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Cardiovascular Flashcards

1
Q

4 Ts and 4 Hs in cardiac arrest?

A

Hypoxia, hypovolaemia, hypo/hyperkalaemia, hypothermia

Thrombosis, tenision pneumothorax, tamponade, toxins

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2
Q

Doses in cardiac arrest?

A
  • 1mg IV adrenaline – repeat in alternate cycles (10ml of 1:10,000)
  • 300mg IV amiodarone – after 3rd shock - flushed with 20ml 0.9% NaCl or 5% dextrose (after 3 shocks)
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3
Q

Drugs in acute LVF?

A

OMFG

  • Oxygen 15L NRBM
  • Morphine 2mg (or Diamorphine 2.5mg) IV (watch RR) and Metaclopramide 10mg IV
  • Furosemide 40-80mg IV slow (more in renal failure)
  • GTN/infusion if systolic >90
    • Salbutamol if wheeze
    • Consider CPAP - forces water back into vasculature
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4
Q

Subsequent managment in acute LVF?

A

Rationalise meds, regular bloods (U+Es – diuretics), strict fluid balance (catheter), falls bundle, consider DNACPR

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5
Q

HTN stages?

A
  • 1 = clinic 140/90, ABPM 135/85
  • 2 = clinic 160/100, ABPM 150/95
  • Severe = 180/110
    • 180/110 + signs of papilloedema and/or retinal haemorrhage – arrange same day admission
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6
Q

Investigations in HTN review?

A
  • Test for presence of protein in urine – albumin:creatinine ratio and haematuria
  • Bloods – plasma glucose, electrolytes, creatinine, eGFR, serum total cholesterol and HDL cholesterol
  • Examine fundi for presence of hypertensive retinopathy
  • 12-lead ECG
  • Full cardiovascular examination
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7
Q

Cardiac problems in HF?

A

Structural –> increased intramural tension and impaired haemodynamics (isovolumentric contraction lost)

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8
Q

Signs of heart failure?

A
  • Tachycardia + Reduced pulse volume
  • Displaced apex beat, 3rd heart sound, gallop rhythm
  • Raised JVP (in RHF)
  • Peripheral oedema
  • Basal crepitations
  • Hepatomegaly and ascites

3rd heart sound = Kentucky – due to increased ventricular filling (HF or mitral regurgitation)

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9
Q

Arrhythmias in HF?

A

Supraventricular arrhythmias common – stretching and irritation of RA.

Ventricular arrhythmias –> sudden death

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10
Q

NHYA classification?

A
  • Class I (mild) - no limitation of physical activity
  • Class II (mild) - slight limitation of physical activity, no dyspnoea at rest but normal activity –> dyspnoea
  • Class III (mod) - ,marked limitation of physical activity, no dyspnoea at rest but less than normal activity –> dyspnoea
  • Class IV (sev) - unable to carry out any physical activity without discomfort - dyspnoea at rest
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11
Q

Management of HF?

A

FUROSEMIDE for symptomatic relief throughout

First Line

  • ACEi + β-blockers

Second line

  • ARB (losartan - if NYHA 2-3)
  • Aldosterone antagonist (spiro - if NYHA 3-4 or recent MI)
  • Hydralazine + nitrate (if afro-caribbean and NYHA 3-4)

Third Line

  • Digoxin (if sedentary)
  • Ivibradine
  • Cardiac transplantation CRT (need LVEF >35%)
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12
Q

Who are ICDs recommended for?

A

People with previous serious ventricular arrhythmia -

  • Survived cardiac arrest by VT/VF
  • Have spontaneous sustained VT –> syncope/ haemodynamic compromise
  • Have sustained VT without syncope or cardiac arrest, and reduction in LVEF of <35%, but symptoms no worse than NYHA class III.
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13
Q

Diagnosis of PVD?

A

Doppler – will show reduced or absent pulse.

