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Cardiology > Abdominal Aortic Aneurysm > Flashcards

Abdominal Aortic Aneurysm Flashcards

1
Q

How does AAA commonly present?

A
  • Severe abdominal and back pain
  • Tachycardia
  • Hypotension
  • Cold, clammy hands and feet
  • Slow capillary refil
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2
Q

What are some common differentials for AAA?

A
  • Perforated viscus: e.g perforated gastric/duodenal ulcer
  • Acute pancreatitis
  • Biliary colic or acute cholangitis
  • Acute mesenteric occlusion (possibly due to an embolus)
  • Ruptured or leaking abdominal aortic aneurysm.

The above are some of the conditions that need to be considered.

Rarely, diseases that originate above the diaphragm: basal pneumonia or an inferior MI also may also present with abdominal pain……so have a very high index of suspicion

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3
Q

How do we investigate a suspected AAA?

A
  • History
  • Examination - tender pulsatile mass in abdomen
  • obs: tachycardic and hypotensive
  • Examine pulse in all limbs - often popliteal is also aneurysmal
  • URGENT USS
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4
Q

What are some important facts surrounding AAAs?

A
  • Ruptured AAA causes generalised shock state and bilateral leg ischaemia. If patient presents with shock and one leg ischaemia, think of dissection or significant peripheral vascular disease (PVD)
  • Always suspect ruptured AAA in men older than 60 years with first presentation of renal colic
  • In patients with GI bleeding and past history of aortic surgery, suspect aorto-enteric fistula until proven otherwise
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5
Q

How do we tell if something is pulsatile vs transmitted?

A
  • If pulsatile, hands will move upwards and outwards

- If transmitted hands will only move upwards

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6
Q

Which artery is frequently ligated during AAA repair?

A

Inferior mesenteric artery

- Can be a source of ‘endoleak’ after EVAR

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7
Q

What are the branches of the coeliac trunk?

A
  • Left gastric artery
  • Splenic artery
  • Common hepatic artery
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8
Q

What are the three different clamping levels used on an AAA?

A

Supra-coeliac clamping:

  • Highest stress on heart
  • Ischaemia to all organs below coeliac artery with subsequent reperfusion injury

Supra-renal clamp:

  • High stress on heart
  • Ischaemic to all organs below the superior mesenteric artery with subsequent reperfusion injury

Infra-renal clamp:

  • Relatively less stress on heart
  • Ischaemia to all organs below kidneys with subsequent reperfusion injury
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9
Q

How do we manage massive haemorrhage in adults?

A
  • Recognise blood loss
  • ABCDE
  • Resuscitate, call for help
  • Stop the bleeding - TXA, PCC
  • Team approach
  • Emergency runner
  • Communicate with lab early and cleary
  • Know where the emergency O- id in your trust
  • Massive haemorrhage packs 1 & 2
  • Monitor coagulation tests and move to goal directed therapy
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10
Q

How do we recognise blood loss?

A
  • Life threatening haemorrhange
  • Patient bleeding/collapses, ongoing bleeding 150mls/min and clinical shock
  • Bleeding rate difficult to assess
  • Blood loss may be hidden
  • Risk of over activation
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11
Q

What measures can be taken to stop bleeding?

A
  • Local measures: pressure, tourniquets
  • Early intervention - damage limitation
  • Reverse anticoagulants eg PCC
  • Tranexamic acid
  • Bloods: FBC, U&Es, LFTs, Ca2+, PT, APTT, fibrinogen, crossmatch, group and save
  • Emergency runner to take sample to lab and collect blood
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12
Q

What should be communicated when a patient has a major bleed?

A
  • State major haemorrhage adult/child/location
  • Request components needed:
  • Red cells
  • FFP
  • Platelets
  • Decide on use of emergency O- uncrossmatched blood, or group specific blood
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13
Q

What are the different options of blood for transfusion?

A

Extreme emergency: Group O RhD neg

~15 mins from sample arriving in lab: group specific, ABO and RhD compatible
- Important antibodies may cause reaction

Safest product if time allows: crossmatched, fully screened for antibodies
~45-60 minutes from sample arriving in lab

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14
Q

What is found in major haemorrhage packs?

