Circulation Flashcards
1
Q
Define the blood pressure?
A
Blood pressure is the product of cardiac output and SVR.
CO = SV x HR
2
Q
How can blood pressure be monitored?
A
Non-invasive = sphygomomanometer Invasive = Direct cannulation of an artery e.g. radial
3
Q
How does invasive monitoring compare to non-invasive.
A
Invasive measures systolic 5mmHg more and diastolic 8mmHg less.
Cons:
- Complications of procedure
- Expensive
- Requires skilled operator for procedure
Pros:
- But allows continuous monitoring
- Accurate even when profoundly hypotensive.
- Can also provide indication of myocardial contractility from ‘arterial swing’
4
Q
Draw the blood pressure waveform..
What is the dicrotic notch?
A
Dicrotic notch = momentary rise in arterial pressure as aortic valve closes
5
Q
How is MAP calculated?
A
Systolic - 0.33(systolic - diastolic)
It is the area beneath the arterial pressure waveform
6
Q
What information can acquired from the arterial waveform?
A
Myocardial contractility - rate of change of pressure by unite time i.e. slope of arterial upstroke
Hypovolaemic - Suggested by narrow waveform and low dicrotic notch.
Peak pressure will also vary with respiration.
7
Q
what is Allens test?
A
Test for competent contralateral vascular supply in the hand, prior to inserting radial line.
Occlude radial and ulnar artery of one hand. Release the ulnar artery and assess if the hand reperfuses well.
Test is +ve if the hand is still blanched after 15 seconds.
8
Q
How does the arterial pressure at the radial artery differ to that at aortic root.
A
In radial the SP is 10mmHg higher, and diastolic 10mmHg lower vs aortic root.
Despite the PP being higher, the MAP is actually 5mmHg lower.
9
Q
How does arterial pressure waveform differ with aortic valve disease?
A
Aortic stenosis = Anacrotic pulse: slow to rise and low amplitude.
Aortic regurgitation = water hammer pulse: Rapid rise + decline, but attains high amplitude.
Mixed aortic valve disease = Pulsus bisferiens: Large amplitude pulse with double peak. Often felt as double pulse at radial
10
Q
What is pulses alternans?
A
Random variation of amplitude of waveform, palpated as strong and weak beats in cardiac cycle.
e.g. left ventricular failure, cardiomyopathy.
11
Q
What is pulses bisferiens?
A
Palpated as a double peak during cardiac cycle. Waveform is high amplitude with double peak. Classically exists in mixed aortic valve disease with dominant regurgitation OR obstructive cardiomyopathy.
12
Q
What is the physiology behind Pulsus bisferiens.
A
Two systolic peaks
First is percussion wave due to rapid ejection of ventricle.
Then get mid systolic peak as MV opens due to Venturi effect and you lose pressure gradient.
Ventricle then overcomes this to give you the second ‘tidal’ wave, which is a reflection of pressure from peripheries.
13
Q
What is Pulsus paradoxus?
Physiology?
A
> 10mmHg reduction in arterial pressure causes by inspiration and may be seen in cardiac tamponade.
During inspiration, you have increased venous return to right atrium = reduced return to left atrium as RA bulges across. this means reduced LV volume = reduced stroke volume = reduced arterial pressure. So have drop in arterial pressure, but <10mmHg
Tight pericardial space lease to reduced LVEDV and therefore stroke volume which causes reduction in pressure further so get a drop >10mmHg.
14
Q
constituents and characteristics of packed RBCs?
Most common additive solution?
A
Volume 220-330ml Stored at 2-6 degrees Shelf life 35 days from donation Hb content 40g Haematocrit 0.5-0.7
Most common additive solution is 100ml saline, adenine glucose and mannitol (SAG-M)
15
Q
How can red cells be treated?
A
Irradiation = for patients at risk of TA-GvHD. Using gamma rays. Shelf life <14 days.
Washing:
Plasma removed and cells resuspended in SAG-M if patients have IgA deficiency.
16
Q
Constituents and characteristics of platelets?
A
Multiple blood donors = centrifuged. 4 donors pooled in plasma of one. Reduces risk of TRALI Volume = 300ml Storage temp = 20-24 degrees Shelf life 5 days Mean platelets 308
Single donor = apheresis Volume 200ml Storage same Shelf life same Mean platelets 280
17
Q
How can platelets be treated?
A
Irradiation if at risk of GvHD
Washing - suspend the platelets In platelet additive solution (PAS)
HLA-selected patients.
