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Conditions-3 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is an abdominal aortic aneurysm?

A

The permanent pathological dilation of the aorta with a diameter >1.5 times the expected anteroposterior (AP) diameter of that segment

*risk of rupture increases significantly >6cm

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2
Q

What are the risk factors of an abdominal aortic aneurysm?

A 
Cigarette smoking *most important*
Family history 
Increased age
Male sex
Female sex- rupture of AAA
Congenital/ connective tissue disorders
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3
Q

What is the aetiology of an abdominal aortic aneurysm?

A

Traditionally, arterial aneurysms were thought to arise from (intimal) atherosclerotic disease. Now- altered tissue metalloproteinases may diminish the integrity of the arterial wall

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4
Q

What is the epidemiology of an abdominal aortic aneurysm?

A

Prevalence among men is 4 to 6 times higher than in women.

Increased prevalence with age and smoking status

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5
Q

What are the presenting symptoms of an abdominal aortic aneurysm?

A 
Can be asymptomatic.
Abdominal and lower back pain may be associated. 
If ruptured: 
Sudden severe pain
Dizziness
Sweating, pale, clammy skin
Shortness of breath 
LOC
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6
Q

What are the signs of an abdominal aortic aneurysm on physical examination?

A

Abdominal Aorta on palpation is pulsatile AND expansile

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7
Q

What are the appropriate investigations for an abdominal aortic aneurysm? Interpret the results

A

1st line:
-*Abdominal ultrasound (abdominal aortic dilation of >1.5 times the expected anterior-posterior diameter of that segment, given the patient’s sex and body size)
Others to consider:
Bloods:
Haematology: FBC (leukocytosis- infectious AAA), ESR (inflammatory AAA)
Biochemistry: CRP (same as ESR)
Microbiology: Blood culture (infectious AAA)
Special tests:
CT angiography/ MRI

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8
Q

What is amyloidosis?

A

A (heterogenous) group of diseases characterised by extracellular deposition of amyloid fibrils.
Progressive deposition of amyloid is disruptive to tissue and organ function and manifests by the dysfunction of those organs in which it deposits

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9
Q

What are the risk factors of amyloidosis?

A

Inflammatory polyarthritis- most common underlying cause of AA amyloidosis (includes rheumatoid arthritis, ankylosing spondylitis, psoriatic arthritis)
Chronic infections (bronchiectasis, chronic UTIs)
IBD- particularly Crohn’s disease
Familial periodic fever syndrome
Monoclonal gammopathy of undetermined significance MGUS- multiple myeloma is the most common disorder, but can increase risk of amyloidosis

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10
Q

What is the aetiology of amyloidosis?

A 
Primary amyloidosis (immunoglobulin light chain amyloidosis-AL): 
aeitiology unknown, no underlying genetic or environmental causes 
Non-familial secondary amyloidosis (AA):
Inflammatory polyarthropathies account for 60% of cases, then chronic infections, IBD. 
Secondary amyloidosis (AA) (familial periodic Mediterranean fever syndrome)
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11
Q

What is the epidemiology of amyloidosis?

A

In the UK, the age-adjusted incidence is between 5.1 and 12.8 per 1 million per year, with around 60 new cases annually- RARE

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12
Q

What are the presenting symptoms of amyloidosis?

A 
PMH of inflammatory conditions (RF)
Chronic infections (RF)
Positive FH (RF)
Fatigue 
Weight loss 
Dyspnoea on exertion
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13
Q

What are the signs of amyloidosis on physical examination?

A

Elevated JVP: High right-sided filling pressure
Lower extremity oedema: High right sided filling pressures in presence of restrictive cardiomyopathy. Present in around half of patients.
Periorbital purpura: skin bleeding around eyes due to vessel wall fragility and damage by amyloid
Macroglossia: (tongue enlargement) most specific sign in AL

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14
Q

What are the appropriate investigations for amyloidosis? Interpret the results

A

1st line:
Serum/ urine immunofixation- presence of monoclonal protein
Immunoglobulin free light chain assay- diagnosing AL
Bone marrow biopsy- clonal plasma cells
Others:
Tissue biopsy, ECG (for conduction abnormalities)

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15
Q

What is aortic dissection?

A

A condition where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, and creating a false lumen.

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16
Q

What are the risk factors of aortic dissection?

A

Hypertension
Aortic atherosclerosis
Connective tissue disease (e.g. SLE, Marfan’s)
Congenital cardiac abnormalities (e.g. aortic coarctation)
Inflammation- aortitis (e.g. Takayasu’s aortitis, tertiary syphilis)
Iatrogenic (e.g. during angiography or angioplasty)
Trauma
Drugs-crack cocaine

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17
Q

What is the aetiology of aortic dissection?

A

Stanford classification divides dissection into:
Type A with ascending aorta tear (most common);
Type B with descending aorta tear distal to the left subclavian artery.

Expansion of the false aneurysm may obstruct the subclavian, carotid, coeliac and renal arteries.

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18
Q

What is the epidemiology of aortic dissection?

A

Most common in males between 40 and 60 years.

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19
Q

What are the presenting symptoms of aortic dissection?

A

Sudden central ‘TEARING’ pain, may radiate to the back (may mimic an MI)
Aortic dissection can lead to occlusion of the aorta and its branches:
Carotid obstruction: Hemiparesis, dysphasia, blackout. Coronary artery obstruction: Chest pain (angina or MI). Subclavian obstruction: Ataxia, loss of consciousness. Anterior spinal artery: Paraplegia.
Coeliac obstruction: Severe abdominal pain (ischaemic bowel).
Renal artery obstruction: Anuria, renal failure.

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20
Q

What the signs of aortic dissection on physical examination?

A 
Murmur on the back below left scapula, descending to abdomen. 
Blood pressure (BP): Hypertension (BP discrepancy between arms of >20 mmHg), wide pulse pressure. If hypotensive may signify tamponade, check for pulsus paradoxus. 
Aortic insufficiency: Collapsing pulse, early diastolic murmur over aortic area. Unequal arm pulses.
There may be a palpable abdominal mass.
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21
Q

What is pulsus paradoxus (paradoxical pulse)?

A

An abnormally large decrease (> 10mmHg) in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration

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22
Q

What are the appropriate investigations for aortic dissection? Interpret the results

A

1st Line:
Bloods-
Haematology: FBC- anaemia present if haemorrhage, cross-match 10 units of blood, clotting.
Biochemistry: U&Es (if renal perfusion is compromised= elevated creatinine and urea), LFTs (if hepatic perfusion is compromised= elevated aspartate transaminase [AST] and alanine transaminase [ALT]), lactate (indicative of malperfusion- elevated or normal), cardiac enzymes- exclude MI
CXR: Widened mediastinum
ECG: Often normal. Exclude MI. May have ST depression in acute dissection.
Echocardiography: Transoesophageal is highly specific- intimal flap (and in CT angiography)
CT-Thorax: False lumen of dissection can be visualized.

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23
Q

What is aortic regurgitation?

A

Reflux of blood from aorta into left ventricle (LV) during diastole.

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24
Q

What are the the risk factors of aortic regurgitation?

A

Bicuspid aortic valve
Rheumatic fever
Endocarditis
Connective tissue disorders- e.g. Marfan’s
Aortitis- secondary to systemic diseases such as syphilis

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25
Q

What is the aetiology of aortic regurgitation?

A

In developing countries rheumatic heart disease is the most common cause.
In developed countries most cases are caused by congenital bicuspid aortic valve and aortic root dilation (connective tissue disorders, aortitis).
Aortic root dissection is an acute cause of AR

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26
Q

What is the epidemiology of aortic regurgitation?

A

Chronic AR often begins in the late 50s, documented most frequently in patients >80 years.

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27
Q

What are the presenting symptoms of aortic regurgitation?

A

Chronic AR: initially asymptomatic. Later, symptoms of heart failure: exertional dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea, weakness, fatigue.
Chest pain.
Occasionally angina.
Severe acute AR: sudden cardiovascular collapse.
Symptoms related to the aetiology, e.g. chest or back pain in patients with aortic dissection.

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28
Q

What are the signs of aortic regurgitation on physical examination?

A

Diastolic murmur
Collapsing ‘water-hammer’ pulse
Thrusting and heaving displaced apex beat- present in chronic AR with LV hypertrophy
Hyperdynamic pulse
Tachypnoea
Jugular venous distension (cariogenic shock)
Cyanosis (acute AR)
Basal lung crepitations (pulmonary oedema)

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29
Q

What is Quincke’s sign*?

A

Visible pulsations on nail-bed

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30
Q

What is de Musset’s sign*?

A

Head nodding in time with pulse

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31
Q

What is Becker’s sign*?

A

Visible pulsations of the pupils and retinal arteries

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32
Q

What is Muller’s sign*?

A

Visible pulsation of the uvula

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33
Q

What is Corrigan’s sign*?

A

Visible pulsations in neck

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34
Q

What are the appropriate investigations for aortic regurgitation? Interpret the results

A

1st line:
ECG: may show non-specific ST-T wave changes, left axis deviation, left ventricular hypertrophy, or conduction abnormalities
CXR: may show cardiomegaly
Echo: may indicate the underlying cause (e.g. aortic root dilation, bicuspid aortic valve) or the effects of AR (left ventricular dilation/dysfunction and fluttering of the anterior mitral valve leaflet)
Doppler echocardiogram: for detecting AR and assessing severity
Other:
Cardiac catheterisation: to assess the presence of coronary artery disease or the functional state of the left ventricle

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35
Q

What is aortic stenosis?

A

Obstruction of blood flow across the aortic valve from the LV due to pathological narrowing

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36
Q

What is the aetiology / risk factors of aortic stenosis?

A

Rheumatic heart disease (commonest worldwide cause)
Calcification of congenital bicuspid aortic valve
Calcification or degeneration of a tricuspid aortic valve in the elderly (RF: age > 60 years)
Chronic kidney disease

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37
Q

Summarise the epidemiology of aortic stenosis

A

Prevalence in 􏰅3% of 75-year-olds.
More common in men than women.
Those with bicuspid aortic valve may present earlier (as young adults).

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38
Q

Recognise the presenting symptoms of aortic stenosis

A

May be asymptomatic initially
(Chest pain) Angina (because of “ oxygen demand of the hypertrophied ventricles)
Syncope or dizziness on exercise
Symptoms of heart failure (e.g. dyspnoea)

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39
Q

Recognise the signs of aortic stenosis on physical examination

A

BP: Narrow pulse pressure.
Pulse: Slow-rising.
Palpation: Thrill in the aortic area (if severe).
Forceful sustained thrusting undisplaced apex beat.
Auscultation:
Harsh ejection systolic murmur at aortic area, radiating to the carotid artery and apex
Second heart sound (A2 component) may be softened or absent (because of calcification)
A bicuspid valve may produce an ejection click.

distinguish from aortic sclerosis and hypertrophied obstructive cardiomyopathy

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40
Q

Identify appropriate investigations for aortic stenosis and interpret the results

A

1st Line:
Transthoracic echocardiogram: visualises structural changes int he valve, measure elevated aortic pressure gradient, measurement of valve area and left ventricular ejection function
ECG: may demonstrate left ventricular hypertrophy and LBBB (and absent Q waves)
Others:
Cardiac MRI- demonstrates stenotic aortic valve
Cardiac catheterisation: elevated aortic pressure gradient
Cardiac angiography: Allows differentiation from other causes of angina, and to assess for concomitant coronary artery disease

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41
Q

Define arterial ulcers

A

an ulcer caused by a reduction in arterial blood flow, leading to decreased perfusion of the tissues and subsequent poor healing.

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42
Q

Explain the aetiology / risk factors of arterial ulcers

A

Atherosclerosis
Hypertension
Others: smoking, diabetes mellitus, hyperlipidaemia, increasing age, positive family history, and obesity and physical inactivity

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43
Q

Recognise the presenting symptoms of arterial ulcers

A

Severe pain, particularly at night

Pain is relieved by dependency

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44
Q

Recognise the presenting symptoms of arterial ulcers

A

likely to give a preceding history of intermittent claudication (pain when they walk) or critical limb ischaemia (pain at night).
Severe pain, particularly at night
Pain is relieved by dependency
Develops over a long period of time with little to no healing

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45
Q

Recognise the signs of arterial ulcers on physical examination

A

On examination:
the limbs will be cold and have reduced or absent pulses. In pure arterial ulcers, sensation is maintained (unlike neuropathic ulcers)
Location: distal, dorsum of foot or toes, over bony prominences
Characteristics: Irregular edge, poor granulation tissue, dry necrotic base, round or punched-out with sharp demarcation
Associated findings:
Trophic changes of chronic ischemia,
Pale, hair loss, atrophic skin, cool feet, thickened nails, necrotic toes
Absence of pulses, prolonged capillary refill (>4–5 s), dependent rubor

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46
Q

Identify appropriate investigations for arterial ulcers and interpret the results

A

Ankle Brachial Pressure Index (ABPI) measurement:
(>0.9 = normal; 0.9-0.8 = mild; 0.8-0.5 = moderate; <0.5 = severe)
Imaging: duplex ultrasound, CT Angiography, and / or Magnetic Resonance Angiogram (MRA)

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47
Q

What does dependency/ dependent position mean?

A

Dependent refers to a means of support, i.e., floor, back of chair, armrest.

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48
Q

What is dependent rubor?

A

A fiery to dusky-red coloration visible when the leg is in a dependent position

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49
Q

What is acute limb ischemia?

A

A surgical emergency

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50
Q

What are the 6P’s of acute limb ischemia?

A 
Pain
Pallor
Pulseless
Perishing cold
Paraesthesia
Paralysis
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51
Q

What is atrial fibrillation?

