MRCP Part 1 Notes
Dermatology
Pemphigus Vulgaris – Site of blisters: Trunk and head. Blisters are flaccid and fragile. 100%
mucosal membrane involvement. Ag: Desmoglein-1+3 (mainly 3)
IgG + C3
Bullous Pemphingoid – Site of blisters: Trunk, flexures, limbs. Tense blisters with occasional
mucosal involvement. Ag: BP-230 + 180.
IgG (70%)
Tx: Steroids + immunosuppression
Dermatitis Herpetiformis – Pruritic papules, vesicular bullae (elbows and buttocks).
Autoimmune process associated with COELIAC DISEASE. Caused by deposition of IgA in
dermis.
Tx: Gluten free diet, If continuous – Dapsone.
Discoid Lupus Erythematous – follicular keratin plugs. Characterised by well demarcated
macular rash with erythema, scales, plaques resulting in SCARRING + ATROPHY.
Tx: First line: Steroids
Second line: Hydroxychloroquine (HCQ)
Erythema Multiforme – Target lesions, resembles bullseye erupts 24-48 hours after
appearance. Type IV hypersensitivity reaction. Symmetrical distribution of lesions over
dorsal surfaces of extensor extremities – minimal mucosal involvement.
Causes: Herpes simplex, mycoplasma
Erythema Nodosum – Inflammation of subQ fat. Tender erythematous, nodular lesions.
Resolves after 6 weeks. Usually over shins.
Causes: Infections: Strep., Tb., Brucellosis
Systemic causes: Sarcoidosis, IBD (Ulcerative colitis), SLE.
Impetigo – Superficial bacterial skin infection usually caused by S. aureus or S. pyogenes.
Golden crusted skin lesions typically found around mouth. Very contagious.
Tx: In limited localisation – Fusidic acid
Extensive localisation – Flucloxacillin. Doxy in pen allergic.
Erysipelas – Caused by S. pyogenes (group A Strep) in deep dermis. Symptoms of tender,
intensely erythematous, indurated plaques with sharply demarcated border.
Tx: IV BenPen. If pen allergic, erythromycin
Lichen Planus – 4 P’s. Purple, Pruritic, Polygonal, Papular. Over flexor surfaces – white lace
patters. Koebner phenomenon : New skin lesions at site of trauma.
,Tx: Topical steroids. If extreme – oral steroids
Lichen Sclerosis – Itchy white spot on vulva of elderly women.
Psoriasis – Associated with HLA-CW6/ HLA-B13.
Salmon coloured plaques with silvery scales – Koebner phenomenon.
AUSPITZ SIGN: Small bleeding spots when scales are scraped off.
Complications: Psoriatic arthropathy, CAD
Triggers: Trauma, ETOH, Beta-blockers, Lithium, Antimalarials
Tx: Potent corticosteroids applied once daily + Vitamin D once daily.
Second line – if after 8/52 no improvements, Vit D analogue BD
Third line – After 8-12/52 no improvements, Steroid BD + Coal preparations.
Tacrolimus/Anti TNF (infliximab, etanercept, adalimumab)
Pityriasis Rosea – Acute self-limiting rash which tends to affect young adults. Caused by
Herpes Hominis Virus-7 (HHV-7). Causes HERALD PATCH (usually on trunk). This is
usually followed by erythematous oral, scaly patches. Gives FIR TREE appearance.
Spares palms and soles. Can be pruritic or asymptomatic.
Tx: Self limiting 4-12 weeks. Moisturisers help with itching.
Pityriasis Versicolour – Superficial cutaneous fungal infection caused by:-
Malassezia Furfur: Mainly affects the trunk. Patches may be hypopigmented –
pink or brown (VERSICOLOUR). Scaling is common as is pruritis,
Tx: Topical antifungals (Ketoconazole)
Second line: Topical selenium sulphide.
Differential diagnosis: Leprosy – main difference is leprosy comes with anaesthesia and
thickened nerves as well as hypopigmentation.
Malignant melanoma – 4 types:
- Lentigo maligna melanoma. Invasive tumour develops
within preexisting lentigo maligna
- Superficial spreading malignant melanoma: large , flat,
irregularly pigmented lesion grows laterally before vertical
invasion
- Nodular – most aggressive. Rapidly growing +
bleeds/ulcerates.
- Acral – Pigmented lesion on palms/soles or under nail.
Presents late – may NOT be related to sun exposure.
BRESLOW THICKNESS is key for prognosis - >4mm 5 year survival ~ 5 year survival
50%.