Human platelet antigen (HPA) selected
18
Q
Basic constituents and characteristics of plasma?
A
Only from male donors, female plasma has increased risk TRALI
Single donor plasma = FFP.
Main components are cryoprecipitate and cryosupernatant containing coag factors, vWF and some plasma proteins e.g. fibrinogen.
Volume 275ml
Storage -25 degrees
Shelf life 36 months, 24 hours after thawing
Mean factor VIIIc 0.83
Multiple donors = solvent detergent FFP pooled from approximately 1500 low risk vCJD donors
Volume 200ml
Storage temp -18 degrees
Shelf life 4 years, transfuse ASAP post thawing
Mean factor VIIIc 0.8, fibrinogen 2.6mg/ml
19
Q
How can plasma be treated?
A
With methylene blue = solvent detergent FFP
Inactivates bacteria and encapsulated viruses
BUT decrease levels of Factor VIII, fibrinogen and protein S
20
Q
Constituents and characteristics of cryoprecipitate ?
A
Supernatant obtained by thawing FFP at 4 degrees
Contains vWF, fibrinogen, factor VIIIc and FXIII
Single donor: Volume = 40ml Storage -25 degrees Shelf life 36 months Mean Factor VIIIc = 105iU Mean fibrinogen = 400mg/pack
Multiple donors = same except 190ml
Mean factor VIIIc = 464iu
Fibrinogen = 1550mg
21
Q
What is HAS and what types are available and their indications?
A
Human albumin solution. Contains no clotting factors to blood group antibodies.
Isotonic solutions 4.5% used I plasma exchange, occasionally in burns but needs ITU consult
Hypertonic 20% used in: Hepatorenal syndrome, SBP, large volume paracentesis
22
Q
What are coag factor concentrates and their use in surgery?
A
One example is prothrombin complex (PCC) which contains factors 2, 7, 9, 10.
It is recommended treatment for rapid reversal of warfarin over FFP now due to its:
Superior efficacy
Lower risk of allergic reaction / fluid overload
Ease of admin
23
Q
Which infections are donated blood screened for?
A
Hep B + C
HIV
HTLV
Syphilis
All blood donations are filtered to remove leucocytes, reducing the risk of vCJD
24
Q
Management of warfarin overdose?
A
Major bleeding: Stop warfarin IV Vitamin K 5mg PCC e.g. Bereplex 50ug/kg In all cases of major haemorrhage discuss with on call haem.
INR >5 with minor bleeding:
Stop warfarin
IV Vitamin K 3-5mg
Recheck, and restart when INR <5
INR >8 no bleeding
Hold warfarin
Oral vitamin K
Restart when <5
INR 5-8 no bleeding:
Withhold warfarin
Restart when <5
25
Purpose of a blood transfusion?
Expected Hb raise per unit?
To restore oxygen carrying capacity of the blood, and improve tissue perfusion
About 4
26
How can we classify complications of blood transfusion?
Complications of massive transfusion / repeated transfusion
Infective complications
Immune complications
27
What is a massive transfusion and what are the complications?
Massive transfusion is total blood volume transfused within 24 hours
1. Volume overload
2. Thrombocytopaenia - following storage there is a reduction in functioning platelets = dilutional effect
3. Coag factor deficiency = can lead to coagulopathy
4. Poor tissue oxygenation as stored blood has reed 2,3-DPG
5. Hypothermia as cold storage
6. Hypocalcaemia due to chelation by the citrate in the additive solution
7. Hyperkalaemia due to K leakage from stored RBCs
28
Which coagulation factors are most affected by storage
V and VIIIc.
Although reduction in FVIIIc may be offset by the metabolic response to stress which increases Factor VIIIc production
29
What infective complications may be seen following transfusion?
Viruses - HBV, HCV and HIV
Bacteria:
G -ve e.g. Yersinia Enterocolitica
G +ve especially staphylococcal following contamination
Syphilis
Tropical disease e.g. Malaria
30
What would make you suspect a unit of RBC has bacterial contamination?
Clots in bag
| High degree of haemolysed red cells
31
How can we classify the immune reactions seen with blood transfusions?
Severe, less severe, delayed
32
Outline the severe acute immune reactions associated with blood transfusions
1. Acute haemolytic transfusion reaction:
ABO incompatibility.
Transfusion of ABO incompatible red cells which react with the patients anti-A/B = intravascular haemolysis.
PC = agitation, fever, shock, DIC + renal failure.
Mx = stop Transfusion and treat DIC
2. Allergic reaction:
This includes a mild urticaria to shock.
