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Year 3 - Diseases > Cardio 2 > Flashcards

Cardio 2 Flashcards

1
Q

Define heart block

A
  • Atrioventricular (AV) block is a cardiac electrical disorder defined as impaired (delayed or absent) conduction from the atria to the ventricles.
  • The severity of the conduction abnormality is described in degrees: first-degree; second-degree, type I (Wenckebach or Mobitz I) or type II (Mobitz II); and third-degree (complete) AV block.
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2
Q

Describe epidemiology of heart block

A
  • More prevalent in African American patients
  • More common over age 50
  • 3rd degree incidence is 0.04%
  • More common in men
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3
Q

Describe aetiology of heart block

A
  • Fibrosis and calcification of the conduction system
  • CAD (including patients with a chronic disease and/or an acute coronary syndrome, right coronary artery)
  • Medication such as AV-nodal blocking agents (i.e., beta-blockers, calcium-channel blockers, digitalis, adenosine), anti-arrhythmic medications such as sodium-channel blockers, and some class III agents (i.e., sotalol and amiodarone).
  • High vagal tone; cardiomyopathy (e.g., hypertrophic, sarcoid, amyloid, haemochromatosis); calcification from adjacent valvular calcification; post catheter ablation for arrhythmias
  • Post-surgical causes (i.e., valve repair or replacement myectomy, septal ethanol ablation); blunt cardiac injury;[10]and some indigenous medicines.
  • Severe electrolyte disturbance, acidosis, or hypoxaemia may result in AV block as well as neuromuscular disorders (myotonic dystrophy, Kearns-Sayre syndrome, Erb dystrophy, peroneal muscular atrophy), myocarditis, infective endocarditis, and Lyme disease.
  • AV block may be congenital as well
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4
Q

List risk factors for heart block

A
  • Age-related degenerative changes in the conduction system
  • Increased vagal tone
  • AV-nodal blocking agents
  • Chronic stable CAD
  • Acute coronary syndrome
  • CHF
  • Hypertension
  • Cardiomyopathy
  • Left ventricular hypertrophy
  • Recent cardiac surgery
  • Acid-base or electrolyte disturbance
  • Neuromuscular disorders
  • Sarcoidosis
  • Myocarditis
  • Infective endocarditis
  • Hypoxemia
  • Blunt cardiac injury
  • Some indigenous medicines
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5
Q

List symptoms of heart block

A

Mobitz 2 and 3rd degree only

  • Fatigue
  • Dyspnoea
  • Chest pain, palpitations, and nausea or vomiting
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6
Q

List signs of heart block

A
  • Hypertension
  • Cannon A waves (3rd degree heart block, irregular large wave of the JVP)
  • Hypoxaemia
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7
Q

Describe diagnosis of heart block

A
  • ECG
  • First degree increased PR interval
  • Mobitz 1 increasing PR interval then dropping a QRS complex
  • Mobitz 2 PR the same with randomly dropped QRS
  • Third degree P and QRS dissociated
  • Troponin may be elevated, measure potassium, calcium, pH
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8
Q

Describe treatment of heart block

A

First degree or Mobitz 1

  • Monitor for development
  • Discontinue AV-nodal blocking medications including beta-blockers, non-dihydropyridine calcium-channel blockers, and digitalis.
  • Pacemaker if symptoms continue

Mobitz II or third degree

  • Discontinue AV blocking drugs
  • Give atropine
  • Pacemaker insertion with or without ICD
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9
Q

List complications of heart block

A

Pacemaker insertion 2-3% risk of

  • Bleeding, infection, vascular trauma, pneumothorax, cardiac tamponade, lead dislodgement, and pocket haematoma development.
  • The risk of MI, stroke, and death is <1%.
  • Long-term complications include pulse generator or lead malfunction and infection, requiring replacement or extraction
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10
Q

Describe prognosis of heart block

A
  • First-degree AV block 2-fold increase in the probability of atrial fibrillation, a 3-fold increase in the probability of pacemaker implantation, and an increase in all-cause mortality.
  • In symptomatic patients with irreversible AV block, symptoms are likely to persist or potentially worsen.
  • Patients with irreversible advanced AV block (type II second-degree or third-degree) are at high risk for progression to third-degree AV block or ventricular asystole.
  • Low rate of pacemaker complications
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11
Q

Describe prognosis of ACS and angina

A
  • Stable angina 58% of patients free of symptoms within 1 year following lifestyle modification and medical therapy
  • non-ST ACS patient mortality after 6 months 4.8%
  • At 12 months, rates of adverse cardiovascular events (MI and death) 10%
  • NSTEMI high risk of morbidity and death, sudden death rate 4-6 times higher than general population
  • STEMI in hospital mortality 4-12% and 1 year mortality 10%
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12
Q

List risk factors for myocarditis

A
  • Infection (non-HIV)
  • HIV infection
  • Smallpox vaccination
  • Autoimmune/immune-mediated diseases
  • Peripartum and postnatal periods
  • Drugs and toxins
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13
Q

Describe diagnosis of myocarditis

A
  • 12-lead ECG (ST and T wave abnormalities, commonly ST elevation/depression)
  • CXR (bilateral pulmonary infiltrates)
  • Serum CK (mildly high)
  • Serum CK-MB (mildly high)
  • Serum troponin (I or T - elevated)
  • Serum B-type natriuretic peptide (elevated in ventricular distention)
  • Two-dimensional echocardiogram (global and regional left ventricular motion abnormalities and dilatation)
  • Endomyocardial biopsy (EMB - myocardial cellular infiltrated and or necrosis)
  • Coronary angiography (normal)
  • Cardiac MRI (early enhancement myocarditis)
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14
Q

Define constrictive pericarditis

A
  • A type of chronic pericarditis (lasts more than 3 months)
  • Characterized by thickening and rigidity of the pericardium, resulting in both backward and forward failure. There is a characteristic pericardial knock on auscultation, which is caused by a sudden stop in ventricular diastolic filling.
  • Effusive-constrictive pericarditis (the other type of chronic pericarditis) is characterized by a thickened pericardium with an effusion; this can lead to cardiac tamponade
    .
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15
Q

Describe aetiology of constrictive pericarditis

A
  • Idiopathic
  • Infectious (most commonly viral e.g., coxsackie B virus), bacterial e.g., Staphylococcus spp., Streptococcus spp., or M. tuberculosis, fungal or toxoplasmosis)
  • Myocardial infarction (Postinfarction fibrinous pericarditis within 1–3 days as an immediate reaction or dressler syndrome within weeks to months following an acute myocardial infarction)
  • Postoperative (postpericardiotomy syndrome): blunt or sharp trauma to the pericardium
  • Uremia (e.g., due to acute or chronic renal failure)
  • Radiation
  • Neoplasm (e.g., Hodgkin lymphoma)
  • Autoimmune connective tissue diseases (e.g., rheumatoid arthritis, systemic lupus, scleroderma)
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16
Q

