Cardiovascular Flashcards
1
Q
4 Ts and 4 Hs in cardiac arrest?
A
Hypoxia, hypovolaemia, hypo/hyperkalaemia, hypothermia
Thrombosis, tenision pneumothorax, tamponade, toxins
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)
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
4
Q
Subsequent managment in acute LVF?
A
Rationalise meds, regular bloods (U+Es – diuretics), strict fluid balance (catheter), falls bundle, consider DNACPR
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
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
7
Q
Cardiac problems in HF?
A
Structural –> increased intramural tension and impaired haemodynamics (isovolumentric contraction lost)
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)
9
Q
Arrhythmias in HF?
A
Supraventricular arrhythmias common – stretching and irritation of RA.
Ventricular arrhythmias –> sudden death
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
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%)
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.
13
Q
Diagnosis of PVD?
A
Doppler – will show reduced or absent pulse.
ABPI - <0.5 = critical limb ischaemia
Angiography may demonstrate an obstruction
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.
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)
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
17
Q
JVP sign in 3rd degree heart block?
A
Cannon A waves (atria and ventricles contract simultaneously)
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
19
Q
Definition of postural hypotension?
A
Drop in systolic blood pressure upon standing of greater than 20 mmHg.
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
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)
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
23
Q
Classification of AF?
A
- First onset
- Paroxysmal
- Persistent
- Long standing persistent
- Permanent
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
25
HAS-BLED?
* 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
26
Criteria for cardioversion in AF?
* 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
27
Anticoagulation in cardioversion?
If \<48 hours from start, risk of thrombus low --\> cardiovert.
If \>48 hours, anticoagulated for 3 weeks before.
28
1st degree heart block?
Prolongation of PR interval (\>0.2s)
29
2nd degree (Mobitz I, Wenckebach)
Progressive lengthening of PR interval with eventual dropped ventricular conduction
30
2nd degree (Mobitz II)
Intermittent dropping of ventricular conduction without progressive prolongation of PR interval
31
2nd degree (2:1 type)
Alternate p-wave not conducted to ventricles
32
3rd degree
Complete dissociation between atria and ventricles – P wave rate around 90/min, QRS rate around 36/min
33
Management of heart blocks?
**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
34
ECG pattern in RBBB?
* Tall R’ wave in V1 (“M” pattern)
* Wide, slurred S wave in V6 (“W” pattern)
35
ECG pattern in LBBB?
* Dominant S wave in V1
* “M" shaped R wave in V5 and V6
36
Causes of RBBB?
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).
37
Causes of LBBB?
Always an indication of heart disease (usually left sided) - coronary artery disease, hypertensive heart disease, cadiomyopathy
38
What is bifascicular block?
AKA anterior hemiblock = LAD + RBBB
39
Pathophysiology of AVNRT?
* 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)
40
Pathophysiology of AVRT (WPW)?
* 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
41
Risk factors for SVT?
* Previous SVT
* Structural cardiac anomaly
* Alcohol
* ↑T4
42
ECG features in SVT?
* Regular tachycardia
* QRS complexes narrow unless BBB
* P waves hidden or after QRS with inversion in II, III and aVF
43
Pathophysiology of VT?
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.
44
What is torsades de pointes?
Distinctive polymorphic VT which QRS amplitude
QRS complexes appear to twist around baselin – associated with long QT
45
ECG features in VT?
* 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
46
Bloods to check in VT?
check urgent U+E (especially K+) and Mg2+
47
Management of VT (with a pulse)?
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
48
Management of SVT with BBB?
Treat as VT
49
Management of Torsades?
Treat with Magnesum 2g IV
50
Causes of aortic stenosis?
Calcification, congenital (bicuspid valve), rheumatic, endocarditis
51
Signs in aortic stenosis?
* Slow-rising pulse – carotid/brachial – duration of ejection prolonged
* JVP normal unless RVF
* Usually in sinus rhythm
* Narrow pulse pressure
52
Investigations in aortic stenosis?