Due to recipient IgA deficiency or anti-IgA IgE.
Mx = slow transfusion + chlorphenamine
3. TRALI:
Due to antibodies in the donor blood to neutrophils, monocytes and pulmonary endothelium
Inflamm cells sequester in the lungs = non-cardiogenic oedema
PC = SOB, cough, b/l infiltrates
Mx = stop transfusion and treat ARDS
```
4. TACO
Acute pulmonary overload
< 6 hours post transfusion
PC = CCF
Mx = slow transfusion, oxygen, diuretic
```
33
Outline less severe acute immune reactions to blood transfusion
1. Febrile non-haemolytic transfusion reaction:
Due to a reaction to leucocyte antigens in donated blood.
PC = <24 hours. Fevers, rigors and shock.
Mx = slow transfusion and paracetamol
34
Outline delayed immune reactions to blood transfusion
1. Delayed haemolytic transfusion reaction:
If patient is immunised to foreign red cell antigens due to previous transfusion can cause delayed reaction = 1-7 days
PC = jaundice, anaemia, fever
2. Post-Transfusion purpura:
occurs at 7-10 days due to reaction to HPA-1a
PC = thrombocytopaenia and purpura
Mx = IVIG and platelets
3. Ta-GvHD:
From 4 days to 1 month
Immunocompetent donor lymphocytes mediate an immune response to recipient cells of different HLA
Mx is steroid based
35
Management of acute haemolytic transfusion reaction?
ABCDE.
Stop transfusion, commence IVF
Bloods - d-dimer, G+S, FBC, cultures
Direct antiglobulin test (Coombes)
36
What is Direct Coombs test?
Direct antiglobulin test
Used for detection of antibodies or complement that have developed in-vivo
Tests for Haemolytic reactions
37
Risks of platelet transfusion?
1. Infection
2. Sensitisation = Rhesus -ve females under 45 should receive Rh-D -ve platelets
3. Allo-immunisation = Development of antibodies to HLA class 1 antigens
38
Anatomic location of SA node and AV node?
SA = Elliptical area at junction of SVC and RA
| AV node = triangular are of RA wall, just above septal cusp of tricuspid valve
39
Where on the body do ECG leads go?
```
Limb leads:
R - right wrist
Y - left wrist
G - right ankle
B - left ankle
```
```
Chest leads:
V1 - 4th ICS right of sternum
V2 = 4th ICS left of sternum
V3 = Between V2 and V4
V4 = Left 5th ICS, MCL
V5 = Level with V4 Anterior axilla
V6 = Level with V4 MAL
```
40
When do the heart sounds occur in relation to the cardiac cycle?
```
HS1 = AV valve closure = r wave on ECG
HS2 = aortic/pulmonary valve closure = end of T wave
```
41
What is the origin of the p wave?
Atrial depolarisation
42
What is PR interval and what it represents?
Beginning of P to beginning of QRS
Corresponds to time taken for impulse to travel from SA node to the ventricle
0.12-0.2 seconds
43
What does QRS represent and upper limit?
QRS = ventricular depolarisation
| Upper limit 0.12s
44
Define the QT interval?
From beginning of Q wave to end of T wave
Represent time of onset of ventricular depolarisation to full repolarisation.
Duration is heart rate dependant
45
What is QTc?
| How calculated?
QT interval corrected for a heart rate of 60bpm
Bazetts formula = QT/_/(RR)
normal is 0.35-0.43
46
What does the t wave represent?
Why is the t wave deflection upwards.
Ventricular repolarisation
As it represents repolarisation one would expect it to be a negative deflection, however repolarisation occurs from epicardium too endocardium. This is the opposite direction to depolarisation. This negative coupled with the negative charge, is a double negative so gives us a positive deflection.
47
J wave vs U wave?
J wave occurs at the ST junction, and is a sign of hypothermia
U wave occurs after the ST segment and is a sign of hypokalaemia
48
Causes of sinus tachycardia?
```
Exercise
Pain
Pyrexia
Shock
Drugs e.g. adrenaline
```
49
Causes of sinus bradycardia?
```
Athletic
Vasovagal
Hypothermia / hypothyroid
Raised ICP
Jaundice
Drugs e.g. BB, digoxin, amiodarone
```
50
Outline the different types of tachyarrhythmias ?
narrow complex or broad, which can each then be divided into regular or irregular
51
outline different types of narrow complex tachyarrhythmias and management?
Generally narrow complex is SVT
1. Regular (AV node dependant)
e. g. paroxysmal SVT, flutter with regular AV conduction, WPW.