List risks for constrictive pericarditis

A
  • Low if idiopathic or viral pericarditis
  • Intermediate risk for autoimmune and neoplastic aetiologies
  • High risk for bacterial aetiologies, especially with TB and purulent pericarditis
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17
Q

Describe epidemiology of constrictive pericarditis

A
  • 9% of patients with acute pericarditis
  • 0.76 cases per 1,000 person-years after acute idiopathic/viral pericarditis
  • 31.7 cases per 1,000 person-years for acute tuberculous pericarditis
  • 52.7 cases per 1,000 person-years for purulent pericarditis
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18
Q

List symptoms and signs of constrictive pericarditis

A

Symptoms of fluid overload (i.e., backward failure)

  • Jugular vein distention
  • Kussmaul sign
  • Hepatic vein congestion: hepatomegaly, painful liver capsule distention, hepatojugular reflux
  • Peripheral edema; or anasarca, ascites with abdominal discomfort

Symptoms of reduced cardiac output (i.e., forward failure)

  • Fatigue, dyspnea on exertion
  • Tachycardia
  • Pericardial knock: sudden cessation of ventricular filling during early diastole that is heard best at the left sternal border
  • Pulsus paradoxus: ↓ blood pressure amplitude by at least 10 mm Hg during deep inspiration
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19
Q

List investigations for constrictive pericarditis and their findings

A
  • Echocardiography (increased pericardial thickness)
  • CT and cardiac MRI (pericardial thickening > 2 mm, calcifications, normal cardiac silhouette)
  • Chest x-ray (heart size normal or slightly increased, pericardial calcifications, clear lung fields)
  • Cardiac catheterization if noninvasive methods have failed to provide a definitive diagnosi (similar pressures in the left and right atria and right ventricle at the end of diastole (e.g., “equalization of pressures”), normal pulmonary artery systolic pressure < 40 mm Hg, mean right arterial pressure > 15 mm Hg)
  • Square root sign - dip-and-plateau waveform, a sudden dip in the right and left ventricular pressure in early diastole followed by a plateau during the last stage of diastole
  • ECG (no conclusive findings: generalized flat/inverted T waves, low QRS voltage, possible AF)
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20
Q

List signs on examination associated with intermittent claudication

A
  • Wet gangrene
  • Shiny hairless skin
  • Ulcers
  • Non-palpable pulses
  • Buergers angle (pale limb under 20 degrees with flushing when the limb is lowered due to overcompensation)
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21
Q

Describe investigations of peripheral vascular disease

A
  • Doppler ultrasound
  • Ankle brachial index (systolic pressure of leg divided by systolic blood pressure of the arm - less than 0.41 is grounds for immediate surgical consultation)
  • HbA1c, lipid screen, u&es, digital subtraction angiogram, cardio exam and lower limb exam
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22
Q

List signs on examination associated with limb ischaemia

A
  • Paralysis
  • Pallor
  • Perrishingly cold
  • Pain
  • Pulseless
  • Paraesthesia
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23
Q

Describe aetiology of limb ischaemia

A

Chronic
- Atherosclerosis (intermittent claudication)

Acute

  • Embolus (eg. mural thrombus, AF, TB, IV drug users, malignant)
  • Thrombotic (Vircows triad - ruptured plaque with clot on it)
  • Aneurysm (eg. marfans)
  • Iatrogenic (eg. air embolis)
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24
Q

Describe vircows triad

A
  • Hypercoagulability (blood clotting due to liver failure, polycythaemoa vera)
  • Stasis (long haul flights, recent surgery)
  • Endothelial trauma (bruising, crush injury, plaque rupture)
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25
Q

Describe arterial ulcers

A
  • Located distally, over bony prominences
  • Severe pain, particularly at night
  • Irregular edge, dry necrotic base, poor granulation tissue, round or punched out with sharp demarcation
  • Trophic changes of chronic ischaemia associated with it
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26
Q

Describe venous ulcers

A
  • Lower third of leg (gaiter area between malleolus and lower calf)
  • Mild pain, relieved by elevation
  • Shallow, irregular shape, granulating base, flat or steep elevation markings, fibrinous material at ulcer bed
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27
Q

List associated signs alongside venous ulcers

A
  • Lipodermatofibrosis/ lipodermatosclerosis
  • Pigmentation
  • Oedema
  • Atrophie blanche
  • Telangiectasia
  • Normal cap refill time
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28
Q

List associated signs alongside arterial ulcers

A
  • Trophic changes of chronic ischaemia
  • Pale
  • Hair loss
  • Atrophic skin
  • Cool feet
  • Absence of pulses
  • Prolongued cap refill
  • ABI less than 0.5
  • Dependent rubor
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29
Q

Describe neurotrophic ulcers

A
  • Under calluses or pressure points
  • Punched out, deep sinus variable depth, seep sinus, may involve bone, tendon, fascia, joint capsule
  • Neuropathy may be associated/ underlying osteomyelitis
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30
Q

List investigations for aortic stenosis

A
  • Transthoracic echocardiogram (including Doppler - elevated aortic pressure gradient; measurement of valve area and left ventricular ejection function - diagnostic modality of choice)
  • ECG (left ventricular hypertrophy and absent Q waves, atrioventricular block, hemiblock, or bundle branch block)
  • Cardiac MRI
  • Cardiac catheterisation
  • ECG exercise stress testing
  • Dobutamine stress echo
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31
Q

Define aortic sclerosis

A

Narrowing of the aorta which causes a murmur but has no functional impairment. Does not radiate to the carotids

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32
Q

Define mitral stenosis

A

A narrowing of the mitral valve orifice, usually caused by rheumatic valvulitis producing fusion of the valve commissures and thickening of the valve leaflets.

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33
Q

Describe aetiology of mitral stenosis

A
  • Rheumatic fever
  • congenital
  • Mucopolysaccharidosis
  • endocardial fibroelastosis
  • Malignant carcinoid
  • Prosthetic valve
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34
Q

List risk factors for mitral stenosis

A
  • Streptococcal infection
  • Female sex
  • Ergot medications
  • Serotogenic medications
  • Amyloidosis
  • Bronchial carcinoid syndrome
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35
Q

Describe epidemiology of mitral stenosis

A
  • Mainly in developing countries as primarily caused by rheumatic fever
  • Highest prevelence in Oceania, South Asia and sub-Saharan Africa
  • Rheumatic heart disease more common in females
  • No longer a notifiable disease in US
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36
Q

List symptoms of mitral stenosis

A
  • Start at diameter below 2cm
  • Pulmonary hypertension causes dyspnoea, haemoptysis chronic bronchitis-like picture
  • Pressure on local structures by enlarged left atrium causes haemoptysis, dysphagia and bronchial obstruction
  • Paroxysmal nocturnal dyspnoea
  • Fatigue, palpatations, chest pain, emboli
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37
Q

List signs of mitral stenosis

A
  • Malar flush due to decreased cardiac output
  • Weak pulse
  • AF
  • Tapping, non-displaced apex beat
  • Loud S1, then opening snap with mid diastolic rumble. Closer to S2/ longer rumble = worse disease. Louder on laying on side and expiration (pre-systolic accentuation)
  • Graham steel murmur may be heard (pulmonary hypertension, high pitched decreascendo diastolic murmur on left sternal border)
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38
Q