ABPI - <0.5 = critical limb ischaemia

Angiography may demonstrate an obstruction

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14
Q

What is superficial thrombophlebitis?

A

Occurs when a superficial vein (usually the long saphenous vein of the leg or its tributaries) becomes inflamed and the blood within it clots.

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15
Q

Risk factors for superficial trombophlebitis?

A

Virchow’s Triad

  • Endothelial damage (trauma, infection, inflammation)
  • Stasis of blood flow
  • Hypercoagulability of blood

Obesity, thrombophilia, smoking, oral contraceptives, pregnancy, IV drug use, IV infusion (especially if irritant substance used)

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16
Q

Management of superficial thrombophlebitis?

A
  • Elevate, warm compress
  • Exercise
  • DVT prophylaxis
  • Topical analgesia (NSAID cream)
  • LMWH for a month –> reduces risk of DVT and reduces recurrence
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17
Q

JVP sign in 3rd degree heart block?

A

Cannon A waves (atria and ventricles contract simultaneously)

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18
Q

Drug management of 3rd degree heart block?

A

Titrate 500mcg atropine (antimuscarinic) IV every 2-3min (max of 3mg), followed by large flush, until HR improves.

If not –> PACING

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19
Q

Definition of postural hypotension?

A

Drop in systolic blood pressure upon standing of greater than 20 mmHg.

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20
Q

Causes of postural hypotension?

A
  • Venous blood pooling (varicose veins, standing)
  • Impaired vasomotor response (diabetic neuropathy)
  • Reduced muscle tone
  • Hypovolaeima Drugs (hypotensive agents, levodopa)
  • Addisonian crisis
  • Idiopthic
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21
Q

How to check for postural hypotension?

A

BP/HR measurement when patient is lying flat, and either standing or at a 45 degree angle (lying/standing BP)

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22
Q

Pathophysiology of atrial flutter?

A

Re-entry circuit within the right atrium

Ventricular rate determined by AV conduction ratio (block) –> usually 2:1 so ventricular rate = 150

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23
Q

Classification of AF?

A
  • First onset
  • Paroxysmal
  • Persistent
  • Long standing persistent
  • Permanent
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24
Q

CHA2DS2-VASc?

A
  • CCF
  • HTN
  • Age >75
  • DM
  • Stroke/TIA/TE
  • Vascular disease
  • Age 65-74
  • Sex category (female)

Anticoagulate if score 2 or higher, or men with 1 or higher

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25
Q

HAS-BLED?

A
  • HTN
  • Abnormal Liver/Renal
  • Stroke
  • Bleeding
  • Labile
  • INR
  • Elderly (>65)
  • Drugs/alcohol

Score of 3 or more indicates increased one year bleed risk on anticoagulation sufficient to justify caution or more regular review

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26
Q

Criteria for cardioversion in AF?

A
  • AF has a reversible cause
  • Heart failure thought to be primarily caused by AF
  • New-onset atrial fibrillation
  • Atrial flutter whose condition is considered suitable for an ablation strategy
  • To restore sinus rhythm in a patient for whom a rhythm control strategy would be more suitable based on clinical judgement
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27
Q

Anticoagulation in cardioversion?

A

If <48 hours from start, risk of thrombus low –> cardiovert.

If >48 hours, anticoagulated for 3 weeks before.

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28
Q

1st degree heart block?

A

Prolongation of PR interval (>0.2s)

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29
Q

2nd degree (Mobitz I, Wenckebach)

A

Progressive lengthening of PR interval with eventual dropped ventricular conduction

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30
Q

2nd degree (Mobitz II)

A

Intermittent dropping of ventricular conduction without progressive prolongation of PR interval

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31
Q

2nd degree (2:1 type)

A

Alternate p-wave not conducted to ventricles

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32
Q

3rd degree

A

Complete dissociation between atria and ventricles – P wave rate around 90/min, QRS rate around 36/min

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33
Q

Management of heart blocks?

