Cardiovascular Flashcards
(244 cards)
1
Q
Acute coronary syndrome
Umbrella term for what?
A
- STEMI
- NSTEMI
- Unstable angina
2
Q
Acute coronary syndrome
Pathophysiology
A
- RFs lead to initial endothelial damage (pro-inflammatory, pro-oxidant, proliferative and reduced NO bioavailability)
- Gradual build-up of atherosclerotic plaques (LDLs) in walls of arteries
- Monocytes migrate from blood and differentiate into macrophages -> phagocytose the oxidised LDL -> large foam cells
- As macrophages die -> further inflammation
- Smooth muscle proliferation and migration from tunic media into intima -> fibrous capsule covering fatty plaque
Leads to:
- gradual narrowing -> angina
- sudden occlusion -> MI
- aneurysm -> rupture
3
Q
Acute coronary syndrome
Risk factors
A
- Male
- Older age
- Fx
- Smoking
- Alcohol
- DM
- HTN
- Hypercholesterolaemia
- Obesity
4
Q
Acute coronary syndrome
Presentation
A
- Central, constricting chest pain
- May radiate to jaw or left arm
- SOB
- Palpitations
- Sweating and clamminess
- Nausea and vomiting
- General observations (HR, BP, SpO2) may all be normal
5
Q
Acute coronary syndrome
Who may have atypical MI?
A
- Elderly
- Diabetic
- Females
6
Q
Acute coronary syndrome
Mainstay investigations
A
First = ECG
- STEMI = ST elevation or new LBBB
- No ST elevation -> do Troponin
Troponin
- Raised +/- other ECG signs (T wave inversion, pathological Q waves, ST depression) -> diagnose NSTEMI
- Normal troponin and ECG -> unstable angina or other cause (e.g. MSK)
7
Q
Acute coronary syndrome
Other investigations
A
- Physical exam
- FBC for anaemia
- U&Es (prior to ACE-Is)
- LFTs (prior to statins)
- Lipid profile
- TFTs
- CXR (other causes of chest pain and pulmonary oedema)
- ECHO (assess functional damage)
- CT coronary angiogram (coronary artery disease)
8
Q
Acute coronary syndrome
STEMI criteria
A
Clinical symptoms consistent with ACS (generally of ≥ 20 minutes duration) with persistent (> 20 minutes) ECG features in ≥ 2 contiguous leads of:
- 2.5 mm (i.e ≥ 2.5 small squares) ST elevation in leads V2-3 in men under 40 years, or ≥ 2.0 mm (i.e ≥ 2 small squares) ST elevation in leads V2-3 in men over 40 years - 1.5 mm ST elevation in V2-3 in women - 1 mm ST elevation in other leads - New LBBB (LBBB should be considered new unless there is evidence otherwise)
9
Q
Acute coronary syndrome
Initial management
A
MONA
Morphine
Oxygen if sats < 94%
Nitrates (SL or IV)
Aspirin 300 mg
10
Q
Acute coronary syndrome
When should nitrates be used with caution?
A
In hypotensive patients
11
Q
Acute coronary syndrome
Complications of MI
A
DREAD
Death Rupture of heart septum or papillary muscles E'Edema' (HF) Arrhythmias, aneurysm Dressler's syndrome
12
Q
Acute coronary syndrome
Poor prognostic factors
A
- Age
- Development (or history) of heart failure
- Peripheral vascular disease
- Reduced systolic blood pressure
- Killip class*
- Initial serum creatinine concentration
- Elevated initial cardiac markers
- Cardiac arrest on admission
- ST segment deviation
CARDIOGENIC SHOCK carries 30-day mortality of 81%
13
Q
Acute coronary syndrome
Secondary prevention
Lifestyle
A
- Stop smoking
- Reduce alcohol consumption
- Mediterrean diet
- Cardiac rehab
- Optimise Tx of other medical conditions (e.g. DM, HTN)
- Sexual activity may resume 4 weeks after an uncomplicated MI. Reassure that sex does not increase likelihood of further MI.
14
Q
Acute coronary syndrome
Secondary prevention
Medications
A
6 A’s
- Aspirin 75 mg OD
- Another antiplatelet (Clopidogrel or Ticagrelor) for up to 12 months
- Atorvastatin 80 mg OD
- ACE-I
- Atenolol (or other beta-blocker)
- Aldosterone antagonist (for those with clinical HF, e.g. Eplerenone) - initiate with 3-12 days and ideally after ACE-I
15
Q
Acute coronary syndrome
STEMI management
Basic principle
A
- PCI within 2 hours
- Thrombolysis within 12 hours if not PCI
16
Q
Acute coronary syndrome
STEMI management
PCI process
A
- Give within 120 minutes
- If patients present after 12 hours and still have evidence of ongoing ischaemia then PCI should still be considered
- Catheter into patients brachial or femoral artery → feeds up to coronary arteries under XR guidance → injects contrast to identify blockage → balloon dilatation or device to remove blockage → stent to keep artery open
17
Q
Acute coronary syndrome
STEMI management
PCI drugs
A
Further antiplatelet prior to PCI (dual antiplatelet therapy - aspirin + another drug)
- If NOT taking an oral anticoagulant → Prasugrel - If taking an oral anticoagulant → Clopidogrel
Drug therapy during PCI:
- If undergoing with radial access: unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - If undergoing with femoral access: bivaluridin with bailout GPI
18
Q
Acute coronary syndrome
STEMI management
Thrombolysis process
A
- Offered within 12 hours of onset if primary PCI not delivered within 120 minutes of the time when fibrinolysis could have been given
- Injecting fibrinolytic medication → break down fibrin → rapidly dissolve the clot
- Significant risk of bleeding
- Repeat ECG after 60-90 minutes, if ECG changes have not been resolved → PCI
19
Q
Acute coronary syndrome
STEMI management
Thrombolysis drugs
A
Streptokinase
Alteplase
Tenecteplase
20
Q
Acute coronary syndrome
NSTEMI / Unstable angina management
Basic treatment
A
BATMAN B: Beta-blocker A: Aspirin T: Ticagrelor (or Clopi) M: Morphine A: Anticoagulant (Fondaparinux) N: Nitrates
Oxygen if sats < 94%
21
Q
Acute coronary syndrome
NSTEMI / Unstable angina management
When might you not use fondaparinux?
A
- High bleeding risk
- Having immediate angiography
- Creatinine > 265
Give unfractionated heparin if either of the bottom two apply.
22
Q
Acute coronary syndrome
NSTEMI / Unstable angina management
What score is used to assess recurrency risk?
A
GRACE score
Assesses 6 month risk of death or repeat MI after NSTEMI
23
Q
Acute coronary syndrome
NSTEMI / Unstable angina management
GRACE Score
A
- Age
- HR/BP
- Cardiac and renal function
- Cardiac arrest on presentation
- ECG changes
- Troponin levels
0-3% = low risk 3-6% = intermediate risk >6% = high risk
PCI > 3% within 72 hours!
24
Q
Acute coronary syndrome
NSTEMI / Unstable angina management
Criteria for angiography (and maybe also PCI)
A
- Clinically unstable, e.g. hypotensive
- Within 72 hrs if GRACE score > 3%
- If ischemia is subsequently experienced after admission
25
Acute coronary syndrome
NSTEMI / Unstable angina management
Conservative drug management
Dual antiplatelet therapy:
- NOT at high risk of bleeding - Ticagrelor
- IS at high risk of bleeding - Clopidogrel
26
Acute coronary syndrome
NSTEMI / Unstable angina management
PCI drugs
- Unfractionated heparin (regardless of already having fondaparinux or not)
- Further antiplatelet (dual therapy):
If not on oral anticoagulant → Prasugrel or Ticagrelor
If they are on oral anticoagulant → Clopidogrel
27
Dressler's Syndrome
What is it? When?