,Tx: Vemurafenib/Dabrafenib
Pyoderma Gangrenosum – Expanding ulcer. Typically on lower limbs
Causes: IBD – Ulcerative colitis/Crohn’s
Kaposi Sarcoma – HHV-8 most common in HIV/immunosuppressed patients. Red/purple
lesion.
Tx: 1st line – Antivirals
2nd line – intralesional injection of Vincristine
3rd line – chemo with liposomal doxorubicin
Tinea
Tinea Capitis – Scalp ringworm – SCARRING ALOPAECIA. Mainly seen in children. If
untreated, spongey mass called KERION forms.
Most common cause – Trichophyton Tonsurians (NO FLUORESCENCE). Can
also be caused by Microsporium Canis (CAUSES GREEN FLUORESCENCE UNCER
WOOD’S LAMP) from cats and dogs.
Diagnosis by scalp scrapings.
Tx: Terbinafine for Trichophyton. Griesofulvin for Microsporium. Topical ketoconazole
shampoo for reduction of transmission.
Tinea Corpus – Caused by TRICHOPHYTON RUBRUM/VERUCOSSUM contact with
cattle.
Tx: Oral fluconazole
Tinea Pedis – Athlete’s foot. Characterised by itching, peeling skin. Common in adolescence.
Tx: Clotrimazole ointment.
Scabies – Caused by Sarcotes scabei and spread by prolonged skin contact. Delayed type IV
hypersensitivity reaction. Occurs in web spaces and nipples.
Tx: 1st line Permethrin 5%
2nd line Malathion 0.5%
Tylosis – Thickened palms and soles, often linked with oesophageal Ca.
Necrolytic Migratory Erythema – Associated with glucagonoma -> shiny, bright red tongue,
weight loss, high BMs, frequent urination, diarrhoea, mood changes.
,Cardiology
Arrhythmias
Atrial Fibrillation
Irregularly irregular pulse. Absence of P waves and varied R-R intervals.
Paroxysmal (up to 7 days) Congestive HF – 1pt
Persistent (> 7 days) Hypertension – 1pt
Permanent. A2ge (>75) – 2pts
CHA2DS2VASC Diabetes – 1pt
0 points = No prophylaxis S2troke – 2pts
1 point = Consider DOAC in men Vascular disease – 1pt
2+ points = Oral anticoag. Age – 1pt
ScEX – Female = 1pt
Non-valvular AF (non-prosthetic valve) treatment of choice is DOAC.
Valvular – treatment of choice is Warfarin
ORBIT Score (Risk of Bleed) Hb <130 in men, <120 in women = 2pts
0-2pts – low risk Age > 74 = 1pt
3pts – Medium risk Bleeding hx = 2pts
4-7pts – High risk Renal impairment = 1pt
Anti-platelet therapy = 1pt
Tx: 1. Rate control – Beta-blocker (bisoprolol) or CCB (Verapamil)
2. Rhythm control – Amiodaronje/fleccanide if no structural heart disease (also used
in paroxysmal AF).
3. DOAC – Apixaban/Warfarin
Digoxin is reserved in patients that do no exercise and have non-paroxysmal AF
If Onset <48 hrs and haemodynamically unstable: SBP = <90 - DC Cardioversion is
required.
If structural heart disease present – Amiodarone.
If AF is greater than 48 hrs DOAC must be given for at least 3/52 prior to cardioversion. Rule
out clot with TOE If high risk of DC failure, 4 weeks of amiodarone must be given prior to
attempt. DOAC for 4/52 after DC cardio version.
,Long QT Interval (>450 ms) – Congenital: Jervell-Lange Nielson syndrome (Autosomal
recessive [AR] comes with hearing impairment.
Romano-Ward Syndrome Autosomal Dominant (AD).
Acquired: Electrolyte abnormalities; hypokalaemia, hypocalcaemia, hypomagnesaemia.
Drug induced: Quinidine, disopyramide, Sotolol, Amiodarone, TCA –
amitriptyline, phenothiazides, haloperidol, olanzapine, macrolides, quinolones, methadone
Poisons: Organophosphates
Tx: Usually happens due to loss of function/bloackage of K+ channels.
1. Withdraw culprit drug(s)
2. Beta blocker (propranolol, metoprolol, Atenolol – NOT SOTOLOL)
3. ICD in high risk cases – previous arrests
4. Left stellate cardiac ganglionectomy
Polymorphic V.Tach
Torsades de Pointes Tx : First line IV MgSO4-
V.tach with pulse TX: Cardioversion; 3S’s Synchronised, Sedate, JouleS (low energy) 3
shocks. If unsuccessful give 300mg IV amiodarone in 10-20mins then repeat shocks.