List investigations for mitral stenosis

A
  • ECG (AF, left atrial enlargement, right ventricular hypertrophy, bifid p waves ‘p-mitrale’/ no p waves)
  • CXR (double right heart border indicating enarged left atrium, prominent pulmonary artery, kerley B lines, mitral valve calcification)
  • Trans-thoracic echocardiography (hockey stick shaped mitral deformity - diagnostic. Stenosis significant if valve orifice <1cm2/m2 body surface area)
  • Trans-oesophageal echocardiography (possible left atrial thrombus)
  • Cardiac catheterisation (high left atrial pressure, low left ventricular pressure and low CO, Indicated if signs of other valve disease, pulmonary hypertension/ calcified mitral valve, angina)
  • Dynamic exercise testing (pressures increase with exercise)
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39
Q

Describe diagnosis of ventricular septal defect

A
  • Chest radiograph
  • ECG
  • Echo
  • Coronary angiogram
  • Swan ganz pulmonary artery catheter
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40
Q

Describe treatment of ventricular septal defect

A
  • Analgesia
  • Urgent transfer
  • Intra-aortic balloon pump
  • Ionotrophic support
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41
Q

Describe signs of ventricular septal defect

A
  • Pan systolic murmur left sternal edge with heaves and thrills
  • Raised JVP
  • Cardiac failure
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42
Q

Compare pericardial effusion with cardiac tamponade

A
  • Both involve fluid in the pericardial space
  • Cardiac tamponade is a pericardial effusion which raises intrapericardial pressure, reducing ventricular filling and dropping cardiac output. Can lead to cardiac arrest
  • For both treat the cause, urgent fluid drainage and send for analysis
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43
Q

Describe management of stable and unstable angina

A
  • Stop smoking, increase exercise, stop alcohol, weight loss, diet modifications
  • Aspirin 75mg if not contraindicated
  • Statin
  • GTN spray/sublingual (SE headache)
  • ACEi
  • B blocker
  • CABG or angioplasty if necessary
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44
Q

Compare aetiology of STEMI and NSTEMI

A
  • NSTEMI subendocardial ischaemia

- STEMI transmural ischaemia

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45
Q

Define aortic dissection

A
  • Intimal layer of wall of the aorta separating resulting in a blood filled lumen
  • Type A ascending aorta
  • Type B descending aorta
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46
Q

List signs and symptoms of aortic dissection

A
  • Acute onset, severe, tearing chest pain radiating from the back. Intense from the onset.
  • Hypertension, dyspnoea
  • Asymmetric upper and lower extremity blood pressure and pulses (absent pulse in one arm)
  • New onset of aortic regurg
  • Paraplegia, paraesthesia
  • Limb pain, abdo pain
  • Left sided decreased breath sounds/dullness
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47
Q

List risk factors for aortic dissection

A
  • Hypertension
  • Atherosclerotic aneurysmal disease
  • Marfan syndrome
  • Ehlers-Danlos syndrome
  • Bicuspid aortic valve
  • Annulo-aortic ectasia
  • Coarctation
  • Smoking
  • Family history of aortic aneurysm or dissection
  • Older age
  • Giant cell arteritis
  • Overlap connective-tissue disorders
  • Vasculitis (takayasus/giant cell)
  • Surgical/catheter manipulation
  • Cocaine/amfetamine use
  • Heavy lifting
  • Infection (syphollis)
  • Pregnancy
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48
Q

Describe epidemiology of aortic dissection

A
  • 0.5-2.95 cases per 100000 annually
  • US 0.2-0.8 per 100000 cases annually, 2000 new cases each year
  • Highest rate in italy, 4.04 per 100000 per year
  • Men predominantly affected, especially over 50 years
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49
Q

Describe aetiology of aortic dissection

A
  • Intimal tear extending into the media of the aortic wall
  • Cystic medial degeneration predisposes to intimal disruption and is characterised by elastin, collagen and smooth muscle breakdown in the lamina media
  • Inherited conditions (eg. marfans and ehlers danlos)
  • Aterosclerosis
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50
Q

List types of aortic dissection

A
  • Type A ascending aorta (always needs surgery)

- Type B descending aorta

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51
Q

Describe diagnosis of aortic dissection

A
  • ECG (look for MI)
  • CXR showing widened mediastinum, possible pericardial effusion
  • Cardiac enzymes usually negative
  • BP in both arms, then transthoracic/oesophageal ultrasound
  • CT angiography (include abdo and pelvis to see extent - shows intimal flap) GOLD STANDARD
  • MRI
  • Renal function tests (elevated creatinine and urea in reduced renal perfusion)
  • LFTs (asparate transaminase and alanine transaminase raised in reduced hepatic perfusion)
  • Lactate
  • FBC
  • Group and save (prepare for surgery)
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52
Q

Describe ECG changes in hypokalaemia

A
  • U wave, elongated PR interval, t wave flattening and inversion and ST depression caused by hypokalaemia.
  • Untreated hypokalaemia causes toursades de points, a form of ventricular tachycardia
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53
Q

Define aortic regurgitation

A
  • The diastolic leakage of blood from the aorta into the left ventricle.
  • It occurs due to inadequate coaptation of valve leaflets resulting from either intrinsic valve disease or dilation of the aortic root.
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54
Q

Describe epidemiology of aortic regurgitation

A
  • Not as common as aortic stenosis and mitral regurgitation
  • 13% prevalence in men and 8.5% in women trace or mild.
  • Prevalence increases with age
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55
Q

Describe aetiology of aortic regurgitation

A
  • Developing countries rheumatic heart disease is the most common cause

Acute:

  • Infective endocarditis
  • Ascending aortic dissection
  • Chest trauma

Chronic

  • Congenital
  • Connective tissue disorders (eg. marfans, Ehlers Danlos)
  • Rheumatic fever
  • Takayasu arteritis
  • Rheumatoid arteritis
  • SLE
  • Appetitie suppressents
  • Arthritides
  • Hypertension
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56
Q

List risks for aortic regurgitation

A
  • Bicuspid aortic valve
  • Rheumatic fever
  • Endocarditis
  • Marfan’s syndrome and related connective tissue disease
  • Aortitis
  • Systemic hypertension
  • Older age
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57
Q

List symptoms of aortic regurg

A
  • Exertional dyspnoea
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Palpitations, angina, syncope
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58
Q

List signs of aortic regurg

A
  • Collapsing (water hammer) pulse
  • Wide pulse pressure
  • Displaced, hyperdynamic apex beat
  • High pitched early diastolic murmur louder on expiration when sitting up in tricuspid region
  • Corrigons sign (caorid pulsation)
  • De mussets sign (head nodding with each heartbeat)
  • Quinckes signs (carotid pulsations in nail bed)
  • Duroziezs sign (in the groin a finger compressing the femoral artery gives a diastolic murmur)
  • Traubes sign (pistol shot sound over femoral arteries)
  • Austin flint murmur (severe AR)
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59
Q