- Occurs 2-3 weeks after MI
- Caused by a local immune response
- Causes pericarditis
28
Dressler's Syndrome
Features
- Pleuritic chest pain
- Low grade fever
- Pericardial rub on auscultation
29
Dressler's Syndrome
Diagnosis
ECG
- Global ST elevation - saddle-shaped ST
- T wave inversion
ECHO - pericardial effusion
Raised inflammatory markers
30
Dressler's Syndrome
Management
- NSAIDs (aspirin, ibuprofen)
- Steroids if severe (e.g. Prednisolone)
- May need pericardiocentesis to remove fluid
31
Dressler's Syndrome
Complications
- Pericardial effusion
| - Pericardial tamponade (fluid constricts heart and prevents function) - rare
32
Hypertension
Definition
- > 140/90 in clinic
| - > 135/85 with ambulatory or home readings
33
Hypertension
Causes of secondary
ROPE
R: Renal: glomerulonephritis, chronic pyelonephritis, adult PCKD, renal artery stenosis
O: Obesity
P: Pregnancy/pre-eclampsia
E: Endocrine: Phaeochromocytoma, Cushing's, Liddle's, Congenital adrenal hyperplasia (11-beta hydroxylase deficiency), acromegaly, PRIMARY HYPERALDOSTERONISM (CONNS) - do renin:aldosterone blood test
Other causes:
- Coarctation of the aorta
Drugs: steroids, NSAIDs, COCP, MAOIs, leflunomide
34
Hypertension
Features
Does not typically present with symptoms unless VERY high (>200/120 mmHg):
- Headaches
- Visual disturbances
- Seizures
35
Hypertension
Diagnosis
- Check BP every 5 years to screen for HTN
- Measure more often in borderline (140/90) or every year in T2DM
- Gold-standard = 24-hour BP readings or home readings
- Check in BOTH arms, if differ by > 20 → repeat readings, take highest reading
36
Hypertension
Monitoring checks
- Fundoscopy - hypertensive retinopathy
- Urine dipstick - renal disease (consequence or cause)
- ECG - LVH or IHD
- HbA1c - co-existing DM
- Lipids - hyperlipidaemia
37
Hypertension
Management
Lifestyle
- Low salt diet (< 6g/day), ideally 3g/day
- Reduced caffeine intake
- Stop smoking, drink less aclohol, eat balance diet, exercise more
38
Hypertension
Management
When to admit?
- Retinal haemorrhage/papilloedema
- New onset confusion
- Chest pain
- Signs of HF
- AKI
- If suspect phaeochromocytoma (labile or postural hypotension, headache, palpitations, pallor and diaphoresis)
39
Hypertension
Management
Medications
Step 1
Patient < 55-years-old or a background of type 2 diabetes mellitus:
- ACE inhibitor or Angiotensin receptor blocker (ACE-i or ARB): (A)
- Angiotensin receptor blockers should be used where ACE inhibitors are not tolerated (e.g. due to a cough)
Patients >= 55-years-old or of black African or African–Caribbean origin:
- Calcium channel blocker (C)
- ACE inhibitors have reduced efficacy in patients of black African or African–Caribbean origin are therefore not used first-line.
40
Hypertension
Management
BP targets
< 80 yrs
Clinic: 140/90
ABPM/HBPM: 135/85
> 80 yrs
Clinic: 150/90
ABPM/HBPM: 145/85
41
Hypertension
Complications
- Ischaemic heart disease
- Cerebrovascular accident (i.e. stroke or haemorrhage)
- Hypertensive retinopathy
- Hypertensive nephropathy
- Heart failure
42
Hypertension
When might you suspect renal tubular acidosis as cause?
If very high BP and not responding to Tx
43
Hypertension
Management
Medications
Step 2
- If already taking A, add C or D (thiazide-like Diuretic)
- If already taking C, add A or D
For those of black African or Afro-Caribbean originally taking a CCB, add ARB in preference to ACE-I
44
Hypertension
Management
Medications
Step 3
Add a third drug:
- If already taking (A+C), then add D
- if already taking (A+D), then add C
45
Hypertension
Management
Medications
Step 4
Either add fourth drug or seek specialist advice
First, check:
- Confirm elevated BP with ABPM/HBPM
- Assess for postural hypotension
- Discuss adherence
Then:
- If K+ < 4.5mmol/l: add low-dose spironolactone
If K+ > 4.5mmol/l: add alpha- (doxazosin) or beta-blocker (propanolol/atenolol)
46
Stable angina
Pathophysiology
- Narrowing of the coronary arteries reduced blood flow to the myocardium
- During times of high demand e.g. exercise, there is insufficient blood supply to meet demand
47
Stable angina
Features
- Constricting chest pain
- +/- radiation to jaw or arms
- Brought on by exercise
- Relieved by GTN
48
Stable angina
Investigations
CT coronary angiography = gold-standard
- Inject contrast and take CT images timed to heart beat
- Detailed view of coornary arteries, higlighting any narrowing
All patients should have baseline:
- Physical examination
- ECG
- FBC (check for anaemia)
- U&Es (prior to ACEi and other meds)
- LFTs (prior to statins)
- Lipid profile
- Thyroid function tests (check for hypo / hyper thyroid)
- HbA1C and fasting glucose (for diabetes)
49
Stable angina
Basic management
```
RAMP:
R: Refer to cardiology
A: Advise them about diagnosis, management and when to call an ambulance
M: Medical treatment
P: Procedural or surgical interventions
```
50
Stable angina
Medical management
Immediate symptom relief:
- GTN, then again at 5 mins, if not relieved after further 5 mins then call ambulance
Long-term symptom relief:
- B-blockers
- CCBs
- Try monotherapy then dual therapy
- Others: isosorbide mononitrate ivabradine, nicorandil, ranolazine
BEWARE patint may develop tolerance to nitrates, necessitating a change in dose regime. Can use asymmetric dosing interval to maintain a daily nitrate-free time of 10-14 hours
Secondary prevention:
- Aspirin
- Atorvastatin
- ACE-I
- Beta-blocker (already on for symptom relief)
51
Stable angina
Surgical management
- PCI with coronary angioplasty
| - CABG
52
Aortic dissection
Pathophysiology
- Break or tear forms in the inner layer of the aorta → allows blood to flow between the layer of the wall of the aorta
- 3 layers of aorta: intima, media, adventitia
- In dissection → blood enters between the INTIMA and MEDIA → creation of a false lumen
53
Aortic dissection
Risk factors
- Hypertension- heavy lifting/cocaine cause sudden increase in BP
- Male
- Older age
- Smoking
- Poor diet
- Reduced physical activity
- Raised cholesterol
- Aortic conditions:
- Biscuspid aortic valve
- Coarctation of the aorta
- Aortic valve replacement
- CABG
- Connective tissue disorders:
- Marfan’s Syndrome
- Ehlers-Danlos Syndrome
54
Aortic dissection
Classifications
The Stanford System:
- Type A: Affects the ascending aorta, before the brachiocephalic artery
- Type B: Affects the descending aorta, after the left subclavian artery
The DeBakey System:
- Type I: Begins in ascending aorta and involves at least the aortic arch (if not whole aorta)
- Type II: Isolated to ascending aorta
- Type IIIa: Begins in descending aorta and involves only the section above the diaphragm
- Type IIIb: Begins in the descending aorta and involves the aorta below the diaphragm
55
Aortic dissection
Features
- Chest/back/abdo pain
- Severe and sharp
- Tearing in nature
- Maximal at onset
- Chest = more common in Type A
- Back = more common in Type B
- Radial pulse deficit
- Difference in BP between arms (> 20 mmHg)
- Aortic regurgitation
- Diastolic murmur
- Hypertension → hypotension as progresses (poor prognosis)
- Collapse/syncope
- Other features from involvement of specific arteries:
- Coronary arteries → angina
- Spinal arteries → paraplegia
- Distal aorta → limb ischaemia
56
Aortic dissection
Investigations
CT angiography of chest, abdo and pelvis = investigation of choice
- Suitable for stable patients and for planning surgery
- False lumen = key finding
```
Transoesophageal echo (TOE)
- More suitable for unstable patients
```
- CXR: widened mediastinum
- ECG: exclude other causes (e.g. MI), but may be normal and therefore falsely reassuring
- Important to exclude MI as Tx for MI (thrombolysis) could cause fatal progression of dissection
57
Aortic dissection
General management
- Surgical emergency!
