Cardiology (3) Flashcards

1
Q

Define varicose veins

A

Subcutaneous permanently dilated veins >3mm diameter when measured in standing position, usually in the superficial veins of the lower leg due to valve insufficiency

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2
Q

Summarise the aetiology of varicose veins

A

Venous valve incompetence allowing backflow of blood and pooling

Primary:
Due to genetic or developmental weakness in the vein wall
Results in increased elasticity, dilatation and valvular incompetence

Secondary:
Due to venous outflow obstruction 
Pregnancy 
Pelvic malignancy 
Ovarian cysts 
Ascites 
Lymphadenopathy 
Retroperitoneal fibrosis 
Due to valve damage (e.g. after DVT) 
Due to high flow (e.g. arteriovenous fistula)
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3
Q

What are the risk factors of varicose veins?

A
Increasing age
Female
Pregnancy
Family history
Caucasian
Obesity
Standing for prolonged periods of time
Crossing knees for prolonged periods of time
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4
Q

Summarise the epidemiology of varicose veins

A
COMMON
Prevalence higher in industrialised and developed regions
Prevalence = 10-15% in men
Prevalence = 20-25% in women
More common in women
Prevalence increases with age
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5
Q

What are the presenting symptoms of varicose veins?

A

Enlarged, tortuous, visible veins in the lower leg
Pain
Pruritis
Fatigue
Heaviness
Patients may complain about the cosmetic appearance
Aching in the legs - worse towards the end of the day or after standing for long periods of time
Swelling
Bleeding
Infection
Ulceration

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6
Q

What are the signs on physical examination of varicose veins?

A

Inspect when STANDING
Swelling of legs
Enlarged tortuous visible veins in the legs
Hyperpigmentation/darkening of leg (haemosiderin deposition)
Venous stasis ulcers
May feel fascial defects along the veins
Cough impulse may be felt over the saphenofemoral junction
Tap Test - tapping over the saphenofemoral junction will lead to an impulse felt distally (this would not happen if the valves were competent)
Palpation of a thrill or auscultation of a bruit would suggest an AV fistula
Leg is elevated and the veins are emptied

Signs of venous insufficiency:
Varicose eczema 
Haemosiderin staining 
Atrophie blanche 
Lipodermatosclerosis
Oedema 
Ulceration
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7
Q

What are the appropriate investigations for varicose veins?

A

Duplex USS - assess for reversed flow, valve closure time (>0.5 seconds indicative of reflux), locates sites of incompetence or reflux and excludes DVT

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8
Q

What is the appropriate management for varicose veins?

A
Conservative:
Elevate legs above heart regularly
Compression stockings to prevent venous stasis
Manual compression
Exercise - improve skeletal muscle pump#
Weight loss
Reduce long periods of standing
Surgical:
Saphenofemoral ligation 
Stripping of the long saphenous vein 
Avulsion of varicosities
Vein transplant
Vein repair
Vein removal
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9
Q

What are the possible complications of varicose veins?

A
Chronic venous insufficiency
Venous ulceration
Haemorrhage of varicose veins
Lipodermatosclerosis
Haemosiderin deposition
Eczema
Superficial thrombophlebitis 

Complications of Sclerotherapy :
Skin staining, local scarring

Complications of Surgery:
Haemorrhage, infection, recurrence, paraesthesia, peroneal nerve injury

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10
Q

What is the prognosis of varicose veins?

A

Slowly progressive

High recurrence

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11
Q

Define pulmonary hypertension

A

An increase in mean pulmonary arterial pressure >25mmHg which can be caused by a variety of other conditions and can lead to originally right ventricular hypertrophy, followed by right heart failure.

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12
Q

Summarise the aetiology of pulmonary hypertension

A
Idiopathic
Chronic lung disease eg COPD
Hypoxia
Left heart failure
Left heart valve failure
Methotrexate leading to lung fibrosis
Chronic thromboembolic events leading to clots constricting pulmonary vessels causing to increased resistance
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13
Q

Summarise the epidemiology of pulmonary hypertension

A

Idiopathic pulmonary hypertension is RARE

More common in severe respiratory and cardiac disease

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14
Q

What are the presenting symptoms of pulmonary hypertension?

