironolactone in small doses
- Tafamidis for peripheral neuropathy
341
What is the treatment for HF-REF?
1st line: ACEi and beta-blockers
2nd line: ARBs
3rd line: Hydralazine/nitrate combination
342
What lifestyle changes are recommended as treatment for HF?
- Avoid large meals
- Weight loss
- Smoking cessation
- Exercise
- Vaccination
343
What is the purpose of an ECG of a patient suspected of HF?
To ascertain the underlying cause:
- Ischaemia
- LVH
- Hypertension
- Arrhythmia