- Analgesia → **morphine**
- BP and HR well controlled to reduce stress on aortic walls → **beta-blockers**
58
Aortic dissection
Management of Type A
- Open surgery (midline sternotomy) to remove section of aorta with defect and replace with graft
- Aortic valve may also need to be replaced during procedure
- BP should be kept at 100-120 mmHg systolic whilst awaiting intervention
59
Aortic dissection
Management of Type B
- Thoracic endovascular aortic repair (TEVAR)
- Conservative management
- Bed rest
- Reduce BP → IV labetalol
60
Aortic dissection
Complications
Backward tear (rare):
- Aortic valve regurgitation
- Cardiac tamponade
- MI: inferior pattern due to R coronary involvement
Forward tear:
- Stroke
- Unequal arm pulses and BP
- Paraplegia
- Renal failure
61
Aortic aneurysm
Types
- True: All 3 layers of the arterial wall are involved
| - False: Only a single layer of fibrous tissue forms the aneurysm wall
62
Aortic aneurysm
Risk factors
- Males
- Increased age
- Smoking
- Hypertension
- Fx
- Existing CVS disease
- Diabetes
- Connective tissue disorders (Marfans, Ehlers-Danlos)
63
Aortic aneurysm
Features
- Most are asymptomatic
- Usually incidental finding on US, Abdo XR, CT
- Non-specific abdo pain
- **Pulsatile and expansile mass** when palpated with two hands
64
Aortic aneurysm
Screening
- All men are offered a screening US at 65 yrs old
| - Patients with an aorta diameter above 3cm are referred to a vascular team (urgently if more than 5.5cm)
65
Aortic aneurysm
Investigations
- US
| - CT angiogram - more detailed picture and helps guide surgery, generally reserved for >5 cm
66
Aortic aneurysm
Management of unruptured aneurysm
- Treat reversible RFs
- Screening and surveillance: yearly for 3 - 4.4 cm, 3 monthly for 4.5 - 5.5 cm
- Surgery: artificial graft, either open laparotomy or endovascular aneurysm repair (EVAR) via femoral artery
67
Aortic aneurysm
Management of ruptured aneurysm
- **Surgical emergency** → 100% mortality without surgery
- Permissive hypotension → lower than normal BP to reduce pressure
- Haemodynamically unstable → **directly to theatre**, do not delay with imaging
- Haemodynamically stable → **CT angiogram first**
- In patients with co-morbidities that make the prognosis with surgery very poor, a discussion needs to be had with senior doctors, the patient and their family about palliative care
68
Aortic aneurysm
Prognosis
- 80% mortality if ruptured
- Poor prognosis if bleeds anteriorly into peritoneal cavity (about 20%)
- 100% mortality if ruptures and no surgery
69
Aortic aneurysm
features of rupture aneurysm
- Severe abdominal pain that may radiate to the back or groin
- Haemodynamic instability (hypotension and tachycardia)
- Pulsatile and expansile mass in the abdomen
- Collapse
- Loss of consciousness
70
Aortic aneurysm
Criteria for elective surgery
- Symptomatic aneurysm
- Diameter growing >1 cm per year
- Diameter > 5.5 cm
71
Coarctation of the aorta
Epidemiology
More common in males (despite association with Turner's syndrome)
72
Coarctation of the aorta
Features
- Infancy: heart failure, poor feeding, grey floppy baby
- Adult: hypertension
- Radio-femoral delay
- Mid systolic murmur, maximal over back
- Apical click from the aortic valve
- LV heave (due to LVH)
- Notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children
Growth failure, tachycardia and tachypnoea in the context of weak femoral pulses = consider coarctation in babies
73
Coarctation of the aorta
Associations
- **Turner's syndrome**
- Bicuspid aortic valve
- Berry aneurysms
- Neurofibromatosis
74
Coarctation of the aorta
What is it and pathophysiology
Congenital condition where there is a narrowing of the aortic arch, usually around the ductus arteriosus.
Narrowing of the aorta reduces the pressure of blood flowing to the arteries that are distal to the narrowing. It increases the pressure in areas proximal to the narrowing, such as the heart and the first three branches of the aorta.