A
Progressive dyspnoea
Orthopnoea
Fatigue
Weakness
Exertional dizziness and syncope
Swelling of legs
Angina and tachyarrhythmia
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15
Q

What are the signs on physical examination of pulmonary hypertension?

A
Hepatomegaly
Raised JVP
Peripheral oedema
Dullness on percussion due to pulmonary oedema
Right ventricular heave
Loud pulmonary second heart sound 
Murmur - pulmonary regurgitation 
Tricuspid regurgitation
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16
Q

What are the appropriate investigations for pulmonary hypertension?

A

Echo - shows elevated pressure in pulmonary arteries and right ventricle
Right heart catheterisation - allows diagnostic measurement of pressure in pulmonary vessels
CXR – exclude other lung diseases
ECG – right ventricular hypertrophy and strain
Pulmonary function tests
LFTs – liver damage - portal hypertension
Lung biopsy – interstitial lung disease

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17
Q

Define ventricular tachycardia

A

A regular broad QRS complex tachycardia, characterised by heart beat greater than 100bpm which originates from a ventricular ectopic focus.

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18
Q

Summarise the aetiology of ventricular tachycardia

A

Idiopathic

Secondary to:
Coronary heart disease
Hypertension
Cardiomyopathy
Post-MI

Electrical impulses arise from a ventricular ectopic focus
Can be caused by infectious diseases such as Chagas’ disease.

Risk Factors:
Coronary heart disease
Structural heart disease
Electrolyte deficiencies (e.g. hypokalaemia, hypocalcaemia, hypomagnesaemia)
Use of stimulant drugs (e.g. caffeine, cocaine)

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19
Q

Summarise the epidemiology of ventricular tachycardia

A

Fairly common
It is one of the shockable rhythms that is seen in cardiac arrest patients
VT incidence peaks in the middle decades of life
Most common cause of sudden cardiac death

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20
Q

What are the presenting symptoms of ventricular tachycardia?

A
Symptoms of hypoperfusion of end organs due to decreased CO
Dizziness
Syncope
Weakness
Palpitations
Fatigue
Chest pain
Dyspnoea
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21
Q

What are the signs on physical examination of ventricular tachycardia?

A
Depends on degree of haemodynamic instability:
Tachycardia
Hypotension
Weak pulse
Impaired consciousness
Cannon A waves
Respiratory distress 
Bibasal crackles
Anxiety
Agitation
Lethargy
Coma
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22
Q

What are the appropriate investigations of ventricular tachycardia?

A

ECG:
Broad QRS complex tachycardia - >120ms
Monomorphic (re-entrant tachy above scar tissue or focal) or polymorphic waves (focal)

Electrolytes:
Hypokalaemia and hypomagnesaemia are associated with torsades-de-pointes

Drug levels to check for digoxin toxicity

Troponin and creatine kinase MB - elevated in MI

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23
Q

What is the management of ventricular tachycardia?

A

Pulseless VT - follow advanced life support algorithm, DEFIBRILLATION (unsynchronised)

Unstable VT - reduced cardiac output:
Synchronised cardioversion
Correct electrolyte abnormalities or other reversible cause
Amiodarone – anti-arrhythmic medication

Stable VT: (no symptoms of haemodynamic compromise)
Correct electrolyte abnormalities
Amiodarone
2nd line if ineffective - Synchronised DC shock

Implantable Cardioverter Defibrillator (ICD) if:
Sustained VT causing syncope
Sustained VT with ejection fraction < 35%
Previous cardiac arrest due to VT or VF
MI complicated by non-sustained VT

Radiofrequency catheter ablation if structural heart disease

24
Q

What are the possible complications of ventricular tachycardia?