A

Rapid, chaotic and ineffective atrial electrical conduction.

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52
Q

What are the three subdivisions of AF?

A

Permanent
Persistent
Paroxysmal

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53
Q

What is the aetiology of AF?

A

There may be no identifiable cause (‘lone’ AF)

Secondary causes lead to abnormal atrial electrical pathways that result in AF

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54
Q

What are the secondary systemic causes of AF?

A

Thyrotoxicosis
Hypertension
Pneumonia
Alcohol

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55
Q

What are the secondary cardiac causes of AF?

A 
Mitral valve disease
Ischaemic heart disease
Rheumatic heart disease
Cardiomyopathy
Pericarditis
Atrial myxoma (benign tumour)
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56
Q

What are the secondary respiratory causes of AF?

A

Bronchial carcinoma

Pulmonary embolism

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57
Q

What is the epidemiology of AF?

A

Very common in the elderly (􏰄5% of those >65 years)

May be paroxysmal- sudden recurrence or intensification of symptoms

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58
Q

What are the presenting symptoms of AF?

A

Often asymptomatic
Some patients experience palpitations or syncope
In secondary cases: symptoms of the cause of AF

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59
Q

What are the signs of AF on physical examination?

A

Irregularly irregular pulse
Difference in apical beat and radial pulse
*Look for thyroid disease and valvular heart disease.

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60
Q

What are the appropriate investigations for AF?

A
  • ECG: Uneven baseline (fibrillations) with absent P waves, irregular QRS complexes.
  • Bloods: Cardiac enzymes, TFTs, lipid profile, U&Es,
  • Echocardiogram: To assess for mitral valve disease, left atrial dilation, left ventricular dysfunction or structural abnormalities
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61
Q

What is the characteristic appearance of atrial flutter on an ECG?

A

Saw tooth baseline

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62
Q

What is the management for AF divided into?

A
  1. Rhythm control
  2. Rate control
  3. Stroke risk stratification
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63
Q

What is involved in the rhythm control management for AF?

A

If the AF is >48h from onset, anticoagulate (at least 3–4 weeks) before attempting cardioversion.
- DC cardioversion: Synchronized DC shock (2x100 J, 1x200 J)
-Chemical cardioversion: Anti-arryhtmic (flecainide or amiodarone)- contraindicated if there is history of ischaemic heart disease and only recommended in dangerous arrythmias
Prophylaxis against AF: Sotalol, amiodarone or flecainide.

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64
Q

What is involved in the rate control management for AF?

A

This is for chronic ‘permanent’ AF:
Ventricular rate control with digoxin, verapamil (calcium channel blocker) and/or B- blockers.
Aim for rate of 􏰄90/min.

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65
Q

What is digoxin?

A

It is a cardiac glycoside that increases the force of myocardial contraction and reduces conductivity within the atrioventricular (AV) node- used to treat AF, atrial flutter and heart failure

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66
Q

Which electrolytes need to be measured in AF, and why?

A

K+, Mg2+, Ca2+

There is a risk of digoxin toxicity if potassium or magnesium are low, or if calcium is high

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67
Q

What is stroke risk stratification management for patients with AF?

A

Low-risk patients: Aspirin

High-risk patients: Require anticoagulation with warfarin

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68
Q

What are the risk factors for being a high stroke risk patient?

A

Previous thromboembolic event (s)
Age 􏰃75 years with hypertension, diabetes or vascular disease, and/or clinical evidence of valve disease, heart failure or impaired left ventricular function

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69
Q

How do you measure stroke risk for patients with AF?

A

CHADS-vasc score

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70
Q

What are the complications of AF?

A

Thromboembolism (embolic stroke􏰄, risk with left atrial enlargement or left ventricular dysfunction)
Worsens any existing heart failure

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71
Q

What is the prognosis for patients with AF?

A

Chronic AF in a diseased heart does not usually return to sinus rhythm

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72
Q

What is cardiac arrest?

A

Acute cessation of cardiac function

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73
Q

What are the reversible causes for a cardiac arrest?

A 
4 Hs and 4Ts:
Hypokalaemia 
Hypothermia 
Hypovolaemia 
Hypoxia

Tamponade
Tension pneumothorax
Thromboembolism
Toxins

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74
Q

What signs would be seen on physical examination for a a patient in cardiac arrest?

A

Unconscious
Patient is not breathing
Absent carotid pulses

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75
Q

What are the 4 cardiac rhythm disturbances?

A

Ventricular fibrillation (VF)
Pulseless ventricular tachycardia (VT)
Pulseless electrical activity
Asystole

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76
Q

What are the appropriate investigations for a cardiac arrest?

A

Cardiac monitor: Classification of the rhythm directs management
Bloods: ABG, U&Es, FBC, cross-match, clotting, toxicology screen, glucose.

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77
Q

What is the management for a cardiac arrest?

A

Safety: approach with caution, defibrillators and oxygen are hazards- call for help

A: Clear and maintain airway with head tilt (if no spinal injury), jaw thrust and chin lift.
B: Assess breathing by look, listen and feel.
If not breathing, give two effective breaths immediately.
C: Assess circulation at carotid pulse for 10 s.
If absent, give 30 chest compressions at rate of 􏰄100/min􏰆. Continue cycles of 30 compressions for every two breaths.
Proceed to advanced life support as soon as possible.

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78
Q

What is the advanced life support for a cardiac arrest?

A
  1. Attach cardiac monitor and defibrillator

2. Assess the rhythm

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79
Q

What cardiac rhythms are shockable?

A

Ventricular tachycardia

Ventricular fibrillation

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80
Q

What is the management for shockable cardiac rhythms?

A
  1. Defibrillate once
  2. Resume CPR immediately for 2 min, and then defibrillate
  3. Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
  4. If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus
    (anti-arrhythmic)
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81
Q

What cardiac rhythms are non-shockable?

A

Pulseless electrical activity

Asystole

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82
Q

What is the management for non- shockable cardiac rhythms?

A
  1. CPR for 2 min, and then return to assessing rhythm
  2. Administer adrenaline (1 mg IV) every 3–5 min.
  3. Atropine (3 mg IV, once only) if asystole or PEA with rate <60/min􏰆
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83
Q

What is the treatment for the reversible causes of cardiac arrest?

A

Hypothermia: Warm slowly
Hypo- or hyperkalaemia: Correction of electrolytes
Hypovolaemia: IV colloids, crystalloids or blood products
Hypoxia: oxygen
Tamponade: Pericardiocentesis under xiphisternum up and leftwards
Tension pneumothorax: Needle into second intercostal space, mid-clavicular line
Thromboembolism: management for PE, MI
Toxins: antidotes

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84
Q

What are the complications of a cardiac arrest?

A

Irreversible hypoxic brain damage, death

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85
Q

What is the prognosis for patients with a cardiac arrest?

A

Resuscitation is less successful in the arrests that occur outside hospital.
Duration of inadequate effective cardiac output is associated with poor prognosis.

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86
Q

What sort of cardiomyopathy do you get in amyloidosis?

A

Restrictive

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87
Q

What is cardiac failure?

A

Inability of the cardiac output to meet the body’s demands despite normal venous pressures

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88
Q

What is the aetiology of low output cardiac failure?

A 
Left heart failure: 
-Ischaemic heart disease
-Hypertension
-Cardiomyopathy
-Aortic valve disease
-Mitral regurgitation
Right heart failure: 
-Secondary to left heart failure
-Infarction
-Cardiomyopathy
-Pulmonary hypertension/embolus/valve disease
-Chronic lung disease
-Tricuspid regurgitation
-Constrictive pericarditis/pericardial tamponade
Biventricular failure: 
-Arrhythmia
-Cardiomyopathy (dilated or restrictive)
-Myocarditis
-Drug toxicity
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89
Q

What is the aetiology of high output cardiac failure?

A 
(High demand)
Anaemia
Beriberi (vitamin B-1 deficiency- thiamine deficiency)
Pregnancy
Paget’s disease
Hyperthyroidism
Arteriovenous malformation
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90
Q

What is the epidemiology of cardiac failure?

A

10% of > 65-year-olds

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91
Q

What are the presenting symptoms of left sided cardiac failure?

A 
Left (symptoms caused by pulmonary congestion): Dyspnoea (New York Heart Association classification):
1. no dyspnoea
2. dyspnoea on ordinary activities
3. dyspnoea on less than ordinary activities
4. dyspnoea at rest
Orthopnoea
Paroxysmal nocturnal dyspnoea
Fatigue
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92
Q

What are the presenting symptoms of right sided cardiac failure?

A 
Swollen ankles
Fatigue
Increased weight (resulting from oedema)
Reduced exercise tolerance
Anorexia
Nausea
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93
Q

What are the signs of left sided cardiac failure on physical examination?

A

Tachycardia
Tachypnoea
Displaced apex beat
Bilateral basal crackles
Third heart sound (’gallop’ rhythm: rapid ventricular filling)
Pansystolic murmur (functional mitral regurgitation)

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94
Q

What are the symptoms and signs of ACUTE left ventricular cardiac failure?

A

Symptoms: Dyspnoea, wheeze, cough and pink frothy sputum
Signs: Tachypnoea, cyanosis, tachycardia, peripheral shutdown, pulsus alternans (strong and weak beats), gallop rhythm, wheeze ’cardiac asthma’, fine crackles throughout the lung

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95
Q

What are the signs of right sided cardiac failure on physical examination?

A 
Raised JVP
Hepatomegaly
Ascites
Ankle/sacral pitting oedema
Signs of functional tricuspid regurgitation
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96
Q

What are the appropriate investigations for cardiac failure?

A

Bloods:

  • Elevated BNP (B type natriuretic peptide, associated with reduced LVEF)
  • FBC (anaemia, high lymphocytes)
  • U&Es baseline (decreased sodium, altered potassium)
  • Serum creatinine: normal to elevated
  • LFTs: normal to elevated (reflects abdominal congestion)
  • TFTs: screening for hypo and hyperthyroidism
  • Others: CRP, glucose, lipids

CXR:

  • Cardiomegaly (heart >50 % of thoracic width)
  • Pulmonary vascular congestion (vascular redistribution, Kerley B lines-interstitial oedema)
  • Pleural effusion (usually right-sided but often bilateral)

ECG: May be normal. May show underlying coronary artery disease, left ventricular hypertrophy, or atrial enlargement

Echocardiogram: To assess ventricular contraction

  • If left ventricular ejection fraction (LVEF) <40%: systolic dysfunction
  • Diastolic dysfunction: reduced compliance leading to a restrictive filling defect

Swan–Ganz catheter (right heart catheterisation):
Allows measurements of right atrial, right ventricular, pulmonary artery, pulmonary wedge and left ventricular end-diastolic pressures (any pulmonary or systemic resistance)

Exercise stress testing/exercise tolerance:
Assess patient’s functional exercise limitation and haemodynamic response to exercise

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97
Q

What are the appropriate investigations for acute cardiac failure?

A

Bloods:
-FBC (anaemia)
-ABG
-Troponin: elevated
-Brain natriuretic peptide (BNP): elevated suggests the
diagnosis of cardiac failure
*A low plasma BNP rules out cardiac failure (90% sensitivity)

ECG: arrhythmia (20% are AF) , ischaemic ST and T wave changes

CXR:

  • Cardiomegaly
  • Pulmonary congestion
  • Pleural effusion
  • Valvular or pericardial calcification

Echocardiogram:
-Abnormal systolic and diastolic function (EF)

Cardiac catheterisation: abnormal coronary artery flow and left ventricular function

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98
Q

What is the management for acute cardiac failure?

A

Cardiogenic shock:
Severe cardiac failure with low BP requires the use of inotropes (e.g. dopamine, dobutamine) and should be managed in ITU
*inotropes: increase the force contractility of the heart

Pulmonary oedema:
Sit up patient, 60–100% O2 and consider CPAP. Other first-line therapies are diamorphine (venodilator and anxiolytic effect), GTN infusion (reduces preload), IV furo- semide if fluid overloaded (venodilator and later diuretic effect)
Monitor BP, respiratory rate, sat. O2, urine output, ECG. Treat the cause, e.g. myocardial infarction, arrhythmia

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99
Q

What is the management for chronic cardiac failure?

A

Treat the cause, e.g. hypertension
Treat exacerbating factors, e.g. anaemia

  1. ACE-inhibitors (e.g. enalapril, perindopril, ramipril):
    Inhibit intracardiac renin-angiotensin system which may contribute to myocardial hypertrophy and remodelling. ACE inhibitors slow progression of the heart failure and improve survival
  2. b-Blockers (bisprolol or carvedilol): Block the effects of chronically activated sympathetic system, slow progression of the heart failure and improve survival. The benefits of ACE inhibitors and b-blockers are additive*
  3. Loop diuretics (e.g. furosemide) and dietary salt restriction to correct fluid overload.
  4. Aldosterone antagonists (spironolactone or, if not tolerated, eplerenone) improve survival. May be used to assist in the management of diuretic-induced hypokalaemia
  5. Angiotensin receptor blockers (ARB) (e.g. candesartan): May be added in patients with persistent symptoms despite ACE inhibitors and b-blockers.
  6. Hydralazine and a nitrate: May be added in patients (particularly in Afro-Caribbeans) with persistent symptoms despite therapy with an ACE inhibitor and b-blocker
  7. Digoxin: Positive inotrope, reduces hospitalization, but does not improve survival
  8. Cardiac resynchronization therapy (CRT): Biventricular pacing improves symptoms and survival in patients with LVEF 􏰅 35%.
    Most patients who meet these criteria are also candidates for an implantable cardiac defibrillator (ICD) and receive a combined device

*Avoid drugs that can adversely affect patients with heart failure due to systolic dysfunction, e.g. NSAIDs, non-dihydropyridine calcium channel blockers (i.e. diltiazem and verapamil)

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100
Q

What are the complications of cardiac failure?