Describe investigations for aortic regurg

A
  • ECG showing left ventricular hypertrophy
  • CXR showing cardiomegaly, dilated ascending aorta, pulmonary oedema
  • Echo is diagnostic
  • Cardiac catheterisation to assess severity of the lesion, anatomy of the aortic root, left ventricular function, coronary artery disease and other valve disease
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60
Q

Define mitral regurgitation

A

Backflow through the mitral valve during systole

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61
Q

Describe aetiology/risks of mitral regurg

A
  • Functional (LV dilation)
  • Annular calcification (elderly)
  • Rheumatic fever
  • Infective endocarditis
  • Mitral valve prolapse
  • Ruptured chordae tendinae
  • Papillary muscle dysfunction/rupture post MI
  • Connective tissue disorders (eg. Ehlers Danlos and Marfans)
  • Cardiomyopathy
  • Congenital
  • Anorectic/dopaminergic drugs
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62
Q

List symptoms of mitral regurg

A
  • Dyspnoea
  • Fatigue
  • Palpitations
  • Symptoms of causitive factor
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63
Q

List investigations for mitral regurg

A
  • ECG showing AF, echo
  • P-mitrale pn ECG if sinus rhythm
  • LVH
  • CXR (large LA and LV, mitral valve calcification, pulmonary oedema)
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64
Q

Define tricupsid regurgitation

A

Backflow of blood through the tricuspid valve in systole

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65
Q

Describe epidemiology of tricuspid regurg

A
  • COmmon incidental finding on imaging
  • 50-60% mild asymptomatic adults
  • 15% moderate
  • In developed countries most commonly ischaemic or degenerative mitral regurg.
  • Developing rheumatic fever
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66
Q

Describe aetiology/risks of tricuspid regurg

A
  • Functional eg. RV dilation eg. due to hypertension induced by LV falure or PE
  • Rheumatic fever
  • Infective endocarditis
  • Cardinoid syndrome
  • Congenital (ASD, AV canal, ebstein)
  • Drugs (ergot)
  • RA, marfans, tricuspid valve prolapse
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67
Q

List symptoms of tricuspid regurg

A
  • Fatigue
  • Hepatic pain on exertion due to congestion
  • Ascites
  • Oedema
  • Symptoms of causative condition
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68
Q

List signs of tricspid regurg

A
  • Giant v wave and prominent y descent on JVP
  • RV heave
  • Pansystolic murmur heard best at lower left sternal border, on inspiration
  • Pulsatile hepatomegaly
  • Jaundice
  • Ascites
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69
Q

Describe investigations for tricuspid regurg

A
  • Echocardiogram (assess left and right heart ejection fraction)
  • ECG (atrial flutter/fib)
  • LFT
  • Serum urea and creatinine
  • FBC
  • CXR (cardiomegaly, pleural or pericardial effusion)
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70
Q

Compare osler nodes and janeway lesions

A
  • Osler nodes are caused by immune complex deposition. Painful in the fingers and toes
  • Janeway lesions are non-tender palmar or plantar nodules due to emboli
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71
Q

List risk factors for atrial fibrillation

A
  • Age over 70
  • Thyrotoxicosis
  • Rheumatic heart disease
  • Alcoholism
  • Left ventricular dysfunction

Also: IHD, post op, hypokalaemia, pneumonia, caffine

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72
Q

Define ventricular fibrillation

A

An arrythmia causing the ventricles to quiver and cause uncoordinated muscle contraction

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73
Q

Describe aetiology/risks for ventricular fibrillation

A
  • MI
  • Increased catecholamines
  • Electrolyte imbalances (torsades de pointes)
  • Hypoxia
  • Acid-base disturbance
  • Hyper/hypothermia
  • Congenital conditions (QT syndrome, Brugada)
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74
Q

List signs and symptoms of ventricular fibrillation

A
  • Chest pain
  • Dizzy
  • SOB
  • Unconscious
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75
Q

List investigations for ventricular fibrillation

A
  • Time dependent
  • ECG showing no recognisible P, QRS or T waves
  • Blood test
76
Q

Describe management of ventricular fibrillation

A
  • CPR/ defibrillation
  • IV adrenalline 1mg every 3-5 mins
  • IV amiodarone 300 mg after 3 shocks
  • IV amiodarone 150mg after 5 shocks
  • Treat hypoxia, hypothermia, hypovolaemia, electrolyte abnormalities, tension pneumothorax, tamponade, thromboembolism
77
Q

Describe prognosis of ventricular fibrillation

A
  • Prognosis poor without intervention in 4-6 minutes
  • Early defib increases prognosis
  • If occuring 48 hours after acute MI high rate of recurrence
78
Q

Describe complications of ventricular fibrillation

A
  • CNS ischaemic injury
  • Myocardial injury
  • Post defib arrythmias
  • Aspiration pneumonia
  • Injuries from CPR
  • Death
79
Q

Describe epidemiology of ventricular fibrillation

A
  • Most common arrythmia in cardiac arrest patients

- Increases age 45-75

80
Q

Define wolf parkinson white syndrome

A

An arrhythmia that occurs due to the presence of an accessory pathway from the atria to the ipsilateral ventricle causing pre-excitation

81
Q

Describe aetiology of WPW

A

Congenital

  • Ebstein’s anomaly (septal and posterior tricuspid leaflets are displaced towards the apex)
  • Heart defect (VSD, transposition of great vessels, hypertrophic cardiomyopathy)
  • Mitral valve prolapse
  • Coarctation of the aorta
  • Marfan’s syndrome
82
Q

List signs and symptoms of WPW

A
  • Palpitations
  • Dizzy
  • Chest pain
  • SOB
83
Q

Describe investigations for wolf parkinson white

A
  • ECG (slurred upstroke of the QRS (delta wave) with short PR)
  • Echo if suspect structural disease
84
Q

Describe epidemiology of WPW

A
  • 1-3 people per 1000 population
  • More common in males
  • Most common in young, previously healthy people. Prevalence decreases with age
85
Q

Define varicose veins

A

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

86
Q

Describe epidemiology of varicose veins

A
  • Increases in prevalence with age, 41% in 60 year olds
  • Genetic risk
  • Higher prevalence in more developed regions. 10-15% in men and 20-25% in women
87
Q

Describe aetiology/risks of varicose veins

A
  • Previous episode of DVT
  • Female sex
  • Prolongued standing
  • Increasing numbers of births
  • Obesity
  • Genetic links
  • Venous valve incompetence, leading to pooling of blood and distention of veins
  • May be caused by obstruction (DVT, fetus, pelvic tumour), AV malformations, overactive muscle pumps
88
Q

List signs and symptoms of varicose veins

A
  • Dilated torturous veins
  • Fatigue with prolongued standing
  • Cramps, heaviness
  • Restless legs
  • Corona phlebactica
  • Itching
  • Ankle swelling
  • Venous ulceration, oedema, eczema, lipodermatosclerosis
  • Tap test (tap on varicose vein and feel a thrill over saphenofemoral junction). Auscultate for bruits
89
Q