V.tach without pulse: Tx: Defib
Adult tachy leads to shock, Syncope, MI, severe HF
Adult Bradycardia
ABCDE approach
Tx: Atropine 1mg IV. Max 3mg. Use glucagon as beta blocker antidote.
Isoprenaline 5mcg in 1min IV if needed
Adrenaline 2-10mcg/min IV
Transcutaneous pacing if all else fails.
Cardiac Arrest
Adrenaline every 3-5 minutes
SHOCKABLE RHYTHMS: V.Fib/Pulseless V.Tach after 3 shocks give amiodarone as above.
NON-SHOCKABLE RHYTHMS: Asystole, Pulseless Electrical Activity
4 Hs and 4 Ts
Hypoxia Toxins
Hyper/hypokalaemia Tamponade
Hypovolaemia Tension pneumothorax
,Hypothermia Thrombus
ECG Leads – blood vessels:
Leads I, avL, V5-V6 - Left circumflex art., V1-V4 - LAD., II, III, avF - RCA
Acute Coronary Syndrome – STEMI, NSTEMI, and Unstable Angina
STEMI needs early loading dose of 300mg aspirin and PCI. If patient going for PCI needs
DAPT:
Prasgural + Aspirin.
If risk of bleed: Ticagrelor + Aspirin
If very high risk bleed: Clopidogrel + Aspirin
ECG: Anterior V3-V5, Septal V1-V2, Lateral I – avL, Inferior II, III, avF, Posterior depression
of V1-V2, Anterolateral V4-V6, I, avL
Complications of MI: Pericarditis (48 hrs after MI), Dressler syndrome
Heart Failure – HF with preserved EF >50%, HF with mid-range EF 40-50% and HF with
reduced EF <40%.
Tx: Acute HF -> Given diuretics
Chronic AF: First Line - ACEi + B-blocker
Second Line – Aldosterone antagonist e.g. spironolactone or eplenerone
Third Line – a) Ivabradine is HR >75bpm
b) Sacubitril/Valsartan if HR <75bpm
c) Hydralazine + Nitrate in Afro-Caribbeans
d) Digoxin if consistent AF
e) Cardiac resynch. therapy
Permanent pacemaker indications:
1) Complete HB (3rd degree)
2) 2nd Degree HB (Mobitz II)
3) Symptomatic HB
4) Sinus pause of >3 sec
HOCM – AD disorder. Mutation in gene encoding of beta-myosin heavy chain protein
MYH7.
Symptoms: Dyspnoea, angina, syncope, palpitations.
Most common cause of SUDDEN CARDIAC DEATH, jerky pulse (large ‘a’ waves), double
apex beat. ESM increases with Valsalva manoeuvre and decreases when squatting.
ECHO: MR. SAM. ASH: Mitral Regurgitation. Systolic Ant. Motion. ASymmetric
Hypertrophy.
,ECG: RBBB, Prolonged PR, T-wave inversion, LVH. Poor prognosis if septum >3cm.
Tx: Amiodarone, B-Blocker, ICD
Catecholaminergic V.Tach – AD. Defect in Ryanodine receptor RYR2.
Symptoms: Develop before 20YO.
Tx: B-blockers, ICD
Arrythmogenic R-ventricular Cardiomyopathy – 2nd most common cause of cardiac arrest in
young after HOCM. AD.
Will see TWI + Epsilon wave after QRS complex.
Tx: B-blockers
Mitral regurgitation (MR) Mitral stenosis (MS)
Pulse NSR/AF AF
Apex Forceful, displaced, systolic thrill Localised, tapping
Sounds Soft S1+S3 Loud S1 + P1
Murmurs Pansystolic Mid diastolic
Valvular Heart Disease
Mitral stenosis comes with low pitched, mid-late diastolic rumbling murmur best heard on
exp. and opening snap.
Features of MS:
1. Increased length of murmur
2. Opening snap becomes closer to S2
3. Calcification of valves greatly increases immobility and loss of snap
4. Lutenbacher’s syndrome MD + ASD
ECG: P-wave mitrale, RVH, AF
CXR: L-atrial enlargement and pulmo. Oedema
Tx: If in AF – B-blockers and diuretics
Surgical intervention: 1. Transeptal balloon valvotomy
2. Open valvotomy
Aortic regurgitation (AR) Aortic stenosis (AS)*
Pulse NSR, large vol., collapsing NSR, slow rising
Apex Displaced, diffuse, forceful Not displaced, sustained
Sounds Ejection click Soft S2
Murmurs Mid diastolic rumble ESM radiating to carotids
3. Mitral valve replacement
*most common in UK. Crescendo and decrescendo murmurs decrease with standing, Valsalva
or handgrips.