A
ICD malfunction
VF
Sudden cardiac death
ICD infection
Congestive cardiac failure
Cardiogenic shock
25
Q

Summarise the prognosis of ventricular tachycardia

A

GOOD if treated RAPIDLY

Long-term prognosis depends on the underlying cause

26
Q

Define peripheral vascular disease

A

A range of arterial syndromes caused by narrowing of vessels, resulting in reduced blood flow. This is most often due to atherosclerosis affecting the arteries of the leg.

27
Q

Summarise the aetiology of peripheral vascular disease

A

The most common cause is ATHEROSCLEROSIS

Types of peripheral vascular disease:
Intermittent claudication - calf pain on exercise
Critical limb ischaemia - pain at rest: the MOST SEVERE manifestation of PVD
Acute limb ischaemia - a sudden decrease in arterial perfusion in a limb, due to thrombotic or embolic causes
Arterial ulcers
Gangrene

Risk factors:
Hypertension
Smoking
Dyslipidaemia
Diabetes
Metabolic syndrome
Age >60 years
Obesity
Physical inactivity
28
Q

Summarise the epidemiology of peripheral vascular disease

A

Incidence increases with age

More common in men

29
Q

What are the presenting symptoms of peripheral vascular disease?

A

INTERMITTENT CLAUDICATION:
Pain, tiredness, numbness of legs which is relieved by rest
Calf claudication = femoral disease
Buttock claudication = iliac disease

Critical limb ischaemia:
Pain in legs at rest, worst when lying down
Relieved by standing
Ulcers
Gangrene 
Night pain

Leriche Syndrome (aortoiliac occlusive disease):
Buttock claudication
Impotence
Absent/weak distal pulses

Progression from asymptomatic, intermittent claudication, rest pain, ulcers and gangrene

30
Q

What are the signs on physical examination of peripheral vascular disease?

A
Hair loss
Pallor
Nail changes - loss, brittle, ridging
Ulcers - dry, painful, punched out, non-healing
Gangrene
Dependent rubor - foot turns red when hanging down
Elevation pallor
Muscular atrophy
Acute ischaemic limb = 6Ps:
Pallor
Parasthesia
Paralysis
Pain
Perishingly cold
Pulseless
31
Q

What are the appropriate investigations for peripheral vascular disease?

A

Ankle brachial pressure index - systolic ankle/systolic arm <0.91
Toe-brachial index <0.6
Doppler ultrasound - FIRST LINE - shows site and degree of stenosis
CT/MR arteriography
Conventional arteriography - gold standard for vascular imaging

DO NOT APPLY PRESSURE BAND - will worsen ischaemia

32
Q

Define ventricular fibrillation

A

Uncoordinated muscle fibre contraction in the ventricles, resulting in an irregular broad-complex tachycardia that can cause cardiac arrest and sudden cardiac death and zero cardiac output.

Ventricular fibrillation is a medical emergency and will result in death within minutes if it is not rapidly identified and managed appropriately.

33
Q

Summarise the aetiology of ventricular fibrillation

A

The ventricular fibres contract randomly causing complete failure of ventricular function
Most cases occur in patients with underlying heart disease

Causes:
Ischaemic Heart Disease/Coronary artery disease (most common)
Idiopathic (progression from idiopathic ventricular tachycardia)
Cardiomyopathy (hypertrophic, arrhythmogenic right ventricular)
Long QT Syndrome
Tissue heterogeneity
Ischaemia
Electrolyte disturbance - hypo or hyperkalaemia
Drugs - methamphetamines, cocaine
Scarring of heart causing anatomical reentrant

34
Q

Summarise the epidemiology of ventricular fibrillation

A

The MOST COMMON arrhythmia identified in cardiac arrest patients
Incidence of VF parallels the incidence of ischaemic heart disease

35
Q

What are the presenting symptoms of ventricular fibrillation?