List investigations for varicose veins

A

Duplux ultrasound, valve closure time of over 0.5 seconds indicative of reflux

90
Q

Describe management of varicose veins

A
  • Specialist referal if bleeding, pain, ulceration, severe impact on quality of life or thrombophlebitis
  • Treat underlying cause
  • Education (avoid standing lots, elevate legs, stockings, lose weight, regular walks)
  • Endovascular treatment (radiofrequency ablation, endovenous laser ablation, injection sclerotherapy)
  • Surgery (eg. saphenofemoral ligation, post op elevation and compression)
91
Q

List possible complications of varicose veins

A
  • Chronic venous insufficiency
  • Haemorrhage
  • Venous ulceration
  • Lipodermatosclerosis
  • Haemosiderin deposition
92
Q

Describe prognosis of varicose veins

A

Resolution of symptoms occurs in over 95% of patients

93
Q

Define venous ulcer

A
  • Abnormal break in the epithelial surface, caused by venous insufficiency
94
Q

Describe epidemiology of venous ulcers

A
  • 70% of leg ulcers

- More common with advancing age, 1-3 per 1000 in general population to 20 per 1000 in 80 plus age group

95
Q

List risk factors for venous ulceration

A
  • Pre-existing varicose veins
  • DVT
  • Phlebitis
  • Previous fracture, trauma or surgery
  • Family history
  • Increasing age
  • Prolongued stanging
  • Obesity
  • Smoking
  • Pregnancy
96
Q

List symptoms of venous ulceration

A
  • Pain relieved by elevation
  • Leg heaviness
  • Aching
  • Swelling
  • Skin dryness
  • Tightness
  • Itching
  • Irritation
  • Muscle cramps
  • Venous claducation
97
Q

List signs of venous ulceration

A
  • Ulcer in lower third of leg (gaiter area), between malleolus and lower calf
  • Shallow, irregular shape, granulating base, slat of steep elevation markers and fibrinous materal at ulcer bed
  • May also see lipodermatofsclerosis (like an upside down wine bottle), pigmentation (hemosiderin deposition), oedema, atrophie blanche, telangiectasia, normal cap refil, stasis eczema
98
Q

Describe investigations of venous ulceration

A
  • Venous duplex ultrasound showing reflux (less than 500 milliseconds superficial veins, 1000 milliseconds for deep veins)
  • ABPI to rule out arterial
  • May swab and biopsy
99
Q

Describe management of venous ulcers

A
  • Graduated compression (reverse venous insufficiency, multilayer dressing)
  • Debridement and cleaning (release trapped pus)
  • Dressing (hydrocolloidal)
  • Antibiotics (if suspician of infection)
  • Pentoxifylline (chronic if it fails to respond after 4 weeks, given for 6 months)
  • Topical steroids for surrounding dermatitis
  • Aspirin
  • Venous surgery
  • Skin grafting if extensive
100
Q

Describe prognosis of venous ulcers

A

Prognosis is improved if the patient is mobile and has no significant comorbidities

101
Q

List complications of venous ulcers

A
  • Recurrent
  • Malignant change
  • Osteomyelitis/sepsis
  • Cellulitis/infection
102
Q

Define arterial ulcer

A

A break in the epithelium of the skin caused by arterial insufficiency

103
Q

Describe epidemiology of arterial ulcers

A
  • Second most common ulcer in the leg
  • 10% of all leg ulcers
  • Both sexes equally affected
104
Q

Describe aetiology of arterial ulcer

A
  • Arterial or arteriolar obstruction leading to ischaemia of skin and subcutaneous tissues
  • Acute imparment may be trauma/thrombosis, chronic impairment atherosclerosis
  • Peripheral vascular disease due to atherosclerosis is the most common cause of arterial ulceration (commonly men over 45 and women over 55)
105
Q

List risk factors for arterial ulcers

A
  • Old age
  • CV risks (smoking, alcohol, obesity, diabetes, HTN, high cholesterol)
  • Vasculitis
  • Sickle cell disease
  • Thalassemia
106
Q

List symptoms and signs of arterial ulcers

A
  • Severe pain, particularly at night which eases when depressing the leg, and intermittent claudication
  • Distal ulcer on the dorsum of foot or toes, over bony prominences
  • Irregular edge, poor granulation tissue, dry necrotic base, round or punched out with sharp demarcation
  • Trophic changes of chronic ischaemia (pale, hair loss, atrophic skin, cool feet, absent pulses, prolongued cap refill, ABI <0.5 rubor
  • Buergers test where there is pain lifting the legs, pallor, and when legs hung over the side skin initially blue, then red due to reactive hyperaemia
107
Q

List investigations for arterial ulcers

A
  • ABI <0.5 severe
  • Buergers test
  • Duplex ultrasound, CT angiography, MRA
108
Q

Define pulmonary hypertension

A
  • Chronically elevated mean pulmonary arterial pressure (mPAP) at rest ≥ 20 mmHg (normal: 10–14 mmHg) or > 30 mmHg with exercise due to chronic pulmonary and/or cardiac disease or unknown reasons
  • Plus elevated pulmonary vascular resistance of ≥ 3 Wood units for patients with pre-capillary pulmonary hypertension (e.g., pulmonary arterial hypertension)
109
Q

Define cor pulmonale

A
  • Altered structure of impaired function of the right ventricle caused by pulmonary hypertension resulting from a primary disorder of the respiratory or pulmonary artery system
110
Q

Describe aetiology of pulmonary hypertension

A

Group 1: pulmonary arterial hypertension

  • Idiopathic
  • Hereditary (BMPR2)
  • Drug induced (amphetamines, cocaine, appetite suppressants)
  • Associated conditions (connective tissue diseases, congenital heart disease, HIV)

Group 2: left heart disease

Group 3: chronic lung diseases and or hypoxemia

  • Obstructive sleep apnea
  • COPD/emphysema
  • Interstitial lung disease
  • High altitude

Group 4: chronic thromboembolic occlusion

Group 5: Unclear (sickle cell, scleroderma, metabolic syndrome, compression of pulmonary vessels by a tumor)

111
Q

Describe epidemiology of pulmonary hypertension

A
  • PAH rare, 10-52 cases per million
  • PH more common in severe respiratory and cardiac disease, 18-50% pateints assessed for transplantation and 7-83% of those with diastolic heart failure
  • 0.5-4% post PE
112
Q

List symptoms of pulmonary hypertension

A
  • Dyspnoea, syncope on exertion
  • Chest pain
  • Fatigue
  • Cyanosis
  • Clinical features of underlying aetiology
  • Hoarseness and cough occur rarely
113
Q

List signs of pulmonary hypertension

A
  • Loud and palpable second heart sound
  • Jugular vein distention
  • RHF (palpitations, oedema)
  • Nail clubbing
  • Parasternal heave
114
Q