A

Pack 1:

  • 4 units red cells
  • 4 units fresh frozen plasma (FFP)

Pack 2:

  • 4 units red cells
  • 4 units FFP
  • 1 dose platelets
  • 2 packs cryoprecipitate
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15
Q

What clotting and blood results should be aimed for in the MH pathway?

A

Fibrinogen >1.5g/L
PT ratio <1.5
APTT ratio <1.5

Hb 80-100g/L
Plts >75 x10^9/L

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16
Q

What should you consider when you stand down during a MH pathway?

A
  • Let the lab know when the haemorrhage is under control
  • Consider patient’s risk of thrombosis and requirement of thromboprophylaxis
  • Record which blood components are given for traceability
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17
Q

What should be examined during a vascular examination?

A
  • Signs of wellness
  • Build
  • Pulse and regularity
  • BP both sides
  • JVP
  • Heart sounds
  • Presence of AAA
  • Warmth and perfusion peripherally
  • Oedema
  • Skin changes
  • Tissue loss
  • Varicose veins
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18
Q

What is peripheral vascular disease?

A
  • Inevitable, degenerative, generalised
  • Consequence of atherosclerosis

Symptoms depend on:

  • Vascular bed affected
  • Rate of development
  • Extent

Risk factors:

  • Increasing age, male sex, family history
  • Smoking, hypertension, cholesterol, diabetes
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19
Q

How does acute ischaemia of tissues present?

A 
PPPPPP
Pale
Perishingly cold
Pulseless
Painful
(at this point reversible)
Paraesthetic
- Muscle tenderness
(threatened)
Paralysed
- Numb
- Mottled
(non-viable)

Causes:

  • Atherosclerosis + thrombosis
  • Embolus (cardiac, aneurysm)
  • Thrombosis (thrombophilia, graft occlusion, aneurysm)
  • Dissection
  • Trauma

NOT SWOLLEN HOT OR TENDER

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20
Q

How do we determine the prognosis when faced with tissue ischaemia?

A
  • Rate of development of ischaemia
  • Collateralisation
  • Acclimatisation of tissues
  • Presentation window
  • Level of occlusion
  • Cause
  • Delay in presentation
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21
Q

How do we grade chronic ischaemia?

A

Fontaine I - asymptomatic
Fontaine II - claudication
Fontaine III - rest pain
Fontaine IV - tissue loss

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22
Q

What symptoms are seen in peripheral vascular disease?

A

Claudication

  • Aching muscles on effort
  • Predictable
  • Worse on hills, with loads, at speed
  • Settles swiftly at rest

Rest pain

  • Icy, burning, constant aching pain in foot
  • Worse on elevation or at night
  • Needs opiates

Tissue Loss
- Ulcers, necrosis, gangrene

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23
Q

How do we manage peripheral vascular disease?

A
  • Stop smoking
  • Antiplatelet therapy (aspirin 75mg od)
  • Blood pressure control (sBP <140)
  • Cholesterol reduction <5 or 25%
  • Regular exercise
  • Weight loss
  • Diabetes HbA1c <7
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24
Q

What is the prognosis of peripheral vascular disease?

A

Prognosis

  • Generally improves over 6-12months
  • Collaterals, lifestyle adaption, muscle metabolism

Lifetime amputation risk ~1%
MI in next 5 years ~30%

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25
Q

How do we investigate cerebrovascular disease?

A

Duplex:

  • Cheap, easy, available, no XR
  • Morphology

Angiography

  • Low flow states, calcification
  • Intracranial/proximal disease

MR, CT yet to be proven
- Brain substance imaging

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26
Q

What are the indications for surgical treatment of cerebrovascular disease?

A
  • Symptomatic patients (in last 6 months)
  • > 70% stenosis ICA
  • 2 year life expectancy
  • Fit for surgery
    NNT = 12
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27
Q

How do we treat asymptomatic cerebrovascular disease?