A

Respiratory failure, cardiogenic shock, death

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101
Q

What is the prognosis of cardiac failure?

A

50% of patients with severe heart failure die within 2 years

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102
Q

What is cardiomyopathy?

A

Primary disease of the myocardium

Cardiomyopathy may be dilated, hypertrophic or restrictive

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103
Q

What is the aetiology of cardiomyopathy?

A

The majority are idiopathic, the different types have different aetiologies

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104
Q

What is the aetiology of dilated cardiomyopathy?

A

Post-viral myocarditis
Alcohol, drugs (e.g. doxorubicin, cocaine)
Familial (􏰄25% of idiopathic cases, usually autosomal dominant)
Thyrotoxicosis
Haemochromatosis
Peripartum

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105
Q

What is the aetiology of hypertrophic cardiomyopathy?

A

Up to 50% of cases are genetic (autosomal dominant) with mutations in b-myosin, troponin T or a-tropomyosin

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106
Q

What is the aetiology of restrictive cardiomyopathy?

A

Amyloidosis, sarcoidosis, haemochromatosis

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107
Q

What is the epidemiology of cardiomyopathy?

A

Prevalence of dilated cardiomyopathy and hypertrophic cardiomyopathy is 􏰄0.05–0.20%
*Restrictive cardiomyopathy is rare

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108
Q

What are the presenting symptoms of dilated cardiomyopathy?

A

Symptoms of heart failure
Arrhythmias
Thromboembolism
Family history of sudden death.

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109
Q

What are the presenting symptoms of hypertrophic cardiomyopathy?

A 
Usually none
Syncope
Angina
Arrhythmias
Family history of sudden death
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110
Q

What are the presenting symptoms of restrictive cardiomyopathy?

A

*Dyspnoea
*Fatigue
Arrhythmias
Ankle or abdominal swelling
Family history of sudden death

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111
Q

What are the signs of dilated cardiomyopathy on physical examination?

A

(similar to heart failure)
Raised JVP
Displaced apex beat
Functional mitral and tricuspid regurgitations
Third heart sound
*auscultation of the lungs: crackles, indicating pulmonary congestion

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112
Q

What are the signs of hypertrophic cardiomyopathy on physical examination?

A

Jerky carotid pulse
Double apex beat
Ejection systolic murmur
*auscultation of the lungs: crackles, indicating pulmonary congestion

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113
Q

What are the signs of restrictive cardiomyopathy on physical examination?

A

Raised JVP (Kussmaul’s sign: further increase on inspiration)
Palpable apex beat
Third heart sound
Ascites
Ankle oedema
Hepatomegaly
*auscultation of the lungs: crackles, indicating pulmonary congestion

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114
Q

What are the appropriate investigations for cardiomyopathy?

A

Bloods:FBC,LFTs,TFTs, BNP (elevated), cardiac enzymes

CXR: May show cardiomegaly, and signs of heart failure (pulmonary oedema)

ECG:
All types: Non-specific ST changes, conduction defects, arrhythmias
-Hypertrophic: Left-axis deviation, signs of left ventricular hypertrophy
-Restrictive: Low voltage complexes

Echocardiography:

  • Dilated: Dilated ventricles with ‘global’ hypokinesia
  • Hypertrophic: Ventricular hypertrophy (disproportionate septal involvement)
  • Restrictive: Non-dilated non-hypertrophied ventricles
  • IN AMYLOIDOSIS: Atrial enlargement, preserved systolic function, diastolic dysfunction, granular or ‘sparkling’ appearance of myocardium

Others:
Cardiac catheterization:
May be necessary for measurement of pressures
Endomyocardial biopsy: May be helpful in restrictive cardiomyopathy (RARE)

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115
Q

What is Pericarditis?

A

Inflammation of the pericardium, may be acute, subacute or chronic

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116
Q

What is the criteria for acute Pericarditis?

A

New-onset inflammation lasting <4-6 weeks

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117
Q

What is the aetiology of Pericarditis?

A

Can be idiopathic or due to an underlying systemic condition (e.g., systemic lupus erythematosus)
As many as 90% of cases are either idiopathic or due to viral infections or systemic autoimmune conditions

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118
Q

What are the risk factors for Pericarditis?

A

Viral or bacterial infection (viral is most common):
-Commonly coxsackie B, echovirus, mumps virus, streptococci, fungi, staphylococci, TB
Systemic autoimmune conditions e.g. rheumatoid arthritis and SLE
Malignancy
Metabolic disorders
Cardiac surgery (4 weeks after coronary artery bypass graft)
Transmural MI:
-post-myocardial infarction (24–72 h)
-Dressler’s syndrome (weeks to months after acute MI)

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119
Q

What is the epidemiology of Pericarditis?

A

Acute pericarditis is more common in adults (typically between 20 to 50 years old) and in men
Uncommon- the clinical incidence is <1 in 100 hospital admissions

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120
Q

What are the presenting symptoms of Pericarditis?

A

Chest pain (most common- 85% of cases)
-Sharp, stabbing, pleuritic, or aching, and can mimic the pain of myocardial ischaemia or infarction
**Almost all patients report relief of pain with sitting up or leaning forward
-Pain radiates to neck or shoulders
-Aggravated by coughing, deep inspiration and lying flat
Others: Dyspnoea, nausea

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121
Q

What are the signs of Pericarditis on physical examination?

A

Fever
Pericardial friction rub (best heard lower left sternal edge, with patient leaning forward in expiration)
Heart sounds may be faint in the presence of an effusion

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122
Q

What are the signs of Constrictive Pericarditis (chronic) on physical examination?

A

Raised JVP with inspiration (Kussmaul’s sign)
Pulsus paradoxus: an abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration (<10 mmHg)
Hepatomegaly
Ascites
Oedema
Pericardial knock (rapid ventricular filling)
AF

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123
Q

What is Constrictive Pericarditis?

A

Impedes (delays) normal diastolic filling and can be a medium to late complication of acute pericarditis

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124
Q

What are the appropriate investigations for Constrictive Pericarditis?

A

*ECG: Widespread ST elevation that is saddle-shaped (most useful diagnostic test)
Bloods:
-Troponin: elevated
-ESR and CRP: elevated consistent with inflammation
-Urea: elevated suggest a urea cause
-FBC: elevated leukocytes
Pericardial fluid/blood culture: positive if infectious cause
(and viral serology, ANA, rheumatoid factor)
CXR: Usually normal unless a large pericardial effusion is present >300 mL effusion: water-bottle-shaped enlarged cardiac silhouette
Chest CT: Pericardial calcification can be seen in constrictive pericarditis:
-pericardial thickness, calcification
-deformed ventricular contours
-dilatation of the inferior vena cava
-angulation of the ventricular septum (lateral CXR or CT)

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125
Q

What is coronary angiography?

A

An invasive diagnostic procedure to assess the structure and function of the heart, using a contrast medium and x-rays of the heart and coronary arteries

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126
Q

What is Percutaneous Coronary Intervention (PCI)?

A

The combination of coronary angioplasty with stenting, widening blocked or narrowed coronary arteries

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127
Q

What are the indications for coronary angiography and PCI?

A

Coronary angiography: diagnosis, treatments and procedures

  • Post MI: where the heart’s blood supply is blocked
  • Diagnose angina: chest pain is caused by restricted blood supply to the heart
  • Plan interventional or surgical procedures – such PCI
  • Diagnose coronary heart disease

PCI: may be required to restore the blood supply to the heart in severe cases where medication is ineffective for MI and angina
-Coronary angioplasties are also often used as an emergency treatment after a heart attack

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128
Q

What are the possible complications of coronary angiography and PCI?

A

Allergic reaction to contrast dye
Bleeding under the skin where the catheter was inserted
Damage to the artery in the arm or leg where the catheter was inserted
Rare: Heart attack, Stroke, Kidney damage and, very rarely, death

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129
Q

What is Coronary artery bypass graft?

A

A surgical procedure used to treat coronary heart disease by diverting blood around narrowed or clogged parts of coronary arteries to improve blood flow and oxygen supply to the heart

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130
Q

What are the indications for a Coronary artery bypass graft?

A

Atherosclerosis causing coronary heart disease

Reduce the risk of MI

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131
Q

What are the possible complications of Coronary artery bypass graft?

A

Arrhythmias
Infection risk
Rare: stroke or heart attack

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132
Q

What is DC cardioversion?

A

A procedure to convert an abnormal heart rhythm to a normal heart rhythm (most commonly AF)

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133
Q

What are the indications for DC cardioversion?

A

Arrhythmias

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134
Q

What are the possible complications of DC cardioversion?

A

Usually temporary:

  • Headaches and dizziness from a drop in your blood pressure from anaesthetic
  • Discomfort in chest where the shock was given
  • Nausea (from anaesthetic)
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135
Q

What is Virchow’s triad?

A

Venous stasis
Vessel wall injury
Blood hypercoagulability

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136
Q

What is deep vein thrombosis (DVT)?

A

Formation of a thrombus within the deep veins (most commonly of the calf or thigh) which may result in impaired venous blood flow and consequent leg swelling and pain

137
Q

What are the risk factors for DVT?

A

Oral contraceptive pill
Surgery
Prolonged immobility
Long bone fractures
Obesity
Pregnancy
Dehydration
Smoking
Polycythaemia
Anti-phospholipid syndrome
Thrombophilia disorders (e.g. protein C deficiency)
Active malignancy

138
Q

What is the epidemiology for DVT?

A

Common, especially in hospitalised patients- yearly incidence of approximately 1 in every 1000 adults
Long-term complications of DVT (venous insufficiency, ulceration) affect 0.5% population
Incidence increases with age (increased medical co-morbidities, declining mobility, and perhaps age-related changes in coagulation)

139
Q

What are the presenting symptoms of DVT?

A

Asymptomatic or lower limb swelling or tenderness

May present with signs/ symptoms of a pulmonary embolus (sudden onset dyspnoea, chest pain)

140
Q

What are the signs of DVT on physical examination?

A

Examine for swelling, calf tenderness:
Severe leg oedema (usually unilateral)
Dilated superficial veins over foot and leg
Cyanosis (phlegmasia cerulea dolens) is rare
*Respiratory examination for signs of a pulmonary embolus (Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain)

141
Q

What are the appropriate investigations for DVT?

A

*Doppler ultrasound: gold standard
-Good sensitivity for femoral veins; less sensitive for calf veins (reduced/absent spontaneous blood flow)
Bloods:
-D-dimers (fibrinogen degradation products) are sensitive but very non-specific and only useful as a negative predictor in low-risk patients
-If indicated (e.g. recurrent episodes), a thrombophilia screen should be sent, prior to starting anticoagulation
-FBC (platelet count prior to starting heparin)
-U&Es and clotting
ECG, CXR and ABG: If there is suggestion that there might be PE

142
Q

What is the Well’s system for DVT?

A

Lower limb trauma or surgery or immobilisation in a plaster cast (+1)
Bedridden for >3 days or surgery within the last 4 weeks (+1)
Tenderness along deep venous system (+1)
Entire limb swollen (+1)
Calf >3 cm bigger circumference; 10 cm below tibial tuberosity (+1)
Pitting oedema (+1)
Dilated collateral superficial veins (non-varicose) (+1)
Malignancy (including treatment up to 6 months previously) (+1)
Alternative diagnosis more likely than DVT (-2)

Clinical probability of DVT:
High >3
Moderate 1–2

143
Q

What is the management for DVT?

A

Anticoagulation:

  • Patients should be treated with heparin while awaiting therapeutic INR from warfarin anticoagulation
  • DVTs not extending above the knee treated with anticoagulation for 3 months, while those extending beyond the knee require anticoagulation for 6 months
  • Recurrent DVTs may require long-term warfarin*
  • If active anticoagulation is contraindicated and/or high risk of embolisation, placement of an IVC filter, e.g. Greenfield filter, by interventional radiology is indicated to prevent embolus to the lungs

Prevention:

  • Use of graduated compression stockings
  • Mobilisation if possible (physical activity)
  • At-risk groups (immobilised hospital patients) should have prophylactic heparin, e.g. low molecular weight heparin if no contraindications
144
Q

What are the complications of DVT?

A

Of the disease:
-Pulmonary embolus
-Damage to vein valves and chronic venous insufficiency of the lower limb (post-thrombotic syndrome)
*Rare: Venous infarction (phlegmasia cerulea dolens)
Of the treatment:
-Heparin-induced thrombocytopaenia
-Bleeding

145
Q

What is the prognosis of DVT?

A

Depends on extent of DVT:

  • Below-knee DVTs lower risk of embolus
  • More proximal DVTs have higher risk of propagation and embolisation, which, if large, may be fatal
146
Q

What is Hypercholesterolaemia?

A

An elevation of total cholesterol (TC) and/or low-density lipoprotein cholesterol (LDL-C)

147
Q

What is Dyslipidaemia?

A

Dyslipidaemia is classified as serum Total cholesterol, LDL-C, triglycerides, apolipoprotein B, or lipoprotein(a) concentrations above the 90th percentile for the general population

148
Q

What is the aetiology of Dyslipidaemia?

A

Primary causes: due to single or multiple gene mutations, resulting in a disturbance of low-density lipoprotein (LDL) and triglyceride production or clearance - most commonly seen in children and young adults
Secondary causes: caused by lifestyle factors or disorders that interfere with blood lipid levels over time such as obesity, chronic renal insufficiency, abdominal obesity, diabetes mellitus and hypothyroidism

149
Q

What is the epidemiology of Dyslipidaemia?