Mx = vagal manœuvres, then adenosine 6,12,12mg.
- in asthmatics use verapamil.
If AV dependant the adenosine should cause AV blockage.
If its AV independent e.g. actually AF but hard to tell, the tachycardia will persist.
2. Irregular (AV node independant)
e. g. AF, flutter in variable AV conduction
Mx = Rate control with BB
If in heart failure consider digoxin or amiodarone
Don't forget to consider anticoagulant
52
outline different types of broad complex tachyarrhythmias and management?
Generally broad complex is ventricular, occasionally SVT with aberrant conduction.
Irregular = AF with bundle branch block, or polymorphic VT
Mx:
Seek expert help
If AF with BBB treats for narrow complex
Regular = VT or SVT with BBB
Amiodarone 300mg IV over 20mins
then 900mg over 24 hours
53
Management of any tachyarrhythmia with adverse features + what are adverse features?
Adverse features = shock, syncope, MI, heart failure
DC shock x3
Amiodarone 300mg IV over 20mins
repeat shock
900mg over 24 hours
54
Management of bradycardias?
Features of asystole risk?
Any adverse features or risk of asystole:
Atropine 500mcg IV repeat to a maximum of 3mg
Isoprenaline 5mcg/min IV
Adrenaline 2-10mcg / min IV
Seek expert help as pacing may be required.
If no adverse features / risk of asystole = observe.
Features of systole risk:
Recent asystole, mobitz type 2, complete HB, ventricular pause >3 seconds
55
Explain the difference between the different heart blocks?
1 = prolonged. PR >0.2 seconds
2. 1 = progressive lengthening of PR interval until QRS dropped
2. 2 Regular prolonged Pr with dropping of QRS in ratio.
3 = complete dissociation between atrial and ventricular contraction
56
How do you asses state of hydration?
Hypovolaemic:
Circulation = Cool peripheries, reduced cap refill, reduced skin turgor, dry mouth, tachycardia, low BP, low UO
Hypervolaemic:
Breathing = tachypnoeic, bibasal creps
Circulation = Raised JVP, peripheral oedema
Assess fluid charts, drains, UO
57
what are the main fluid compartments of the body?
```
Intracellular = 28L
Extracellular = 14L
```
Extracellular:
3L plasma, 10L interstitium, 1L transcellular fluid
58
Why do we need to give fluid therapy?
1. To satisfy basal fluid requirements
2. Replace lost fluids and electrolytes
3. Support arterial pressure due to shock
4. Increase oxygen carrying capacity of blood If giving RBC's
59
Colloids vs crystalloids?
Colloids have greater osmotic pressure as contain larger insoluble molecules. So they remain intravascular
Crystalloids are aqueous solutions of mineral salts so pass more easily between compartments.
60
Which fluid type should you use in an emergency setting?
Controversial but studies show colloids require less volume to maintain similar monitoring parameters
61
Types of crystalloids and contents of each?
Saline 0.9% = 150mmol/L of Na and Cl
```
Hartmanns:
131 Na
5 K
111 Cl
29 Bicarb
2 Ca
```
Hartmann's has an osmolality of 280 and pH 6.5, so is more physiological
Dextros 5% = 50g/L glucose, which is rapidly metabolised by the liver and the fluid then rapidly redistributed = useless for resuscitation.
62
Precautions of using crystalloids?
1. Metabolic acidosis due to hyperchloremia in excess NaCl = chloride shift:
If chloride rises, it forces bicarbonate into cells to balance the negative ionic change. This means extracellularly there is no pH buffer
2. Hyperkalaemia in Hartmann's use
3. Hypernatraemia NaCl
4. Oedema, particularly with dextrose.
63
What type of colloids are available?
HAS
Dextrans = branched polysaccharides. Often used as antiaggregant in microvascular surgery
Gelatins:
Succinylated gelatins e.g. Gelofusin
Urea crossed gelatins e.g. Haemaccel
Starches
64
Risk of colloids?
1. Disease transmission e.g. HAS
2. Coagulopathy - dextran and. gelatine can. interfere with platelet adhesion and vWF as well as decrease coag factors
3. Interaction with blood transfusion e.g. the calcium content of haemaccel can cause blood to clot if used in same cannula
4. Immune reactions - Dextran and gelatins can cause anaphylaxis
5. Volume overload
65
Which jugular vein is used for JVP exam and why?
IJV is used due to its lack of valves, providing a single column of blood directly affected by RA
66
What info can be obtained from JVP?