List investigations for pulmonary hypertension

A
  • Doppler echocardiography (hypertrophy of right ventricle, dilation of coronary sinus, estimation of pulmonary arterial pressure)
  • Right heart catheterisation (mPAP >20mmHg at rest, if pre capillary pulmonary vascular resistance over 3 wood units)
  • Electrocardiography right axis deviation, RBBB, p pulmonale
  • CXR right heart hypertrophy, vascular changes (increased diameter of pulmonary arteries)
  • LFTs, TFT, autoimmune screening
115
Q

List the grades of hypertensive retinopathy

A
  • Grade 1 tortuosity of retinal arteries with increased reflectiveness (silver wiring).
  • Grade 2 grade 1 plus arteriovenous nipping (thickened retinal arteries pass over retinal veins).
  • Grade 3 additional flamed shaped haemorrhage and cotton wool exudates due to small infarct.
  • Grade 4 additional papilloedema (blurry margin of optic disc)
116
Q

List side effects of spironolactone

A
  • Hyperkalaemia

- Gynaecomastia

117
Q

List side effects of b blockers

A
  • Bronchospasm
  • Heart failure
  • Lethargy
118
Q

List the mid diastolic murmurs

A
  • Mitral stenosis

- Tricuspid stenosis

119
Q

List the pan systolic murmurs

A
  • Tricuspid regurg
  • Mitral regurg
  • VSD
120
Q

List mid systolic murmurs

A

Aortic stenosis

121
Q

List late systolic murmurs

A

Valve prolapse

122
Q

List early diastolic murmurs

A
  • Aortic regurg

- Pulmonary regurg

123
Q

Describe austin flint murmurs

A
  • Occurs in severe aortic regurg

- Low pitch rumbling and mid-diastolic murmur best heard at the apex

124
Q

Define cardiac arrest

A
  • A sudden state of circulatory failure due to a loss of cardiac systolic function
  • The result of 4 specific rhythm disturbances - VF, pulseless VT, pulseless electrical activity and asystole
125
Q

Describe epidemiology of cardiac arrest

A
  • 84 per 100000 population per year in Europe out of hospital considered for resus
  • US 110.8 per 100000 out of hospital arrest
126
Q

Describe aetiology of cardiac arrest

A
  • Ischaemic heart disease (62%)
  • Unspecified cardiovascular disease (12%)
  • Cardiomyopathy/dysrhythmias (9%)
  • 4 arrythmias: VT, VF, PEA, asystole
  • VT and VF most common, due to ischaemic heart disease, left vent dysfunction, premature ventricular beats
  • PEA MI, hypovolaemia, PE
  • Other causes: hypoxia, hyper/hypokalaemia, acidosis, hypothermia, glucose abnormalities, trauma, tamponade, tension pneumothorax
127
Q

List risk factors for cardiac arrest

A
  • Coronary artery disease
  • Left ventricular dysfunction
  • HCM
  • Arrythmogenic right ventricular dysplasia
  • Long QT syndrome
  • Acute emergency
  • Illicit substances
  • Brugada syndrome
  • Valvular heart disease
  • Smoking
  • ED
128
Q

List signs and symptoms of cardiac arrest

A
  • Patient unresponsive
  • Absence of normal breathing
  • Absence of circulation
  • Cardiac rhythm disturbance
129
Q

List investigations for cardiac arrest

A
  • Continuous cardiac monitoring to identify shockable rhythm (VF or VT) or non-shockable rhythm (asystole or pulseless electrical activity)
  • FBC (haemorrhage)
  • Serum electolytes (for potassium abnormalities)
  • ABG
  • Cardiac biomarkers (positive)
  • Echo (tamponade, valve disorders, assess left ventricular function)
  • ECG once circulation returned
  • Coronary angiography
  • CXR
130
Q

Describe management of cardiac arrest

A
  • CPR
  • Defibrillation if shockable
  • Adrenaline (IV), anti-arrythmic (amiodarone), magnesium (torsades de pointes)
  • Post resus care - rewarming, prevent recurrence
131
Q

List complications of cardiac arrest

A
  • Death
  • Rib fracture
  • Anoxic brain injury
  • Ischaemic liver injury
  • Renal tubular necrosis
  • Recurrent cardiac arrest
132
Q

Describe prognosis of cardiac arrest

A
  • Poor - early CPR increases survival
  • Survival <20% out of hospital VF
  • Survival <10% all patients out of hospital cardiac arrest
  • 36% in hospital VF/VT survival to discharge
133
Q

Define cardiomyopathy

A
  • Cardiomyopathies are diseases of the muscle tissue of the heart.
  • Types of cardiomyopathies include dilated, hypertrophic, restrictive, and arrhythmogenic right ventricular cardiomyopathy
  • Dilated cardiomyopathy (DCM) is the most common type of cardiomyopathy.
  • Unclassified: arrythmia induced, left ventricular non-compaction
134
Q

Describe aetiology of dilated cardiomyopathy

A

Dilated

  • Idiopathic
  • TTN gene mutation
  • IHD
  • Infections (coxsackie B virus, chagas, HIV)
  • Systemic disorders (sarcoidosis, haemochromatosis, thiamine deficiency)
  • Peripartum
  • Toxic substances (cocaine, alcohol, medication)
  • Valvular disease (aortic stenosis, aortic regurg, mitral regurg)
135
Q

Describe aetiology of hypertrophic cardiomyopathy

A
  • Autosomal dominant

- Mutation of myosin binding protein C and B-Myosin heavy chain

136
Q

Describe aetiology of restrictive cardiomyopathy

A
  • Idiopathic
  • Systemic disorders (amyloidosis, sarcoidosis, haemochromatosis, systemic sclerosis)
  • Heart disease (Loffler endocarditis eospinophilic, endocardial fibroelastosis first 2 years of life)
  • Post radiation fibrosis
137
Q

Describe epidemiology of cardiomyopathy

A
  • Dilated 6/100000 per year, most common cardiomyopathy. 3:1 male to female
  • Restrictive least common
  • Arrythmogenic right ventricular cardiomyopathy most common in young adults (mean age 30), 1:1000-2000 prevalence
138
Q

List symptoms and signs of hypertrophic cardiomyopathy

A
  • Asymptomatic
  • Signs of LHF (dyspnoea, syncope, dizziness)
  • Arrythmias (ejection systolic murmur)
  • Jerky carotid pulse
  • S4 gallop
  • Mitral regurg
  • Sudden death
139
Q

List symptoms and signd of dilated cardiomyopathy

A
  • Exertional dyspnoea, ankle oedema, ascites, angina pectoris
  • Mitral or tricuspid regurg
  • S3 gallop
  • Left ventricular impulse displacement
  • JVP raised
  • Rales
  • Palpitations
  • Diffuse oedema
140
Q

Describe investigations for dilated cardiomyopathy

A
  • BNP raised in HF
  • Troponin and CK-MB to rule out MI
  • Echo - atrial and/or ventricular dilatation, reduced LVEF, wall motion abnormalities
  • CXR cardiomegaly, pulmonary oedema
  • ECG (disorders of condition, arrhythmias, change of cardiac axis, reduced QRS)
  • Histology (fibrosis without inflammation, more extensive in subendocardium)
141
Q