,Causes: Degenerative calcification in patients >65YO. Congentital bicuspid valves in patients
<65YO.
Management: Coronary angio. AV replacement, TAVI if fit
AR signs: Corrigan’s pulse: visible and vigorous arterial pulsations on neck
Musset’s sign: Bobbing of head due to arterial neck pulsations
Quincke’s sign: Capillary pulsations of nail bed
Muller’s sign: Pulsation of uvula
Traube’s sign: Pistol shot murmurs in femoral arteries
Duroziez sign: Diastolic murmur prox. to femoral art
Severity indications: 1) Collapsing pulse
2) Wide pulse pressure
3) Oedema
Tx: AVR in all symptomatic patients with severe AR.
Infective Endocarditis (IE) – When there is a fever and new onset of murmur, ?IE.
Modified Duke’s criteria:
MAJOR CRITERIA:
1. +ve blood cultures in 2 separate cultures. OR Persistently +ve cultures in 3 >12 hrs
apart.
2. Single +ve Coxiella culture
3. +ve ECHO finding of vegetation, abscess
Minor Criteria:
1. Predisposition
2. Fever >38
3. Vasc issues eg emboli
4. Osler’s nodes
Causes: S. aureus (most common and acute presentation in IVDU). S. viridans can cause it
with good prognosis. S. mitis post dental procedure. S. epidermidis due to prosthetic valves,
S. bovis (or gallolyticus) usually secondary to bowel Ca.
Tx: Indications for surgery : aortic abscess (often indicated by PR prolongation).
Blind therapy: Fluclox. + gent.
If prosthetic valves in situ and this is S. aureus; vanc. Gent, and rifampicin.
If S. aureus with native valves use fluclox. 4/52
Strep infections: BenPen1.2g 4hrly IV 4-6 weeks. Add gent if less penicillin sensitive
microbe.
,Enterococci – Amox + gent
HACEK microbes – Ceftriaxone 4/52, 6/52 if prosthetic valves
Vanc in lieu of penicillin in pen allergies.
Fungals: Candida – Amphotericin B. Aspergillus – Voriconazole
Rheumatic Fever – JONES Criteria
MAJOR CRITERIA: Joint Pain, Carditis, SubQ Nodules, Erythema marginatum,
Sydenham’s chorea
Minor Criteria: Fever, arthralgia, previous RF, raised ESR/CRP, first degree HB
Consider previous strep infection: SCARLET FEVER
Raised antistrptolysin O
HTN –
Step 1: <55 YO or hx of DM give ACEi
>55YO or Afro-Caribbean give CCB
Step 2: Add CCB
Step 3: Add diretic + A+C
Step 4: If K+ <4.5 add spironolactone. If >4.5 add indapamide (thiazide-like diuretic)
If not responding THEN add either alpha/beta-blockers.
Emergency HTN -> End organ damage. Urgent HTN does not lead to end organ damage.
Pulmonary HTN Tx: USE ACUTE VASODILATOR TESTING:
- If +ve CCB
- If -ve Endothelin Receptor antagonist eg Bosentan
Prostacyclin analogiues: Ilioprost, Trepostinil
JVP Waves
- a Wave: Atrial contraction
- c Wave: Closure of tricuspid valve
- v Wave: Due to passiVe filling of blood against closed
tricuspid valve
- x descent: Fall in atrial pressure during ventricular systole
- y descent: Opening of tricuspid valve
Pathologies: Absent a Waves – AF.
Cannon a Waves – Complete HB
Giant v Waves – Tricuspid regurgitation
Steep x descent – Cardiac tamponade or Constrictive pericarditis
, Steep y descent – absent in tamponade
Pulses:
Paradoxus: >10mmHg drop in SBP inspiration. Occurs in severe asthma, cardiac tamponade.
