Critical Care Flashcards

0
Q

What is the function of a chronotrope?

A

To increase the heart rate

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1
Q

What is the function of an inotrope?

A

To increase the contractile force of the cardiac muscle, thereby increasing stroke volume

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2
Q

What is the function of a vasopressor?

A

Constrict the arterial tree, increasing systemic vascular resistance

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3
Q

Where are alpha1 adrenergic receptors located, and what is their function?

A

Located in vascular smooth muscle, hence activation causes vasoconstriction

Also located in heart, and increases duration of contraction without increasing chronotropy

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4
Q

Where are beta adrenergic receptors located?

A

Beta1 in the heart, increasing inotropy and chronotropy without vasoconstriction

Beta2 in blood vessels and cause vasodilation

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5
Q

Where are dopamine receptors located and what is their function?

A

In renal, splanchnic (mesenteric), coronary, cerebral vascular beds.
Induces vasodilation

Second subtype causes vasoconstriction by inducing norepinephrine release

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6
Q

What receptors does adrenalin act on, and therefore what are its effects and uses?

A

Beta 1- adrenaline acts strongly on this receptor to increase inotropy and chronotropy

Beta 2, alpha 1- adrenaline acts moderately on these receptors

Used in anaphylaxis and second line in septic shock

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7
Q

What receptors does dobutamine act on and what effect does it have?

A

Beta 1 and beta 2- increases inotropy and chronotropy, reduces LV filling pressure

Has no vasopressor effects as has no action on alpha 1 receptors

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8
Q

What receptors does noradrenaline act on and what effect does it have?

A

Alpha 1 and beta 1 receptors

Producing vasoconstriction and inotropic effects

At low doses, a reflex bradycardia in response to increased mean arterial pressure, which cancels out the mild chronotropic effect and therefore there is no increase in heart rate!

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9
Q

What receptors does phenylephrine act on and what effect does it have?

A

Alpha 1 only

So purely vasoconstriction!

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10
Q

In septic shock, which is the first line vasoactive agent?

A

Noradrenalin

As it causes vasoconstriction to counteract the vasodilation from sepsis

Pure vasoconstriction alone can cause reflex bradycardia and reduce cardiac output, so the inotropic effects of noradrenalin helps to counteract this.

The inotropic effects of noradrenalin also helps to counteract the decrease in cardiac function which typically occurs in septic shock

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11
Q

What vasoactive drug is first line in anaphylactic shock?

A

Adrenalin

Vasopressin is second agent

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12
Q

What vasoactive drug is used in neurogenic shock?

A

Phenylephrine as it has purely vasoconstriction effects

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13
Q

What is the most appropriate vasoactive drug in cardiogenic shock

A

Norepinephrine

After establishing adequate perfusion, dobutamine can be added, as it is a potent inotropic drug, and it’s effects on beta 2 receptors causes vasodilation, so the heart has less pressure to pump against

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14
Q

What is a level 0 patient?

A

A patient whose needs can be met through normal ward care - eg observations greater than four hourly

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15
Q

What is a level 1 patient?

A

A patient at risk of their condition deteriorating, or recently discharged from a higher level of care.

Patients requiring additional monitoring <4 hour obs, clinical interventions or advice from critical care outreach.

16
Q

What is a level 2 patient?

A

Patients needing pre-operative optimisation or extended postoperative care.

Patients stepping down from level 3 care.

Patients requiring single organ support! Greater than 50% oxygen or NiV
Vasoactive drugs/CVP monitoring
Renal replacement therapy
ICP monitoring 
Dermatological support - burns

This is achieved on HDU

17
Q

What is a level 3 patient?

A

Patients requiring advanced respiratory support alone - invasive mechanical ventilation

Patients requiring more than one organ supported

This is achieved on ICU

18
Q

What are some early complications of endotracheal intubation?

A
Trauma to mouth, teeth etc
Aspiration of stomach contents
Tube malposition
Airway obstruction
Hypoxia from prolonged attempts
19
Q

What are some late complications of endotracheal intubation?