75
Coarctation of the aorta
Management
- In babies: Prostaglandin E is used keep the ductus arteriosus open whilst awaiting surgery
- Surgery is then performed to correct the coarctation and to ligate the ductus arteriosus
76
Cardiac arrest
Shockable rhythms
- Ventricular fibrillation
- Pulseless ventricular tachycardia
(VF/pulseless VT)
77
Cardiac arrest
Non-shockable rhythms
- Asystole
- Pulseless-electrical activity
(asystole/PEA)
78
Cardiac arrest
Chest compressions:ventilation ratio
- Ratio of chest compressions to ventilation = 30:2
79
Cardiac arrest
Defibrillation
- A single shock for VF/pulseless VT
- Followed by 2 mins of CPR
- If witnessed cardiac arrest in a monitored patient (e.g. cardiac ward) --> three quick successive (stacked) shocks instead
80
Cardiac arrest
Drugs
Delivery routes
- IV access = first-line
| - If not --> intraosseous route
81
Cardiac arrest
Drugs used and when
Adrenaline (1 mg):
- Non-shockable: ASAP
- Shockable: Once chest compressions have restarted after the third shock
- Repeat adrenaline 1mg every 3-5 minutes
Amiodarone:
- Shockable: 300 mg given after 3 shocks, further 150 mg after 5 shocks
- Lidocaine used as alternative
Thrombolytic drugs
- Given if PE is suspected
- Prolonged CPR for 60-90 minutes if given
82
Cardiac arrest
Reversible causes
4 H's:
- Hypoxia
- Hypovolaemia
- Hyperkalemia, hypokalaemia, hypoglycaemia, hypocalcemia, acidaemia (and other metabolic disorders)
- Hypothermia
4 T's:
- Toxins
- Tamponade (cardiac)
- Thrombus
- Tension pnuemothorax (PEA)
83
Atrial flutter
Define
Form of supraventricular tachycardia characterized by a succession of rapid atrial depolarisation waves
- Re-entrant rhythm
- Electrical signal re-circulates in self-perpetuating loop due to extra electrical pathway
- Goes round and round atrium without interruption
84
Atrial flutter
ECG findings
- SAWTOOTH appearance
- Atrial rate of 300 bpm
- Ventricular rate of 150 bpm (signal conducts every second lap)
85
Atrial flutter
Associated conditions
- Hypertension
- Ischaemic heart disease
- Cardiomyopathy
- Thyrotoxicosis
86
Atrial flutter
Management
- Rate/rhythm control with beta-blockers or cardioversion
- Treat underlying reversible conditions (e.g. htn, thyrotoxicosis)
- Radiofrequency ablation of the tricuspid valve - curative for most
- Anticoagulation based on CHA2DS2VASc
87
Aortic stenosis
Pathophysiology
- Outflow obstruction of the left ventricle
- Pressure gradient builds between left ventricle and aorta
- INCREASES the AFTERLOAD
- Initially, LV function is maintained by compensatory pressure HYPERTROPHY
- When compensatory mechanisms are exhausted → decline of LV function
88
Aortic stenosis
Features
- Normally asymptomatic
- Features tend to appear when 1/4 of size
- normal size = 3-4cm
SAD
S: Syncope - exertional
A: Angina
D: Dyspnoea - exertional
89
Aortic stenosis
Murmur
- **EJECTION SYSTOLIC MURMUR**
- Crescendo-descendo character
- Radiates to carotids
- Loudness does **not** correlate with severity
90
Aortic stenosis
Other signs
- Narrow pulse pressure
- Slow rising pulse
- Delayed ESM
- Soft-absent S2
- Thrill
- LVH or failure
91
Aortic stenosis
Investigations
- Transthoracic ECHO
| - Valvular gradient (doppler-derived)
92
Aortic stenosis
Management
- Asymptomatic → observe
- Advise about dental hygiene
- Consider IE prophylaxis in dental procedures
- Symptomatic → valve replacement
- **TAVI** (transcatheter aortic valve implantation)
93
Aortic stenosis
Criteria for surgery
- Symptomatic with severe AS
- Decreasing ejection fraction
- Undergoing CABG with moderate AS
Consider in asymptomatic patients with valvular gradient > 40 mmHg and features such as LV systolic dysfunction
94
Aortic stenosis
Causes
- **DEGENERATIVE CALCIFICATION** (most common >65 yrs)
- **CONGENITAL BISCUSPID** (most common <65 yrs)
- Rheumatic heart disease
- William’s syndrome (supravalvular aortic stenosis)
- Subvalvular: hypertrophic obstructive cardiomyopathy (HOCM)
95
Mitral regurgitation
Pathophysiology
- Mitral valve does not close properly
- Backflow of blood from LV → LA during systole
- Compensatory mechanisms = LA enlargement and LVH
- As it becomes more severe → body’s oxygen demand may exceed what the heart can supply → myocardium may thicken over time → may eventually feel more fatigued as a thicker myocardium becomes less efficient → finally results in congestive heart failure
96
Mitral regurgitation
Risk factors
- Female
- Low BMI
- Age - idiopathic weakening
- Renal dysfunction
- Prior MI
- Prior mitral stenosis or valve prolapse
- Collagen disorders, e.g Ehler-Danlos, Marfans
97
Mitral regurgitation
Causes
- IHD or post-MI: papillary muscles or chordae tendinae may be affected by cardiac insult
- Mitral valve prolapse - due to myxomatous degeneration
- Infective endocarditis: vegetations from organisms colonise the valve and prevent it from closing properly
- Rheumatic fever: inflammation of the valves
- Congenital
98
Mitral regurgitation
Features
- Most are asymptomatic
- Features tend to be due to LV failure, arrhythmias or pulmonary hypertension
- Fatigue
- Dyspnoea
- Oedema
99
Mitral regurgitation
Murmur
- **PAN-SYSTOLIC MURMUR**
- Heard best at apex and radiating into axilla
- High-pitched
- Whistling
- Soft S1 sound
- May hear a third heart sound (severe)
- Displaced hyperdynamic apex beat
- Loudness **DOES** correlate with severity
100
Mitral regurgitation
Investigations
- ECG: Broad P wave (left atrial enlargement)
- CXR: Cardiomegaly (enlarged left atrium and ventricles)
- ECHO: Crucial to diagnosis
101
Mitral regurgitation
Management
- Medical management
- Nitrates
- Diuretics
- Positive inotropes
- Intra-aortic balloon pump to increase CO
- If HF → ACE-Inhibitors along with beta-blockers and spironolactone
- Degenerative → repair (valvuloplasty) is more effective than replacement
102
Mitral regurgitation
Criteria for surgery
- Acute and severe
- ANY symptoms (at rest or on exertion)
- Asymptomatic but ejection fraction <60% (regardless of symptoms)
- Asymptomatic but new-onset AF or raised pulmonary artery pressure (PAP)
103
Aortic regurgitation
Pathophysiology
- Leakage of blood from aorta into LV during diastole
- Combined pressure and volume overload
- Compensatory mechanisms: LV dilation and hypertrophy to maintain cardiac output
- Progressive dilation may lead to HF
104
Aortic regurgitation
Causes
Due to valve disease:
- Rheumatic fever
- Infective endocarditis
- Bicuspid aortic valve
- Idiopathic age related weakness
- Connective tissue disorders, e.g. Ehler-Danlos, Marfan’s, SLE
Due to aortic root disease:
- Aortic dissection
- Spondyloarthropathies (AS)
- Hypertension
- Syphilis
105
Aortic regurgitation
Features
- Asymptomatic until 4th/5th decade
- Exertional dyspnoea, orthopnoea, paroxysmal dyspnoea
- Palpitations
- Angina
106
Aortic regurgitation
Murmur
- **EARLY DIASTOLIC, SOFT BLOWING MURMUR**
- Heard at the left sternal border
- Can also cause **Austin Flint** murmur → heard at apex, early diastole, **rumbling**
107
Aortic regurgitation
Other signs
- **Corrigan’s pulse** - collapsing pulse
- Wide pulse pressure
- Displaced apex beat
- HEAD BOBBING (de musset's sign)
- Quincke's sign (nailbed pulsation)
108
Aortic regurgitation
Investigations
- ECG: LVH
- CXR: Cardiomegaly (LV and aortic root enlargement)
- ECHO
109
Aortic regurgitation
Management
- Infective endocarditis prophylaxis
- ACE-Is
- Serial ECHOs
- Surgery → TAVI
110
Aortic regurgitation
Surgery indications
- Symptoms worse
- Enlarging heart
- ECG deterioration (T wave inversion in lateral leads)
111
Mitral stenosis
Pathophysiology
- Narrow mitral valve prevents proper filling during diastole from LA → LV
- Raised LA pressure causes LA hypertrophy and dilation
- Increased pressure in the lungs
- Pulmonary hypertension
112
Mitral stenosis
Causes
- Rheumatic heart disease
- Infective endocarditis
- Mitral calcification
113
Mitral stenosis
Other signs
- Low volume pulse
- Atrial fibrillation
- Malar flush
- Additional ‘a’ wave in JVP (pulmonary HTN)
114
Mitral stenosis
Investigations
- ECG: AF, LA enlargement, **P-mitrale** (broad, bifid P-waves in Lead 2)
- CXR: LA enlargement
- ECHO: A tight mitral valve would be <1 sq cm
115
Mitral stenosis
Management
- Anticoagulation in AF (Warfarin)
- Monitor asymptomatic patients with serial ECHOs
- Symptomatic → percutaneous mitral balloon valvotomy or mitral valve commissurotomy or replacement
116
Mitral stenosis
Management
- Anticoagulation in AF (Warfarin)
- Monitor asymptomatic patients with serial ECHOs
- Symptomatic → percutaneous mitral balloon valvotomy or mitral valve commissurotomy or replacement
117
Myocarditis
Pathophysiology
inflammation of the myocardium
118
Myocarditis
Causes
- viral: coxsackie B, HIV
- bacteria: diphtheria, clostridia
- spirochaetes: Lyme disease
- protozoa: Chagas' disease, toxoplasmosis
- autoimmune
- drugs: doxorubicin
119
Myocarditis
Features
- Usually young patient with an acute history
- Chest pain
- Dyspnoea
- Arrhythmias
120
Myocarditis
Investigations
Bloods
↑ inflammatory markers in 99%
↑ cardiac enzymes
↑ BNP
ECG
- Tachycardia
- Arrhythmias
- ST/T wave changes including ST-segment elevation and T wave inversion
121
Myocarditis
Management
- Treatment of underlying cause e.g. antibiotics if bacterial cause
- Supportive treatment e.g. of heart failure or arrhythmias
122
Myocarditis
Complications
- Heart failure
- Arrhythmia, possibly leading to sudden death
- Dilated cardiomyopathy: usually a late complication
123
Venous leg ulcers
Causes
- Venous hypertension (secondary to chronic venous insufficiency) = MOST COMMON
- Calf pump dysfunction
- Neuromuscular disorders
124
Venous leg ulcers
Pathophysiology
- Form due to capillary fibrin cuff or leucocyte sequestration
125
Chronic venous insufficiency
Features
- Oedema
- Brown pigmentation
- Lipodermatosclerosis
- Eczema
126
Venous leg ulcers
Features
- Occur in the GAITER area
- Occur after minor injury to leg
- Larger than arterial ulcers
- More superficial than venous ulcers
- Irregular, sloping border
- More likely to bleed
- Less painful
- Pain = relieved by elevation
- Pain = worse on lowering the leg
127
Venous leg ulcers
What is deep venous insufficiency related to?