A
  • Medical therapy
  • Operation in selected circumstance
  • No real evidence for benefit overall
  • NNT = 50, stroke risk 2%pa to 1%pa
  • Younger patients
  • CABG aortic surgery
  • Cerebral perfusion concerns
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28
Q

What is an aneurysm?

A
  • Abnormal dilation of an artery
  • Greater than 50% of its transverse diameter
  • Ectasia = dilation of up to 50%
  • Ateriormegaly = generalised dilation

Aneurysm = atherosclerotic infrarenal abdominal aortic aneurysm (AAA)

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29
Q

What is the aetiology of an aneurysm?

A
  • Atherosclerotic
  • Mycotic
  • Inflammatory
  • Connective tissue disorder
  • False
30
Q

What are some complications of aneurysms?

A
  • Can be simple
  • Ureteric compression
  • AV fistula
  • Aortoenteric fistula
  • Rupture
  • Thrombosis/embolism
31
Q

In which arteries do aneurysms occur?

A
  • Aortic
  • Iliac (branches of aorta!)
  • Visceral
  • Intracerebral
32
Q

What are the symptoms of aneurysms?

A
  • Asymptomatic!!
  • Back pain
  • Tenderness
  • Limb ischaemia
33
Q

What are the shapes of aneurysms?

A
  • Fusiform

- Saccular

34
Q

What is the relevance of the size of an aneurysm?

A

Threshold of surgery

35
Q

What is the normal diameter of the aorta?

A

2.5cm

36
Q

How do we categorise different sizes of AAA?

A

Normal = 2.5cm
Ectasia < 3.5cm
Small AAA < 4.5cm
Large AAA >5.5cm

37
Q

What interventions are performed on aneurysms?

A

Symptoms: intervene regardless of size
Under 5.5cm: surveillance scan (ultrasound)
Over 5.5cm: intervene on risk balance

Open surgery: replace affected segment with plastic graft, tube or bifurcate

  • GA
  • Major cardiovascular stress from XC
  • Mortality 5% and upwards, usually cardiac

Endovascular surgery: reline aorta

  • Spinal
  • Reduced CV stress
  • Mortality: ~2%
38
Q

What is endovascular repair (EVAR)?

A

Only ~70% of aneurysms suitable (Approx)
- Proximal infrarenal aortic neck
- Iliac arteries
Lifelong followup with CT of duplex

6-8% per annum failure rate
- Endoleak: sac pressurisation
Endovascular reinterventions usually possible

39
Q

What surveillance is performed for aneursyms?

A

Ultrasound

40
Q

When should we suspect an aneurysm rupture

A

Suspect rupture in triad of:

  • Collapse
  • Hypotension
  • Lower back or flank pain
41
Q

What are some other forms of aneurysm?

A

Thoracic aneurysms

  • Stanford classification, Types I-IV
  • NOT THE SAME AS DISSECTION
  • Open repair is extremely hazardous (death, paralysis, organ failure)
  • Endoluminal repair if at all possible

Suprarenal aneurysms

  • Between thoracic and standard AAA for risks
  • Require more dissection and suprarenal/coeliac XC
  • Open repair or fenestrated stents

Popliteal aneurysms

  • Often bilateral, associated with AAA, familial
  • Limb ischaemia rather than rupture
  • Repair by surgery if > 2.5cm or symptoms
  • Stents if unfit
42
Q

What is an aortic dissection?

A

Life-threatening condition:

A separation in the layers of the wall of the aorta

43
Q

What are the three tunica (layers) of the aorta?

A 
Outer = tunica adventitia
Middle = tunica media (thich muscular)
Inner = tunica intima (thin)
44
Q

How do aortic dissections happen?

A
  • Blood flow through the aorta is very strong and high-pressured
  • This creates stress on the innermost tunica (layer) which is thin
  • A tear in the intima
  • Blood gets between intima and media
  • Strong blood flow continues pushing through between the layers
  • Dissection keeps getting bigger and wider
  • Blood can either pool in the layers (false lumen), or create an exit tear through which it leaves back into the lumen

If blood continuously propagates into the tear between layers, less blood reaches tissues, causing symptoms of blood loss (hypotension, shock)

45
Q

What are the causes of aortic dissection?