List signs and symptoms of restrictive cardiomyopathy

A
  • Duspnoea
  • JVP raised
  • Peripheral oedema, ascites
  • Hepatomegaly
  • Kussmal sign = paradoxical rise in JVP during inspiration
  • S4 sound
142
Q

Describe diagnosis of restrictive cardiomyopathy

A
  • Echo (diastolic dysfunction - rapid early but reduced diastolic filling, near normal or elevated EF, atrial enlargement)
  • ECG (low voltage, LBBB)
  • CXR (pulmonary congestion, underlying disease)
    Cardiac catheterisation (high atrial pressure, abnormal vnetricular)
  • Biopsy (fibrosis)
143
Q

List investigations for hypertrophic cardiomyopathy

A
  • Echo showing decreased LV cavity size, normal EF, increased wall thickness, outflow obstruction and reduced diastolic filling
  • ECG - left ventricular hypertrophy (deep S in V1/2, tall R in V5/6, S in V1+R in V5 or V6 over 7 large squares), left axis deviation, q waves
144
Q

Describe signs and symptoms of arrythmogenic right ventricular cardiomyopathy

A
  • Variable, most asymptomatic
  • Angina
  • Dyspnoea
  • Peripheral oedema
  • Ascited, hepatic and splenic congestion
  • Palpitations, syncope, sudden death
145
Q

Describe investigations for arrythmogenic right ventricular cardiomyopathy

A
  • AHA - dysfunction and structural abnormalities of RV, histological characteristics, abnormal repolarisation, conduction abnormalities, arrythmias, family history
  • ECG epilson wave in right precordial leads, increased QRS duration, ventricular tachycardia, ventricular extrasystoles
  • Echo (RV enlargement, RV wall motion abnormalities, reduced EF, localised RV aneurysms)
  • Biopsy fibrofatty replacement
  • Genetic testing myltiple genetic abnormalities (JUP, DSP.ect)
146
Q

Define gangrene

A
  • A complication of necrosis characterised by the decay of body tissues.
  • There are two major categories: infectious gangrene (wet gangrene) and ischaemic gangrene (dry gangrene).
147
Q

Describe epidemiology of gangrene

A
  • 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.
  • Type II necrotising fasciitis has an annual incidence of 5 to 10 cases per 100,000 in the US.
  • Approximately, half of the cases of streptococcal necrotising fasciitis occur in young and previously healthy people.
  • Gas gangrene 3000 annual cases US
  • Atheroembolism 0.3-3.5% incidence.
148
Q

Describe aetiology/risks of gangrene

A

Infectious

  • Necrotising fasciitis (strep, staph, enterobacteriaecaea)
  • Gas (C. perfringes - spore baring)
  • Surgery/trauma, malnutrition, immunosuppression

Ischaemic

  • Atherosclerosis, diabetes associated microangiopathy. Hypercoagulable states (drug abuse, malignancy, antiphospholipid syndrome)
  • Inadequate blood supply due to venous obstruction. Phlegmasia cerulea dolens (complete venous obstruction)
149
Q

Describe symptoms and signs of gangrene

A
  • Pain (sudden onset)
  • Oedema
  • Skin discolouration (ecchymoses, purpura, blebs, haemorrhagic bullae)
  • Crepitus (gas gangrene)
  • Diminished pedal pulses and ABI (ischaemic)
  • Low grade fever and chills (infectious)
150
Q

List investigations for gangrene

A
  • FBC (leukocytosis, haemoconcentration, anaemia)
  • Metabolic panel (acidosis, liver derangement, renal failure)
  • LDH (haemolytic anaemia)
  • Coagulation
  • Blood cultures
  • Serum CRP
  • X rays (gas in soft tissues (gas gangrene))
  • CT, MRI (abscess, enhancement, oedema, thickening of fascia)
  • Doppler ultrasonography (obstruction)
  • CT angiogram (artheroemboli)
  • Surgical exploration, skin biopsy (determine involvement of fascia)
  • Cryofibrinogens, cryoglobulin, ANA, lupud and anticardolipin for antiphospholipid syndrome
151
Q

Define pressure sore

A

Pressure ulcers have been defined by the National Pressure Ulcer Advisory Panel and the European Pressure Ulcer Advisory Panel as localised injury to the skin and/or underlying tissue usually over a bony prominence, as a result of pressure or of pressure in combination with shear.

152
Q

Describe epidemiology of pressure ulcers

A
  • 4.7-32.1% prevalence in hospitalised patients
  • 0.58 per 100 person years among elderly patients in UK
  • Most are on sacrum, coccyx and heels
153
Q

Describe aetiology/risks of pressure sores

A
  • Pressure, shear, friction and moisture
  • Circulation and tissue perfusion
  • Most commonly over bony prominances
  • Risks include increased age, reduced mobility, malnurishment, history of ulcers, neurological impairment, and conditions that prevent normal self positioning
154
Q

List signs and symptoms of pressure sores

A
  • Localised skin changes (non-blanching erythea or discolored skin which may be painful, firm, mushy, boggy, or altered temp)
  • Shallow open wound or tissue loss on aread under pressure (grade 2)
  • Full thickness with some slough grade 3
  • Full thickness with major tissues involved (bone, tendon or muscle - grade 4)
  • Localised tenderness and warmth (infection)
  • Exudate and foul odour (infection)
155
Q

Describe investigations for pressure sores

A
  • Clinical diagnosis
  • Wound swab
  • ESR (osteomyelitis), WBC (osteomyelitis), glucose
  • Deep tissue biopsy (infection)
  • MRI (bony involvement)
156
Q

Define coronary angiography and PCI

A
  • Coronary angiography is a prodedure where a contrast dye, containing iodine, is is injected. Then a catheter tube is inverted into a blood vessel (arm, groin, thigh) and moved to your cooronary artery. Dye is injected through the catheter to highlight blockages, and X rays are taken of the heart.
  • PCI is where the catheter is used to pace a stent in blood vessels that have narrowed to open them up. THis uses a baloon to open the vessel, which is then deflated.
157
Q

List indications for coronary angiography and PCI

A
  • Diagnose ischaemic chest pain (abnormal ECG, sudden cardiac arrest, chest pain, abnormal stress test)
  • Increasing angina
  • Heart defect you were born with
  • Valvular defect
158
Q

List complications of coronary angiography and PCI

A
  • Bleeding
  • Reaction to contrast
  • Blood vessel damage
  • Arrythmias
  • Infection
  • Blood clot formation (heart attack or stroke)
  • Higher risk in older people and those with CKD/diabetes
  • Restenosis
  • Cholesterol embolisation
159
Q

Define CABG

A

Revascularisation technique used to treat patients with significant, symptomatic stenosis of the coronary artery.