Can measure CVP clinically and observe the waveform giving information about the hearts rhythm and function
67
How can JVP be distinguished from the carotid pulse?
- JVP has two venous pulsations (a and v)
- Venous pulse is also obliterated with light pressure
- Height of JVP varies with respiratory cycle
68
Draw the normal JVP waveform and explain the differing wave reflections?
a wave = atrial contraction, will be larger if increased atrial pressure
c wave is due to the closure of tricuspid valves and bulging into the RA at beginning of ventricular systole
x descent is fall in atrial pressure during systole
V wave is due to passive filling of RA against closed tricuspid
Y descent is open of tricuspid valve and passive ventricular filling PRIOR to atrial contraction.
69
What abnormalities can we see with the JVP waveform: a wave, V wave and Y descent.
1. Absent a wave = AF
2. Large a wave = any. cause of RVH e.g. pulmonary stenosis/HTN, tricuspid stenosis
3. Cannon a wave = atrial contraction against closed tricuspid during complete heart block.
1. Prominent v wave = tricuspid regurgitation
1. Slow y descent = tricuspid stenosis, RA myxoma
2. Steep y descent = RVF, constrictive pericarditis, tricuspid regurgitation.
70
Causes of raised JVP?
Obstruction of RA outflow e.g. lung tumour, mediastinal mass, large goitre
Disease of tricuspid valve e.g. stenosis, regurgitation or RA myxoma
Compressed right ventricle e.g. tamponade or constructive pericarditis
71
Why does JVP vary with respiration?
During inspiration intrathoracic pressure decreases. This increases venous return. to the heart. This causes a reduction in JVP as blood flows into the heart.
72
What is Kussmauls sign?
Kussmauls sign is a paradoxical rise in JVP during inspiration.
It occurs when the RA cannot accommodate the. increased venous return e.g. constrictive pericarditis or tamponade.
73
How can we classify aortic dissection?
Stanford system is useful as guides management.
Type A = ascending aorta, and can extend to arch and descending as well
Type B = descending aorta
74
What are. the pathological hallmarks of dissection?
Microscopically:
1. Myxoid degeneration = loss of elastic fibres and replacement of musculo-elastic tissue with proteoglycan rich matrix
2. Cystic medial necrosis
Macroscopically:
Dissection is due to an intimal layer transverse tear along the greater curvature of the aorta, and propagation of the blood into the media.
75
RF's for aortic dissection?
Non-modifiable:
Age, male, connective tissue disorders
Modifiable:
Bicuspid aortic valve, HTN, pregnancy, trauma
Cocaine use
Iatrogenic - Cardiac catheterisation, aortic valve replacement
76
What are the effects of an aortic dissection?
Location dependant:
Abdominal
- gut ischaemia if mesenteric vessels involved or renal failure if renal vessels
- Intercostal and Lumbar vessel involvement can cause spinal cord ischaemia
Carotids = ischaemic stroke
Cardiac:
Coronaries can lead to MI/Angina
Rupture into the pericardium / pleura can cause cardiac tamponade or haemothorax.
77
Clinical signs and symptoms of dissection?
PC = tearing central chest pain, radiates to back.
May auscultate new aortic regurgitation
signs of shock = low BP, tachycardia. May measure different blood pressure in both arms.
May see features of tamponade = muffled heart sounds, Pulsus paradoxus, raised JVP
neurological dysfunction if spinal cord / carotid involvement
78
Investigations in aortic dissection?
ECG looking for ischaemic changes
CXR for signs of dissection = depression left main bronchus, prominent aortic knuckle, widened mediastinum
CT/MRI
Echo
79
How is aortic dissection managed?
ABCDE approach
Type A = surgical management:
replacement of the diseased segment with a prosthetic graft.
If root is involved it may require valve replacement, preimplantation of coronaries.
If arch is involved will require deep hypothermic circulatory arrest during repair to maintain cerebral function.
Type B is medical management.
IVF, Systolic <130mmHg using BB.
80
Indications for type B dissection to receive surgical management?
persistent intractable pain
Aneurysmal expansion
Peripheral complications
Rupture
81
What is cardiogenic shock?
Criteria?
Inadequate tissue perfusion, as a result of myocardial dysfunction.
Criteria:
Cardiac Index <2.2
PACWP >18mmHg
Systolic BP <90mmHg
82
Complications of STEMI?