* 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
Management of aortic stenosis?
* 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
Causes of aortic regurgitation?
* Congenital bicuspid valve
* Rheumatic valvulitis
* Endocarditis
* Root dilatation (isolated, Marfan’s, syphilis, ank spond, HTN)
55
Signs in aortic regurgitation?
* 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
Investigations in aortic regurg?
* 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
Management of aortic regurgitation?
* 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
Grading of murmurs?
* 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
Extra heart sounds?
3rd (Kentucky) = CCF/dilated cardiomyopathy
4th (Tennessee) = hypertrophic cardiomyopathy, AS, HTN
60
Causes of mitral stenosis?
Rheumatic fever (99%) – 4x more common in females
61
Investigations in mitral stenosis?
* CXR – LA enlargement, pulmonary congestion
* ECG – P mitrale (bifid P wave lead II)
* AF in 60-70%
* Echo – diagnosis and assessment of severity
62
Management of mitral stenosis?
* Anticoagulation
* Rate control – digoxin/beta blocker
* Diuretics – lessen pulmonary venous pressure
* Balloon valvuloplasty
* Surgical mitral valvotomy or replacement
63
Causes of mitral regurgitation?
**Primary** – redundant cusp, mitral leaflet prolapse, rheumatic, IHD, cardiomyopathy in papillary muscle, CTD
**Secondary** – due to dilated LV
64
Signs in mitral regurg?
AF - because backlog to RA --\> knacks up SAN.
65
Investigations in mitral regurg?
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
Management of mitral regurg?
* Rate control
* Diuretics/ACEi – if LVF
* Abx – infective endocarditis prophylaxis
* Anticoagulation - if AF or dilated LA
* Mitral valve replacement/repair
67
Organisms causing infective endocarditis?
* Strep Viridans (50%)
* Enterococcal (10% - GI/GU disease)
* Staph aureus (20% - IVDUs)
* Fungi (Candida, Aspergillus, Histoplasma)
68
Sources of infection in infective endocarditis?
Dental caries
Bladder catheterisation
IV drug abuse
Indwelling venous lines,
Colonic problems
Skin pressure sores
Surgery/dental treatment
Septicaemia
69
Types of infective endocarditis?
ACUTE
* Staphylococcus aureus (prosthetic, IVDU)
* Equally prevalent on normal and abnormal valves
* Rare
SUBACUTE
* Streptococcus viridans
* Affects abnormal valves
* More common
70
Risk factors for infective endocarditis?
* 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
Classic triad of infective endocarditis?
1. Persistent fever
2. Emobli
3. New or changing murmurs
72
Symptoms of infective endocarditis?
Fever, low grade fever, malaise, anorexia, weight loss, HF symptoms, embolism symptoms, confusion
73
Signs of infective endocarditis?
* 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
Complications of infective endocarditis?
Aortic root abscess, septic emboli, sepsis, HF, arrhythmias, MI
75
Diagnostic criteria for IE?
Duke’s Criteria
76
Investigations in IE?
* 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
Management in IE?
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
ECG findings in PE?
* Sinus tachy
* RBBB
* Inverted T waves V1-V4
* S1Q3T3
79
Anticoagulation after PE?
Oral anticoagulation for 3 months if provoked, 6 months if unprovoked
LMWH for 5 days whilst warfarin/NOAC commenced
80
Definition of AAA?
Enlargement of the aorta of at least 1.5 times its normal diameter or greater than 3 cm diameter in total
81
Classification of AAA?
Suprarenal
Pararenal
Infrarenal
82
Risk factors for AAA?
* 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
Location of AAA rupture and prognosis?
Posterolateral wall rupture into retroperitoneal space – most alive when reach hospital.
Anterolateral into peritoneal cavity – dead at scene
84
Criteria for AAA surveillance?
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
Medical management of AAA?