A

1st degree

  • No treatment usually required

2nd degree

  • Episodes of dimming or loss of consciousness associated with bradycardia are an indication for pacing.
  • Asymptomatic Mobitz I = no treatment.
  • Mobitz II = pacemaker

3rd degree

  • Permanent pacing – dual chamber pacing usually preferred
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34
Q

ECG pattern in RBBB?

A
  • Tall R’ wave in V1 (“M” pattern)
  • Wide, slurred S wave in V6 (“W” pattern)
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35
Q

ECG pattern in LBBB?

A
  • Dominant S wave in V1
  • “M” shaped R wave in V5 and V6
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36
Q

Causes of RBBB?

A

RBBB patterns with normal duration of QRS complex are common in healthy people.

Can indicate pathology in the right side of the heart - right ventricular strain (pulmonary embolism).

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37
Q

Causes of LBBB?

A

Always an indication of heart disease (usually left sided) - coronary artery disease, hypertensive heart disease, cadiomyopathy

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38
Q

What is bifascicular block?

A

AKA anterior hemiblock = LAD + RBBB

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39
Q

Pathophysiology of AVNRT?

A
  • Functional re-entry circuit within the AV node.
  • Premature impulse (beat) reaches the end of the slow pathway while fast pathway is still refractory – impulse is allowed to recycle retrogradely up the fast pathway.
  • Leads to circus movement –> impulse cycles around the two pathways, activating Bundle of His anterogradely and atria retrogradely.
  • Means P wave after QRS complex (pseudo R-wave)
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40
Q

Pathophysiology of AVRT (WPW)?

A
  • Anatomical re-entry circuit (Bundle of Kent) – an accessory pathway which allows ‘pre-excitation’ of the ventricles by impulses bypassing the AV node.
  • A reentry circuit is formed by the normal conduction system and the accessory pathway resulting in circus movement
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41
Q

Risk factors for SVT?

A
  • Previous SVT
  • Structural cardiac anomaly
  • Alcohol
  • ↑T4
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42
Q

ECG features in SVT?

A
  • Regular tachycardia
  • QRS complexes narrow unless BBB
  • P waves hidden or after QRS with inversion in II, III and aVF
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43
Q

Pathophysiology of VT?

A

Two distinct conduction pathways with a conduction block in one pathway, and a region of slow conduction in the other.

Develops due to abnormal myocardial scarring usually due to prior ischemia or infarction.

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44
Q

What is torsades de pointes?

A

Distinctive polymorphic VT which QRS amplitude

QRS complexes appear to twist around baselin – associated with long QT

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45
Q

ECG features in VT?

A
  • Broad complex tachycardia
  • AV dissociation (P/QRS complexes at different rates)
  • Rate usually >150 Absence of typical RBBB and LBBB morphology
  • Extreme axis deviation (“northwest axis”) — QRS is positive in aVR and negative in I + aVF
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46
Q

Bloods to check in VT?

A

check urgent U+E (especially K+) and Mg2+

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47
Q

Management of VT (with a pulse)?

A

Restoration of sinus rhythm with either drugs (sotalol, amiodarone) or DC cardioversion (under sedation unless unconscious)

Amiodarone 300mg IV over 20-60 min then 900mg over 24h

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48
Q

Management of SVT with BBB?

A

Treat as VT

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49
Q

Management of Torsades?

A

Treat with Magnesum 2g IV

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50
Q

Causes of aortic stenosis?

A

Calcification, congenital (bicuspid valve), rheumatic, endocarditis

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51
Q

Signs in aortic stenosis?

A
  • Slow-rising pulse – carotid/brachial – duration of ejection prolonged
  • JVP normal unless RVF
  • Usually in sinus rhythm
  • Narrow pulse pressure
52
Q

Investigations in aortic stenosis?

A
  • ECG – left ventricular hypertrophy (peaked R waves laterally)
  • CXR - left ventricle is normal sized until there is left ventricular failure
  • Echo - left ventricular thickening of the free wall and septum (>1cm).
  • Cardiac Catheterisation - gradients
53
Q

Management of aortic stenosis?