A

Collapse, fainting and loss of consciousness are most common presentations

Preceding symptoms:
Chest pain
Nausea
Vomiting
Palpitations
Dizziness
SOB
History of associated conditions:
Coronary artery disease
Cardiomyopathy
Valvular heart disease
Long QT syndrome
Wolff-Parkinson-White syndrome
Brugada syndrome
36
Q

What are the signs on physical examination of ventricular fibrillation?

A
Tachycardia
Hypotension
Weak pulses
Presyncope
Syncope
Airway compromise
Diminished responsiveness
Dyspnoea
37
Q

What are the appropriate investigations for ventricular fibrillation?

A

ECG:
No clear P, Q, R, S or T waves
Rate 150-500bpm
Chaotic irregular deflections of varying amplitude

Cardiac enzymes (e.g. troponins) - check for recent ischaemic event

Electrolytes - derangement can cause arrhythmias, including VF

Drug levels and toxicology screen - anti-arrhythmics and cocaine can cause arrhythmia

TFTs - hyperthyroidism can cause tachyarrhythmias

Coronary angiography - if patient survives VF, to check the integrity of coronary arteries

38
Q

What is the management of ventricular fibrillation?

A

Urgent defibrillation and CPR
Cardioversion

ICD implantation if VF is due to irreversible cause

Patients who survive need full assessment of left ventricular function, myocardial perfusion and electrophysiological stability

Empirical beta-blockers
Some patients may be treated with radiofrequency ablation (RFA)

39
Q

What are the possible complications of ventricular fibrillation?

A
Ischaemic brain injury due to loss of cardiac output
Myocardial injury 
Post-defibrillation arrhythmias 
Aspiration pneumonia 
Skin burns 
Death
40
Q

Summarise the prognosis of ventricular fibrillation

A

Depends on the time between onset of VF and medical intervention
Early defibrillation is essential (ideally within 4-6 mins)
Anoxic encephalopathy is a major outcome of VF

41
Q

Define supraventricular tachycardia

A

A narrow-complex tachycardia with absent p waves which has a supraventricular origin.
AF is a type of SVT
Typically involves AVNRT and AVRT - regular narrow complex, paroxysmal SVT

42
Q

Describe the aetiology of supraventricular tachycardia

A

AVRT - accessory pathway forms between atria and ventricles, allowing electrical impulse to pass back up from the ventricle to the atria, causing a re-entry circuit. Common type of this is Wolff-Parkinson-White syndrome with Bundle of Kent

AVNRT - accessory pathway is in or around the AV node (localised re-entry circuit)

Risk factors:
Nicotine
Alcohol
Caffeine
Previous MI
Digoxin toxicity
43
Q

Summarise the epidemiology of supraventricular tachycardia

A

Twice as common in females

More common in younger patients

44
Q

What are the presenting symptoms of supraventricular tachycardia?

A

Paroxysmal
Abrupt onset and termination of symptoms

Dyspnoea
Dizziness
Chest pain
Syncope
Pre-syncope
Fatigue
Palpitations
45
Q

What are the signs on physical examination of supraventricular tachycardia?

A

Tachycardia - 150-250bpm
AVNRT - normal except tachycardia

Wolff-Parkinson-White:
Tachycardia
Secondary cardiomyopathy (S3 gallop, RV heave, displaced apex beat)

46
Q

What are the appropriate investigations for supraventricular tachycardia?

A

ECG:
Narrow complex tachycardia, absent p waves
Differentiating between AVNRT and AVRT – once the SVT has been terminated and normal rate and rhythm are re-established:
AVNRT – appears normal
AVRT – delta-waves (slurred upstroke of the QRS complex)

24 hr ECG monitoring - will be required in patients with paroxysmal palpitations

Cardiac Enzymes: Check for features of MI (especially if there is chest pain)
Electrolytes: can cause arrhythmia
TFTs: can cause arrhythmia
Digoxin Level: for patients on digoxin
Echocardiogram: check for structural heart disease

47
Q

What is the appropriate management of supraventricular tachycardia?