DVT
128
Venous leg ulcers
What is superficial venous insufficiency related to?
Varicose veins
129
Venous leg ulcers
Investigations
- ABPI - assess for poor arterial flow, could impair healing
- Bloods to look for infection (FBC/CRP)
- Bloods for co-morbidities (HbA1c, FBC for anaemia, albumin for malnutrition)
- Charcoal swabs to look for causative organism
- Skin biopsy (if skin cancer suspected) - 2 week wait
- Doppler US to look for reflux
- Duplex US to look at anatomy/flow of veins
130
Venous leg ulcers
Management
- 4 LAYER COMPRESSION BANDAGING (after exclusion of arterial disease or surgery)
- Oral pentoxifylline, a peripheral vasodilator, improves healing rate
- Cleaning, debridement and dressing of wound
- If fails to heal within 12 weeks or > 10 cm -> may need grafting
- Tissue viability in complex/non-healing ulcers
- Pain killers or pain team if painfuk
- Diabetes team if diabetic
- Abx if infection
131
Arterial ulcers
Associations
- PAD
| - Absent pulses, pallor and intermittent claudication
132
Arterial ulcers
Features
- Occur distally, toes or dorsum of foot (heel)
- Smaller than venous ulcers
- Deeper than venous ulcers
- Well-defined borders
- Punched-out appearance
- Pale due to poor blood supply
- Less likely to bleed
- Painful
- Worse at night (when elevated)
- Pain improved by lowering leg
- May be areas of gangrene
- Low ABPI measurements
- Cold, no palpable pulses
133
ABPI interpretation
- Normal ABPI = 0.9 - 1.2
- Values below 0.9 indicate arterial disease
- Interestingly, values above 1.3 may also indicate arterial disease, in the form of false-negative results secondary to arterial calcification (e.g. In diabetics)
134
Arterial ulcers
Management
- Same as PAD
- Urgent referral to vascular to consider surgical revascularization
- If the underlying arterial disease is treated, the ulcer should heal rapidly
Debridement and compression are NOT used in arterial ulcers
135
Complication of diabetic foot ulcer?
Osteomyelitis
136
What score is used for pressure ulcers?
Waterlow Score
137
Tricuspid regurgitation
Signs
- Pan-systolic murmur
- Prominent/giant *V waves* in JVP
- Pulsatile hepatomegaly
- Left parasternal heave
138
Tricuspid regurgitation
Causes
- Right ventricular infarction
- Pulmonary hypertension, e.g. COPD
- Rheumatic heart disease
- Infective endocarditis
- Ebstein's anomaly
- Carcinoid syndrome
139
Ebstein's Anomaly
Pathophysiology
- Congenital heart defect
- Low insertion of the tricuspid valve
- Results in large atrium and small ventricle
- Sometimes referred to as atrialisation of the right ventricle
- Poor flow from right atrium to right ventricle -> poor flow to pulmonary vessels
140
Ebstein's Anomaly
Associations
- Patent foramen ovale (PFO) or atrial septal defect (ASD) is seen in at least 80% of patients, resulting in a shunt between the right and left atria
- Wolff-Parkinson White syndrome
- Exposure to lithium in-utero
141
Ebstein's Anomaly
Features
- Cyanosis
- SOB
- Tachypnoea
- Poor feeding if baby
- Prominent 'a' wave in the distended jugular venous pulse,
- Hepatomegaly
- Tricuspid regurgitation
- Pansystolic murmur, worse on inspiration
right bundle branch block → widely split S1 and S2 (S3 and S4 = gallop rhythm)
- Collapse/cardiac arrest
142
JVP
'a' wave
= Atrial contraction
- large if atrial pressure e.g. tricuspid stenosis, pulmonary stenosis, pulmonary hypertension
- absent if in atrial fibrillation
143
JVP
Cannon 'a' wave
- caused by atrial contractions against a closed tricuspid valve
- are seen in complete heart block, ventricular tachycardia/ectopics, nodal rhythm, single-chamber ventricular pacing
144
JVP
'c' wave
- closure of the tricuspid valve
| - not normally visible
145
JVP
'v' wave
- due to passive filling of blood into the atrium against a closed tricuspid valve
- giant v waves in tricuspid regurgitation
146
JVP
'x' descent
fall in atrial pressure during ventricular systole
147
JVP
'y' descent
opening of tricuspid valve
148
JVP
Non-pulsatile JVP
Vena cava obstruction
149
JVP
Kussmaul's sign
- Paradoxical rise in JVP on inspiration
| - Seen in constrictive paricarditis
150
Ejection systolic murmur
Louder on expiration causes
- Aortic stenosis
| - Hypertrophic obstructive cardiomyopathy
151
Ejection systolic murmur
Louder on inspiration causes
- Pulmonary stenosis
| - Atrial septal defect
152
Pansystolic murmur
Causes
High-pitched and blowing in character
- Mitral regurgitation
- Tricuspid regurgitation- louder during inspiration
Harsh in character
- Ventricular septal defect
153
Late systolic murmur
Causes
- Mitral valve prolapse
| - Coarctation of aorta
154
Early diastolic murmur
Causes
High-pitched and blowing in nature
- Aortic regurgitation
- Graham-Steel murmur (pulmonary regurgitation)
155
Mid-late diastolic murmur
Causes
- Mitral stenosis ('rumbling' in character)
| - Austin-Flint murmur (severe aortic regurgitation, again is 'rumbling' in character)
156
Continuous machine-like murmur
Causes
Patent ductus arteriosus
157
Ebstein's Anomaly
Investigations
ECHO
158
Ebstein's Anomaly
Managegenmt
- Treat arrhythmias and HF
- Prophylactic Abx for infective endocarditis
- Definitive surgical correction of defect
159
Infective endocarditis
Risk factors
Things that can introduce infectious material:
- IVDU
- Poor dental hygiene
- Dental treatment
- IV cannula
- Cardiac surgery
- Recent piercings
Others:
- Prosthetic valves
- Valve disease (including rheumatic)
- Congenital heart defects
- Elderly
160
Infective endocarditis
Causative organisms
- STAPH. AUREUS = MOST COMMON (IVDUs, DM, surgery)
- Strep viridans (poor dental hygeine, dental procedure)
- Staph epidermidis (indwelling lines, prosthetic valve surgery). MOST COMMON if < 2 months of valve surgery.
