Circulation Flashcards
Define the blood pressure?
Blood pressure is the product of cardiac output and SVR.
CO = SV x HR
How can blood pressure be monitored?
Non-invasive = sphygomomanometer Invasive = Direct cannulation of an artery e.g. radial
How does invasive monitoring compare to non-invasive.
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’
Draw the blood pressure waveform..
What is the dicrotic notch?
Dicrotic notch = momentary rise in arterial pressure as aortic valve closes
How is MAP calculated?
Systolic - 0.33(systolic - diastolic)
It is the area beneath the arterial pressure waveform
What information can acquired from the arterial waveform?
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.
what is Allens test?
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.
How does the arterial pressure at the radial artery differ to that at aortic root.
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.
How does arterial pressure waveform differ with aortic valve disease?
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
What is pulses alternans?
Random variation of amplitude of waveform, palpated as strong and weak beats in cardiac cycle.
e.g. left ventricular failure, cardiomyopathy.
What is pulses bisferiens?
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.
What is the physiology behind Pulsus bisferiens.
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.
What is Pulsus paradoxus?
Physiology?
> 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.
constituents and characteristics of packed RBCs?
Most common additive solution?
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)
How can red cells be treated?
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.
Constituents and characteristics of platelets?
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
How can platelets be treated?
Irradiation if at risk of GvHD
Washing - suspend the platelets In platelet additive solution (PAS)
HLA-selected patients.
Human platelet antigen (HPA) selected
Basic constituents and characteristics of plasma?
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
How can plasma be treated?
With methylene blue = solvent detergent FFP
Inactivates bacteria and encapsulated viruses
BUT decrease levels of Factor VIII, fibrinogen and protein S
Constituents and characteristics of cryoprecipitate ?
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
What is HAS and what types are available and their indications?
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
What are coag factor concentrates and their use in surgery?
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
Which infections are donated blood screened for?
Hep B + C
HIV
HTLV
Syphilis
All blood donations are filtered to remove leucocytes, reducing the risk of vCJD
Management of warfarin overdose?
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
Purpose of a blood transfusion?
Expected Hb raise per unit?
To restore oxygen carrying capacity of the blood, and improve tissue perfusion
About 4
How can we classify complications of blood transfusion?
Complications of massive transfusion / repeated transfusion
Infective complications
Immune complications
What is a massive transfusion and what are the complications?
Massive transfusion is total blood volume transfused within 24 hours
- Volume overload
- Thrombocytopaenia - following storage there is a reduction in functioning platelets = dilutional effect
- Coag factor deficiency = can lead to coagulopathy
- Poor tissue oxygenation as stored blood has reed 2,3-DPG
- Hypothermia as cold storage
- Hypocalcaemia due to chelation by the citrate in the additive solution
- Hyperkalaemia due to K leakage from stored RBCs
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
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
What would make you suspect a unit of RBC has bacterial contamination?
Clots in bag
High degree of haemolysed red cells
How can we classify the immune reactions seen with blood transfusions?
Severe, less severe, delayed
Outline the severe acute immune reactions associated with blood transfusions
- 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 - Allergic reaction:
This includes a mild urticaria to shock.
Due to recipient IgA deficiency or anti-IgA IgE.
Mx = slow transfusion + chlorphenamine - 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
Outline less severe acute immune reactions to blood transfusion
- 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
Outline delayed immune reactions to blood transfusion
- 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 - Post-Transfusion purpura:
occurs at 7-10 days due to reaction to HPA-1a
PC = thrombocytopaenia and purpura
Mx = IVIG and platelets - 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
Management of acute haemolytic transfusion reaction?
ABCDE.
Stop transfusion, commence IVF
Bloods - d-dimer, G+S, FBC, cultures
Direct antiglobulin test (Coombes)
What is Direct Coombs test?
Direct antiglobulin test
Used for detection of antibodies or complement that have developed in-vivo
Tests for Haemolytic reactions
Risks of platelet transfusion?
- Infection
- Sensitisation = Rhesus -ve females under 45 should receive Rh-D -ve platelets
- Allo-immunisation = Development of antibodies to HLA class 1 antigens
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
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
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
What is the origin of the p wave?
Atrial depolarisation
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
What does QRS represent and upper limit?
QRS = ventricular depolarisation
Upper limit 0.12s
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
What is QTc?
How calculated?
QT interval corrected for a heart rate of 60bpm
Bazetts formula = QT/_/(RR)
normal is 0.35-0.43
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.
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
Causes of sinus tachycardia?
Exercise Pain Pyrexia Shock Drugs e.g. adrenaline
Causes of sinus bradycardia?
Athletic Vasovagal Hypothermia / hypothyroid Raised ICP Jaundice Drugs e.g. BB, digoxin, amiodarone
Outline the different types of tachyarrhythmias ?
narrow complex or broad, which can each then be divided into regular or irregular
outline different types of narrow complex tachyarrhythmias and management?
Generally narrow complex is SVT
- 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.
- 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
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
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
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