A
  • Symptomatic –> replacement (AVR/TAVI)
  • Asymptomatic –>if the systolic gradient across valve >70 mm Hg, replacement indicated. If unfit for surgery –> percutaneous transluminal valvuloplasty
  • Prophylactic abx against infective endocarditis
  • Avoid exercise
54
Q

Causes of aortic regurgitation?

A
  • Congenital bicuspid valve
  • Rheumatic valvulitis
  • Endocarditis
  • Root dilatation (isolated, Marfan’s, syphilis, ank spond, HTN)
55
Q

Signs in aortic regurgitation?

A
  • Waterhammer pulse (wide pulse pressure)
  • Quinke’s sign – pulsing nailbed
  • De Musset’s sign = head bobbing with systole
  • Pistol shot femorals
  • Visible pulse in carotids (Corrigan’s sign)
  • Raised JVP if HF
  • Apex displaced if volume overload
  • Usually in AF
56
Q

Investigations in aortic regurg?

A
  • BP – wide pulse pressure (Larger amount of blood than normal in aorta during systole, less than normal during diastole)
  • ECG – left ventricular hypertrophy
  • CXR – dilated LV and dilated ascending aorta
  • Echo + doppler – dilated LV
  • Cardiac Catheterisation/Angiocardiography
57
Q

Management of aortic regurgitation?

A
  • Anticoagulation sometimes
  • Diuretic if needed
  • Digoxin if AF
  • Abx prophylaxis (endocarditis)
  • Replacement/repair – if low diastolic blood pressure, dilated left ventricle and evidence of left ventricular hypertrophy
58
Q

Grading of murmurs?

A
  • I = barely audible
  • II = audible but soft
  • III = easily audible
  • IV = easily audible + thrill
  • V = easily audible + thrill + steth only lightly on chest
  • VI = easily audible + thrill + steth off chest
59
Q

Extra heart sounds?

A

3rd (Kentucky) = CCF/dilated cardiomyopathy

4th (Tennessee) = hypertrophic cardiomyopathy, AS, HTN

60
Q

Causes of mitral stenosis?

A

Rheumatic fever (99%) – 4x more common in females

61
Q

Investigations in mitral stenosis?

A
  • CXR – LA enlargement, pulmonary congestion
  • ECG – P mitrale (bifid P wave lead II)
  • AF in 60-70%
  • Echo – diagnosis and assessment of severity
62
Q

Management of mitral stenosis?

A
  • Anticoagulation
  • Rate control – digoxin/beta blocker
  • Diuretics – lessen pulmonary venous pressure
  • Balloon valvuloplasty
  • Surgical mitral valvotomy or replacement
63
Q

Causes of mitral regurgitation?

A

Primary – redundant cusp, mitral leaflet prolapse, rheumatic, IHD, cardiomyopathy in papillary muscle, CTD

Secondary – due to dilated LV

64
Q

Signs in mitral regurg?

A

AF - because backlog to RA –> knacks up SAN.

65
Q

Investigations in mitral regurg?

A

CXR – cardiac enlargement

ECG – AF, LVH, p mitrale (enlarged LA)

Echo – enlargement of LA/LV, abnormal valve.

Cardiac catheterisation – quantifies gradient across the valve

66
Q

Management of mitral regurg?

A
  • Rate control
  • Diuretics/ACEi – if LVF
  • Abx – infective endocarditis prophylaxis
  • Anticoagulation - if AF or dilated LA
  • Mitral valve replacement/repair
67
Q

Organisms causing infective endocarditis?

A
  • Strep Viridans (50%)
  • Enterococcal (10% - GI/GU disease)
  • Staph aureus (20% - IVDUs)
  • Fungi (Candida, Aspergillus, Histoplasma)
68
Q

Sources of infection in infective endocarditis?