- Strep bovis (colorectal cancer)
- Non-infective = SLE (Libman-Sacks), malignancy (marantic endocarditis)
Culture-negative causes:
- Prior Abx therapy
- Coxiella burnetti
- Bartonella
- Brucella
- HACEK = Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella
161
Infective endocarditis
Modified Duke Criteria
Major criteria
- Positive blood culture (x2 12 hrs apart, x3 for less specific like s.aureus) or positive serology for culture-negatives
- Positive echocardiogram
- New valvular regurgitation murmur
162
Infective endocarditis
Modified Duke Criteria
Minor criteria
- Predisposing heart condition or IVDU
- Microbiological evidence does not meet major criteria
- Fever > 38
- Vascular phenomena - major emboli, splenomegaly, clubbing, splinter haemorrhages, Janeway lesions, petechia or purpura
- Immunological phenomena - glomerulonephritis, Osler's nodes, Roth spots
163
Infective endocarditis
Modifed Duke Criteria
Pathological critera
- Positive histology or microbiology of pathological material obtained at autopsy or cardiac surgery
- E.g. valve tissue, embolic fragments, intracardiac abscess content
164
Infective endocarditis
Modifed Duke Criteria
Score interpretation
Infective endocarditis diagnosed if:
- Pathological criteria positive, or
- 2 major criteria, or
- 1 major and 3 minor criteria, or
- 5 minor criteria
165
Infective endocarditis
Poor prognostic factors
- Staph.aureus infection
- Prosthetic valve
- Culture negative endocarditis
- Low complement levels
166
Infective endocarditis
Management
Initial blind therapy
Own valve:
- Amoxicillin (consider adding low-dose gentamicin)
Penicillin allergic:
- Vancomycin + low-dose gentamicin
Prosthetic valve:
- Vancomycin + rifampicin + low-dose gentamicin
167
Infective endocarditis
Specific Tx
Staphylococci:
- Own valve: Flucloxacillin
- Own valve and PA: Vanc + rifampicin
- Prosthetic valve: Flucloxacillin + rifampicin + low-dose gent
- Prosthetic and PA: Vanc + rifampicin + low-dose gent)
Streptococci:
- Own valve: Benzylpenicillin
- Own valve and PA: Vanc + low-dose gent
- Prosthetic valve: Benzylpenicillin + low-dose gent
- Prosthetic and PA: Vanc + low-dose gent
PA = penicillin allergy
168
Infective endocarditis
Indications for surgery
- Severe valvular incompetence
- Aortic abscess (lengthened PR)
- Infections resistant to Abx/fungal infections
- HF
- Recurrent emboli after Abx
169
Infective endocarditis
Indications for prophylaxis
- Any episode of infection in people at risk of IE
- If a person at risk of infective endocarditis is receiving antimicrobial therapy because they are undergoing a gastrointestinal or genitourinary procedure at a site where there is a suspected infection they should be given an antibiotic that covers organisms that cause infective endocarditis
170
DVT
Risk factors
- Immobility
- Recent surgery
- Long haul travel
- Pregnancy
- Hormone therapy with oestrogen (combined oral contraceptive pill and hormone replacement therapy)
- Malignancy
- Polycythaemia
- Systemic lupus erythematosus
- Thrombophilia
171
DVT
Thrombophilias
- MAIN = ANTIPHOSPHOLIPID SYNDROME (recurrent VTEs and recurrent miscarriages, blood test fr antiphospholipid antibodies)
- Factor V Leiden
- Antithrombin deficiency
- Protein C or S deficiency
- Hyperhomocysteinaemia
- Prothombin gene variant
- Activated protein C resistance
172
DVT
Features
- Almost always unliateral
- Bilateral symptoms are more likely to be chronic venous insufficiency or HF
- Lower limb swelling
- Dilated superficial veins
- Tenderness to the calf
- Oedema
- Colour changes to the leg
To examine for leg swelling, measure the calf 10cm below the tibial tuberosty. >3 cm difference is significant.
173
DVT
Diagnosis
- WELLS SCORE
If Wells >=2 (DVT likely):
- Proximal leg vein USS
- If positive -> diagnosed
- If negative -> D-Dimer
- If USS can not be carried out within 4 hrs then give anticoagulation and do D-Dimer whilst waiting
- If positive D-Dimer but negative scan and Wells+, stop anticoagulation and offer repeat USS 1 week later
If Wells < 1 (unlikely):
- Perform a D-Dimer within 4 hrs
- Give anticoagulation in interim if not within 4 hrs
- Negative -> DVT unlikely
- Positive -> proximal leg USS within 4 hrs
- If USS not within 4 hrs, anticoagulate and do it within 24hrs
174
DVT
Other things that may cause a raised D-Dimer
- Pregnancy
- Pneumonia
- Malignancy
- HF
- Surgery
175
DVT
Initial management
- Apixaban or Rivoraxaban
- Started immediately
If neither are suitable:
- LMWH followed by dabigatran or edoxaban
OR
- LMWH followed by a vitamin K antagonist (VKA, i.e. warfarin)
176
DVT
When might you consider catheter-directed thrombolysis?
- Symptomatic ileofemoral DVT
| - Symptoms lasting < 14 days
177
DVT
Management in active cancer
DOAC unless CI
178
DVT
Management in renal impairment
If severe, e.g. < 15/min:
| - LMWH, unfractionated heparin or LMWH followed by a VKA (Warfarin)
179
DVT
Management in antiphospholipid syndrome
- LMWH followed by VKA (Warfarin)
180
DVT
How long do you continue anticoagulation for?
- 3 months: Reversible cause (then review)
- 3+ months (often 6 months, exact time based on HASBLED): Unclear cause, recurrent VTE, an irreversible underlying cause (e.g. thrombophilia)
- 3-6 months: Active cancer (then review)
181
DVT
Further management for recurrent PEs that are unsuitable for anticoagulation
IVC filter
| - Catch blood clots travelling from the venous system
182
DVT
What should you check for in patients with unprovoked DVT or PE that are about to finish anticoagulation?
- Antiphospholipid syndrome (check antiphospholipid antibodies)
- Hereditary thrombophilias (only if they have a first-degree relative also affected by a DVT or PE)
183
DVT
What should you check in patients presenting with their first VTE without a clear cause?