A
  • Hypertension
  • Connective tissue disease (marfan’s, Ehlers-Danlos)
  • Pre-existing aneurysm
  • Chest trauma
  • Male and age are risk factors
  • Peak 50-65 years
46
Q

How are aortic dissections classified?

A

Stanford system
A = Before left subclavian artery origin
B = After left subclavian artery origin

B is more easily medically managed, A surgically

47
Q

What are the two most common sites of aortic dissection?

A

Right after the aortic valve (type A)
Right after left subclavian origin (type B)

These two sites have the most shear stress on the layers of the aorta
Blood is more turbulent at the start of the aorta

48
Q

What symptoms are seen in aortic dissection?

A
  • Sharp tearing chest pain towards back
  • Sweating
  • Nausea
  • Shortness of breath
  • Weakness
  • Syncope
49
Q

How do we diagnose aortic dissection?

A

GOLD STANDARD:
CT with contrast - full length of aorta, and contrast makes things more clear

TOE - transoesophageal echocardiogram (quick and cheap)
MRA (magnetic resonance angiogram - 100% sensitive and specific

50
Q

How do cardiac output and blood pressure change in a patient who is losing blood?

A
  • Body is able to maintain pressure (at the expense of cardiac output and tissue blood flow) until a large volume of blood has been lost
  • Only when compensatory mechanisms are unable to cope that BP falls

Therefore, any patients (especially young) who have a low blood pressure in the context of acute blood loss, are extremely ill and need urgent medical attention

51
Q

What is shock?

A

An acute clinical syndrome initiated by ineffective perfusion and cellular hypoxia, resulting in severe dysfunction of organs vital to survival

52
Q

What are the key features of shock?

A
  • Acute tissue/organ hypoperfusion
  • Impaired delivery of oxygen to cells
  • Supply inadequate to meet demand
  • Generalised cellular hypoxia
  • Consequences for cellular respiration
  • Haemodynamic abnormalities but shock isn’t simply the presence of hypotension
  • Oxygen utilisation may be abnormal
53
Q

What are the four types of shock?

A
  • Hypovolaemic
  • Cardiogenic
  • Distributive
  • Obstructive
54
Q

How can we classify the different types of shock?

A

Hypovolaemic - reduced intravascular volume
Distributive - vasodilation and malperfusion
Cardiogenic - intrinsic cardiac (pump) failure
Obstructive - failure of circulatory flow

55
Q

What are some examples of each type of shock?

A

Hypovolaemic:
- Haemorrhage
- Burns
GI losses (vomiting, diarrhoea, fistula)
- Dehydration (heat exposure, polyura (DKA))

Distributive:

  • SIRS related - sepsis, pancreatitis, trauma, burns
  • Neurogenic - spinal cord injury
  • Anaphylaxis

Cardiogenic:

  • Myocardial infarction/ischaemic
  • Arrhythmia
  • Acute valve pathology

Obstructive:

  • Tension pneumothorax
  • Peripcardial tamponade
  • Pulmonary embolism
56
Q

What is hypovolaemia?

A
  • Sudden, severe blood loss
  • Reduction in venous return
  • Fall in stroke volume and cardiac output
  • Hypotension
  • Hypoperfusion of organs
  • Onset of organ dysfunction
57
Q

What is the physiological response to hypovolaemia?

A
  • Sympathetic system activated
  • Adrenal catecholamine release
  • Compensatory cardiovascular responses (increase vascular tone)
  • Sodium and water retention
  • Coagulation system activation
  • Cortisol release
  • Increased contractility of the heat
  • Increased heart rate
58
Q

What clinical manifestations are seen in hypovolaemia?

A
  • Haemodynamic changes
  • Narrowing of pule pressure but maintenance of systolic BP initially
  • Effects of circulatory redistribution and signs of organ hypoperfusion:
  • Skin
  • Oligouria
  • Cognitive changes
  • Metabolic acidosis
59
Q

How do we manage hypovolaemia?