A

Dental caries

Bladder catheterisation

IV drug abuse

Indwelling venous lines,

Colonic problems

Skin pressure sores

Surgery/dental treatment

Septicaemia

69
Q

Types of infective endocarditis?

A

ACUTE

  • Staphylococcus aureus (prosthetic, IVDU)
  • Equally prevalent on normal and abnormal valves
  • Rare

SUBACUTE

  • Streptococcus viridans
  • Affects abnormal valves
  • More common
70
Q

Risk factors for infective endocarditis?

A
  • Congenital lesions = VSD, ToF, coarctation of aorta, patent ductus
  • Vascular abnormalities
  • IV drug abuse
  • Abortion
  • Prosthetic valve replacement
  • Cardiac/urinary catherization
  • Any invasive diagnostic or surgical procedure (dental, upper resp, urological, lower GI, upper GI, gynae)
71
Q

Classic triad of infective endocarditis?

A
  1. Persistent fever
  2. Emobli
  3. New or changing murmurs
72
Q

Symptoms of infective endocarditis?

A

Fever, low grade fever, malaise, anorexia, weight loss, HF symptoms, embolism symptoms, confusion

73
Q

Signs of infective endocarditis?

A
  • Pyrexia of unknown origin
  • New/changing murmurs
  • signs of HF/embolism (cerebral, pulmonary, popliteal)
  • Osler’s nodes, splinter haemorrhages, Janeway lesions
  • clubbing (1-2 months)
  • Anaemia (normochromic, normocytic)
  • ESR usually raised
  • Splenomegaly (6 weeks)
  • Roth’s spots (Fundoscopy)
74
Q

Complications of infective endocarditis?

A

Aortic root abscess, septic emboli, sepsis, HF, arrhythmias, MI

75
Q

Diagnostic criteria for IE?

A

Duke’s Criteria

76
Q

Investigations in IE?

A
  • Blood Cultures – 3 different sets from 3 different sites to diagnose! At least 12 hours between each
  • Echocardiography, cardiac doppler
  • Urine - Microscopic haematuria/proteinuria common
  • Bloods
  • CXR - RHF/emboli ECG - ?MI due to emboli
77
Q

Management in IE?

A

S.viridans

  • IV benzylpenicillin + IV gentamicin for 2 weeks.
  • If emboli/complications – 6 weeks.

Surgical (indications =)

  • Acute valvular regurgitation with pulmonary oedema, dehiscence of a prosthetic valve, and abscess formation.
78
Q

ECG findings in PE?

A
  • Sinus tachy
  • RBBB
  • Inverted T waves V1-V4
  • S1Q3T3
79
Q

Anticoagulation after PE?

A

Oral anticoagulation for 3 months if provoked, 6 months if unprovoked

LMWH for 5 days whilst warfarin/NOAC commenced

80
Q

Definition of AAA?

A

Enlargement of the aorta of at least 1.5 times its normal diameter or greater than 3 cm diameter in total

81
Q

Classification of AAA?

A

Suprarenal

Pararenal

Infrarenal

82
Q

Risk factors for AAA?

A
  • Age (men >50, women 60-70)
  • Familial risk (4x higher risk)
  • Sex
  • Smoking (associated with ↑growth and rupture)
  • HTN
  • Ethnicity (white people)
  • Hypercholesterolaemia
  • Obesity
  • Pre-existing atherosclerotic occlusive disease
83
Q

Location of AAA rupture and prognosis?

A

Posterolateral wall rupture into retroperitoneal space – most alive when reach hospital.

Anterolateral into peritoneal cavity – dead at scene

84
Q

Criteria for AAA surveillance?

A

All men aged 65 offered screening

  • If <5.5cm – if greater, should be referred to vascular.
  • 4cm - 5.4cm = surveillance evevery 3-12 months
  • <4.0cm = every 2-3 years
85
Q

Medical management of AAA?