Cardiogenic shock
Arrhythmias:
LAD = complete heart block
RCA = infarction of AV node = 1st degree / 2nd degree HB
Mechanical:
VSD
Free wall rupture = cardiac tamponade (due to thinness of apical wall due to necrosis)
Papillary muscle rupture = mitral regurgitation
LV aneurysm
Chronic heart failure
Immunological = Pericarditis (dresslers)
83
Causes of cardiogenic shock?
Cardiac causes:
MI is main one
Also acute arrhythmias
Non-cardiac causes:
Obstruction to cardiac output = tension, tamponade or PE
Iatrogenic = Post cardiac surgery / prolonged cardiopulmonary bypass
84
Clinical features of cardiogenic shock?
Reduced cardiac index = cool peripheries, reduced cap refill, reduced UO, reduced consciousness
Elevated CVP = Volume overload, increased JVP, hepatomegaly
Reduced MAP = low BP
Auscultation may illicit gallop rhythm, bibasal creps, peripheral oedema on palpation.
85
Cardiac output in cardiogenic vs septic shock?
Cardiogenic is reduced
| Septic is increased = bounding pulse, warm peripheries.... but eventually drop BP
86
Pathophysiology of cardiogenic shock?
Primary issue is pump failure and reduced cardiac output, which in turn causes:
1. Increased sympathetic activity:
a) increased contractility and HR = increased myocardial demand = further pump failure
b) activates RAAS = increased sodium and water retention
= Peripheral oedema + ascites, as well as increased afterload = pump failure.
2. Increased pulmonary venous pressure = pulmonary oedema
87
Investigations for cardiogenic shock?
ABCDE
ECG for ischaemia
CXR for pulmonary oedema, widened mediastinum in dissection / tamponade
Echo
CT - for PE or dissection
Monitoring = pulmonary artery catheter (Swan Ganz) to measure PACWP and CO.
Catheter to measure UO.
88
What information can an echo provide?
Structural = valve lesions
Functional = ventricular function, end diastolic measurements, flow through defects
89
Findings in pulmonary artery catheter in cariogenic shock?
Cardiac index <2.2
PACWP >18mmHg
Raised CVP >10mmHg
Mixed venous congestion saturation
90
Basic components of normal haemostatic function?
- Normal vascular endothelium
- Normal platelet number/function
- Normal coagulation factor amount / function
- Presence of essential agents e.g. vitamin K / calcium
91
What is platelet function and what is their origin?
Origin = Formed in bone marrow and released by megakaryocyte fragmentation
1. Vasoconstriction:
this allows flow of blood to slow, allowing contact activation of platelets and coagulation factors
2. Formation of primary haemostat plug:
Adhesion of platelets to exposed collagen and the release of their cytoplasmic granules = thromboxane A2, ADP, fibrinogen, as well as aggregation of platelets
3. Factor binding:
Platelet membrane phospholipid binds. factors 2,7,9,10 = concentrates more factors .
92
What is von willebrands factor?
Molecule synthesised in megakaryocytes and endothelial cells.
Essential cofactor in platelet adhesion, and is a carrier of Factor VIIIc and protects it from inactivation and cleavage.
93
Intrinsic pathway factors?
10, 8, 9, 11, 12.
94
Extrinsic pathway factors?
3, 7, 10
95
Common pathway.
10, 5, 2, 1, 13
96
What. is the function of vitamin K?
Vitamin K is a fat soluble vitamin involved inn the gamma carboxylation of factors 2, 7, 9, 10.
This allows them to bind to calcium and hence platelet surfaces.
97
What is the end goal of the coagulation cascade?
For fibrinogen (Factor 1) to be converted to fibrin (F13), and form a stable cross linked network around primary platelet plug.
98
Can you think of any reasons surgical patients may develop coagulopathy?
Iatrogenic:
- HIT
- Massive transfusion = reduced platelets, reduce factors.
- Hypothermia due to IVF = dysfunctional platelets
Sepsis = DIC
99
How can a coagulopathy be recognised?
Clinically:
Most common sign is bleeding.
1. Pre-op may be from catheter or cannulas
2. Intra-op = persistent microvascular bleeding despite adequate haemostasis
3. Post-op = Surgical drains, purpuric rash
Biochemistry:
Low platelet count
Coag times raised
D-dimer raised
100
What is the pathophysiology of DIC?
Normal:
TF exposed to vascular system = extrinsic pathway. which triggers intrinsic. Coagulation makes fibrin = clot. Fibrinolytic system then breaks down fibrinogen and fibrin = plasmin
In DIC:
Pathological activation of coag cascade, which releases cytokines and further tissue factors.
this is followed by pathological activation of fibrinolytic system.