A
  • Restore tissue perfusion and oxygen delivery to cells and rapidly as possible
  • ABCDE
  • Administer oxygen
  • Give IV fluids
  • Treat the cause
  • Resuscitation begins concurrently or ahead of diagnostic process
  • Aim to prevent irreversible organ injury and failure
60
Q

What fluids might be given in hypovolaemia?

A

Large bore cannula

  • 1l warmed Hartmann’s stat
  • Colloids
  • Bloods requested
61
Q

What investigations are performed in hypovolaemia shock?

A

Blood tests:

  • Cross matched red cells
  • Haematology (FBC, clotting)
  • Biochemistry (U&Es, glucose, liver, bone, lactate)
  • Arterial blood gases
  • ECG
  • Ultrasound of abdomen (FAST scan)
  • Measure and maintain core temperature
62
Q

What would be the fluid management involved in hypovolaemic shock?

A
  • Consider type of fluid that has been lost
  • Initial therapy with crystalloids or colloids
  • In major blood loss will need blood urgently
  • Fluid administration initially guided by frequent assessment of clinical response (HR, skin, mental state, BP, urine output)
  • Beware hypothermia! (coagulation)
  • Failure to response appropriately - think again
63
Q

What are the differences between crystalloids and colloids, and what are some examples of each?

A

Crystalloids:

  • Normal saline
  • Hartmann’s solution
  • Ringer’s lactate
  • Glucose solutions
  • Electrolytes (solutes) dissolved in water (solvent)
  • Electrolytes and waster distribute into ECF

Colloids:

  • Gelofusine
  • Starch solutions
  • Dextran
  • Blood, plasma, platelets
  • Large molecules suspended in a solution
  • Colloid particles and fluid remain predominantly intravascular
64
Q

What should we consider if a patient does not respond to fluids as expected (in hypovolaemia)?

A
  • Unable to keep up with blood loss?
  • Missing something?
  • Wrong diagnosis?
  • Specific therapy required?
  • MI, sepsis, PE?
  • Continued failure to restore perfusion = bad
  • Indicates increased severity of problem
  • Need for higher level of care
65
Q

What are some important differential diagnoses to consider if a patient has symptoms of hypovolaemia?

A
  • Tension pneumothorax
  • Pericardial tamponade
  • Pulmonary embolism
  • Acute myocardial infarction
  • Identify using ECG and CXR and echo
66
Q

What further management can be used in shock?

A
  • Surgery
  • Fluid management
  • Invasive lines
  • Drugs (inotropes)
  • Monitoring
  • ICU
67
Q

How do we monitor response to therapy?

A
  • Oxygen delivery
  • Markers of aerobic metabolism
  • Monitor for compromised end-organ function
68
Q

What are the consequences of shock?

A

Mortality is high (even with advanced care)

  • Septic 30-50%
  • Cardiogenic 60-80%
  • Hypovolaemic - variable (attributable to underling aetiology)
  • Prolonged organ hypoperfusion and tissue hypoxia
  • Cellular injury and death
  • Multi-organ dysfunction then failure
  • Early recognition and management considerably improves outcome
69
Q

What is sepsis?

A
  • Widespread inflammation due to infection
  • Vasodilatation and capillary leak
  • When severe can rapidly progress to shock
  • Treatment principles same as shock
  • Piperacillin/tazobactam
70
Q

Why might a patient develop abnormal clotting following a massive blood transfusion?

A
  • Dilution of platelets and clotting factors cause state of coagulopathy
  • Patients receiving massive transfusions require careful monitoring of coagulation status and transfusion of blood products
  • Monitor platelets, FFP, cryoprecipitate and single clotting factors
  • Always seek advice of haematologists
71
Q

What are some complications of spending a significant duration in a critical care unit?

A
  • Muscle weakness and wasting
  • Nutritional deficiencies
  • Sleep disorders
  • Inability to swallow effectively and microaspiration of food
  • Recurrent chest infections
  • Overall risk of morbidity
  • High risk for re-admission
  • Need special attention by ward staff!

Cardiology (4 decks)

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