A
  • Smoking cessation
  • Statins
  • Antihypertensives
  • Beta blockers
  • Antiplatelets
86
Q

Surgical management of AAA?

A

Elective surgical repair – recommended when diameter reaches 5.5cm.

Open Repair

  • Large incision in the abdomen and inserting a prosthetic graft above and below the aneurysmal tissue (to replace the damaged section of the aorta) – can be done laparoscopically.

Endovascular Repair (EVAR)

  • Stent–graft inserted through a small incision in the femoral artery in the groin
  • Lower operative mortality and morbidity than open repair
87
Q

Predisposing factors for varicose veins?

A
  • Obesity in women (not in men)
  • Prolonged standing
  • Parity (following 2nd or 3rd pregnancy) – impaired venous return (pressure on iliac veins of uterus)
  • High level of progesterone (affects collagen structure and relaxes smooth muscle)
  • Previous DVT – valves damaged when veins recanalize
88
Q

Symptoms of varicose veins?

A
  • Disfigurement – poor cosmetic appearance
  • Pain – after prolonged standing Itching – varicose eczema
  • Heaviness
  • Ulceration
89
Q

Complications of varicose veins?

A
  • Haemorrhage – due to high venous pressure
  • Superficial thrombophlebitis
  • Venous HTN can cause…
    • Ankle oedema
    • Varicose eczema
    • Lipdermatosclerosis
    • Atrophie blanche
    • Severe excoriation from scratching
    • Venous ulceration
90
Q

Investigations in varicose veins?

A

Doppler Flow Studies – ‘backflow’ through incompetent valves

Only used in those with:

  • recurrent VVs, history of DVT/thrombophlebitis, varicose eczema, ulceration etc.
91
Q

Conservative management of varicose veins?

A
  • Encourage walking
  • Discourage prolonged sitting or standing
  • Keep legs elevated when sitting to increase venous return
  • Lose weight, if appropriate
  • Wear supporting elastic stockings which compress superficial veins and prevent reflux from deep veins: Should extend from the distal metatarsals to just below the knee
92
Q

Interventions in varicose veins?

A

In order of preference

  1. Endothermal ablation/endovenous laser treatment of long saphenous vein
  2. Ultrasound-guided foam scleropathy (permanent obliteration of varices)
  3. Surgery (removal of varices with ligation of incompetent perforators)
93
Q

6 Ps of limb ischaemia? Other signs of limb ischaemia?

A

Pain, pallor, paralysis, paraesthesia, pulseless, perishingly cold

  • Venous guttering
  • Buerger’s test +ve
  • Trophic skin changes – thin, hairless, shiny skin, arterial ulcers, gangrene
94
Q

Other main differential for PVD?

A

Spinal claudication – pain may be worse on prolonged rest, flexion of spine relieves pain.

95
Q

Investigations in PVD?

A
  • Ankle Brachial Pressure Index (ABPI) - <0.89 = arterial disease
  • Imaging Duplex ultrasound = first line
  • Contrast-enhanced magnetic resonance angiography
  • CT angiography
96
Q

Management of PVD?

A

Conservative

  • Lifestyle measures + supervised exercise programme

Medical

  • Manage lipids, diabetes, hypertension and give antiplatelet therapy.
  • Naftidrofuryl oxalate (vasodilator) – when exercise programme not satisfactory improvement

Surgical

  • Angioplasty/Stenting = first line surgery
  • Bypass surgery and grafts – when angioplasty unsuccessful
97
Q

What is accelerated/malignant hypertension?

A

Recent significant increase over baseline BP associated with target organ damage.

Usually seen as vascular damage on fundoscopy, such as flame-shaped hemorrhages or soft exudates.

98
Q

Symptoms of accelerated hypertension?

A
  • Visual disturbance
  • Headache
  • Breathlessness
  • Hypertensive encephalopathy (↓conscious level, coma, epileptic seizures)
99
Q

Signs of accelerated hypertension?