  • Uses a midline sternotomy
  • The stenosed artery is bypassed using an arterial (internal thoracic, internal mammary, radial) or venous (great saphenous vein) autograft), re-establishing bloodflow to ischaemic areas of the myocardium
160
Q

List indications for CABG

A
  • High grade left main stem coronary artery stenosis
  • Significant stenosis (>70%) of the proximal left anterior descending artery, with 2 vessel or 3 vessel disease
  • Symptomatic 2 vessel or 3 vessel disease
  • Disabling angina despite medical treatment
  • Poor left ventricular function
  • Post-infarct angina
  • NSTEMI
  • STEMI with inadequate response to all non-surgical therapy
  • Failed PCI
161
Q

List complications of CABG

A
  • Myocardial dysfunction
  • Post-pericardiotomy syndrome (autoimmune pericarditis or pleuritis, treated with NSAIDs and drainage)
  • Postoperative cardiac tamponade with shock
  • Bypass occlusion
  • Arrythmias
  • Postoperative acute mediastinitis (surgical debridement, antibiotics)
  • Mediastinal haemorrhage (ventilation)
162
Q

Define DC cardioversion

A
  • Direct current cardioversion is a procedure used to convert an abnormal heart rhythm to a normal heart rhythm
  • Uses defibrillator pads and administers a controllec electrical current while the patient is under general anaesthetic
163
Q

List indications for DC cardioversion

A
  • Treatment of a tachycardia present for less than 24 hours with the aim to revert back to sinus rhythm
  • Treatment of a tachyarrythmia present for less than 24 hours when pharmacological measures have failed
  • Treatment of tachyarrythmia where the patient shows signs of decompensation (chest pain, hypotension, or signs of heart failure)
  • Atrial fibrillation or atrial flutter
  • Ventricular and sypraventricular tachycardia
164
Q

List complications of DC cardioversion

A
  • Skin soreness
  • Arrythmia
  • Stroke
  • Unsuccessful in 50%
  • Dislodging bloood clots
165
Q

Define implanted cardiac defibrillator

A
  • An implanted device that prevents sudden cardiac death by delivering electrical impulses to convert heart rhythm back to normal sinus rhythm, and continually monitoring the heart
  • Subcutaneous is under the skin
  • It can perform pacing, cardioversion, and defibrillation
  • Inserted under local anaesthetic, just under the collarbone
166
Q

List indications for an implated cardiac defibrillator

A
  • Previous life threatening abnormal heart rhythm (Cardiac arrest, V fib, V flutter)
  • Risk of life threatining abnormal heart rhythm (cardiomyopathy, long QT, brugada syndrome)
  • Heart failure (EF<35%)
167
Q

List complications of implantable cardiac defibrillator

A
  • Bleeding from incision
  • Damage to blood vessel
  • Infection
  • Cardiac tamponade
  • Collapsed lung
  • Post surgery: lead complications, movement of the generator causing pain, innapropriate shocks
168
Q

Define permanent pacing

A
  • An electronic device that monitores the heart rhythm and stimulates the heart when indicated (low or absent intrinsic activity)
  • Single chamber one lead in the right atrium/ventricle
  • Dual chamber 2 leads one in right ventricle and one in right atrium
  • Biventricular pacing is a extra lead in the coronary sinus for left ventricular pacing
169
Q

List indications for permanent pacing

A
  • Sinus node dysfunction and high-grade AV block (three or Mibitz II)
  • Chronic bi-fascicular block
  • Post acute MI
  • Hypersensitive carotid sinus syndrome
  • Post cardiac transplant
  • Prevent tachycardia, AF
  • Congenital heart disease
  • Hypertropic cardiomyopathy
  • Cardiac resynchronisation in severe systolic HF
170
Q

List complications of permanent pacing

A
  • Haematoma
  • Lead dislodgement
  • Infection
  • Lead perforation
  • Dysrhythmias
  • Pneumothorax, pericarditis
  • Venous thrombosis
  • Failure to output or capture
  • Pacemaker syndrome (atrial and ventricular contractions are simultaneous)
171
Q

List signs of longstanding hypertension

A
  • Left ventricular hypertrophy
  • Heave
  • S4 atria contracting forcefully to overcome an abnormally stiff or hypertrophic ventricle
  • Bruits
172
Q

List the 4H and 4T reversible causes of cardiac arrest

A
  • Hypothermia
  • Hypovolaemia
  • Hypoxia
  • Hyper/hypokalaemia
  • Toxins
  • Tension pneumothorax
  • Cardiac tamponade
  • Thromboembolic
173
Q

List causes and left and right BBB

A

Left BBB

  • Hypertension
  • IHD
  • MI
  • Aortic stenosis

Right BBB

  • Congenital heart disease
  • PE
  • Fibrosis of conduction system
  • Cor pulmonale
174
Q

List signs of cardiac tamponade

A

Becks triad

  • Muffled heart sounds
  • Distended neck veins
  • Hypotension
175
Q

Describe management of prinzmetal angina

A
  • CCB

- Nitrates

176
Q

Describe arrythmogenic cardiomyopathy

A
  • Progressive fatty and fibrous replacement of the ventricular myocardium
  • Inherited (autosomal dominant
177
Q

Describe takotsubo cardiomyopathy

A
  • Sudden temporary weakening of heart muscle after a significant stressor
  • ”Broken heart syndrome”
178
Q

List risk factors for cardiac tamponade

A
  • Vasculitis
  • Trauma
  • MI
179
Q

List investigations and management for cardiac tamponade

A
  • ECG (electrical alternans)
  • CXR (globular)
  • Eco
  • Management: emergency needle pericardiocentesis
180
Q

Describe ECG changes in right vs left ventricular hypertrophy

A
  • Right has tall R in V1 and deep S in V6, RAD, right ventricular strain (ST depression V1-4)
  • Left deep S in V1 and tall R in V6
  • TO be significant, must be S+R>7 squares
181
Q

COmpare intermittent claudication and critical limb ischaemia

A

Intermittent claudication

  • Does not require intervention unless lifestyle impaired
  • Pain upon movement eased by rest
  • Pain is a cramping nature

Critical limb ischaemia

  • Pain at rest, requiring opioid analgesia
  • Over 2 weeks or presense of tissue loss
  • Pain at night
  • Gangrene, ulceration
  • Pain is a burning nature
182
Q

Describe ECG changes in posterior STEMI

A
  • Horizontal ST depression in V1-3
  • Prominent R in V2-3. R/S >1
  • Positive T in V1-3
183
Q

Describe brugada syndrome

A

Type 1

  • Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave.
  • This is Brugada Sign

Type 2
- >2mm of saddleback shaped ST elevation.

Type 3
- Can be the morphology of either type 1 or type 2, but with <2mm of ST segment elevation.

184
Q

List signs of severe aortic stenosis

A
  • Late-peaking murmur
  • Paradoxically split S2 or inaudible A2
  • Small and delayed carotid pulses (pulsus parvus et tardes)
  • LV heave,
  • An audible (and occasionally palpable) S4.
185
Q

Describe management of bradycardia

A
  • Where there is no clear reversible cause, use atropine

Year 3 - Diseases (27 decks)

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