cardiovascular Flashcards
define arterial ulcer
- localised area of damage and breakdown of skin
- due to inadequate arterial blood supply
- typically feet of patients with sever atheromatous narrowing of arteries supplying leg
aetiology of arterial ulcers
- caused by lack of blood flow to capillary beds of lower extremities
- prevalence increases with age and obesity
risk factors:
- coronary heart disease
- Hx of stroke/TIA
- DM
- peripheral arterial disease
- immobility
symptoms + signs of of arterial ulcers
- punched out appearance with clearly defined edges
- eliptical shape
- mainly on foot dorsum/toes
- grey granulomatous tissue
- ischaemic signs: hairlessness, pale skin, absent pulses, nail dystrophy, calf muscle wasting
- night pain
- pain is worse in supine because arterial blood flow is further reduced
investigations for arterial ulcers
1. doppler US of lower limbs
- assess latency of arteries
- assess potential for revascularisation/bypass surgery
- ABPI - <0.9= PAD, <0.5- critical limb ischaemia
- percutaneous angiography
- ECG
- fasting serum lipids
- fasting blood glucose + HbA1c
- FBC (anaemia can worsen ischaemia)
management of arterial ulcer
Immediate:
- pain relief
surgery
- angioplasty (balloon => widen arteries in atherosclerosis)
- stenting
- bypass grafts
- amputate
define cardiac arrest
acute cessation of cardiac function
aetiology and risk factors of cardiac arrest
reversible:
- hypothermia
- hypoxia
- hypovolaemia
- hypo/hyperkalaemia
- toxins
- thromboembolic
- tamponade
- tension PTX
presenting symptoms of cardiac arrest
sudden; management precede/concurrent to Hx
preceding symptoms:
- fatigue
- fainting
- blackouts
- dizziness
physical examination findings of cardiac arrest
unconscious
absent breathing
absent carotid pulses
investigations for cardiac arrest case
cardiac monitor
- classification of rhythm
bloods:
- FBC
- ABG
- U&E
- cross match
- clotting screen
- toxicology screen
- blood glucose
management of cardiac arrest
approach arrest scene with caution
* cause of arrest may pose threat
BLS
- if arrest is witnessed, consider precordial thump
- clear and maintain airway
- assess breathing, if absent, 2 rescue breaths
- assess carotid pulse for 10 seconds, if absent, 30 chest compressions
advanced life support
advanced life support management of cardiac arrest with shockable rhythm
cardiac monitor + defibrillator
assess rhythm
shockable rhythms: pulseless VT/VF
- defibrillates once (150-360J biphasic, 360J monophasic)
- resume CPR for 2 mins
- reassess and shock again if no change
- 1mg IV adrenaline after 2nd defibrillation
- 1mg IV adrenaline every 3-5 mins
*persistant shockable rhythm after 3rd shock
- 300mg IV bolus amiodarone
advanced life support management of cardiac arrest with asystole/PEA
cardiac monitor + defibrillator
assess rhythm
pulseless electrical activity (PEA)/asystole:
- CPR for 2 mins
- reassess
- 1mg IV adrenaline every 3-5 mins
*asystole or PEA + <60bpm, 3mg IV atropine once only
during CPR for cardiac arrest
check electrodes, paddle positions, and contacts
secure airway
consider magnesium, bicarbonate, and external pacing
stop CPR and check pulse ONLY IF change in rhythm or signs of life
treatment of reversible causes of cardiac arrest
hypothermia
- warm slowly
hypovolaemia
- IV colloids
- IV crystalloids
- blood products
hypo/hyperkalaemia
- give insulin (+dextrose) increase K+uptake
toxins
- toxin antidote
thromboembolic
- treat as PE/MI
tamponade
- pericardiocentesis
tension PTX
- aspiration/chest drain
complications of cardiac arrest
irreversible hypoxic brain damage
death
prognosis of cardiac arrest
resus less successful if cardiac arrest occurs outside hospital
increased duration of inadequate effective CO = poor prognosis
define DVT
thrombus formation within deep veins of usually calf or thigh
deep veins in leg more prone due to blood stasis (Virchow’s triad)
DVT risk factors
- polycythaemia
- thrombophilia
- OCP
- post surgery
- prolonged immobility/ long flights
- obesity
- pregnancy
- dehydration
- smoking
- malignancy
presenting symptoms of DVT
- asymmetrical swollen leg
- may be painless
examination findings of DVT
- local erythema, warmth, and swelling
- varicosities (dilated superficial veins)
- skin colour changes
- +/- unilateral leg pain
- Homan’s sign
what is Homan’s sign