A
  • Acute ↑BP - diastolic greater than 130 mm Hg
  • Hypertensive retinopathy - with haemorrhages and exudates visible on the retina
  • Papilloedema - from cerebral oedema
  • Renal failure - with proteinuria
  • Cardiac failure
  • Rarely, haemoglobinuria, jaundice and anaemia (microangiopathic haemolytic anaemia)
100
Q

Management of accelerated hypertension?

A
  • 180/110 + signs of papilloedema/retinal haemorrhage –> refer immediately to hospital.
  • Use labetolol/nifedipine to reduce BP quickly – not too rapidly because of potential cerebral infarction in watershed areas.
101
Q

Causes of pericarditis?

A

Infective

  • Viral
    • (coxsackie, mumps, EBV, CMV, HIV, rubella, parvovirus)
  • Bacterial
    • (pneumococcus, meningococcus, chlamydia, gonorrhoea) TB

MI

  • Dressler’s syndrome = autoimmune pericarditis +/- effusion 2-14 weeks post MI

Uraemic Malignant (locally invasive)

Post-cardiac surgery

102
Q

Signs of pericarditis>

A

Pericardial friction rub –> intermittent, positional, louder during inspiration, left sternal edge

Pericardial effusion may develop – rise in venous pressure

103
Q

ECG in pericarditis?

A
  • 10% normal, sinus tachycardia
  • AF/flutter/atrial ectopics, concave (saddle-shaped) ST elevation in 2+ limb leads or all chest leads
  • Prominent peaked T-waves (flatten/invert over following days)
  • PR depression
  • Pericardial effusion –> decreased QRS amplitude in all leads
  • NO pathological Q waves – unlike MI
104
Q

What is Ewart’s sign?

A

Dullness to percussion over left subscapular area due to compression of left lung base due to pericardial effusion

105
Q

Investigations in pericardial effusion?

A
  • Echo = diagnostic (echo-free zone surrounds heart)
  • CXR = large lobular heart – “water-bottle heart”
  • ECG = loss of QRS voltages; alternating QRS morphologies
  • Diagnostic pericardiocentesis = cytology may show malignant cells etc
106
Q

Definition of aortic dissection?

A

Tear in intima –> “intimal flap” –> blood enters space between intima and media, continues to separate the two layers down the length of the aorta –> true lumen and false lumen.

  • True = lined by intima on both sides
  • False = between intima and media

Propagation of tear (dissection gets bigger), or blood re-enters lumen through another ‘exit tear’.

107
Q

Causes and risk factors for aortic dissection?

A

Causes

  • HTN
  • Connective tissue disease (Marfan’s, Ehlers Danlos)
  • Aneurysm
  • Trauma

Risk Factors

  • Smoking
  • Obesity
  • DM
  • ↑BP
  • ↑cholesterol
  • FH
  • Previous IHD
  • Pregnancy
  • Connective tissue disease (Marfan’s, Ehler’s danlos)
108
Q

Signs of aortic dissection?

A
  • Unequal radial pulses
  • Tachycardia
  • Hypotension/hypertension
  • Difference in brachial pressures >15 mmHg
  • Aortic regurgitation
  • Pleural effusion (L>R)
  • Neurological deficits from carotid artery dissection
109
Q

Investigations in aortic dissection?

A

ECG – may be normal or show LV strain/ ischaemia

CXR – classically widened mediastinum >8cm (rarely seen), irregularity of aortic knuckle and small left pleural effusion can develop from blood tracking down.

Echo – May show aortic root leak, aortic valve regurgitation or pericardial effusion.

Also consider MRI/CT/conventional angiography.

Bloods – D-dimer to rule out PE

110
Q

Classification of aortic dissection and how it affects management?

A

Stanford Classification

  • Type A – ascending aorta = surgical management
  • Type B – descending aorta = medical management
111
Q

Types of cardiomyopathy?

