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PBL > Albert Smith > Flashcards

Albert Smith Flashcards

1
Q

How does a ruptured aortic aneurysm present?

A
  • Abdominal and back pain
  • Syncope- fainting
  • Vomiting
  • Haemodynamically compromised- hypotensive, tachycardic, diaphoretic- sweating
  • Pulsatile abdominal mass
  • Tenderness
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2
Q

What are the differential diagnoses of paleness and clamminess of the skin?

A
  • Anxiety attack
  • MI
  • Heat exhaustion
  • Internal bleeding- shock
  • Low blood oxygen
  • Sepsis
  • Anaphylaxis
  • Pain
  • Hyperhidrosis
  • Menopause- hot flushes
  • Fever
  • Hyperthyroidism
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3
Q

4 types of aneurysm

A
  • True- all layers of the vessel are dilated
  • Pseudoaneurysm aka false aneurysm- hole in one layer
  • Fusiform
  • Saccular- common in abdomen, less elastin in abdominal aorta than in thoracic.
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4
Q

What is Starling’s law

A
  • Increased venous return increases the ventricular filling (end-diastolic volume) and therefore preload, which is the initial stretching of the cardiac myocytes prior to contraction. Myocyte stretching increases the sarcomere length, which causes an increase in force generation and enables the heart to eject the additional venous return, thereby increasing stroke volume.
  • This phenomenon can be described in mechanical terms by the length-tension and force-velocity relationships for cardiac muscle. Increasing preload increases the active tension developed by the muscle fibre and increases the velocity of fibre shortening at a given afterload and inotropic state.
  • One mechanism to explain how preload influences contractile force is that increasing the sarcomere length increases troponin C calcium (helps form cross bridges) sensitivity, which increases the rate of cross-bridge attachment and detachment, and the amount of tension developed by the muscle fibre (see Excitation-Contraction Coupling). Other mechanisms are undoubtedly involved. The effect of increased sarcomere length on the contractile proteins is termed length-dependent activation.
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5
Q

What is CVP

A

pressure in thoracic vena cava nearest the right atrium

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6
Q

CVP and pressure in the … are pretty much equal

A

RA

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7
Q

BP= …. x ….

A

TPR X CO

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8
Q

What is poiseulle’s law

A

explains the role of radius on resistance- greater radius= less resistance

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9
Q

what is the myogenic response?

A

intrinsic response is: increased distension of vessel leads to constriction and decreased pressure causes vasodilation.

Protective mechanism- ensures good blood flow even when there is low BP

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10
Q

3 things that affect viscosity of blood

A

blood velocity
vessel diameter
haematocrit

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11
Q

What effect does a fall in blood pressure have on HR, ventricular contractility, tone in the resistance vessels and capacitance vessels?

A
  • HR: increase
  • ***Ventricular contractility: decreases. There is less ventricular filling.
  • Tone in resistance vessels (arteries): vasodilation, leading to reduced TPR myogenic response
  • Tone in capacitance vessels (veins): decrease. There is a reduced pressure gradient so there will be less pressure in the veins and the tone will decrease.
  • Baroreceptor reflexes- activate sympathetic adrenoceptors to increase HR and contractility and cause vasoconstriction and increasing vascular resistance. The brain benefits from the increased resistance- redistribution from less important organs
  • Chemoreceptor reflexes- vasoconstriction causes systemic acidosis, chemoreceptors recognise this and further stimulate the SNS response.
  • Circulating vasoconstrictors
  • Renal reabsorption of sodium and water- RAAS system
  • Activation of thirst mechanisms
  • Reabsorption of tissue fluids- reduced capillary hydrostatic pressure
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12
Q

How does blood loss lead to shock?

A
  • Hypovolemia
  • Leads to decreased BP- less blood to pump
  • Tachycardia due to adrenaline release
  • Vasoconstriction causes pallor
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13
Q

MOA of ACh

A

o Parasympathetic nervous system
o Bind to muscarinic receptors (M2) on SAN and AVN cells- Gai causing hyperpolarisation by increasing K efflux
o Increases vagal activity to SAN, decreasing firing rate

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14
Q

MOA of adrenaline and noradrenaline

A

o Binds to both alpha- and beta-adrenergic receptors
 alpha 1: vasoconstriction via Gaq
 alpha 2: vasoconstriction via Gai
 beta: increase HR, impulse conduction, increase contraction and vasodilation via Gas

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15
Q

example of mAch antagonist

A

atropine

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16
Q

example of indirect AchR agonist

A

neostigmine

17
Q

example of a1 adrenergic receptor agonist

A

phenylephrine

18
Q

difference between adrenaline and noradrenaline

A
  • Noradrenaline is the main neurotransmitter of the sympathetic nerves in the cardiovascular system- secreted by the nerves.
  • Adrenaline is the main hormone secreted by the adrenal medulla.
  • Noradrenaline has more specific effects- only works on a receptors
  • Adrenaline has more widespread effects both a and b receptors
19
Q