A

Common, particularly in developing countries
Strong correlation between body mass index and coronary heart disease
Primary causes are common in children and young adults whereas secondary is seen more in adults

150
Q

What are the presenting symptoms of Dyslipidaemia?

A

Excess body weight
PMH Diabetes Mellitus Type 2 or cardiovascular disease
Consumption of saturated fats
FH of early onset of coronary heart disease or Dyslipidaemia

151
Q

What are the signs of Dyslipidaemia on physical examination?

A

Xanthelasmas: Yellow plaques that occur most commonly near the inner canthus of the eyelid
Tendinous xanthomas: Slowly enlarging subcutaneous nodules (on tendons or ligaments)

152
Q

What are the appropriate investigations for Dyslipidaemia?

A

Lipid profile:
-total cholesterol (TC) >5.18 mmol/L (>200 mg/dL)
-LDL-cholesterol >2.59 mmol/L (>100 mg/dL)
-triglycerides >1.7 mmol/L (>150 mg/dL)
Fasting (12h) triglycerides: ≥2.3 mmol/L (200 mg/dL)
Thyroid stimulating hormone: elevated in primary hypothyroidism
Lipoprotein (a): values >50 mg/dL or >125 nmol/L are considered high

153
Q

What is the management of Dyslipidaemia?

A

Combination of lifestyle changes to diet and exercise, medications, and dietary supplements

Lifestyle changes: dietary reduction in total and saturated fat, weight loss in overweight patients, aerobic exercise

Drug therapy: Statins inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase, a key enzyme in cholesterol synthesis, which leads to up-regulation of LDL receptors and increased LDL clearance

154
Q

What are the complications of Dyslipidaemia?

A

Atherosclerosis:
Ischaemic heart disease
Peripheral vascular disease
Acute coronary syndrome
Stroke
Erectile dysfunction (endothelial dysfunction)

155
Q

What is the prognosis of Dyslipidaemia?

A

The rate of adverse outcomes has been significantly reduced with the use of statins
Useful in the rid reduction of coronary heart disease

156
Q

What is Hypertriglyceridaemia?

A

Having a fasting plasma triglyceride level of ≥2.3 mmol/L (≥200 mg/dL)

157
Q

What is an exclusive sign of Hypertriglyceridaemia on physical examination?

A

Eruptive xanthomas: Small yellowish papules, frequently surrounded by an erythematous base, that appear predominantly on the buttocks, elbows, and other pressure-sensitive areas

158
Q

What is Gangrene?

A

A complication of necrosis characterised by the decay of body tissues. There are two major categories:

  • Infectious gangrene (wet gangrene)
  • Ischaemic gangrene (dry gangrene)
159
Q

What is the aetiology of Gangrene?

A

May result from ischaemia, infection, or trauma (or a combination of these processes)
Ischaemia may result from either arterial or venous compromise, and may be an acute or chronic process (or a combination of both)
*Critically insufficient blood supply is the most common cause of gangrene, and is often associated with diabetes and long-term smoking

160
Q

What is the epidemiology of Gangrene?

A

Gangrene occurs equally in men and women
Type I necrotising fasciitis occurs most commonly in patients with diabetes and patients with peripheral vascular disease- it is the most common form of necrotising fasciitis in the general population

161
Q

What are the presenting symptoms of Gangrene?

A

Pain
Affected area may become swollen
Skin discolouration
Low grade fever and chills (infectious gangrene)

162
Q

What are the signs of Gangrene on physical examination?

A

Oedema with overlying erythema
Skin discolouration: ecchymoses (bleeding underneath the skin), purpura, skin blebs, and haemorrhagic bullae
Gas gangrene- crepitus (uncommon)
Diminished pedal pulses and ankle-brachial index: Suggests chronic arterial insufficiency

163
Q

What are the appropriate investigations for Gangrene?

A

Bloods:
-FBC: leukocytosis and anaemia
-CRP: elevated
-LDH: elevated if haemolytic anaemia and gas gangrene
-Metabolic profile: may indicate metabolic acidosis, liver derangement, renal failure
Blood cultures: positive for infectious organism

Imaging:

  • Plain X-rays: for gas gangrene- may demonstrate gas in the soft tissues and/or indicate underlying osteomyelitis
  • CT/MRI of affected site: may reveal abscess formation or evidence of enhancement, oedema, or thickening in the fascia
  • Doppler ultrasound: may indicate presence and severity of arterial or venous obstruction

Others:

  • Skin biopsy
  • CT angiography: region of obstruction
  • CT chest/abdomen: if suspected malignancy
164
Q

What is Heart Block?

A

Impairment of the atrioventricular (AV) node impulse conduction, as represented by the interval between P wave and QRS complex

165
Q

What is first degree Heart Block?

A

Prolonged conduction through the AV node

166
Q

What is second degree Heart Block (Mobitz type 1- Wenchebach)?

A

The progressive prolongation of AV node conduction culminating in one atrial impulse failing to be conducted through the AV node. The cycle then begins again

167
Q

What is second degree Heart Block (Mobitz type 2)?

A

Intermittent or regular failure of conduction through AV node
Also defined by the number of normal conductions per failed or abnormal one (e.g. 2 : 1 or 3 : 1)

168
Q

What is third degree Heart Block?

A

Also known as complete heart block
No relationship between atrial and ventricular con- traction
Failure of conduction through the AV node leads to a ventricular contraction generated by a focus of depolarization within the ventricle (ventricular escape)

169
Q

What is the aetiology of Heart Block?

A

Most common cause: MI or ischaemic heart disease
Other causes:
-Infection e.g. rheumatic fever, infective endocarditis
-Drugs e.g. digoxin ,b-blockers, Ca2+ channel blockers
-Metabolic e.g. hyperkalaemia, cholestatic jaundice, hypothermia
- Infiltration of conducting system e.g. sarcoidosis, cardiac neoplasms, amyloidosis
-Degeneration of the conducting system

170
Q

What is the epidemiology of Heart Block?

A

The majority of pacemakers implanted annually are for heart block
First degree heart block is associated with increased risk of AF

171
Q

What are the presenting symptoms of Heart Block?

A 
First degree: Asymptomatic 
Wenchebach: Usually asymptomatic 
Mobitz type II and third-degree block: 
-May cause Stokes–Adams attacks (syncope caused
by ventricular asystole)
-Dizziness
-Palpitations
-Chest pain
-Heart failure
172
Q

What are the signs of Heart Block on physical examination?

A 
Often normal
Complete heart block: 
-Slow large volume pulse
-JVP may show ‘cannon waves’
Mobitz type II and third-degree block: 
Signs of a reduced cardiac output (e.g. hypotension, heart failure)
173
Q

What are the ECG findings for First degree Heart Block?

A

Prolonged PR interval (>0.2 s)

174
Q

What are the ECG findings for Second degree Mobitz 1 (Wenchebach) Heart Block?

A

Progressively prolonged PR interval, culminating in a P wave that is not followed by a QRS
The pattern then begins again

175
Q

What are the ECG findings for Second degree Mobitz 2 Heart Block?

A

Intermittently a P wave is not followed by a QRS
There may be a regular pattern of P waves not followed by a QRS (e.g. two P waves per QRS, indicating 2 : 1 block)

176
Q

What are the ECG findings for Third degree (complete) Heart Block?

A

No relationship between P waves and QRS complexes
If QRS initiated by focus in the bundle of His, the QRS is narrow- the QRS initiated more distally are wide and slow rate (􏰄30 beats/min)

177
Q

What are the appropriate investigations for Heart Block?

A

ECG: different findings
CXR: may show hilar lymphadenopathy, cardiac enlargement, pulmonary oedema
Bloods:
-TFTs: hypo or hyperthyroidism
-Digoxin level: identify cause
-Cardiac enzymes, troponin: may be elevated
Echocardiogram:
Ventricular dysfunction or hypertrophy, valvular disease, wall-motion abnormalities

178
Q

What is the management for asymptomatic first-degree AV block or type I second-degree Heart Block?

A

No specific treatment is required
Patients are at low risk for progression to higher-degree AV block

179
Q

What is the management for symptomatic chronic Heart Block?

A

First line of treatment is to stop all AV-nodal blocking medications: beta-blockers, non-dihydropyridine calcium-channel blockers, and digoxin.
While discontinuing these medicines may improve AV conduction, they are not likely to completely reverse a clinically significant AV block
If severe: Permanent pacemakers should be considered (recommended in patients with third-degree heart block, advanced Mobitz type II and symptomatic Mobitz type I)

180
Q

What is the management for acute Heart Block (e.g. secondary to MI)?

A

If associated with clinical deterioration, IV
Atropine (anti-muscarinic) and consider temporary (external) pacemaker

181
Q

What are the complications of Heart Block?

A

Asystole- cardiac arrest
Heart failure
Complications of any pacemaker inserted

182
Q

What is the prognosis for Heart Block?

A

Mobitz type II and third-degree block (advanced) usually indicate serious underlying cardiac disease whereas first degree and Mobitz type I have a low risk

183
Q

What is Hypertension?

A

Defined as systolic BP >140mmHg and/or diastolic BP >90mmHg measured on three separate occasions

184
Q

What is malignant hypertension?

A

Defined as BP 􏰃200/ 130 mmHg

185
Q

What is the aetiology of Hypertension?

A

Primary: Essential or idiopathic hypertension (Commonest, >90% of cases)

Secondary:

  • Renal: Renal artery stenosis, chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney disease, chronic renal failure.
  • Endocrine: DM, hyperthyroidism, Cushing’s syndrome, Conn’s syndrome, hyperparathyroidism, phaeochromocytoma, congenital adrenal hyperplasia, acromegaly
  • Cardiovascular: Aortic coarctation, increase in intravascular volume.
  • Drugs: Sympathomimetics, corticosteroids, OCP
  • Pregnancy: Pre-eclampsia
186
Q

What is the epidemiology of Hypertension?

A

Very common- 10–20% of adults in the Western world

187
Q

What are the presenting symptoms of Hypertension?

A

Often asymptomatic

If secondary, symptoms of the cause

188
Q

What are the signs of Hypertension on physical examination?

A

BP: measure on two to three different occasions before diagnosing hypertension and record lowest reading (>140/90mmHg)
Longstanding hypertension: retinopathy (retinal vascular changes)

189
Q

What is the Keith–Wagner classification of retinopathy?

A

(I) ‘silver wiring’
(II) as above, plus arteriovenous nipping
(III) as above, plus flame haemorrhages and cotton wool exudates
(IV) as above, plus papilloedema

190
Q

What are the appropriate investigations for Hypertension?

A

ECG: May show signs of left ventricular hypertrophy or ischaemia
Ambulatory BP monitoring: Excludes ‘white coat’ hypertension, allows monitoring of treatment response
Fasting metabolic profile with estimated GFR:
-may show renal insufficiency, hyperglycaemia, hypokalaemia, hyperuricaemia, or hypercalcaemia
Lipid panel: metabolic syndrome, high LDL/triglycerides
Urinalysis: proteinuria (end organ damage from albumin excretion)
Bloods: U&Es, glucose, lipids (secondary causes)

191
Q

What is the management of Hypertension?

A

Lifestyle modification (conservative): Stop smoking, lose weight, reduce alcohol, reduce dietary salt

Medical:
*-Thiazide diuretics (e.g. bendrofluamethiazide): Recommended first line, especially in >55 year-olds or black patients
-ACE inhibitors (e.g. ramipril) or angiotensin-II antagonist (e.g. losartan): First line in <55 year-olds, diabetic patients, heart failure or left ventricular dysfunction
*-Ca2+ channel antagonists (e.g. amlodipine): Recommended first line, especially in >60-
year-olds or black patients
-b-Blockers (e.g. atenolol): Not preferred initial therapy, but may be considered in younger patients. Avoid combining with thiazide diuretic to reduce patient risk of developing diabetes. May increase risk of heart failure
*-a-Blockers (e.g. doxazosin): Fourth-line agent. May be useful for patients with prostatism

Severe hypertension (diastolic BP > 140 mmHg): Atenolol or nifedipine

192
Q

What are the complications of Hypertension?

A 
Heart failure
Coronary artery disease and MI
Cerebrovascular accident 
Peripheral vascular disease
Thomboembolism
Retinopathy
Renal failure
Uncommon:
-Hypertensive encephalopathy
-Posterior reversible encephalopathy syndrome (PRES)
-Malignant hypertension
193
Q

What is the prognosis of Hypertension?

A

*Good, if BP controlled
Uncontrolled hypertension linked with increased mortality (6x􏰇 stroke risk and 3􏰇x cardiac death risk)
Treatment reduces incidence of renal damage, stroke and heart failure

194
Q

What is an Implanted cardiac defibrillator?

A

A machine that is placed under the skin to monitor heart rate. If it detects an arrhythmia it can deliver one or more of:

  • Pacing: a series of low-voltage electrical impulses (paced beats) at a fast rate to try and correct the heart rhythm
  • Cardioversion: one or more SMALL electric shocks to try and restore the heart to a normal rhythm
  • Defibrillation: one or more LARGE electric shocks to try and restore the heart to a normal rhythm
195
Q

What are the indications for an Implanted cardiac defibrillator?

A

Arrhythmias
Other cardiac conditions such as cardiomyopathy or Heart Block
Cardiac failure

196
Q

What are the possible complications of an Implanted cardiac defibrillator?

A

Infection at the implant site
Allergic reaction to the medications used during the procedure
Swelling, bleeding or bruising where ICD was implanted
Damage to the vein
Bleeding around heart (pericardium), which can be life-threatening
Blood leaking through the heart valve where the ICD lead is placed
Pneumothorax

197
Q

What is Infective Endocarditis?