- Medical history
- Baseline bloods
- Physical examination for evidence of cancer
184
PE
CTPA vs V/Q scanning in pregnancy
CTPA:
- Slight increased risk of maternal breast cancer
- Pregnancy makes breast cancer more sensitive to radiation
V/Q Scanning:
- Slight increased risk of childhood cancer compared with CTPA
185
Antiphospholipid syndrome
Pathophysiology
- Acquired disorder
- Predisposes to venous and arterial thromboses, recurrent foetal loss and thrombocytopenia
- May occur as primary disorder or secondary to other conditions, particularly **SLE**
186
Antiphospholipid syndrome
Features
- Venous/arterial thrombosis - stroke/MI/renal thrombosis
- Recurrent foetal loss
- Livedo reticularis (reddish/blue mottled rash, worse on cold)
- Thrombocytopenia (low platelets)
- Prolonged APTT (paradoxical)
- Pre-eclampsia
- Pulmonary hypertension
187
Antiphospholipid syndrome
Associations
- SLE
- Other autoimmune disorders
- Lymphoproliferative disorders
- Phenothiazines (RARE)
- VTEs
188
Antiphospholipid syndrome
Diagnosis
Hx of thrombosis or pregnancy complication PLUs peristent antibodies:
- Lupus anticoagulant
- Anticardiolipin antibodies
- Anti-beta-2 glycoprotein I antibodies
189
Antiphospholipid syndrome
Management
Primary, secondary and pregnancy
Primary thromboprophylaxis:
- Low-dose aspirin
Secondary thromboprophylaxis:
- Initial VTE or arterial thrombosis -> lifelong warfarin, target INR 2-3
- Recurrent VTE -> lifelong warfarin, target INR 3-4
Pregnancy:
- LMWH plus aspirin to reduce risk of complications
- Warfarin CI in pregnancy
190
Antiphospholipid syndrome
Target INRs
- Initial VTE/arterial thrombosis: 2-3
| - Recurrent VTE: 3-4
191
Haemochromatosis
Pathophysiology
- Autosomal recessive
- Disorder or iron absorption and metabolism
- Mutation in HFE gene (human haemochromatosis protein)
- Located on chromosome 6
192
Haemochromatosis
Epidemiology
- 1 in 10 people in Europe carry mutation
- More common that CF
- Usually presents after age of 40 yrs (iron overload becomes symptomatic)
- Presents later in females due to loss of iron through menstruation
193
Haemochromatosis
Features
Early on:
- Fatigue
- Erectile dysfunction
- Arthralgia (esp. hands)
Others:
- Bronze skin pigmentation
- DM
- Stigmata of chronic liver idisease
- Cardiac failure (2nd to dilated cardiomyopathy)
- Hypogonadism (2nd to cirrhosis and pituitary dysfunction - hypogonadotropic hypogonadism)
- Arthritis, especially of hands
- Hair loss
- Cognitive symptoms (memory and mood disturbances)
- Amenorrhoea
194
Haemochromatosis
Diagnosis
- Serum ferritin level (HIGH - > 500ug/l)
- Transferring saturation (HIGH >55% men, 50% women)
- LOW TIBC
- Genetic testing = gold-standard
- Liver biopsy with Perl's stain
- CT abdo
- MRI - liver deposits of iron, iron deposits in heart
195
Haemochromatosis
Complications
- T1DM
- Cardiomyopathy (iron deposits in heart)
- Hepatocellular carincoma
- Hypothyroidism (iron in thyroid)
- Cirrhosis
- Chondrocalcinosis, pseudogout
- Iron deposits in pituitary and gonads -> endocrine and sexual problems
196
Haemochromatosis
Management
- Venesection (weekly protocol of removing blood to decrease total iron) = first-line
- Monitoring of serum ferritin and transferrin saturation: TS < 50%, SF < 50 ug/l
- Desferrioxamine = second-line
- Avoid alcohol
- Genetic counseling
- Monitor and treat complications
197
Thoracic aortic aneurysm
Pathophysiology
- Dilation of the thoracic aorta
- Most commonly affected area = ascending aorta
- Diameter is normally < 4.5 cm for ascending and 3.5 cm for descending
- First symptoms may be when it ruptures (extremely high mortality)
198
Thoracic aortic aneurysm
Features
- Chest or back pain
- Trachea or left bronchus compression may cause cough, shortness of breath and stridor
- Phrenic nerve compression may cause hiccups
- Oesophageal compression may cause dysphagia (difficulty swallowing food)
- Recurrent laryngeal nerve compression may cause a hoarse voice
- May result in aortic regurgitation
199
Thoracic aortic aneurysm
Diagnosis
- Echocardiogram
| - CT or MRI angiogram
200
Thoracic aortic aneurysm
Management
- Reduce modifiable RFs
- Surveillance to monitor size
- TEVAR (thoracic endovascular aortic repair) - catheter via femoral artery to insert stent graft
- Open surgery (remove damaged aorta and replace with synthetic graft)
201
Thoracic aortic aneurysm
Complications
- Aortic dissection
- Rupture aneurysm
- Aortic regurgitation (if aortic valve is affected)
202
Thoracic aortic aneurysm
Rupture features
- Severe chest pain or back pain
- Haemodynamic instability (hypotension and tachycardia)
- Collapse
- Death (often patients do not reach hospital)
May be bleeding into:
- Oesophagus, causing haematemesis (vomiting blood)
- Airways or lungs, causing haemoptysis (coughing up blood)
- Pericardial cavity, causing cardiac tamponade (compression of the heart)
203
Thoracic aortic aneurysm
Rupture management
Emergency open surgery
| Often patients do not reach hospital
204
Peripheral arterial disease (PAD)
Pathophysiology
- Narrowing of the arteries supplying the limbs and peripheries
- Reducing the blood flow to these areas
- Usually refers to lower limbs, resulting in symptoms of CLAUDICATION
205
Peripheral arterial disease (PAD)
Umbrella term for what
- Intermittent claudication
- Critical limb ischaemia
- Acute limb-threatening ischaemia
206
Intermittent claudication
What is it
- The symptom of ischaemia in a limb
207
Intermittent claudication
Features
- Occurs during exertion
- Relieved by rest (within minutes)
- Crampy, achey pain in the calf, thigh or buttock
- Muscle fatigue when walking beyond a certain intensity (usually a predictable distance)
208
All peripheral arterial disease (PAD)
Assessment
- Check femoral, popliteal tibialis and dorsalis pedis pulses
- ABPI
- Duplex USS = First-line
- MRA (MR angiography) or CTA prior to any intervention
- Check for aterial/venous ulcers
209
ABPI interpretation
ABPI = Ratio of systolic BP in ankle compared to arm
Taken manually using doppler probe
E.g. Ankle SBP of 80, arm SBP of 100 = 0.8 ratio
0.9 - 1.3 = Normal
0.6 - 09 = Claudication (mild PAD)
0.3 - 0.6 = Rest pain (mod-sev PAD)
< 0.3 = Impending (critical ischaemia)
> 1.3 can indicate calcification of the arteries (DM)
210
Critical limb ischaemia
Features
- Typically a burning pain
- Worse at night when leg is raised, patients often hang legs out of bed to relieve pain
- 1 or more of:
- Rest pain in foot >2 weeks
- Ulceration
- Gangrene
211
Acute limb-threatening ischaemia
Features
6 P's
- Pain
- Pallor
- Pulseless
- Paralysis
- Paraesthesia
- Perishingly cold
212
Intermittent claudication
Management
- Lifestyle changes
- Exercise training
Medicine:
- Atorvastatin
- Clopidogrel
- Naftidofurly oxalate (peripheral vasodilator)