* Smoking cessation
* Statins
* Antihypertensives
* Beta blockers
* Antiplatelets
86
Surgical management of AAA?
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
Predisposing factors for varicose veins?
* 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
Symptoms of varicose veins?
* Disfigurement – poor cosmetic appearance
* Pain – after prolonged standing Itching – varicose eczema
* Heaviness
* Ulceration
89
Complications of varicose veins?
* 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
Investigations in varicose veins?
Doppler Flow Studies – ‘backflow’ through incompetent valves
Only used in those with:
* recurrent VVs, history of DVT/thrombophlebitis, varicose eczema, ulceration etc.
91
Conservative management of varicose veins?
* 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
Interventions in varicose veins?
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
6 Ps of limb ischaemia? Other signs of limb ischaemia?
**Pain, pallor, paralysis, paraesthesia, pulseless, perishingly cold**
* Venous guttering
* Buerger's test +ve
* Trophic skin changes – thin, hairless, shiny skin, arterial ulcers, gangrene
94
Other main differential for PVD?
Spinal claudication – pain may be worse on prolonged rest, flexion of spine relieves pain.
95
Investigations in PVD?
* Ankle Brachial Pressure Index (ABPI) - \<0.89 = arterial disease
* Imaging Duplex ultrasound = first line
* Contrast-enhanced magnetic resonance angiography
* CT angiography
96
Management of PVD?
**_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
What is accelerated/malignant hypertension?
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
Symptoms of accelerated hypertension?
* Visual disturbance
* Headache
* Breathlessness
* Hypertensive encephalopathy (↓conscious level, coma, epileptic seizures)
99
Signs of accelerated hypertension?
* 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
Management of accelerated hypertension?
* 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
Causes of pericarditis?
**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
Signs of pericarditis\>
Pericardial friction rub --\> intermittent, positional, louder during inspiration, left sternal edge
Pericardial effusion may develop – rise in venous pressure
103
ECG in pericarditis?
* 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
What is Ewart's sign?
Dullness to percussion over left subscapular area due to compression of left lung base due to pericardial effusion
105
Investigations in pericardial effusion?
* 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
Definition of aortic dissection?
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
Causes and risk factors for aortic dissection?
**_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
Signs of aortic dissection?
* 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
Investigations in aortic dissection?
**_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
Classification of aortic dissection and how it affects management?
**_Stanford Classification_**
* Type A – ascending aorta = surgical management
* Type B – descending aorta = medical management
111
Types of cardiomyopathy?
**_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
Presentation of dilated cardiomyopathy?
* Congestive heart failure
* thromboembolism
* arrhythmias
* Apex beat displaced/diffuse
* Soft S1 (mitral/tricuspid incompetence)
* loud P2 Gallop rhythm (failure)
113
Presentation of hypertrophy cardiomyopathy?
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
Presentation of restrictive cardiomyopathy?
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
Classic presentation of mesenteric ischaemia?
IRREGULAR PULSE + ABDO PAIN = MESENTERIC ISCHAMIEA
116
Where does mesenteric ischamie usually occur?
occlusion of superior mesenteric artery (usually) – small bowel affected uncommonly.
117
Distributions of coeliac trunk, IMA and SMA?
* **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
Presentation of mesenteric ischaemia?
* 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
Causes of SVC obstruction/thrombosis?
Most common cause = lymph node metastases from primary bronchial carcinoma
* Lymphadenopathy
* Thymoma
* Mediastinal tumour
* Retrostenal goitre
* Thoracic aortic aneurysm
* Mediastinal fibrosis
120
Classification of Raynaud's?
**_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
Presentation of Rayanud's?
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
Complications of MI?
123
Hollistic management of HF?
124
125
Posterior STEMI?
**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
Reciprocal changes
**PAILS (next to letter is leads with ST depression)**
* Posterior = Anterior
* Anterior = Inferior
* Inferior = Lateral/Septal