A

Dilated

  • Progressive dilatation of all heart chambers. Mostly AD inheritance, large numbers of mutations

Hypertrophic

  • Unexplained, asymmetical or concentric hypertrophy of the undilated left ventricle

Restrictive

  • Diastolic dysfunction of the heart –> ventricular walls are excessively rigid and ventricular filling is impeded
112
Q

Presentation of dilated cardiomyopathy?

A
  • Congestive heart failure
  • thromboembolism
  • arrhythmias
  • Apex beat displaced/diffuse
  • Soft S1 (mitral/tricuspid incompetence)
  • loud P2 Gallop rhythm (failure)
113
Q

Presentation of hypertrophy cardiomyopathy?

A

Symptoms

  • Angina, dyspnoea, palpitations, syncope, sudden death

Signs

  • JVP (large A waves), double impulse @ apex, loud 4th heart sound, third heart sound Late systolic murmur (outflow tract obstruction with/without mitral regurgitation)
114
Q

Presentation of restrictive cardiomyopathy?

A

Restriction to filling –> dependent oedema, ascited and enlarged liver.

  • Raised JVP
  • Kussmaul’s sign may be detected
  • Apex beat usually palpable
  • Distant heart sounds S3/S4 may be present
115
Q

Classic presentation of mesenteric ischaemia?

A

IRREGULAR PULSE + ABDO PAIN = MESENTERIC ISCHAMIEA

116
Q

Where does mesenteric ischamie usually occur?

A

occlusion of superior mesenteric artery (usually) – small bowel affected uncommonly.

117
Q

Distributions of coeliac trunk, IMA and SMA?

A
  • Coeliac trunk – first portion of duodenum
  • SMA– distal portion of duodenum + large bowel up to splenic flexure
  • IMA – remainder of large bowel and part of rectum
118
Q

Presentation of mesenteric ischaemia?

A
  • Often a history of vascular disease or diabetes – may sometimes follow aneurysm surgery and ligation of IMA.
  • Cramp-like, left sided abdominal pain – lasts for a few hours and is followed by rectal bleeding.
  • Bleeding is dark red, often without faeces, may occur 2-3 times over a period of 12 hours.
119
Q

Causes of SVC obstruction/thrombosis?

A

Most common cause = lymph node metastases from primary bronchial carcinoma

  • Lymphadenopathy
  • Thymoma
  • Mediastinal tumour
  • Retrostenal goitre
  • Thoracic aortic aneurysm
  • Mediastinal fibrosis
120
Q

Classification of Raynaud’s?

A

PRIMARY

  • Raynaud’s phenomenon.
  • Teens/early 20s
  • Symmetrical involvement, no tissue necrosis/gangrene, ESR normal, normal nail fold capillaries, negative for anti-nuclear antibodies.

SECONDARY

  • Due to underlying condition (systemic sclerosis (SSc), SLE, vasculitis, atherosclerosis and hypothyroidism)
  • >30 years
  • Digital ulceration/year-round symptoms, pain/discomfort higher in severity, abnormal nail fold capillaries, assymetric upper limb pulses, puffiness/tightness of finger skin, raised ESR, positive ANA or other antibodies.
121
Q

Presentation of Rayanud’s?

A

Triphasic colour change in extremities

  • WHITE- ischaemia
  • BLUE - (deoxygenation) rewarming with a slow blood flow
  • RED - (reperfusion) normal colour returns; may be accompanied by throbbing pain and swelling due to reactive hyperaemia
122
Q

Complications of MI?

123
Q

Hollistic management of HF?

125
Q

Posterior STEMI?

A

V1-V3

  • Horizontal ST depression (ST elevenation)
  • Tall broad R waves (Q waves)
  • Upright T waves (T wave inversion)
  • Dominant R wave in V2

ST elevation and Q waves in V7-V9

126
Q

Reciprocal changes

A

PAILS (next to letter is leads with ST depression)

  • Posterior = Anterior
  • Anterior = Inferior
  • Inferior = Lateral/Septal

- FINALS (24 decks)

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