Collapsing pulse: AR, PDA
Pulsus alternans: LVF
Jerky Pulse: HOCM
Heart Sounds:
Loud S1 – MS, Short PR Wide fixed Splitting S2 – ASD
Soft1 – MR, prolongd PR Wide splitting S2 – RBBB, PS, VSD, LV pacing
Loud2 – HTN Reversed splitting S2 – LBBB, PDA, AS
Soft2 – AS
Dermatology
Pemphigus Vulgaris – Site of blisters: Trunk and head. Blisters are flaccid and fragile. 100%
mucosal membrane involvement. Ag: Desmoglein-1+3 (mainly 3)
IgG + C3
Bullous Pemphingoid – Site of blisters: Trunk, flexures, limbs. Tense blisters with occasional
mucosal involvement. Ag: BP-230 + 180.
IgG (70%)
Tx: Steroids + immunosuppression
Dermatitis Herpetiformis – Pruritic papules, vesicular bullae (elbows and buttocks).
Autoimmune process associated with COELIAC DISEASE. Caused by deposition of IgA in
dermis.
Tx: Gluten free diet, If continuous – Dapsone.
Discoid Lupus Erythematous – follicular keratin plugs. Characterised by well demarcated
macular rash with erythema, scales, plaques resulting in SCARRING + ATROPHY.
Tx: First line: Steroids
Second line: Hydroxychloroquine (HCQ)
Erythema Multiforme – Target lesions, resembles bullseye erupts 24-48 hours after
appearance. Type IV hypersensitivity reaction. Symmetrical distribution of lesions over
dorsal surfaces of extensor extremities – minimal mucosal involvement.
Causes: Herpes simplex, mycoplasma
Erythema Nodosum – Inflammation of subQ fat. Tender erythematous, nodular lesions.
Resolves after 6 weeks. Usually over shins.
Causes: Infections: Strep., Tb., Brucellosis
Systemic causes: Sarcoidosis, IBD (Ulcerative colitis), SLE.
Impetigo – Superficial bacterial skin infection usually caused by S. aureus or S. pyogenes.
Golden crusted skin lesions typically found around mouth. Very contagious.
Tx: In limited localisation – Fusidic acid
Extensive localisation – Flucloxacillin. Doxy in pen allergic.
Erysipelas – Caused by S. pyogenes (group A Strep) in deep dermis. Symptoms of tender,
intensely erythematous, indurated plaques with sharply demarcated border.
Tx: IV BenPen. If pen allergic, erythromycin
Lichen Planus – 4 P’s. Purple, Pruritic, Polygonal, Papular. Over flexor surfaces – white lace
patters. Koebner phenomenon : New skin lesions at site of trauma.
,Tx: Topical steroids. If extreme – oral steroids
Lichen Sclerosis – Itchy white spot on vulva of elderly women.
Psoriasis – Associated with HLA-CW6/ HLA-B13.
Salmon coloured plaques with silvery scales – Koebner phenomenon.
AUSPITZ SIGN: Small bleeding spots when scales are scraped off.
Complications: Psoriatic arthropathy, CAD
Triggers: Trauma, ETOH, Beta-blockers, Lithium, Antimalarials
Tx: Potent corticosteroids applied once daily + Vitamin D once daily.
Second line – if after 8/52 no improvements, Vit D analogue BD
Third line – After 8-12/52 no improvements, Steroid BD + Coal preparations.
Tacrolimus/Anti TNF (infliximab, etanercept, adalimumab)
Pityriasis Rosea – Acute self-limiting rash which tends to affect young adults. Caused by
Herpes Hominis Virus-7 (HHV-7). Causes HERALD PATCH (usually on trunk). This is
usually followed by erythematous oral, scaly patches. Gives FIR TREE appearance.
Spares palms and soles. Can be pruritic or asymptomatic.
Tx: Self limiting 4-12 weeks. Moisturisers help with itching.
Pityriasis Versicolour – Superficial cutaneous fungal infection caused by:-
Malassezia Furfur: Mainly affects the trunk. Patches may be hypopigmented –
pink or brown (VERSICOLOUR). Scaling is common as is pruritis,
Tx: Topical antifungals (Ketoconazole)
Second line: Topical selenium sulphide.
Differential diagnosis: Leprosy – main difference is leprosy comes with anaesthesia and
thickened nerves as well as hypopigmentation.
Malignant melanoma – 4 types:
- Lentigo maligna melanoma. Invasive tumour develops
within preexisting lentigo maligna
- Superficial spreading malignant melanoma: large , flat,
irregularly pigmented lesion grows laterally before vertical
invasion
- Nodular – most aggressive. Rapidly growing +
bleeds/ulcerates.
- Acral – Pigmented lesion on palms/soles or under nail.
Presents late – may NOT be related to sun exposure.
BRESLOW THICKNESS is key for prognosis - >4mm 5 year survival ~ 5 year survival
50%.