seen in patients with DVT
forced passive dorsiflexion of ankle causes deep calf pain
how to stratify risk of PE in case of DVT
stratified using Well’s PE criteria
2 or more = high risk
- history: breathlessness, cough, haemoptysis
- check RR, pulse oximetry, and pulse rate
investigations for DVT
Use Wells score for DVT (<2 = low risk)
doppler US - gold standard
bloods:
- *- D dimer** (if low = unlikely to be DVT)
- thrombophilia screen if indicated
impedance plethysmography
- changes in blood volume causes changes in electrical resistance
if suspected PE:
- ECG
- CXR
- ABG
management plan for DVT
confirmed DVT + not pregnant
- 3 months anticoagulation (DOACs- apixaban/ rivaroxiban) -LMWH as alternative
- physical activity
- compression stockings
Confirmed DVT + preganant
- LMWH- anticoagulation
- physical activity
- compression stockings
*recurrent DVT = long term warfarin
if anticoagulation contraindicated (bleeding, haemorrhage, major trauma, aortic dissection) => IVC filter
* DVTs that DO extend above knee => anticoagulation for 6 months
prevention of DVT
graduated compression stockings
mobilisation
prophylactic heparin if high risk
possible complications of DVT
- PE
- venous infarction (death of tissue due to poor perfusion)
- thrombophlebitis- inflammed vein due to clot (from recurrent DVTs)
- chronic venous insufficiency
prognosis of DVT
depends on extent of DVT
below knee = good
proximal DVT = greater risk of embolisation
define vasovagal syncope
loss of consciousness from transient drop in blood flow to brain caused by excessive vagal discharge
aetiology/risk factors of vasovagal syncope
common cause of fainting
precipitated by
- emotions
- orthostatic stress
presenting symptoms of vasovagal syncope
short loss of consciousness
vagal symptoms
- sweating
- dizziness
- light headedness
before episode
twitching during episode
quick recovery
signs on physical examination of vasovagal syncope
usually no signs
investigations for vasovagal syncope
checking for causes
ECG - arrhythmias
echocardiogram - outflow obstruction
lying/standing BP - orthostatic hypotension
fasting blood glucose - DM/hypoglycaemia
define venous ulcers
- large, shallow, sometimes painful
- usually superior to medial malleoli
- caused by incompetent valves in lower limbs - leads to venous stasis and ulceration
aetiology and risk factors of venous ulcers
caused by incompetent valves in lower limbs
- leads to venous stasis and ulceration
risk factors:
- obesity
- immobility
- recurrent DVT
- varicose veins
- previous injury/surgery to leg
- age
presenting symptoms + signs of venous ulcers
- large, shallow, sometimes painful ulcers
- irregular margin
- swelling, itching, aching
- in gaiter region (superior to medial malleoli => mid calf)
associated signs of venous insuffiency with venous ulcers
- stasis eczema
- lipodermatosclerosis (champagne bottle)
- haemosiderin deposition (dark colour)
- atrophie blanche (blood deposits)
investigations for venous ulcers
- ABPI (excuse arterial ulcer) - if ABPI <0.8, DO NOT apply pressure bandage
- Duplex USS of lower legs (GOLD-STANDARD)
- measure surface area of ulcer for monitoring of progression
- microbiology swab samples
- biopsy if suspected Marjolin’s ulcer
management of venous ulcers
- graduated compression to reduce venous stasis- must exclude DM, neuropathy, and PVD before attempt
- debridement and cleaning
- Abx if infected
- topical steroids to treat surrounding dermatitis
complications and prognosis of venous ulcers
- recurrence
- infection
good prognosis
- better results if mobile with few comorbidities
Define Ischaemic heart disease
Ischaemic heart disease is when myocardial demand exceeds oxygen supply resulting in chest pain (angina pectoris)
=> present as stable angina or ACS
Causes of IHD ( A VASE)
when myocardial demand exceeds oxygen supply
usually due to:
- Atherosclerosis
- Vasculitis
- Arteritis
- coronary artery Spasm (cocaine)
- Embolism
Risk factors of IHD
- male
- Diabetes mellitus
- FHx
- Hypertension
- Hyperlipidaemia
- Smoking
- older age
- Obesity
- sedentary lifestyle
- cocaine
Pathophysiology of atherosclerosis
- endothelial damage causes monocytes/ LDLs to migrate into subendothelial space
- free LDLs bind to matrix proteoglycans
- monocytes differentiate => macrophages release free radicals that oxidise LDLs.