A

Infection involving the endocardial surface of the heart, including the valvular structures, the chordae tendineae, sites of septal defects, or the mural endocardium

198
Q

What is the aetiology of Infective Endocarditis?

A

The endocardium can be colonized by virtually any organism, but the most common are:

  1. Streptococci (40%): Mainly a-haemolytic
  2. Staphylococci(35%):Staphylococcusaureus
  3. Enterococci (20%)

Historical sources of bacteraemia should be considered, such as indwelling vascular catheters, recent dental work, and intravenous drug use

RF: prosthetic heart valves, congenial heart disease, valvular disease, IV drug use

199
Q

What is the epidemiology of Infective Endocarditis?

A

Incidence 16–22 per million per year, around 50% are over 60 years old
Incidence increases with age

200
Q

What are the presenting symptoms of Infective Endocarditis?

A 
Fever with sweats/chills/rigors (may be relapsing and remitting)
Malaise
Fatigue
Weight loss
Headache
Arthralgia
Myalgia
Dyspnoea
Confusion (particularly in elderly)
Skin lesions
201
Q

What are the signs of Infective Endocarditis on physical examination?

A

Pyrexia, tachycardia, signs of anaemia
Clubbing (if long-standing)
New regurgitant murmur or muffled heart sounds:
Frequency: Mitral > aortic > tricuspid > pulmonary
Splenomegaly
Vasculitic lesions:
-Petechiae particularly on retinae (Roth’s spots)
-Pharyngeal and conjunctival mucosa
-Janeway lesions (painless palmar macules, which blanch on pressure)
-Osler’s nodes (tender nodules on finger/toe pads)
-Splinter haemorrhages (nail-bed haemorrhages)

202
Q

What are the appropriate investigations for Infective Endocarditis?

A

Bloods:
-FBC (leukocytosis, normocytic anaemia)
-Raised ESR and CRP
-U&Es: mildly elevated urea
-Rheumatoid factors: may be positive (minor criteria for diagnosis)
-Complement levels: decreased
Blood culture: At least three sets 1h apart: bacteraemia or fungaemia

ECG: progression of the infection may lead to conduction system disease

Imaging:
Echocardiography: Should be performed in all cases of suspected IE, detection of vegetations and valve abscess, diagnosis of prosthetic valve endocarditis and assessment of embolic risk
CT/CXR: valvular abnormalities and vegetations, septic pul- monary emboli: focal lung infiltrates

203
Q

What is Dukes’ classification of Infective Endocarditis?

A

Major criteria:
Positive blood culture in two separate sample
-Positive echocardiogram (vegetation, abscess, prosthetic valve dehiscence, new valve regurgitation)

Minor criteria:

  • High-grade pyrexia (temperature >38􏰂C)
  • Risk factors (abnormal valves, IV drug use, dental surgery)
  • Positive blood culture, but not major criteria
  • Positive echocardiogram, but not major criteria
  • Vascular signs
204
Q

What is the management for Infective Endocarditis?

A

ABC approach
1. Broad-spectrum antimicrobial therapy is required empirically on clinical suspicion:
-Benzylpenicillin + gentamicin (empirical treatment)
2. Streptococci: Continue as above (alternatives – ceftriaxone, vancomycin)
3. Staphylococci: Flucloxacillin/vancomycin + gentamicin (for prosthetic valves: vancomycin + gentamicin + rifampin)
Enterococci: Ampicillin + gentamicin

Surgery: If poor response or deterioration, urgent valve replacement is indicated.
*Antibiotic prophylaxis for patients with a PMH of infective endocarditis undergoing high risk procedures

205
Q

What are the complications of Infective Endocarditis?

A 
Valve incompetence
Intracardiac fistulae or abscesses
Aneurysm formation
Heart failure
Renal failure
Glomerulonephritis
Arterial emboli from the vegetations (brain, kidneys, lungs, spleen)
206
Q

What is the prognosis for Infective Endocarditis?

A

Fatal if untreated

Even when treated, 15–30% mortality (mortality is greater in older patients)

207
Q

What is Ischaemic heart disease?

A

Characterized by reduced blood supply (ischaemia) to the heart muscle resulting in chest pain known as angina pectoris. Can present as:

  • Stable angina
  • Acute coronary syndrome (ACS)
208
Q

What can Acute coronary syndrome (ACS) be divided into?

A

Unstable angina (no cardiac injury)
Non-ST-elevation myocardial infarction (NSTEMI)
ST-elevation MI (STEMI, transmural infarction)
*MI refers to cardiac muscle necrosis resulting from ischaemia

209
Q

What is the aetiology of angina pectoris?

A

Occurs when myocardial oxygen demand exceeds oxygen supply
The most common cause is atherosclerosis
Other causes of coronary artery narrowing are: RARE
-Spasm (e.g. from cocaine)
-Arteritis
-Emboli

210
Q

What is the aetiology of a myocardial infarction?

A

Caused by sudden occlusion of a coronary artery due to rupture of an atheromatous plaque and thrombus formation

211
Q

What is the aetiology of atherosclerosis?

A
  1. Endothelial injury
  2. Migration of monocytes into subendothelial space and differentiation into macrophages
  3. Macrophages accumulate LDL lipids in the subendothelium and become foam cells
  4. They release growth factors, which stimulate smooth muscle proliferation, production of collagen and proteoglycans
  5. This leads to the formation of an atheromatous plaque
212
Q

What are the risk factors for Ischaemic heart disease?

A 
Male
Diabetes mellitus
FH of MI
Hypertension
Hyperlipidaemia
Smoking
PMH MI
213
Q

What is the epidemiology of Ischaemic heart disease?

A

Common, prevalence is >2%
More common in males
Annual incidence of MI in the United Kingdom is 􏰄5 in 1000

214
Q

What are the presenting symptoms of Acute Coronary Syndrome?

A

Chest pain or discomfort of acute onset
Central heavy tight ‘gripping’ pain that radiates to arms (usually left), neck, jaw or epigastrium
Occurring at rest, increased severity and frequency of previously stable angina
Associations:
-Breathlessness
-Sweating
-Nausea and vomiting

Can be silent in elderly or in patients with diabetes

215
Q

What are the presenting symptoms of stable angina?

A

Chest pain bought on by exertion and relieved by rest

216
Q

What are the signs of acute coronary syndrome on physical examination?

A

May have no clinical signs
Pale, sweating, restless, low-grade pyrexia
Check both radial pulses for aortic dissection
Arrhythmias, disturbances of BP
New heart murmurs (e.g. pansystolic murmur of mitral
regurgitation from papillary muscle rupture or ventricular septal defect)
Signs of complications, i.e. acute heart failure, cardiogenic shock (hypotension, cold peripheries, oliguria)

217
Q

What are the appropriate investigations for Ischaemic heart disease?

A

Bloods: FBC, U&Es, CRP, glucose, lipid profile, cardiac enzymes:
-CK-MB and troponin-T or I1 (sensitive marker of cardiac injury, increase after 12 h), amylase (pancreatitis may mimic MI), TFTs. AST and LDH increase after 24 and 48 h, respectively; occasionally used only to make retrospective diagnosis

ECG:
Unstable angina or NSTEMI:
-May show ST depression, T-wave inversion (Q waves in these patients may indicate old MIs)
-ST-elevation (Q-wave)
MI:
-Hyperacute T waves, ST elevation (>1 mm in limb leads, >2 mm inchest leads), new-onset LBBB
-Later: T inversion (hours) and Q waves (days)
CXR: To look for signs of heart failure.
Exercise ECG testing (treadmill test)2: To determine prognosis and management (for patients with troponin-negative ACS, or stable angina with an intermediate or
high pretest probability of coronary heart disease)

Radionuclide myocardial perfusion imaging (rMPI):
Can be performed under stress (exercise or pharmacological) or at rest
*Stress testing would show low uptake in ischaemic myocardium
Rest testing can be used in patient with ACS, no previous MI but non-diagnostic troponin and ECGs

Echocardiogram:

  • Measure LVEF (early measurements may be misleading because of myocardial stunning)
  • Exercise (or dobutamine stress) echocardiography may detect inducible wall motion abnormalities

Pharmacologic stress testing:

  • For patients who cannot exercise or if the exercise test is inconclusive. Pharmacological agents such as dipyridamole, adenosine or dobutamine can be used to induce a tachycardia
  • Various imaging modalities (e.g. rMPI, echocardi- ography) can be used to detect ischaemic myocardium. *Dipyridamole and adenosine are contraindicated in AV block and reactive airway disease

Cardiac catheterization/angiography:
In ACS with positive troponin or if high risk on stress testing

218
Q

What is the management of stable angina?

A

Minimize cardiac risk factors:
-Control BP, hyperlipidaemia and diabetes. Provide advice onsmoking, exercise, weight loss and low-fat diet. *All patients should receive aspirin (75 mg/ day) unless contraindicated

Immediate symptom relief:
-GTN as a spray or sublingually.

Long-term treatment:
b-Blockers, e.g. atenolol, unless contraindicated (contraindications include acute heart failure, cardiogenic shock, bradycardia, heart block, asthma), calcium channel blockers (e.g. verapamil, diltiazem), nitrates (e.g. isosorbide dinitrate). Dual therapy may be indicated if monotherapy is ineffective

Percutaneous coronary intervention (PCI):
For localized areas of stenosis, in patients with angina not controlled despite maximal tolerable medical therapy Re-stenosis rate is 􏰄25% at 6 months

Coronary artery bypass graft (CABG): For more severe cases (three-vessel disease). The rates of MI and overall survival are generally similar between PCI and CABG

219
Q

What is the management for Unstable angina/NSTEMI?

A

Admit to coronary care unit (CCU), oxygen, IV access, monitor vital signs and serial ECG
- Analgesia: GTN (initially sublingual, IV infusion if persistent chest pain), morphine sulphate/
diamorphine, antiemetic (metoclopramide).
- Aspirin (loading): 300 mg chewed. Maintenance: 75 mg, indefinite.
- Clopidogrel (loading-anti-platelet): 300 mg. Maintenance: 75 mg for at least 1 year if troponin positive or high risk
- Low-molecular-weight heparin (e.g. enoxaparin or dalteparin).
- b-Blocker (e.g. metoprolol) if not contraindicated.
- Glucose–insulin infusion if blood glucose >11 mmol/L.
- Consider glycoprotein (GP) IIb/IIIa inhibitors, e.g. tirofiban in patients:
. undergoing PCI; or
. at high risk for further cardiac events (troponin positive, TIMI risk score 􏰃4, continuingischaemia or other high-risk features)
*If little improvement, consider urgent angiography 􏰁with revascularization

220
Q

What is the management for a STEMI?

A

Admit to CCU, oxygen, IV access, monitor vital signs and serial ECG.
- Analgesia: GTN
- Aspirin (loading): 300 mg chewed.
- Clopidogrel (loading): 600 mg if patient going to primary PCI, 300 mg if undergoing thrombolysis and 􏰅75 years of age, 75 mg if undergoing thrombolysis and >75 years of
age. Maintenance: 75 mg, for at least 1 year
- b-Blocker (e.g. metoprolol)
- If undergoing primary PCI: IV heparin (plus GP IIb/IIIa inhibitor) or bivalirudin (an antithrombin). If undergoing thrombolysis with recombinant tissue plasminogen
activator (rtPA): IV heparin.
- Glucose–insulin infusion if blood glucose >11 mmol/L
-Primary PCI
-Thrombolysis: Using fibrinolytics such as streptokinase or rtPA (alteplase, reteplase,tenecteplase) if within 12h of chest pain with ECG changes (ST elevation, new-onset LBBB or posterior infarction) and not contraindicated.
Rescue PCI: If continued pain or ST elevation after thrombolysis (<50% decrease of the initial ST-segment elevation on a follow-up ECG 60–90 min after fibrinolytic therapy)

221
Q

What are the other managements for Ischaemic heart disease?

A

Secondary Prevention:
-Antiplatelet agents (aspirin and clopidogrel)
-ACE inhibitors, b-blockers and statins
-Control other risk factors (smoking, diabetes, hypertension)
Advice:
Not to drive for 1 month following MI
Education by cardiac rehabilitation team:
-lifestyle changes (e.g. exercise, stop smoking, changing diet)
CABG for patients with left main stem or three-vessel disease

222
Q

What are the complications of Ischaemic heart disease?

A 
At risk of MI and other vascular diseases (e.g. stroke, peripheral vascular disease)
Cardiac injury can lead secondarily to heart failure and arrhythmias
Early complications of MI (24–72 h): 
-Death
-Cardiogenic shock
-Heart failure
-Ventricular arrhythmias
-Heart block
-Pericarditis
-Myocardial rupture
-Thromboembolism
Late complications of MI: 
-Ventricular wall (or septum) rupture
-Valvular regurgitation
-Ventricular aneurysms
-Tamponade
-Dressler’s syndrome (pericarditis)
-Thromboembolism
223
Q

What is the prognosis of Ischaemic heart disease?

A

ACS: TIMI score (range 0–7) can be used for risk stratification (high scores are associated with high risk of cardiac events within 30 days), consists of:
(1) >65 years;
(2) known coronary artery disease;
(3) aspirin in last 7 days;
(4) severe angina (>2 episodes in 24 h); (5) ST deviation >1 mm;
(6) elevated troponin levels;
(7) >3 coronary artery disease risk factors
(hypertension, hyperlipidaemia, family history, diabetes, smoking)

Killip classification of acute MI:
Class I: no evidence of heart failure.
Class II: mild to moderate heart failure (S3, crepitations

224
Q

What is Mitral Regurgitation?

A

The retrograde flow of blood from LV to left atrium during systole

225
Q

What is the aetiology of Mitral Regurgitation?