,Tx: Vemurafenib/Dabrafenib
Pyoderma Gangrenosum – Expanding ulcer. Typically on lower limbs
Causes: IBD – Ulcerative colitis/Crohn’s
Kaposi Sarcoma – HHV-8 most common in HIV/immunosuppressed patients. Red/purple
lesion.
Tx: 1st line – Antivirals
2nd line – intralesional injection of Vincristine
3rd line – chemo with liposomal doxorubicin
Tinea
Tinea Capitis – Scalp ringworm – SCARRING ALOPAECIA. Mainly seen in children. If
untreated, spongey mass called KERION forms.
Most common cause – Trichophyton Tonsurians (NO FLUORESCENCE). Can
also be caused by Microsporium Canis (CAUSES GREEN FLUORESCENCE UNCER
WOOD’S LAMP) from cats and dogs.
Diagnosis by scalp scrapings.
Tx: Terbinafine for Trichophyton. Griesofulvin for Microsporium. Topical ketoconazole
shampoo for reduction of transmission.
Tinea Corpus – Caused by TRICHOPHYTON RUBRUM/VERUCOSSUM contact with
cattle.
Tx: Oral fluconazole
Tinea Pedis – Athlete’s foot. Characterised by itching, peeling skin. Common in adolescence.
Tx: Clotrimazole ointment.
Scabies – Caused by Sarcotes scabei and spread by prolonged skin contact. Delayed type IV
hypersensitivity reaction. Occurs in web spaces and nipples.
Tx: 1st line Permethrin 5%
2nd line Malathion 0.5%
Tylosis – Thickened palms and soles, often linked with oesophageal Ca.
Necrolytic Migratory Erythema – Associated with glucagonoma -> shiny, bright red tongue,
weight loss, high BMs, frequent urination, diarrhoea, mood changes.
,Cardiology
Arrhythmias
Atrial Fibrillation
Irregularly irregular pulse. Absence of P waves and varied R-R intervals.
Paroxysmal (up to 7 days) Congestive HF – 1pt
Persistent (> 7 days) Hypertension – 1pt
Permanent. A2ge (>75) – 2pts
CHA2DS2VASC Diabetes – 1pt
0 points = No prophylaxis S2troke – 2pts
1 point = Consider DOAC in men Vascular disease – 1pt
2+ points = Oral anticoag. Age – 1pt
ScEX – Female = 1pt
Non-valvular AF (non-prosthetic valve) treatment of choice is DOAC.
Valvular – treatment of choice is Warfarin
ORBIT Score (Risk of Bleed) Hb <130 in men, <120 in women = 2pts
0-2pts – low risk Age > 74 = 1pt
3pts – Medium risk Bleeding hx = 2pts
4-7pts – High risk Renal impairment = 1pt
Anti-platelet therapy = 1pt
Tx: 1. Rate control – Beta-blocker (bisoprolol) or CCB (Verapamil)
2. Rhythm control – Amiodaronje/fleccanide if no structural heart disease (also used
in paroxysmal AF).
3. DOAC – Apixaban/Warfarin
Digoxin is reserved in patients that do no exercise and have non-paroxysmal AF
If Onset <48 hrs and haemodynamically unstable: SBP = <90 - DC Cardioversion is
required.
If structural heart disease present – Amiodarone.
If AF is greater than 48 hrs DOAC must be given for at least 3/52 prior to cardioversion. Rule
out clot with TOE If high risk of DC failure, 4 weeks of amiodarone must be given prior to
attempt. DOAC for 4/52 after DC cardio version.
,Long QT Interval (>450 ms) – Congenital: Jervell-Lange Nielson syndrome (Autosomal
recessive [AR] comes with hearing impairment.
Romano-Ward Syndrome Autosomal Dominant (AD).
Acquired: Electrolyte abnormalities; hypokalaemia, hypocalcaemia, hypomagnesaemia.
Drug induced: Quinidine, disopyramide, Sotolol, Amiodarone, TCA –
amitriptyline, phenothiazides, haloperidol, olanzapine, macrolides, quinolones, methadone
Poisons: Organophosphates
Tx: Usually happens due to loss of function/bloackage of K+ channels.
1. Withdraw culprit drug(s)
2. Beta blocker (propranolol, metoprolol, Atenolol – NOT SOTOLOL)
3. ICD in high risk cases – previous arrests
4. Left stellate cardiac ganglionectomy
Polymorphic V.Tach
Torsades de Pointes Tx : First line IV MgSO4-
V.tach with pulse TX: Cardioversion; 3S’s Synchronised, Sedate, JouleS (low energy) 3
shocks. If unsuccessful give 300mg IV amiodarone in 10-20mins then repeat shocks.