A

Haemodynamically unstable = DC cardioversion
Haemodynamically stable = vagal manouvere and chemical cardioversion

AVNRT:
Vagal manouveres (blocks AV node) - carotid sinus massage, Valsalva manouvere (forced exhalation in acute attack
If unresponsive to vagal manouveres:
Adenosine

AVRT:
Acute: Same as AVNRT, avoid long acting AV nodal blockers e.g. digoxin, verapamil
Medical: Procainamide and Flecainide

Long term - radiofrequency ablation

48
Q

What are the possible complications of supraventricular tachycardia?

A
Haemodynamic compromise
Congestive heart failure
Systemic embolism
Cardiac tamponade
DVT 
Syncope 
MI
Tachycardia-induced angina
49
Q

Summarise the prognosis of supraventricular tachycardia

A

Dependent on the presence of underlying structural heart disease
If structurally normal heart – GOOD PROGNOSIS
People with pre-excitation have a small risk of sudden death

50
Q

Define Ischaemic Heart Disease

A

Characterised by decreased blood supply to the heart muscle resulting in chest pain (angina pectoris).
May present as stable angina or acute coronary syndrome.
ACS can be further subdivided into:
Unstable angina - chest pain at rest due to ischaemia but without cardiac injury
NSTEMI
STEMI - ST elevation with transmural infarction

51
Q

Summarise the aetiology of Ischaemic Heart Disease

A

Angina pectoris occurs when myocardial oxygen demand exceeds oxygen supply, usually due to atherosclerosis

Rare causes of angina pectoris:
Coronary artery spasm (e.g. induced by cocaine), arteritis and emboli

Risk Factors:
Male
Diabetes mellitus
Family history
Hypertension
Hyperlipidaemia
Smoking
52
Q

Summarise the epidemiology of Ischaemic Heart Disease

A

Common

More common in males

53
Q

What are the presenting symptoms of Ischaemic Heart Disease?

A
Crushing central chest pain
Pain radiates to jaw and down left arm
Develops during exercise and relieved with rest - stable angina
Nausea
Sweating
Fatigue
Dyspnoea
54
Q

What are the signs on physical examination of Ischaemic Heart Disease?

A

ACS: There may be NO CLINICAL SIGNS

Pale
Sweating
Restless
Low-grade pyrexia

Check both radial pulses to rule out aortic dissection
Arrhythmias, disturbances of BP and new heart murmurs
Signs of complications (e.g. acute heart failure, cardiogenic shock)

55
Q

What are the appropriate investigations for Ischaemic Heart Disease?

A

Troponin - elevated if STEMI or NSTEMI
AST - raised 24 hours post-MI
LDH - raised 48 hours post-MI

ECG:
ST depression - NSTEMI
New onset LBBB - STEMI
ST elevation in leads V1-V4 - anterior - left anterior descending artery
ST elevation in leads II, III, aVF - inferior - right coronary artery
ST elevation in leads V5, V6, aVL, I - lateral - left circumflex artery

Posterior MI - ST depression V1-V3, tall R wave

56
Q

Summarise the management of Ischaemic Heart Disease

A
Stable angina:
Symptomatic - GTN spray
Anti-anginals - beta blockers, CCB
Risk factor control
Aspirin 75mg/day
ACS management:
Morphine
Oxygen
Anticoagulants - aspirin, clopidogrel
Nitrates

Beta blockers
ACEi
Statins
Heparin

STEMI:
If <12 hours since symptom onset - urgent PCI
If >12 hours, coronary angiography followed by PCI if necessary

STEMI = aspirin, clopidogrel, PCI
NSTEMI = aspirin, clopidogrel, LMWH
57
Q

What are the possible complications of ischaemic heart disease?

A
Death
Arrhythmia - VT
Rupture
Tamponade
Heart failure
Valve disease
Aneurysm
Dressler's syndrome
Embolism
Reinfarction