A

Mitral valve damage or dysfunction:

  • Rheumatic heart disease (most common)
  • Infective endocarditis
  • Mitral valve prolapse (prolapse of mitral valve leaflets into the left atrium during systole)
  • Papillary muscle rupture or dysfunction (secondary to ischaemic heart disease or cardiomyopathy)
  • Chordal rupture and floppy mitral valve associated with connective tissue diseases (e.g. Marfan’s syndrome, SLE)

*Functional mitral regurgitation may be secondary to left ventricular dilation

226
Q

What is the epidemiology of Mitral Regurgitation?

A

Affects 􏰄5% of adults

Mitral valve prolapse is more common in young females

227
Q

What are the presenting symptoms of Mitral Regurgitation?

A

Acute MR:
May present with symptoms of left ventricular failure (dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea and fatigue)
Chronic MR:
May be asymptomatic or present with exertional dyspnoea, palpitations if in AF and fatigue (decreased exercise tolerance)
Mitral valve prolapse:
Asymptomatic or atypical chest pain or palpitations

228
Q

What are the signs of Mitral Regurgitation on physical examination?

A

Pulse may be normal or irregularly irregular (AF)
Apex beat may be laterally displaced and thrusting (left ventricular dilation)
*Pansystolic murmur, loudest at apex, radiating to axilla (palpable as a thrill)
S1 is soft; S3 may be heard (rapid ventricular filling in early diastole)
*Signs of left ventricular failure in acute mitral regurgitation (pulsus alternans (strong and weak beats), gallop rhythm)

229
Q

What are the appropriate investigations for Mitral Regurgitation?

A

*Transthoracic echo: visualises presence and severity of MR; other structural and flow abnormalities
ECG:
Normal or may show AF or broad bifid p wave (p mitrale) indicating delayed activation of left atrium due to left atrial enlargement
CXR:
-Acute mitral regurgitation may produce signs of left ventricular failure
-Chronic mitral regurgitation shows left atrial enlargement, cardiomegaly (caused by left ventricular dilation) or mitral valve calcification in rheumatic cases
Echocardiography:
Every 6–12 months for moderate–severe MR to assess the LV ejection fraction and end-systolic dimension

230
Q

What is Mitral Stenosis?

A

The mitral valve narrowing causing obstruction to blood flow from the left atrium to the ventricle

231
Q

What is the aetiology of Mitral Stenosis?

A 
Most common cause is rheumatic heart disease (90%)- untreated streptococcal pharyngitis infection
Rarer causes are:
-Congenital mitral stenosis
-SLE, rheumatoid arthritis, amyloidosis
-Endocarditis
-Atrial myxoma (rare cardiac tumour)
232
Q

What is the epidemiology of Mitral Stenosis?

A

Incidence is declining because of declining incidence of rheumatic fever
Women are 3x more likely than men

233
Q

What are the presenting symptoms of Mitral Stenosis?

A

May be asymptomatic
Presents with fatigue, shortness of breath on exertion or lying down (orthopnoea). Palpitations (related to AF)
RARE CAUSES:
-Cough
-Haemoptysis
-Hoarseness caused by compression of the left
laryngeal nerve by an enlarged left atrium

234
Q

What are the signs of Mitral Stenosis on physical examination?

A

*May have peripheral or facial cyanosis (malar flush)
Pulse:
*May be ‘thready’ or irregularly irregular (AF)
Palpation:
*Apex beat is undisplaced and tapping
Parasternal heave (right ventricular hypertrophy and pulmonary hypertension)
Auscultation:
*Loud first heart sound with opening snap
*Mid-diastolic murmur (presystolic accentuation if in sinus rhythm)
Evidence of pulmonary oedema on lung auscultation (if decompensated)

235
Q

What are the appropriate investigations for Mitral Stenosis?

A

ECG:
May be normal, broad bifid p wave (p mitrale) caused by left atrial hypertrophy
AF or evidence of right ventricular hypertrophy in cases of severe pulmonary hypertension
CXR:
-Double right heart border indicating enlarged left atrial , cardiac enlargement, pulmonary congestion
-prominent pulmonary artery; Kerley B lines (interstitial oedema)
-Mitral valve may be calcified in rheumatic cases

Transthoracic Echocardiography:
To assess functional and structural impairments: hockey stick-shaped mitral deformity
Transoesophageal gives better valve visualization (presence of possible left atrial thrombus)

Cardiac catheterization: high left atrial pressure, low left ventricular pressure, and low cardiac output

236
Q

What is Myocarditis?

A

Acute inflammation and necrosis of cardiac muscle (myocardium) in the absence of the predominant acute or chronic ischaemia characteristic of coronary artery disease

237
Q

What is the aetiology of Myocarditis?

A

Usually unknown (idiopathic)
Infection:
-Viruses: e.g. Coxsackie B, echovirus, EBV, CMV
-Bacterial: e.g. post-streptococcal, tuberculosis, -diphtheria, Lyme disease
-Fungal: e.g. candidiasis.
-Protozoal: e.g. trypanosomiasis (Chagas disease)
Non-infective:
-Systemic disorders (e.g. SLE, sarcoidosis, polymyositis)
-Hypersensitivity myocarditis (e.g. sulphonamides)
Drugs:
-Chemotherapy agents (e.g. doxorubicin, streptomycin) Others: Cocaine abuse, heavy metals, radiation

238
Q

What is the epidemiology of Myocarditis?

A

True incidence is unknown, as many cases are not detected at the time of acute illness
Coxsackie B virus is a common cause in Europe and the USA but in South America Chagas disease is the common cause
*Patients with myocarditis tend to be younger (<50 years) than those presenting with more common cardiac conditions such as acute coronary syndrome

239
Q

What are the presenting symptoms of Myocarditis?

A 
Prodromal ‘flu-like’ illness
Fever
Malaise
Fatigue
Lethargy
Breathlessness (pericardial effusion/myocardial dysfunction) and orthopnoea
Palpitations
Sharp chest pain (suggesting associated pericarditis)
240
Q

What are the signs of Myocarditis on physical examination?

A

Atrial and ventricular arrhythmias
Sinus tachycardia
S3 gallop
Signs of concurrent pericarditis:
-Pericardial friction rub (best heard lower left sternal edge, with patient leaning forward in expiration)
-Heart sounds may be faint in the presence of an effusion

241
Q

What are the appropriate investigations for Myocarditis?

A

12 lead ECG: anyone who resents with chest pain, Non-specific T wave and ST changes, widespread saddle-shaped ST elevation in pericarditis

Bloods:

  • FBC (raised WCC in infective causes)
  • U&Es, BNP, raised ESR or CRP, cardiac enzymes e.g. creatinine kinase, troponin (may be elevated)
  • To identify the cause (viral or bacterial serology, antistreptolysin O titre, ANA, serum ACE, TFT)

CXR: May be normal or show cardiomegaly with or without pulmonary oedema (frequently reveals bilateral pulmonary infiltrates in the setting of myocarditis-induced CHF)

Echocardiography: Assesses systolic/diastolic function, wall motion abnormalities, pericardial effusion: global and regional left ventricular motion abnormalities and dilatation

Myocardial biopsy: Rarely required, show histological findings of myocardial cellular infiltrates ± myocardial necrosis

242
Q

What is Peripheral Vascular Disease?

A

A range of arterial syndromes that are caused by atherosclerotic obstruction of the lower-extremity arteries

243
Q

What is the aetiology of Peripheral Vascular Disease?

A

The most common cause is atherosclerosis
Rarer causes of claudication are aortic coarctation, arterial fibrodysplasia, arterial tumour, arterial dissection, arterial embolism, thrombosis, vasospasm, and trauma

244
Q

What is the epidemiology of Peripheral Vascular Disease?

A

The prevalence of PAD increases with age, beginning after 40 years of age
Prevalence is equal in men and women and is often under- recognised and under-treated

245
Q

What are the presenting symptoms of Peripheral Vascular Disease?

A

Most patients are asymptomatic and diagnosis is based on risk factors
Pain in one leg:
-Intermittent claudication: ask patients about walking impairment, claudication symptoms, ischaemic rest pain, or presence of non-healing wound/foot ulcer
-Pain in the thigh or buttock with walking which is relieved on rest: larger muscle groups
Erectile dysfunction: early sign of narrowing of the internal iliac arteries

246
Q

What are the signs of Peripheral Vascular Disease on examination?

A
  • Diminished pulse in lower extremities: assessment of pulse in all extremities- palpation of pulses at the brachial, radial, ulnar, femoral, popliteal, dorsalis pedis, and posterior tibial artery is essential
  • Non-healing wound/ulcer
  • Muscle atrophy
  • Loss of hair
247
Q

What are the 6Ps of Acute Limb Ischaemia?

A 
P-pain
P-pallor
P-paraesthesias
P- pulselessness
P-perishingly cold
P-paralysis
248
Q

What are the appropriate investigations for Peripheral Vascular Disease?

A

Ankle-brachial index: ABI ≤0.90
Toe-brachial index: TBI <0.6 (in patients with an unreliable ABI)
Segmental pressure examination: gradient of >20 mmHg between adjacent segments (determine the location and magnitude of stenosis)
Duplex ultrasound: Peak systolic velocity ratio >2.0 = stenosis >50% (assess location and degree of stenosis)
Continuous wave doppler ultrasound: Provides an accurate location and severity of PAD
Exercise ABI: determine the magnitude of walking limitations in symptomatic patients
Angiography: invasive but provides superior resolution for stenosis
CT/MR angiogram: presence of significant stenosis

249
Q

What is permanent pacing?

A

Pacemakers are electronic devices that stimulate the heart with electrical impulses to maintain or restore a normal heartbeat

250
Q

What are the indications for permanent pacing?

A

Sinus node dysfunction (SND) and high-grade atrioventricular (AV) block
Others:
Hypertrophic cardiomyopathy
Pacing to detect and terminate tachycardia
Cardiac resynchronization therapy in patients with severe systolic heart failure
Patients with congenital heart disease

251
Q

What are the possible complications of permanent pacing?

A 
Lead complications are the main reason for the re-implantation of the pacemaker
Other complications include: 
-Infections
-Hematoma formation
-Pericardial effusion or tamponade
-Pneumothorax
-Coronary sinus dissection
-Perforation
252
Q

What is a pulmonary embolism?

A

Occlusion of pulmonary vessels, most commonly by a consequence of thrombus formation within a deep vein of the body, most frequently in the lower extremities

253
Q

What is the aetiology of a pulmonary embolism?

A

Thrombus (>95% originating from DVT of the lower limbs and rarely from right atrium in patients with AF)
Other agents that can embolize to pulmonary vessels include amniotic fluid embolus, air embolus, fat emboli, tumour emboli and mycotic emboli from right-sided endocarditis

254
Q

What are the risk factors for developing a pulmonary embolism?

A 
Surgery
Immobility 
Obesity 
PMH of DVT 
OCP 
Pregnancy 
Heart failure 
Malignancy
255
Q

What is the epidemiology of pulmonary embolism?

A

Relatively common, especially in hospitalized patients, they occur in 10–20% of those with a confirmed proximal DVT
The incidence and direct mortality from PE increases with age

256
Q

What are the presenting symptoms of a pulmonary embolism?

A

Depends on the size and site of the pulmonary embolus:

  • Small: May be asymptomatic.
  • Moderate: Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain.
  • Large (or proximal): All of the above plus severe central pleuritic chest pain, shock, collapse, acute right heart failure or sudden death.
257
Q

What are the presenting symptoms of a pulmonary embolism?

A

Depends on the size and site of the pulmonary embolus:

  • Small: May be asymptomatic
  • Moderate: Sudden onset dyspnoea, cough, haemoptysis and pleuritic chest pain
  • Large (or proximal): All of the above plus severe central pleuritic chest pain, shock, collapse, acute right heart failure or sudden death
  • maybe fever
258
Q

What are the appropriate investigations for pulmonary embolism?

A

Low probability: Use D-dimer blood test (cross-linked fibrin degradation products, highly sensitive but poor specificity)
High probability: Requires imaging
Additional initial investigations:
-Bloods: ABG, consider thrombophilia screen.
-ECG: May be normal or more commonly show a tachycardia, right axis deviation or RBBB.
-CXR: Often normal but to exclude other differential diagnoses

  1. Spiral CT pulmonary angiogram: Poor sensitivity for small emboli, but very sensitive for medium to large emboli
  2. Ventilation-perfusion (VQ) scan: identifies any areas of ventilation and perfusion mismatch (infarction)
  3. Pulmonary angiography: Gold standard, but invasive
  4. Doppler USS of the lower limb: To examine for venous thrombosis
  5. Echocardiogram: May show right heart strain
259
Q

What scoring system is used to predict probability for pulmonary embolisms and to guide further investigation and management?

A 
WELL'S SCORE (>4 high probability, 􏰅3 probability):
Clinically suspected DVT 3.0 
PE is most likely diagnosis 3.0 
Recent surgery (4 weeks) 1.5 
Immobilization 1.5 
Tachycardia 1.5 
History of DVT or PE 1.5 
Haemoptysis 1.0 
Malignancy 1.0
260
Q

What is the management for pulmonary embolism?

A

Primary prevention:

  • Graduated pressure stockings (TEDs) and heparin prophylaxis in those at risk (e.g. undergoing surgery)
  • Early mobilization and adequate hydration post-surgery

If haemodynamically stable:
-O2, anticoagulation with heparin or LMW heparin, changingto oral warfarin therapy (INR 2–3) for a minimum of 3 months. Analgesics for pain

If haemodynamically unstable (massive PE):
-Resuscitate, give oxygen, IV fluid resuscitation, thrombolysis with tPA can be considered on clinical grounds alone if cardiac arrest is imminent (50 mg bolus of tPA)- Tissue plasminogen activator to break down clots

Surgical or radiological:

  • Embolectomy (when thrombolysis is contraindicated)
  • IVC filters (Greenfield filter) may be inserted for recurrent pulmonary emboli despite adequate anticoagulation or when anticoagulation is contraindicated
261
Q

What are the complications of pulmonary embolism?