101
What effects does Dic have not he body?
1. shock:
hypovloaemic (bleeding) and an cardiogenic shock (PE) = hypotension = poor tissue perfusion.
2. Bleeding:
Decreased clotting factors and platelets = bleeding from mucosal surfaces
3. Thrombosis:
Small and large vessel occlusion leading to shock and organ failure.
102
what can trigger DIC?
1. Severe sepsis
2. Malignancy
3. Trauma - burns, fat embolism, multiple trauma
4. Organ dysfunction - liver failure, pancreatitis
5. Obstetric - amniotic fluid embolism, eclampsia
103
What type of anaemia is seen in DIC?
Microangiopathic haemolytic anaemia, due to red cell fragmentation as a result of fibrin deposition.
104
What will bloods show in DIC?
Raised d-dimer
Low platelets, coag factors
Abnormal clotting screen = raised PT and APTT
105
What blood products are useful in management of DIC?
Platelets and FFP
| RBCs if anaemia severe enough.
106
What is the aetiology of fat embolism?
Fracture of long bones - closed fracture have higher incidence
Major burns
Pancreatitis
Diabetes mellitus
107
Pathophysiology of fat embolism?
2 theories...
Mechanical theory
1. On fracture of long bones lipids are released into the circulatory system = embed in terminal vascular beds = ischaemia and tissue injury. This does not however, explain the non-traumatic causes
Biochemical Theory
2. during stress, stress hormones related which activate lipases. These hydrolyse circulating platelet bound lipids into FFA and glycerol.
These FFA induce pulmonary damage and increase capillary permeability.
108
Clinical features of fat embolism?
Triad = cerebral signs, respiratory insufficiency and petechial rash.
Cerebral:
Encephalopathy or distinct peripheral deficit.
- due to micro vessel embolisation of fat, plus activated lipases damage lipid rich platelet cerebral matter.
Respiratory:
- Pulmonary vascular occlusion = V/Q mismatch.
- Pneumonitis due to mediator release leading to increased capillary permeability and atelectiasis > pulmonary oedema > ARDS
Petechial residue to thrombocytopaenia.
109
Which feature of fat embolism is pathognomic?
Presence of petechial rash in right clinical setting.
110
Management of fat embolism?
Generally supportive measures:
Respiratory support e.g. PEEP
Fluid and electrolyte balance
DVT prophylaxis
Specific therapies:
HAS - albumin can bind FFA, but if it leaks through permeable capillaries can cause worsening pulmonary oedema.
111
Can you prevent fat embolism
Yes
Oxygen therapy = prompt CPAP
Steroids = evidence early. sue can be beneficial
Manage #
112
What is the definition of haemorrhage shock?
Circulatory failure resulting in adequate tissue perfusion, secondary to bleeding.
113
What are the difference types of shock?
Cardiogenic
Septic
Hypovolaemic - often due to haemorrhage
Anaphylactic - Type 1 IgE mediated reaction.
Neurogenic
114
Common causes of haemorrhagic shock?
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Trauma:
Pelvis = 1-3L
Each femur = 1-2L
Tibia <1L
Thoracic or abdominal trauma
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Spontaneous e.g. aneurysm rupture
Obstertic - placental ablution retained products, placenta accreta
Iatrogenic - clips slipping, vascular damage intra-op.
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What is haematocrit and normal level?
haemotcrit is the blood volume that is red cells.
0. 4-0.54 in males
0. 37-0.47 in females
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What influences haematocrit?
Plasma volume
Red cell volume
Venous haematocrit is slightly higher than arterial.
This is due to the carrying of CO2 means bicarb is produced and chloride ions enters cells in exchange for bicarb.
Chloride ions entering draws water in.
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How can we classify haemorrhage?
Class 1 = <15%, normal obs
Class 2 = 15-30%, PP reduced and tachycardic.
Agitated
Class 3 = 30-40%, Also reduced UO and BP, with raised RR. Starting to see reduced consciousness / confusion
Class 4 = >40%.
Obs highly deranged, pale cold and low GCS.
No UO
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Why do we see a bradycardia in decompensation during haemorrhage?
Reduced ventricular filling deforms the ventricular wall.
This stimulates myocardial vagal C-fibres.
This causes bradycardia.
119
Whats is the autonomic response to blood loss?
1. Baroreceptors = detect low pressure causing increased sympathetic activity.
This leads to compensatory tachycardia, increased stroke volume and increased PVR.
Increasing CO and maintaining BP.