- macrophages engulf oxidised LDLs => foam cells
- foam cells release growth factors + cytokines => smooth muscle proliferation, collagen production, proteoglycan production
- forms atherosclerotic plaque
presenting symptoms of Stable angina
- chest pain on exertion and relieved by rest
Examination findings of stable angina
- mainly check for risk factors
Investigations for IHD (ACS)
Bloods:
- FBC
- U&Es, TFTs
- CRP
- glucose
- lipid profile
- amylase (exclude pancreatitis)
- AST/ LDH (1-2 days post)
- cardiac enzymes (troponins + Creatine Kinase-MB)
- ECG (+ exercise ECG)
- radionuclide scan
- CT
- MRI
- Coronary angiography
- CXR - check for HF signs (cardiomegaly, pulmonary oedema, widened mediastinum)
Prognosis of IHD
- TIMI score (0-7 thrombolysis in MI)- high scores = high risk of cardiac events within 30 days of MI
define Acute coronary syndromes
type of IHD (atherosclerosis causing partial/total occlusion of coronary arteries)
- unstable angina (RARE)
- NSTEMI
- STEMI
Pathophysiology of ACS
- unstable angina- unstable coronary plaque, disrupts fibrous cap => forms incomplete thrombus
- NSTEMI- incomplete thrombus forms => partial artery occlusion
- STEMI- coronary plaque ruptures => complete thrombus formation => complete artery occlusion, transmural infarction
presenting symptoms of ACS
- acute-onset chest pain lasting >20mins
- central, heavy, tight crushing chest pain
- pain radiates to arm, neck, jaw, epigastrium
Associated symptoms:
- breathlessness
- sweating
- palpitations
- nausea
- vomiting
Symptoms of silent infarcts in elderly/ diabetics
- no chest pain
- syncope
- pulmonary oedema
- epigastric pain
- vomiting
Examination findings of ACS
- may not be signs
- pale, sweaty, restless, fever
- high/low bp
- arrhythmias
- new heart murmurs
- signs of heart failure (raised JVP, S3, basal crepitations)
*rule out aortic dissection (check radial pulses)
Investigations for ACS
- bloods (FBC, U&Es, AST/LDH, lipid profile, glucose, amylase (exclude pancreatitis), CARDIAC ENZYMES (raised troponin/ myoglobin/ CK-MB)
*troponin not raised in unstable angina
- ECG
- radionuclide scans
- CT coronary angiography
- MRI
Investigations for stable angina
- bloods (FBC, lipid profile, AST/LDH, cardiac enzymes: troponin, myoglobin, CK-MB, BNP)
- ECG (usually normal)
- CT coronary angiography (check for arterial stenosis)
- exercise tolerance test
ECG findings for
- Unstable angina/ NSTEMI
- STEMI
- ST depression/ T wave inversion
- ST elevation, hyperacute T waves -tall (later T wave inversion), new-onset LBBB
Management for stable angina
- reduce cardiac risk factors (lower bp/cholesterol, diabetes, stop smoking, exercise)
Immediate
- 75mg/day aspirin
- symptom relief: GTN spray
Long term
- beta blockers (not for acute heart failure, cardiogenic shock, bradycardia, heart block, asthma)
- CCBs
- nitrates
Surgical:
- PCI (if medication doesn’t work)
- CABG
Mangement for unstable angina/ NSTEMI (MONABASH)
- Morphine (give metoclopramide for nausea)
- Oxygen (only if sats >95%)
- Nitrates (GTN)
- Antiplatelets (Aspirin, Clopidogrel)
- Beta-blockers
- ACE-inhibitors
- Statins
- Heparin
Surgery (no improvement) => angioplasty +/- revascularisation (PCI/ CABG)
Management for STEMI
- antiplatelet (ASPIRIN 300mg) + anticoagulants (heparin)
- primary PCI or thrombolysis
- Long term (beta-blockers, ACE-inhibitors, statins, antiplatelets (aspirin + clopidogrel), lifestyle changes, cardiac rehabilitation)
Complications of MI (DARTH VADER)
- death
- arrhythmias
- rupture (septum/outer walls)
- tamponade
- heart failure
- valve disease
- aneurysm
- Dressler’s syndrome (autoimmune pericarditis)
- Embolism
- Reinfarction
Pathophysiology of peripheral vascular disease
caused by atherosclerosis => stenosis of arteries => poor perfusion to limbs => ischaemia => pain
- chronic limb ischaemia (intermittent claudication / critical limb ischaemia)
- acute limb ischaemia