V.tach without pulse: Tx: Defib
Adult tachy leads to shock, Syncope, MI, severe HF
Adult Bradycardia
ABCDE approach
Tx: Atropine 1mg IV. Max 3mg. Use glucagon as beta blocker antidote.
Isoprenaline 5mcg in 1min IV if needed
Adrenaline 2-10mcg/min IV
Transcutaneous pacing if all else fails.
Cardiac Arrest
Adrenaline every 3-5 minutes
SHOCKABLE RHYTHMS: V.Fib/Pulseless V.Tach after 3 shocks give amiodarone as above.
NON-SHOCKABLE RHYTHMS: Asystole, Pulseless Electrical Activity
4 Hs and 4 Ts
Hypoxia Toxins
Hyper/hypokalaemia Tamponade
Hypovolaemia Tension pneumothorax
,Hypothermia Thrombus
ECG Leads – blood vessels:
Leads I, avL, V5-V6 - Left circumflex art., V1-V4 - LAD., II, III, avF - RCA
Acute Coronary Syndrome – STEMI, NSTEMI, and Unstable Angina
STEMI needs early loading dose of 300mg aspirin and PCI. If patient going for PCI needs
DAPT:
Prasgural + Aspirin.
If risk of bleed: Ticagrelor + Aspirin
If very high risk bleed: Clopidogrel + Aspirin
ECG: Anterior V3-V5, Septal V1-V2, Lateral I – avL, Inferior II, III, avF, Posterior depression
of V1-V2, Anterolateral V4-V6, I, avL
Complications of MI: Pericarditis (48 hrs after MI), Dressler syndrome
Heart Failure – HF with preserved EF >50%, HF with mid-range EF 40-50% and HF with
reduced EF <40%.
Tx: Acute HF -> Given diuretics
Chronic AF: First Line - ACEi + B-blocker
Second Line – Aldosterone antagonist e.g. spironolactone or eplenerone
Third Line – a) Ivabradine is HR >75bpm
b) Sacubitril/Valsartan if HR <75bpm
c) Hydralazine + Nitrate in Afro-Caribbeans
d) Digoxin if consistent AF
e) Cardiac resynch. therapy
Permanent pacemaker indications:
1) Complete HB (3rd degree)
2) 2nd Degree HB (Mobitz II)
3) Symptomatic HB
4) Sinus pause of >3 sec
HOCM – AD disorder. Mutation in gene encoding of beta-myosin heavy chain protein
MYH7.
Symptoms: Dyspnoea, angina, syncope, palpitations.
Most common cause of SUDDEN CARDIAC DEATH, jerky pulse (large ‘a’ waves), double
apex beat. ESM increases with Valsalva manoeuvre and decreases when squatting.
ECHO: MR. SAM. ASH: Mitral Regurgitation. Systolic Ant. Motion. ASymmetric
Hypertrophy.
,ECG: RBBB, Prolonged PR, T-wave inversion, LVH. Poor prognosis if septum >3cm.
Tx: Amiodarone, B-Blocker, ICD
Catecholaminergic V.Tach – AD. Defect in Ryanodine receptor RYR2.
Symptoms: Develop before 20YO.
Tx: B-blockers, ICD
Arrythmogenic R-ventricular Cardiomyopathy – 2nd most common cause of cardiac arrest in
young after HOCM. AD.
Will see TWI + Epsilon wave after QRS complex.
Tx: B-blockers
Mitral regurgitation (MR) Mitral stenosis (MS)
Pulse NSR/AF AF
Apex Forceful, displaced, systolic thrill Localised, tapping
Sounds Soft S1+S3 Loud S1 + P1
Murmurs Pansystolic Mid diastolic
Valvular Heart Disease
Mitral stenosis comes with low pitched, mid-late diastolic rumbling murmur best heard on
exp. and opening snap.
Features of MS:
1. Increased length of murmur
2. Opening snap becomes closer to S2
3. Calcification of valves greatly increases immobility and loss of snap
4. Lutenbacher’s syndrome MD + ASD
ECG: P-wave mitrale, RVH, AF
CXR: L-atrial enlargement and pulmo. Oedema
Tx: If in AF – B-blockers and diuretics
Surgical intervention: 1. Transeptal balloon valvotomy
2. Open valvotomy
Aortic regurgitation (AR) Aortic stenosis (AS)*
Pulse NSR, large vol., collapsing NSR, slow rising
Apex Displaced, diffuse, forceful Not displaced, sustained
Sounds Ejection click Soft S2
Murmurs Mid diastolic rumble ESM radiating to carotids
3. Mitral valve replacement
*most common in UK. Crescendo and decrescendo murmurs decrease with standing, Valsalva
or handgrips.