A

Death
Pulmonary infarction
Pulmonary hypertension
Right heart failure

262
Q

What is the prognosis for pulmonary embolism?

A

30% untreated mortality, 8% with treatment (due to recurrent emboli or underlying disease)
Patients have increased risk of future thromboembolic disease

263
Q

What is Pulmonary Hypertension?

A

A consistently increased pulmonary arterial pressure (>20mmHg) under resting conditions

264
Q

What is the aetiology of Pulmonary Hypertension?

A

Primary: Idiopathic
Secondary:
-Left heart disease (mitral valve disease, left ventricular failure, left atrial myxoma/thrombosis)
-Chronic lung disease (COPD)
-Recurrent pulmonary emboli
-Increased pulmonary blood flow (atrial septal defect, ventricle septal defect, patent ductus arteriosus)
-Connective tissue disease (e.g. SLE, systemic sclerosis)
-Drugs (e.g. amiodarone- anti-arrhythmic)

265
Q

What is the epidemiology of Pulmonary Hypertension?

A

Primary pulmonary hypertension is usually seen in young females (rare)
Age 20-50 years

266
Q

What are the presenting symptoms of Pulmonary Hypertension?

A 
*Dyspnoea (on exertion)
Chest pain
Syncope
Tiredness
Symptoms of the underlying cause (e.g. chronic cough)
267
Q

What are the signs of Pulmonary Hypertension on physical examination?

A

Raised JVP (Prominent a wave in the JVP waveform)
Palpation:
Left parasternal heave (right ventricular hypertrophy)
Auscultation:
*Loud pulmonary component of S2 (S3/S4 may be heard), an early diastolic murmur caused by pulmonary regurgitation
*Tricuspid regurgitation (pansystolic murmur)
Signs of the underlying condition, or right heart failure in severe cases

268
Q

What are the appropriate investigations for Pulmonary Hypertension?

A

CXR:

  • Cardiomegaly (right ventricular enlargement, right atrial dilation)
  • Prominent main pulmonary arteries (which taper rapidly)
  • Signs of the cause (e.g. COPD, calcified mitral valves)

ECG:

  • Right ventricular hypertrophy (right-axis deviation)
  • Right atrial enlargement (peaked P wave ‘P pulmonale’)

Echocardiography:

  • Pulmonary artery systolic pressure (sPAP) is considered equal to right ventricular systolic pressure (RVSP) in the absence of pulmonic valve stenosis and outflow tract obstruction
  • To visualize tricuspid regurgitation
  • Estimated RVSP >35 mmHg
  • Right ventricular and right atrial dilation
  • Pericardial effusion

Cardiac catheterization: (required to confirm the presence of pulmonary hypertension)

  • Mean pulmonary arterial pressure >25 mmHg at rest or >30 mmHg with exercise
  • Assess severity, right heart pressures and response to vasodilators.

Lung function tests: To assess for chronic lung disease
VQ scan: To assess for pulmonary embolism
High resolution CT-thorax: Images pulmonary arteries and to diagnose lung disease
Lung biopsy: Assesses structural lung changes

269
Q

What is Rheumatic Fever?

A

An inflammatory (autoimmune) multisystem disorder, occurring following group A b-haemolytic streptococci (GAS) throat infection

270
Q

What is the aetiology of Rheumatic Fever?

A

Streptococcal pharyngeal infection is required, and genetic susceptibility may be present for the autoimmune response to be triggered

271
Q

What is the epidemiology of Rheumatic Fever?

A

Peak incidence: between 5-15 years. More common in the Far East, Middle East, eastern Europe and South America
The mean incidence is 19/100 000.
Despite the decline in incidence over time in the West, the incidence rates remain relatively high in non-Western countries

272
Q

What are the presenting symptoms of Rheumatic Fever?

A 
2–5 weeks after GAS infection- recent sore throat
General: 
Fever
Malaise
Anorexia
Joints: 
Painful, swollen, reduced movement/function
Cardiac:
Breathlessness, chest pain, palpitations
273
Q

What are the signs of Rheumatic Fever on physical examination?

A

Duckett Jones criteria: Positive diagnosis if at least two major criteria, or one major plus two minor criteria are present

Major criteria:

  • Arthritis: Migratory or fleeting polyarthritis with swelling, redness and tenderness of large joints
  • Carditis: New murmur, e.g. Carey Coombs murmur (mid-diastolic murmur due to mitral valvulitis), pericarditis, pericardial effusion or rub, cardiomegaly, cardiac failure, ECG changes
  • Chorea (Sydenham’s): Rapid, involuntary, irregular movements with flowing or dancing quality. May be accompanied by slurred speech. More common in females
  • Nodules: Small firm painless subcutaneous nodules seen on extensor surfaces, joints and tendons.
  • Erythema marginatum (20% cases): Transient erythematous rash with raised edges, seen on trunk and proximal limbs. They may form crescent- or ring-shaped patches

Minor criteria:

  • Pyrexia
  • PMH rheumatic fever
  • Arthralgia (only if arthritis is not present as major criteria)
  • Recent streptococcal infection (supported by positive throat cultures or raised antistreptolysin O titre)
  • Elevated inflammatory markers (ESR, CRP or WCC)
  • Prolonged PR and QT intervals on ECG (only if carditis not present as major criteria)
274
Q

What are the appropriate investigations for Rheumatic Fever?

A

Bloods:
-FBC (elevated WCC)
-Elevated ESR/CRP
-Elevated or rising antistreptolysin O titre
*Throat swab: Culture for GAS, rapid streptococcal antigen test
ECG:
-Prolonged PR interval is a minor criterion of acute rheumatic fever
-Features of pericarditis
-Arrhythmias
Echocardiogram:
-Pericardial effusion
-Myocardial thickening or dysfunction
-Valvulardysfunction
CXR: may demonstrate cardiomegaly and/or congestive cardiac failure

275
Q

What is Supraventricular Tachycardia?

A

An abnormally fast heart rhythm arising from improper electrical activity in the upper part of the heart (atria or AVN)
There are four main types:
1. Atrial fibrillation
2. Paroxysmal supraventricular tachycardia (PSVT)
3. Atrial flutter
4. Wolff–Parkinson–White syndrome.

276
Q

What is the aetiology of Supraventricular Tachycardia?

A

It can occur in healthy people, although often there is underlying cardiac pathology
Associated conditions include cardiomyopathies, ischaemic heart disease, previous cardiac surgery, and hyperthyroidism
Exogenous stimulants can also cause SVT such as amphetamines, cocaine, and acute alcohol intoxication

277
Q

What is the epidemiology of Supraventricular Tachycardia?

A

Atrial fibrillation is the most common arrhythmia in clinical practice, with an estimated prevalence of 0.4% to 1% in the general population and increasing with age

278
Q

What are the presenting symptoms of Supraventricular Tachycardia?

A

Supraventricular tachycardia may come and go suddenly, and symptoms can last anywhere from a few minutes to a few days. Some people have no symptoms at all

Rapid heartbeat (palpitations)
Dyspnoea
Fatigue
Weakness
Lightheadedness or dizziness
Sweating
A pounding sensation in the neck
Syncope or near fainting
279
Q

What are the signs of Supraventricular Tachycardia on physical examination?

A

Heart rate ≥100 bpm
Rales
Oedema

280
Q

What are the appropriate investigations for Supraventricular Tachycardia?

A

ECG: regular tachycardia that does not vary in rate, P waves may be unusual (or not present)
CXR: abnormalities suggestive of cardiac disease e.g. cardiomegaly that would predispose to arrhythmias
Bloods:
-U&Es: electrolyte imbalance
-Toxicology screen: identify cause e.g. amphetamines
-Digoxin level
-TFTs: hyperthyroidism
Echocardiogram: may show underlying cause such as valvular disease or cardiomyopathy

281
Q

What is the management of Supraventricular Tachycardia?

A
  • Adenosine: rapid reversion to sinus rhythm of paroxysmal supraventricular tachycardias:
  • Initially 6 mg, administer into central or large peripheral vein and give over 2 seconds, cardiac monitoring required
  • Followed by 12 mg after 1–2 minutes if required, then 12 mg after 1–2 minutes if required, increments should not be given if high level AV block develops at any particular dose

Other medications:

  • beta blockers or calcium channel blockers
  • override pacing
  • Re-entry arrhythmias will often require direct current (DC) cardioversion and, possibly, amiodarone
282
Q

What are the complications of Supraventricular Tachycardia?

A

Patients with sustained tachycardia may develop congestive heart failure
Rare complication: cardiomyopathy

283
Q

What is the prognosis of Supraventricular Tachycardia?

A

Prognosis depends on the ability to control the arrhythmia
This is further influenced by the patient’s age, underlying cause of the arrhythmia, tolerance of adverse effects of the chosen treatment, and co-morbidities

284
Q

What is Tricuspid Regurgitation?

A

The backflow of blood from the right ventricle to the right atrium during systole

285
Q

What is the aetiology of Tricuspid Regurgitation?

A

The most clinically significant form is secondary in nature, commonly due to left-sided cardiac pathology in the form of advanced mitral, aortic, and left ventricular myocardial disorders

Congenital: Ebstein anomaly (malpositioned tricuspid valve)
Functional:
-Consequence of right ventricular dilation (e.g. in pulmonary hypertension)
-Valve prolapse
Rheumatic heart disease: Associated with other valvular disease
Infective endocarditis:
-Common in IV drug users
-Usually staphylococcal
Other:
-Carcinoid syndrome, trauma, cirrhosis (long-standing), iatrogenic (e.g. radiotherapy to the thorax)

286
Q

What is the epidemiology of Tricuspid Regurgitation?

A

Infective endocarditis probably most common cause

287
Q

What are the presenting symptoms of Tricuspid Regurgitation?

A 
Fatigue
Dyspnoea
Palpitations
Headaches
Nausea
Anorexia
Jaundice
Lower limb swelling
Symptoms due to gut congestion related to reduced cardiac output and associated with right-sided heart failure:
-Epigastric pain made worse by exercise
-Early satiety
-Dyspepsia
-Indigestion
288
Q

What are the signs of Tricuspid Regurgitation on physical examination?

A

Pulse: May be irregularly irregular due to AF (may occur with right atrial enlargement)
Inspection:
-Raised JVP with giant v waves which may oscillate the earlobe
-caused by transmission of right ventricular pressure to the great veins
Palpation: Parasternal heave
Auscultation:
-Pansystolic murmur heard best at the lower left sternal edge, louder on inspiration (Carvallo sign)
-Loud P2 component of second heart sound
Chest:
-Pleural effusion
Causes of pulmonary hypertension (e.g. emphysema) Abdomen:
-Palpable liver (tender, smooth, pulsatile), ascites
Legs: Pitting oedema

289
Q

What are the appropriate investigations for Tricuspid Regurgitation?

A

Bloods:
-FBC: anaemia (e.g., anaemia of chronic disease, renal failure), thrombocytopenia (e.g., due to liver failure and cirrhosis)
-LFTs: patients with chronic severe TR often develop ascites from advanced liver disease, from chronic congestion or fibrosis (cardiac cirrhosis)
-cardiac enzymes
-Blood cultures
ECG:
-Tall P wave (right atrial hypertrophy) if in sinus rhythm
-Changes indicative of other cardiac disease (may show atrial flutter/fibrillation; presence of previous MI)
CXR:
-Right-sided enlargement of cardiac shadow
-Pleural or pericardial effusion
-Presence of pacemaker
Echocardiography:
-Extent of regurgitation estimated by colour flow Doppler. -May be able to detect tricuspid valve abnormality (e.g. prolapse), right ventricular dilation
-Assessment of left and right heart ejection fraction/dilation
Right heart catheterization:
Rarely necessary but may be considered to assess pulmonary artery pressure (helps to differentiate between choosing to repair valve or replace it)

290
Q

What are Varicose Veins?

A

They are subcutaneous, permanently dilated veins 3 mm or more in diameter when measured in a standing position; however, they may not be visible

291
Q

What is the aetiology of Varicose Veins?

A 
Venous valve incompetence is the most common aetiology
Predisposing factors include:
-Gender
-Pregnancy
-Occupation (with prolonged standing)
-Weight
-Ethnicity 
Causative factors:
-Previous episode of deep vein thrombosis
-Genetic links (FH)
292
Q

What is the epidemiology of Varicose Veins?

A

Generally, prevalence rates are higher in industrialised countries and in more developed regions
Prevalence increases with age
Greater prevalence in women than in men

293
Q

What are the presenting symptoms of Varicose Veins?

A

Visible bulges in legs
Leg fatigue or aching with prolonged standing (not present at the beginning fo the day)- improves with elevation
Nocturnal leg cramps
Restless legs
Itching
Ankle swelling
Overlying skin changes: Lipodermatosclerosis: redness, swelling, and a tapering of the legs above the ankles

294
Q

What are the signs of Varicose Veins on physical examination?

A

Dilated tortuous veins (examine the patient standing)
Lipodermatosclerosis (indication of high risk for ulceration and is the result of haemosiderin (venous HTN) causing inflammation and damaging the soft tissues-this leads to scarred and fibrotic tissues)
Ulceration

295
Q

What are the appropriate investigations for Varicose Veins?