Risk factors for peripheral vascular disease
- hypertension
- smoker
- FHx of CVD
- diabetics
- elderly
- hyperlipidemia
- sedentary lifestyle
Presenting symptoms of intermittent claudication
- intermittent claudication (leg pain after exercise + relived on rest immediately
- Calf claudication = femoral disease
- Buttock claudication = iliac disease
- erectile dysfunction
- poor/ slow wound healing
- gangrene
- presecence of risk factors
- reduced/ absent pulses
Presenting symptoms of critical limb ischaemia
- gangrene
- ulcers
- pain at rest
- night pain (relieved by dangling legs off the bed)
Investigations for peripheral vascular disease
Bedside:
- ECG
- ABPI (ankle brachial pressure index SBP of ankle/brachial)- <0.9 = abnormal, <0.5 = critical limb ischaemia
Bloods
- FBC
- U&E (check for renal disease)
- fasting glucose (check in diabetics)
- lipid levels
- D-dimer (fibrin degradation product)
- thrombophillia screen
- troponins
- CRP/ESR (raised indicates thrombophlebitis)
Imaging
- Colour duplex ultrasound of pulses (check stenosis)
- CT angiography/CTA(detetct location + stenosis)- need contrast
- Magnetic resonance angiogaphy/MRA (detect stenosis)
- Trancutaneous pressure of oxygen (perfusion to foot)
Why do diabetics/renal failure have a raised ABPI normally?
calcification of arteries result in high ankle pressures due to incompressible arteries
Management of peripheral arterial disease (intermittent claudication)
non-lifestyle limiting claudication
- anti-platelets (aspirin, clopidogrel)
- exercise
- reduce risk factors (low fat/cholesterol diet, exercise, stop smoking/alcohol, optimise diabetes)
lifestyle limiting claudication
- anti-platelets
- exercise (supervised exercise therapy)
- symptom relief VASOACTIVE drugs (naftidrofuril)- reduces pain on walking
- adjunct revascularisation (PTA - percutaneous transluminal balloon angioplasty or BYPASS)
- amputation
Define ischaemic limb
- Can be acute or acute and chronic
- thrombotic (absent/diminished pulses Hx of intermittent claudication)
- embolic (suddent/more severe- no established collaterals)
Presenting symptoms of acute limb ischaemia (6Ps)
- pale
- pulselessness
- perishingly cold
- pain
- paralysis
- parasthesia
Other
- hair loss
- skin atrophy
- punched out ulcers
- leg colour change when raised to buerge’s angle
Management of acute limb ischaemia
Immediate
- analgesia
- anticoagulants (heparin)
Surgery
- Revascularisation (within 4hrs)- endovascular revascularisation/ fasciotomy
- Amputation
Define abdominal aortic aneurysm (AAA)
abnormal dilation of aorta (>50% normal size) across all layers of aorta wall
Screening progroamme for <65 males
- >3mm => surveillance
- >5.5mm => repair
risk factors for AAA
- modifiable (smoking, hypertension, dyslipidemia)
- non-modifiable (MALE, older, Family Hx)
- connective tissue disorders (Marfan’s, Ehlers Danos)
- Inflammatory disorders (Behcet’s disease-vessel inflammation)
Different types of aneurysms
- true aneurysm= dilation across all layers of aorta wall
- false/pseudoaneurysm = dilation only across part of aorta wall (adventitia)
- location = aortic, iliac, popliteal
- morphology = saccular / fusiform
- aetiology = athelosclerosis, inflammatory, inherited, mycotic (infection by fungi/bacteria)
- Presenting symptoms of AAA
- Presenting symptoms of ruptured AAA
unruptured
- usually asymptomatic
- abdominal/groin/back pain (pressure related)
ruptured:
- abdominal pain => radiates to back
- syncope/ light headed (reduced cerebral perfusion)
- cold, sweaty, nausea - activation of sympathetic response
- pallor
- Pressure (back pain)
- Rupture (high mortality rate)
- Thrombosis (acute limb ischaemia)
- Embolisation (ischaemic symptoms)
Examination signs of AAA
- pulsatile, expansile pulse in abdominal aorta palpation
- shock signs (tachycardia, low bp) in RUPTURED AAA
- +/- aortic bruits
- pallor
- abdominal distension