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
Summarise the prognosis of ventricular tachycardia
GOOD if treated RAPIDLY | Long-term prognosis depends on the underlying cause
26
Define peripheral vascular disease
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
Summarise the aetiology of peripheral vascular disease
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
Summarise the epidemiology of peripheral vascular disease
Incidence increases with age | More common in men
29
What are the presenting symptoms of peripheral vascular disease?
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
What are the signs on physical examination of peripheral vascular disease?
``` 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
What are the appropriate investigations for peripheral vascular disease?
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
Define ventricular fibrillation
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
Summarise the aetiology of ventricular fibrillation
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
Summarise the epidemiology of ventricular fibrillation
The MOST COMMON arrhythmia identified in cardiac arrest patients Incidence of VF parallels the incidence of ischaemic heart disease
35
What are the presenting symptoms of ventricular fibrillation?
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
What are the signs on physical examination of ventricular fibrillation?
``` Tachycardia Hypotension Weak pulses Presyncope Syncope Airway compromise Diminished responsiveness Dyspnoea ```
37
What are the appropriate investigations for ventricular fibrillation?
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
What is the management of ventricular fibrillation?
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
What are the possible complications of ventricular fibrillation?
``` Ischaemic brain injury due to loss of cardiac output Myocardial injury Post-defibrillation arrhythmias Aspiration pneumonia Skin burns Death ```
40
Summarise the prognosis of ventricular fibrillation
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
Define supraventricular tachycardia
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
Describe the aetiology of supraventricular tachycardia
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
Summarise the epidemiology of supraventricular tachycardia
Twice as common in females | More common in younger patients
44
What are the presenting symptoms of supraventricular tachycardia?
Paroxysmal Abrupt onset and termination of symptoms ``` Dyspnoea Dizziness Chest pain Syncope Pre-syncope Fatigue Palpitations ```
45
What are the signs on physical examination of supraventricular tachycardia?
Tachycardia - 150-250bpm AVNRT - normal except tachycardia Wolff-Parkinson-White: Tachycardia Secondary cardiomyopathy (S3 gallop, RV heave, displaced apex beat)
46
What are the appropriate investigations for supraventricular tachycardia?
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
What is the appropriate management of supraventricular tachycardia?
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
What are the possible complications of supraventricular tachycardia?
``` Haemodynamic compromise Congestive heart failure Systemic embolism Cardiac tamponade DVT Syncope MI Tachycardia-induced angina ```
49
Summarise the prognosis of supraventricular tachycardia
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
Define Ischaemic Heart Disease
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
Summarise the aetiology of Ischaemic Heart Disease
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
Summarise the epidemiology of Ischaemic Heart Disease
Common | More common in males
53
What are the presenting symptoms of Ischaemic Heart Disease?
``` 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
What are the signs on physical examination of Ischaemic Heart Disease?
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
What are the appropriate investigations for Ischaemic Heart Disease?
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
Summarise the management of Ischaemic Heart Disease
``` 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
What are the possible complications of ischaemic heart disease?
``` Death Arrhythmia - VT Rupture Tamponade Heart failure Valve disease Aneurysm Dressler's syndrome Embolism Reinfarction ```