2. Hormones:
- Adrenal medulla is stimulated to produce catecholamines such as adrenaline which cause peripheral vasoconstriction
- Adrenal CORTEX releases mineralocorticoids (cortisol), to stimulate water retention and salt retention = maintain BP.
- RAAS system is also activated to stimulate renin release = further salt and water retention.
120
What is the purpose of an arterial line?
Which vessels are commonly used?
Intra-arterial blood pressure.
ABG analysis
Radial, ulnar
121
Pre-procedure checks for arterial line?
Laboratory - PT and platelet count
122
What is the equipment needed and steps require for insertion of arterial line?
Equipment = Arterial cannula, giving set, NaCl, pressure bag connecting tubing and electrical equipment.
1. Position - sat with palms face up, wrist extended
2. Marking - mark site. usually readily palpable radial
3. Prep and drape = betahistadine then drape
4. Infiltration = LA bleb, then 10-15ml subcut.
5. Insertion of arterial line = Seldinger technique, at 30 degrees to skin. Passed freely never forced.
6. Security = suture in place
7. Transducer - saline bag in pressure bag pressurised to prevent back flow. continuous slow flushing system at 3-4ml/hour to prevent clotting.
123
Complications of arterial line insertion?
Contraindications?
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Immediate = bleeding, neurological damage, pain
Early/late = Occlusion, infection, embolism.
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contraindications = digital vasculitis, patients who are going to have radial artery harvested for bypass graft.
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How do arterial lines work?
Column of saline in tubing transmits the pressure changes associate with changes in BP = electrical waveform
125
What does the term arterial swing mean?
If hypovolaemic the arterial waveform peaks will vary with the respiratory cycle.
126
What is the purpose of a central line?
Short term:
1. CVP
2. Pulmonary artery flotation catheter = PACWP and calculate derived measures e.g. SV
3. Fluid balance
4. Drug administration e.g. drugs irritant to veins such as amiodarone or inotropes.
5. Haemodialysis
6. Cardiac pacing
Long term:
1. Venous access - blood sampling in immunocompromised patients
2. Chemotherapy admin
3. TPN
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Which vessels are sued for central line?
IJV
Subclavian vein
Femoral Vein
128
What is the CVP and how is it determined?
normal CVP value?
Measure of RA pressure
Can estimate clinically measuring JVP or directly via central line
2-6mmHg
129
How useful is CVP as a measure of circulating volume?
Measure of CVP itself is not particularly useful
However its response to a fluid challenge provides good information on fluid status
130
Pre-procedure checks for a central line?
Laboratory = PT and platelet count.
Radiology = CXR mandatory due to the risk of iatrogenic lung injury.
131
What is the equipment for a central line and outline the procedure?
Sterile pack, gauze, anaesthetic, catheter, ultrasound and dressings
1. Position = head down and feet up = trendelenburgs position, to increased venous size for IJV / subclavian
2. Markings - Surface landmark identified before US usage.
IJV approached as it lies between 2 heads of SCM.
Subclavian approach is infra-clavicular.
3. Prep and drape
4. Anaesthetic infiltration
5. Insertion of CVC, using seldigner technique.
needle and guide wire introduced directed inferiorly, parallel to saggital plane at 30degrees to the skin.
Advanced under US guidance, applying negative pressure awaiting for flashback.
6. Secure line
7. Collect samples.
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Surface landmarks for IJV?
Runs from lobule of ear, inferiorly to medial end of clavicle. Then lies between two head of SCM. Behind SCJ it unites with subclavian to form right brachiocephalic.
Left and right brachiocephalic then join, being right 1st costal cartilage to form SVC.
This then enters RA at 3rd intercostal cartilage
133
What is the seldinger technique?
Technique of cannulation using introducing needle and guide wire, then inserting catheter over that guide wire.
134
Complications of central line insertion?
Early: Haemothroax, pneumothorax, chylothorax, tamponade
Late = emboli, infection
135
Indications for removal of CVC?
1. Cessation of cardiac support
2. Resolution of acute presentation / discharge
3. Discontinuation of RRT
4. Line sepsis
136
Which two ways can central line information be presented?
one as a continuous waveform using a transducer, or measured intermittently using a manometer
137
What formula governs the rate of flow through tubes?
Hagen-Poiseuille:
flow = Pr^4xPi / (8uL)
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P = pressure difference at two ends
r = radius
u = viscosity
L = tube length
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So you can see. that radius has the. greatest effect on flow as it is to the power of four.
Means central line is not greatest for fast flow i.e. fluid delivery, as it is potentially long, with a small radius.