A

Infection
Mucosal damage to mouth or trachea from cuff pressure
Injury to vocal cords
Tracheal stenosis

20
Q

What are early complications of tracheostomy?

A
Haemorrhage
Pneumothorax
Tube misplacement
Surgical emphysema
Blockage with secretions
Stomal infections
Mucosal ulceration or perforations
Tracheoeseophageal fistula
21
Q

What are late complications of tracheostomy?

A
Late haemorrhage
Tracheal granulomata
Tracheal stenosis
Scarring persistent sinus
Tracheal necrosis
22
Q

What precautions and monitoring should be taken when using vasoactive drugs?

A

Administered by central venous catheter

Haemodynamic monitoring via arterial and central venous catheters

23
Q

How can death be defined?

A

The irreversible loss of the capacity to breath combined with the irreversible loss of the capacity for consciousness

These capacities reside in the brainstem, in the medulla and reticular activating system respectively

24
Can brainstem dead patients move?
Yes! They may demonstrate residual limb movement due to intact spinal cord reflexes. These do not require intact higher centres.
25
What are the cardiovascular criteria for diagnosing death?
The simultaneous and irreversible onset of apnoea and unconsciousness in the absence of a circulation AND The individual meets the criteria for not attempting CPR OR Attempts at CPR have failed OR Life sustaining treatments have been withdrawn in the best interests of the patient
26
How can you assess if the patient meets the cardiovascular criteria for death?
The individual should be observed for a minimum of five mins Absence of central pulse on palpation Absence of heart sounds on auscultation No cardiac activity on ECG, echo etc If continuous cardio respiratory arrest for five mins, move on to assess pupillary light reflexes, corneal reflexes, motor response to supra-orbital pressure
27
Why conditions must be excluded to diagnose brainstem death?
Must be due to irreversible brain damage of known aetiology! Exclude reversible causes of coma: Depressant drugs Hypothermia- core temp above 34 deg Metabolic/endocrine disturbance Exclude reversible causes of apnoea: Neuromuscular blockers High cervical cord injury
28
What five brainstem reflexes can be used to exclude brainstem death?
The pupils are fixed and non responsive to light There is no corneal reflex Absent oculo-vestibular reflexes No motor response to supra orbital pressure No gag reflex/cough reflex Basically all the cranial nerve reflexes!
29
What is the apnoea test for the diagnosis of brain stem death?
Assessing the respiratory response of the brainstem to hypercapnoea Do not perform if previous tests have suggested brainstem activity! Set fi02 to 1.0 Commence apnoiec oxygenation If no response, check ABG has demonstrated paCO2 has risen by 0.5kpa Then reconnect ventilator
30
At what age are the adult criteria for brainstem death applied?
Over 2 months
31
How many doctors are needed to assess brain stem death
Two, both registered for five years At least one consultant No members of the transplant team
32
How many times must the tests for brainstem death be repeated?
Twice
33
At what point when diagnosing death in a brain stem dead patient is the legal time of death confirmed?
The legal time of death is the time at which the first set of tests is completed
34
What are the physiological causes of type 1 respiratory failure?
``` Ventilation perfusion mismatch Due to either: Under ventilated alveoli Venous blood bypasses ventilated alveoli (right to left cardiac shunts) Low inspired oxygen fraction Low barometric pressure ```
35
What are the physiological causes of type 2 respiratory failure?
Reduced central respiratory drive Hypo ventilation due to abnormalities of motor nerves, muscles, chest wall, spinal cord Abnormalities of airways and lungs
36
What is acute respiratory distress syndrome?
A common condition which can affect all adult patients. It occurs when non cardiogenic pulmonary oedema (secondary to acute damage to the alveoli ) leads to respiratory failure
37
What is the diagnostic criteria for ARDS? Three things
Acute onset after lung injury CXR shows bilateral infiltrates Refractory hypoxaemia: pa02 : fiO2 ratio is less than 200
38
How is ARDS managed?
CPAP may be effective, but usually mechanical ventilation is required