A

Tourniquet test (Trendelenburg): when patient stands the veins do not fill
Duplex ultrasond:
-Two sound heard, when the blood flows up the vein when the calf is squeezed and then when released the blood that flows back down the incompetent vein
Assesses for reversed flow;
-valve closure time >0.5 second is indicative of reflux
-valve closure time >1.0 second is indicative of reflux in the deep system
*can also be used to exclude DVT

296
Q

What is the management of Varicose Veins?

A 
Interventional treatment:
-Endovenous ablation
-Foam sclerotherapy
-Phlebectomy-  removal of the veins
-Open surgery (stripping and ligation) 
If interventional treatment is unsuitable e.g. pregnant :
-Compression stockings

If the superficial axial system (the great saphenous vein, the small saphenous vein, or the anterior accessory saphenous vein) is involved: endovenous thermal ablation (radiofrequency or laser ablation) is offered as a first-line option

297
Q

What are the complications of Varicose Veins?

A

Chronic venous insufficiency: Increased dilation of venous system leading to axial system reflux
Erosion of varices can lead to haemorrhage (low)
Venous ulceration
Lipodermatosclerosis
Haemosiderin deposition: Capillaries become elongated, fibrotic, and leaky

298
Q

What is the prognosis of Varicose Veins?

A

Generally resolution of symptoms occurs in >95% of patient who are treated
However, patients need to be counselled that new varicosities will very likely occur with time, as varicose veins are a progressive disease

299
Q

Where do most Varicose Veins occur?

A

Long saphenous vein: groin to the medial aspect of the lower leg
Short saphenous vein: popliteal fossa along the calf to the lateral malleolus

300
Q

What are the indications for surgical treatment of Varicose Veins?

A

Oedema
Skin changes- Lipodermatosclerosis
Venous eczema and ulceration

301
Q

What is Vasovagal syncope?

A

Neurally mediated reflex syncope (NMRS): A group of related conditions or scenarios in which symptomatic hypotension occurs as a result of neural reflex vasodilation and/or bradycardia
Vasovagal syncope: a particular type of NMRS also known as the common faint, and is generally considered to encompass faints triggered by emotional upset, fear, and pain, as well as those occurring in less well-defined circumstances

302
Q

What is the aetiology of Vasovagal syncope?

A

Syncope has many possible causes commonly grouped in 3 main groups:
-Neurally-mediated reflex syncopal syndromes
-Orthostatic
-Cardiovascular
In susceptible people, vasovagal syncope may be triggered by:
-Prolonged periods of upright posture
-Relative dehydration
-Excessively warm, closed-in environments
-Extreme emotions

303
Q

What is the epidemiology of Vasovagal syncope?

A

These neurally mediated reflex faints, especially the vasovagal faint, are the most common causes of syncope overall and are particularly prevalent in people without evidence of underlying heart disease or vascular disease

304
Q

What are the presenting symptoms of Vasovagal syncope?

A

PMH of recurrent faints: (especially beginning in youth) and not associated with structural cardiovascular disease
Provocative factors: include painful or emotionally upsetting experiences, excessive dehydration, after vigorous exercise

Characteristics of Vasovagal syncope:

  • Pallor
  • Diaphoresis: sensation of feeling sweaty and experiencing a coldness and/or clammy sensation
  • Fatigue after episode

Other features:

  • Diminished hearing or vision
  • Nausea
  • Light headedness (occurs in many conditions)
305
Q

What are the signs of Vasovagal syncope on examination?

A

Bradycardia: Slow heart rates are a common finding at the time of vasovagal syncope

306
Q

What are the appropriate investigations for Vasovagal syncope?

A

12 lead ECG: exclude AV block, bradycardia, asystole, Bundle branch block
Bloods:
-FBC: exclude syncope caused by anaemia
-Blood glucose: exclude syncope caused by hypoglycaemia
-Serum B-hCG: exclude syncope caused by pregnancy
-Cardiac enzymes: exclude MI
-D-dimer: exclude PE
-Serum cortisol: exclude syncope caused by adrenal insufficiency
-U&Es: dehydration
Echo: excludes hypertrophic cardiomyopathy (enquire about FH of sudden death), aortic stenosis, poor ventricular function

*Tilt-table test: Used only if there is suspicion of vasovagal syncope (VS) but the medical history is not convincing on its own- reproduction of symptoms/syncope, bradycardia, hypotension

307
Q

What are venous ulcers?

A

Ulcers that are caused by venous insufficiency. They often appear shallow with irregular borders and a granulating base, characteristically located over the medial malleolus

308
Q

What is the aetiology of venous ulcers?

A

Impaired venous return
This results in venous hypertension causing the “trapping” of white blood cells in capillaries and the formation of a fibrin cuff around the vessel hindering oxygen transportation into the tissue.
The white blood cells subsequently become activated, with the release of inflammatory mediators leading to resultant tissue injury, poor healing, and necrosis

309
Q

What are the risk factors of venous ulcers?

A 
Increasing age
Pre-existing venous incompetence or history of venous thromboembolism (including varicose veins)
Pregnancy - increased clotting
Obesity or physical inactivity
Severe leg injury or trauma
310
Q

What is the epidemiology of venous ulcers?

A

Venous leg ulcers are the most common type of leg ulcer; they are prone to infection and can present with associated cellulitis

311
Q

What are the presenting symptoms of venous ulcers?

A

Associated symptoms of chronic venous disease, such as aching, itching, or a bursting sensation, will be present often before venous leg ulcers appear.

312
Q

What are the signs of venous ulcers on physical examination?

A 
Shallow, irregular shape
Granulating base
Flat or steep elevation margins
Fibrinous material at ulcer bed
Pain is relieved by elevation
Associated findings:
-Lipodermatosclerosis
-Pigmentation
-Oedema
-Telangiectasia
-Normal capillary refill time and normal pulses
313
Q

What are the appropriate investigations for venous ulcers?

A

Doppler ultrasound: venous insufficiency- DVT, varicose veins
ABI: arterial insufficiency
Bloods:
-FBC: anaemia, high WCC indicates infection
-ESR/CRP: inflammation
-U&Es: high urea levels may indicate dehydration, which may impair healing
-Albumin: low albumin may be associated with protein loss and malnutrition, which may delay healing.
-HbA1c: to assess for diabetes mellitus
Bacterial swab: only when clinical evidence of infection

314
Q

What is the management for venous ulcers?

A

Compression therapy:
-Ulcer should be cleaned and dressed before
Consider prescribing pentoxifylline to aid ulcer healing:
-Pentoxifylline is an effective adjunct to compression bandaging for treating venous leg ulcers
Assess complications: oedema and eczema and treat if infected
*After a venous leg ulcer has healed: lifestyle advice and graduated compression stockings to prevent recurrence

315
Q

What are the complications of venous ulcers?

A

Chronic pain
Impaired mobility (often due to pain)
Infection, including osteomyelitis and septicaemia
Allergic contact dermatitis (caused by allergens in creams and dressings and medications, steroids, antibiotics)
Malignant transformation in the ulcer bed (Marjolin’s ulcer)
Negative impacts on quality of life and daily functioning: time off work, psychological distress, loss of independence, and social isolation

316
Q

What is the prognosis of venous ulcers?

A

Six-month healing rates have been reported as 45% for those treated in the community (about 80% of people with venous leg ulcers), and 70% for those treated in specialist clinics
But: repeat cycles of ulceration, healing, and recurrence are common

317
Q

What is Ventricular Fibrillation?

A

Considered the most serious cardiac rhythm disturbance (medical emergency):

  • Disordered electrical activity causes the ventricles to quiver, or fibrillate, instead of contracting normally
  • This prohibits the heart from pumping blood, causing collapse and cardiac arrest
318
Q

What is the aetiology of Ventricular Fibrillation?

A

Cann have several root causes, including:

  • Insufficient blood flow to the heart muscle
  • Damage to the heart muscle (e.g MI)
  • Cardiomyopathy
  • Problems with the aorta
  • Drug toxicity
  • Sepsis (severe body infection)
319
Q

What is the epidemiology of Ventricular Fibrillation?

A

Considered the most serious cardiac rhythm

Life threatening

320
Q

What are the presenting symptoms/signs of Ventricular Fibrillation on physical examination?

A

Sudden cardiac arrest (SCA), which requires immediate medical attention
Signs of cardiac arrest include:
-Loss of responsiveness
-No normal breathing

321
Q

What are the appropriate investigations for Ventricular Fibrillation?

A

Cardiac monitor e.g. ECG: determine rhythm-classification of the rhythm directs management

322
Q

What is the management of Ventricular Fibrillation?

A

Ventricular fibrillation is a SHOCKABLE rhythm:
1. Defibrillate once
2. Resume CPR immediately for 2 min, and then defibrillate
3. Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
4. If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus
(anti-arrhythmic)

323
Q

What are the complications of Ventricular Fibrillation?

A

(same as cardiac arrest)

Irreversible hypoxic brain damage, heart failure, death

324
Q

What is the prognosis of Ventricular Fibrillation?

A

Resuscitation is less successful in the arrests that occur outside hospital
Duration of inadequate effective cardiac output is associated with poor prognosis

325
Q

What is Ventricular Tachycardia?

A

An abnormally fast heart rhythm as a result of improper electrical activity in the ventricles- a broad complex tachycardia originating from a ventricular ectopic focus

326
Q

What is the aetiology of Ventricular Tachycardia?

A

Caused by a disruption in the normal electrical impulses that control the rate of your heart’s pumping action

Causes include:

  • Abnormalities of the heart that result in scarring of heart tissue (sometimes called “structural heart disease”), the most common cause is a prior heart attack
  • Poor blood flow to the heart muscle due to coronary artery disease
  • Congenital heart conditions, including long QT syndrome
  • Imbalance of electrolytes necessary for conducting electrical impulses
  • Medication side effects
  • Use of drugs such as cocaine or methamphetamine
327
Q

What are the presenting symptoms/signs of Ventricular Tachycardia on physical examination?

A

Brief episodes of ventricular tachycardia may not cause any symptoms in some people or may cause:

  • Dizziness
  • Shortness of breath
  • Lightheadedness
  • Palpitations
  • Chest pain (angina)

Sudden cardiac arrest (SCA), which requires immediate medical attention is caused by sustained or more severe episodes of VT:
Signs of cardiac arrest include:
-Loss of responsiveness
-No normal breathing

328
Q

What are the appropriate investigations for Ventricular Tachycardia?

A

Cardiac monitor e.g. ECG: determine rhythm-classification of the rhythm directs management

329
Q

What is the management of Ventricular Tachycardia?

A

Ventricular fibrillation is a SHOCKABLE rhythm:
1. Defibrillate once
2. Resume CPR immediately for 2 min, and then defibrillate
3. Administer adrenaline (1 mg IV) after second defibrillation and again every 3–5 min.
4. If ‘shockable rhythm’ persists after third shock, administer amiodarone 300 mg IV bolus
(anti-arrhythmic)

330
Q

What are the complications of Ventricular Tachycardia?

A

(same as cardiac arrest)

Irreversible hypoxic brain damage, heart failure, death

331
Q

What is the prognosis of Ventricular Fibrillation?

A

Resuscitation is less successful in the arrests that occur outside hospital
Duration of inadequate effective cardiac output is associated with poor prognosis

332
Q

What is Wolff-Parkinson-White syndrome?

A

Occurs when one or more strands of myocardial fibres capable of conducting electrical impulses (known as accessory pathways or bypass tracts) connect the atrium to the ipsilateral ventricle across the mitral or tricuspid annulus
Conduction from the atrium reaches the adjacent ventricle earlier via the AP, and a part of the ventricle is pre-excited
*predisposes supraventricular tachycardias (SVT)

333
Q

What is the aetiology of Wolff-Parkinson-White syndrome?

A 
Accessory pathway (bundle of Kent) bypasses the atrioventricular node causing ventricular pre-excitation
Approximately 90% of APs are rapidly conducting, resulting in circus movement tachycardia involving the atrium and ipsilateral ventricle (AV re-entrant tachycardias)
334
Q

What are the associated conditions with Wolff-Parkinson-White syndrome?

A 
Ebstein's anomaly: malformation of the tricuspid valve and right ventricle characterised by adherence of the septal and posterior tricuspid leaflets to the underlying myocardium (strong RF)
Hypertrophic cardiomyopathy
Mitral valve prolapse
Atrial septal defect
Ventricular septal defect
Transposition of the great vessels
Coarctation of the aorta
Dextrocardia (heart points toward the right side rather than left)
Coronary sinus diverticula
Right and left atrial aneurysms
Cardiac rhabdomyomas (primary tumour: as seen in patients with tuberous sclerosis)
Marfan's syndrome
335
Q

What is the epidemiology of Wolff-Parkinson-White syndrome?

A

The exact prevalence of ventricular pre-excitation is difficult to estimate because most patients are asymptomatic
Slight male predominance (2:1)

336
Q

What are the presenting symptoms of Wolff-Parkinson-White syndrome?

A 
Palpitations
Dizziness
Dyspnoea
Chest pain
Syncope (uncommon)
337
Q

What are the signs of Wolff-Parkinson-White syndrome on physical examination?

A

Arrhythmia:

  • Most common: atrioventricular re-entrant tachycardia (AVRT)- 70-80%
  • Atrial fibrillation (irregularly irregular)
  • Atrial flutter
338
Q

What are the appropriate investigations for Wolff-Parkinson-White syndrome?

A

*12-lead ECG: Short PR interval and ‘Delta’ wave
Cardiac electrophysiology: location and physiology of the accessory pathway (AP)
Echocardiogram (to detect any associated cardiac anomalies: associated structural heart disease such as hypertrophic cardiomyopathy, Ebstein’s anomaly and other congenital heart disease)
Treadmill exercise test: intermittent pre-excitation or disappearance of pre-excitation, determine risk of sudden death

Conditions-3 (18 decks)

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