Surgery:
- Endovascular angioplasty and stenting
- Endarterectomy - cut open and remove atheromatous plaque
- Bypass surgery
213
Critical limb ischaemia
Management
Urgent referral to vascular team
Surgery:
- Endovascular angioplasty and stenting
- Endarterectomy - cut open and remove atheromatous plaque
- Bypass surgery
- Amputation if not possible to restore blood supply
214
Acute limb-threatening ischaemia
Management
REVASCULARISE WITHIN 4-6 HRS
- Endovascular thrombolysis
- Endovascular thrombectomy
- Surgical thrombectomy
- Endarterectomy - cut open and remove atheromatous plaque
- Bypass surgery
- Amputation if not possible to restore blood supply
215
PAD
Factors suggestive of thrombus
- Pre-existing claudication with sudden deterioration
- No obvious source for emboli
- Reduced or absent pulses in contralateral limb
- Evidence of widespread vascular disease (e.g. MI, stroke, TIA, previous vascular surgery)
216
PAD
Factors suggestive of emboli
- Sudden onset leg pain (< 24 hrs)
- No Hx of claudication
- Clinically obvious source of embolus (e.g. AF, recent MI)
- No evidence of PAD (normal pulses in contralateral limb)
- Evidence of proximal aneurysm (e.g. abdominal or popliteal)
217
PAD
Buergers test
Part 1
- Lying on back
- Lift leg to 45 degrees at hip and hold for 1-2 mins
- Pallor would indicate inadequate arterial supply
- Buergers angle refers to angle in which the legs go pale
Part 2
- Sit patient up and hang legs off bed
- Blood will flow back into legs
- In health patient -> legs will remain pink
- In PAD they will go:
- BLUE initially as ichaemic tissue deoxygenates the blood
- DARK RED (RUBOR) after short time due to vasodilation in response to waste products of anaerobic respiration
218
Acute pericarditis
Causes
- Viral infections (Coxsackie)
- Tuberculosis
- Uraemia
- Trauma
- Post-MI
- Dressler's syndrome
- Connective tissue disease (SLE, RA)
- Hypothyroidism
- Malignancy
219
Acute pericarditis
Features
- Sudden onset of SHARP pain
- Worse on inspiration and lying flat
- relief when leaning forwards (differentiate from MI)
- Radiates to arm and trapezius ridge
- Dyspnoea
- Fever
- Irritation of phrenic nerve (cough, hiccups)
- Cardiac tamponade
220
Acute pericarditis
Investigations
ECG:
- Saddle-shaped ST elevation
- Global/widespread changes (differentiate from MI)
- PR depression = most specific marker!!
Trans-thoracic echo
- For ALL patients with suspected acute pericarditis
221
Acute pericarditis
Management
- Treat underlying cause
- NSAIDs and COLCHICINE
- Steroids if not improving
222
Constrictive pericarditis
Causes
- Any causes of acute pericarditis
| - Especially TB
223
Constrictive pericarditis
Features
- Dyspnoea
- RHF - raised JVP, ascites, oedema, hepatomegaly
- JVP shows x and y descent
- Pericardial knock (Loud S3)
- Kussmaul's sign = positive
224
What is Kussmaul's sign
Increased jugular venous pressure with inspiration
225
Constrictive pericarditis
Pathophysiology
The heart is encased in rigid fibrotic pericardium -> prevents diastolic filling of ventricles
226
Constrictive pericarditis
Investigations
CXR: pericardial calcification
227
Constrictive pericarditis
Management
Surgical excision of the pericardium
228
Constrictive pericarditis vs Cardiac tamponade
JVP:
- CT - absent Y descent
- CP - X+Y descent present
TAMponade = TAMpaX
Pulsus paradoxus:
- CT - present
- CP - absent
Kussmaul's sign
- CT - rare
- CP - present
Characteristic features
- CP - pericardial calcification on CXR
229
Cardiac tamponade
Pathophysiology
Accumulation of pericardial fluid under pressure
230
Cardiac tamponade
Features
BECK'S TRIAD
- Hypotension
- Raised JVP
- Muffled heart sound
Others:
- Dyspnoea
- Tachycardia
- Absent Y descent on JVP
- Pulsus paradoxus - large drop in BP during inspiration
231
Cardiac tamponade
Investigations
- ECG: electrical alternans
| = Alternating QRS amplitude in any or all leads
232
Cardiac tamponade
Management
Urgent pericardiocentesis
233
Dilated cardiomyopathy
Pathophysiology
- Most common type of cardiomyopathy
- Dilated heart primarily causes systolic dysfunctions
- All four chambers are dilated but left ventricle more than right ventricle
- Deterioration of the heart muscle (myocardium) to contract
- Electrical and mechanical functions are affected
- Arrhythmia risk
- Eccentric hypertrophy
- Can be genetic --> Autosomal dominant
234
Dilated cardiomyopathy
Causes
- Idiopathic = most common
- Myocarditis - Coxsackie B, HIV, dipththeria, Chagas disease
- IHD
- Peripartum (pregnancy)
- HTN
- Iatrogenic, e.g. doxorubicin
- Substance abuse - alcohol, cocaine
- Inherited - autosomal dominant, or Duchenne muscular dystrophy
- Infiltrative (haemochromatosis, sarcoidosis)
235
Dilated cardiomyopathy
Features
- HF findings
- Systolic murmur - stretching of valves may result in mitral and tricuspid regurgitation
- S3
236
Dilated cardiomyopathy
Investigations
- CXR: balloon heart
- ECHO
- ECG: T wave flattening, poor R wave progression, tachycardia
- BNP
- Low sodium - poor prognostic factor
237
Dilated cardiomyopathy
Management
- Bed rest
- HF meds: ACE-I, Beta-blockers, diuretics, digoxin
- Bi-ventricular pacing
- ICD
- Heart transplant
238
Hypertrophic obstructive cardiomyopathy (HOCM)
Pathophysiology
- Most common = mutation in beta-myosin heavy chain protein or myosin-binding protein C
- Results primarily in diastolic dysfunction (LVH -> decreased compliance -> decreased CO)
- Characterised by myofibrillar hypertrophy with chaotic and disorganised fashion myocytes (disarray) and fibrosis on biopsy
239
Hypertrophic obstructive cardiomyopathy (HOCM)
Features
- Often asymptomatic
- Exertional dyspnoea
- Angina
- Syncope (usually exertional)
- Sudden death (due to ventricular arrhythmias)
- Jerky pulse
240
Hypertrophic obstructive cardiomyopathy (HOCM)
Associations
- Wolff-Parkinson-White syndrome
| - Friedrich's ataxia
241
Hypertrophic obstructive cardiomyopathy (HOCM)
Examination findings
- Jerky pulse
- Large 'a' waves
- Double apex beat
- Ejection systolic murmur
242
Hypertrophic obstructive cardiomyopathy (HOCM)
Investigations
ECHO - MR SAM ASH
- MR = mitral regurgitation
- SAM = systolic anterior motion of anterior mitral valve
- ASH = asymmetric hypertrophy
ECG
- LVH
- Non-specific ST and T wave abnormalities
- Progressive T wave inversion
- Deep Q waves
- AF occasionally
243
Hypertrophic obstructive cardiomyopathy (HOCM)
Management
ABCDE
- A: Amiodarone
- B: Beta-blocker or verapamil
- C: Cadioverter defibrillator
- D: Dual chamber pacemaker
- E: Endocarditis prophylaxis (maybe?)
AVOID:
- Nitrates
- ACE-Is
- Inotropes
244
Causes of AF?
* *SMITH**
- **S:** Sepsis
- **M**: Mitral valve pathology (stenosis)
- **I:** Ischaemic heart disease
- **T:** Thyrotoxicosis
- **H:** Hypertension