How to stabilise a patient with a suspected AAA

A
  • Immediate high flow oxygen
  • IV access- 2x large bore cannula
  • Urgent bloods- FBC, U&Es, clotting
  • Cross matching for minimum 6 units
  • Treat the shock carefully- don’t want to dislodge a clot that is tamponading the rupture- aim to keep systolic BP <100mmHg- known as permissive hypotension to prevent excess blood loss.
  • Inform vascular registrar, consultant and anaesthetist
  • If patient is stable- CT angiogram
  • In unstable- open surgical repair
20
Q

What is a fluid challenge, including the amounts given and time frames

A
  • A diagnostic intervention used to decide if a patient with haemodynamic compromise will benefit from further fluid replacement.
  • A small amount of fluid is administered in a short period of time. Assess whether the patient has the preload reserve that can be used to increase SV with more fluid.
  • A positive response to a fluid challenge would be an increase in SV of >10%.
  • A negative response would be an increase in PAOP with an increase of SV of <10%.
  • Bolus of 500ml over less than 15 minutes (NICE guidelines) use colloid fluids
21
Q

What are “packed RBCs”?

A
  • Made by removing the plasma from blood.
  • Contain WBCs, platelets and residual plasma.
  • Indicated for anaemia and can be used to treat haemorrhagic stroke when administered with volume expanders.
  • Used to improved oxygen carrying capacity and blood volume
22
Q

What does cryoprecipitate contain?

A
  • Precipitate of thawed FFP FFP is repeatedly frozen and thawed to produce a liquid rich in clotting factors.
  • High in FVIII and fibrinogen
  • Precipitate of thawed FFP FFP is repeatedly frozen and thawed to produce a liquid rich in clotting factors.
  • High in FVIII and fibrinogen
23
Q

Where is a central line inserted

A

• Internal jugular vein is preferred but can use the subclavian vein less likely to cause a pneumothorax.

24
Q

Reasons for a central line

A

o Administration of medications that require central access e.g. amiodarone, inotropes
o Fluid balance monitoring with CVP
o IV access for long term e.g. chemo

25
Q

Complications of central line

A 
o	Infection
o	Haemothorax
o	Pneumothorax
o	Haematoma
o	Arterial puncture 
o	Air embolism
o	Arrhythmias 
o	Thrombosis
26
Q

3 examples of sympathetic agonists

A

salbutamol
dobutamine
epinephrine

27
Q

5 effects of sympathetic agonists

A 
increased HR, contractility
bronchodilation 
sphincter contraction
increased glycogenolysis 
venoconstriction 
peripheral vasdilation
28
Q

4 types of sympathetic antagonist

A

a blockers

b blockers

a2 adrenergic agonists

monoamine-depleting agents

29
Q

2 effects of a blockers

A

o Decrease vasoconstriction via a1r and increase vasodilation via b2r- Decrease BP
o Increased renin secretion via b1r - Increase water retention

30
Q

effect of b blockers

A

mainly inhibit b1r in heart- decrease HR, contractility and AV conduction

31
Q

effect of a2 adrenergic agonists

A

o Activate a2r in presynaptic sympathetic neurons in CNS increasing negative fb. This leads to less catecholamine release- dopamine and norepinephrine. Reduced sympathetic tone, reduced vasoconstriction and lower BP

32
Q

effect of monoamine- depleting agents

A

o Inhibit uptake of norepinephrine and dopamine into presynaptic vesicles of adrenergic neurons.
o This reduces catecholamine release, decreasing CO and BP
o Less vasoconstriction leads to lower BP

33
Q

2 groups of parasympathetic agonist

A

muscarinic receptor agonist

cholinesterase inhibitors

34
Q

effect of muscarinic receptor agonist

A

o a decrease in heart rate and in atrial contraction
o indirect vasodilatation due to stimulation of NO from vascular endothelial cells
o contraction of smooth muscle of the gastrointestinal tract along with relaxation of the sphincters
o stimulation of exocrine glands leading to gastric acid secretion, salivation, lacrimation and sweating
o contraction of the detrusor muscle and relaxation of the bladder sphincters, leading to urination
o constriction of the pupil and the ciliary muscle of the eye, leading to miosis and decreased intraocular pressure

35
Q

example of parasympathetic antagonist

A

muscarinic receptor antagonist

36
Q

4 effects of muscarinic receptor antagonist

A

o to cause pupil dilation to facilitate eye examinations (e.g. atropine; tropicamide)
o to cause relaxation of bronchial smooth muscle in COPD (e.g. ipratropium)
o to decrease gastric motility (e.g. hyoscine)
o to decrease bladder emptying (e.g. oxybutynin)

PBL (15 decks)

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