,Causes: Degenerative calcification in patients >65YO. Congentital bicuspid valves in patients
<65YO.
Management: Coronary angio. AV replacement, TAVI if fit
AR signs: Corrigan’s pulse: visible and vigorous arterial pulsations on neck
Musset’s sign: Bobbing of head due to arterial neck pulsations
Quincke’s sign: Capillary pulsations of nail bed
Muller’s sign: Pulsation of uvula
Traube’s sign: Pistol shot murmurs in femoral arteries
Duroziez sign: Diastolic murmur prox. to femoral art
Severity indications: 1) Collapsing pulse
2) Wide pulse pressure
3) Oedema
Tx: AVR in all symptomatic patients with severe AR.
Infective Endocarditis (IE) – When there is a fever and new onset of murmur, ?IE.
Modified Duke’s criteria:
MAJOR CRITERIA:
1. +ve blood cultures in 2 separate cultures. OR Persistently +ve cultures in 3 >12 hrs
apart.
2. Single +ve Coxiella culture
3. +ve ECHO finding of vegetation, abscess
Minor Criteria:
1. Predisposition
2. Fever >38
3. Vasc issues eg emboli
4. Osler’s nodes
Causes: S. aureus (most common and acute presentation in IVDU). S. viridans can cause it
with good prognosis. S. mitis post dental procedure. S. epidermidis due to prosthetic valves,
S. bovis (or gallolyticus) usually secondary to bowel Ca.
Tx: Indications for surgery : aortic abscess (often indicated by PR prolongation).
Blind therapy: Fluclox. + gent.
If prosthetic valves in situ and this is S. aureus; vanc. Gent, and rifampicin.
If S. aureus with native valves use fluclox. 4/52
Strep infections: BenPen1.2g 4hrly IV 4-6 weeks. Add gent if less penicillin sensitive
microbe.
,Enterococci – Amox + gent
HACEK microbes – Ceftriaxone 4/52, 6/52 if prosthetic valves
Vanc in lieu of penicillin in pen allergies.
Fungals: Candida – Amphotericin B. Aspergillus – Voriconazole
Rheumatic Fever – JONES Criteria
MAJOR CRITERIA: Joint Pain, Carditis, SubQ Nodules, Erythema marginatum,
Sydenham’s chorea
Minor Criteria: Fever, arthralgia, previous RF, raised ESR/CRP, first degree HB
Consider previous strep infection: SCARLET FEVER
Raised antistrptolysin O
HTN –
Step 1: <55 YO or hx of DM give ACEi
>55YO or Afro-Caribbean give CCB
Step 2: Add CCB
Step 3: Add diretic + A+C
Step 4: If K+ <4.5 add spironolactone. If >4.5 add indapamide (thiazide-like diuretic)
If not responding THEN add either alpha/beta-blockers.
Emergency HTN -> End organ damage. Urgent HTN does not lead to end organ damage.
Pulmonary HTN Tx: USE ACUTE VASODILATOR TESTING:
- If +ve CCB
- If -ve Endothelin Receptor antagonist eg Bosentan
Prostacyclin analogiues: Ilioprost, Trepostinil
JVP Waves
- a Wave: Atrial contraction
- c Wave: Closure of tricuspid valve
- v Wave: Due to passiVe filling of blood against closed
tricuspid valve
- x descent: Fall in atrial pressure during ventricular systole
- y descent: Opening of tricuspid valve
Pathologies: Absent a Waves – AF.
Cannon a Waves – Complete HB
Giant v Waves – Tricuspid regurgitation
Steep x descent – Cardiac tamponade or Constrictive pericarditis
, Steep y descent – absent in tamponade
Pulses:
Paradoxus: >10mmHg drop in SBP inspiration. Occurs in severe asthma, cardiac tamponade.
Collapsing pulse: AR, PDA
Pulsus alternans: LVF
Jerky Pulse: HOCM
Heart Sounds:
Loud S1 – MS, Short PR Wide fixed Splitting S2 – ASD
Soft1 – MR, prolongd PR Wide splitting S2 – RBBB, PS, VSD, LV pacing
Loud2 – HTN Reversed splitting S2 – LBBB, PDA, AS
Soft2 – AS
