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PHYSIO 4th yr > ICU > Flashcards

ICU Flashcards

1
Q

Name the 2 types of blunt injury

A

Deceleration injury
Compression injury

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2
Q

Name 2 types of penetrating injury

A

Low-velocity injuries
High-velocity injuries

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3
Q

List 6 lethal injuries

A

Airway obstruction
Tension pneumothorax
Open pneumothorax
Massive haemothorax
Flail chest
Cardiac temponade

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4
Q

What is the primary survey provided in ER

A

ABCDE approach to rescuitation
Lethal 6 injuries
Abdominal injury (identify and manage internal bleeding)

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5
Q

What is the secondary survey for ER

A

Head to toe evaluation and history taking
Placement of lines and continuation of care from primary survey
Radiological investigations

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6
Q

List 6 hidden injuries

A

Pulmonary contusion
Myocardial contusion
Traumatic disruption of the aorta
Traumatic diaphragmatic rapture
Tracheobronchial injury
Oesophogeal trauma

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7
Q

Precautions and contraindications related to abdominal injury

A

Analgesia
Caution with drainage tubes
Caution with manual chest therapy over anterior basal lung segments
Vigorous chest percussions may cause alveolar collapse
Wound support during suction and coughing
Open abdomen - restric head tilt to 25 degrees
If abdominal compartment syndrome develops no turning of patient

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8
Q

What is a TBI

A

An alteration in brain function or other evidence of brain pathology caused by external force

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9
Q

What categories can TBI be classified based on

A

Mechanics of injury
Location of injury
Extent of injury
Severity of injury

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10
Q

What is epidural haematoma

A

Blood accumulates between the skull and dura mater
Arterial bleeding from middle meningeal artery
Temporal or temporo-parietal region often affected

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11
Q

What is subdural haematoma

A

Blood accumulated between dura mater and arachnoid meninges
Haematoma occurs due to damage occurring cerebral cortex and venous sinus

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12
Q

What is subarachnoid haematoma

A

Bleeding in the subarachnoid space
Ruptured aneurysms occur here (can be Traumatic or not)

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13
Q

What is intracerebral haematoma

A

Collection of fluid in the brain tissue
Majority of lesions occur in the frontal and temporal lobes

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14
Q

What is primary head injury

A

The initial Traumatic force applied to the head that causes neuronal damage due to contusion, damage to blood vessels and axonal injury

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15
Q

What is a secondary head injury

A

The delayed non-mechanical damage that develops hours and days after the primary injury

The degree of secondary damage depends on duration of cerebral ischemia and intracranial hypertension

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16
Q

What are the factors that lead to ischemia

A

Hypoxaemia
Systemic hypotension
Cerebral hypo-perfusion
Inflammatory processes
Cerebral oedema
Hypercapnia

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17
Q

Factors that influence outcomes of a patient following a TBI

A

Severity of primary and secondary injuries
Low GCS findings on presentation
Advanced age
Presence of comorbidities

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18
Q

What is the GCS rating of Severity of TBI

A

Mild (13,14)
Moderate (9-12)
Severe (3-8)

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19
Q

What is intracranial pressure

A

Pressure within three cranium
Influenced by :
Blood volume, brain tissue and CSF in rigid skull

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20
Q

Name the ICP monitoring devices

A

Epidural sensor
Subdural bolt
Subarachnoid bolt
Parenchymal catheter
Intraventricular catheter

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21
Q

Factors that may increase ICP

A

Suction
Head movements
Turning
Head down positions
MHI
manual techniques
Seizures
Pain
Anxiety
Increased BP and abdominal pressure

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22
Q

Late signs of raised ICP

A

GCS of 3/10 or 3/15
Abnormal motor response (abnormal posture or flaccidity)
Cushing’s response (hypertension, bradycardia, increased temp and altered respiratory pattern)

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23
Q

What is cerebral perfusion pressure

A

The BP gradient across the brain

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24
Q

Contraindications for physiotherapy management

A

Cardiovascular instability
Neurological instability I.e seizures
Non-reactive dialted pupils
Temp above 40 degrees
Nasal suction with base of skull fracture
Haematological instability (platelets lower than 50x10^9L)

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25
Q

Define DIC (Disseminated intravascular coagulation)

A

A condition in which small blood clots develop throughout the bloodstream blocking small blood vessels due to overactive proteins

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26
Q

What is phase 1 of DIC

A

Thrombotic phase
Numerous small thrombi and emboli form throughout the microvasculature causing blockage of circulation and ischemic organ damage.

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27
Q

What is phase 2 of DIC

A

Fibrinolytic phase
The fibrin degradation products suppress thrombin and have an anti-haemostatic effect aggravating bleeding

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28
Q

Risk factors for the development of DIC

A

Blood transfusion reaction
Cancer
Pancreatitis
Liver disease
Infection of blood
Pregnancy complications
Recent surgery or anesthesia

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29
Q

Signs and symptoms of excessive blood clotting

A

Chest pain with shirtless of breath (PE)
Pain, swelling and redness if DVT
Headaches, speech changes, paralysis and dizziness (stroke)
Heart attack

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30
Q

Signs and symptoms of internal bleeding

A

Blood in your urine
Blood in stools (dark, tarry colour)
Headaches, double vision and seizures

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31
Q

Define acute renal failure

A

Sudden loss of the ability of the kidneys to excrete waste, concentrated urine, conserve electrolytes and maintain fluid balance in the body

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32
Q

Comorbidities associated with development of ARF

A

Hypertension
Diabetes
Chronic heart failure
Liver disease
Obesity
Chronic infection
Autoimmune disease

33
Q

Clinical presentation of ARF

A

Decreased urine output
Swelling of the legs, ankle and feet
Shortness of breath
Fatigue
Fever
Loss of appetite
Arrhythmia
Nausea and vomiting
Confusion
Joint pain
Coma and seizures
Nosebleed

34
Q

Symptoms of ARDS

A

cyanosis
Decreased respiratory compliance
Hypoxemia
Acute onset of severe dyspnoea

35
Q

Risk factors for development of ARDS

A

Sepsis
Multiple blood transfusions
Pnuemonia
Drug overdose
Near drowning
DIC
multiple trauma
Diabetes

36
Q

Classification of ARDS

A

Primary or secondary

37
Q

Primary ARDS

A

Failure of lungs alone
Direct pulmonary injury e.g near drowning, gastric Aspiration

38
Q

Secondary ARDS

A

Failure of lungs due to systemic disease
Sepsis
Multiple trauma
Multiple transfusions

39
Q

List the 3 stages of ARDS

A

Exudative
Poliferative
Fibrotic

40
Q

Exudative phase

A

1st week of onset symptoms
Increased pulmonary vascular permeability leading to alveolar oedema
Intrapulmonary shunt causes severe hypoxemia
Surfactant lost due to oedema
Damage to type 1 and 2 pnuemocytes
Decreased lung compliance
Pt presents with dyspnoea and tachypnoea

41
Q

Poliferative phase

A

Week 1-2
Activation of type 2 pnuemocytes and fibroblasts
Lung compliance decreased and become heavy
Airway and lung tissue resistance increase

42
Q

Fibrotic phase

A

More than 2 weeks
Macroscopically coarse cobble-stoned lungs
Excessive depositions of collagen and diffuse fibrosis
Further decreased lung compliance

43
Q

Benefits of prone position

A

Decrease intrapulmonary shunt
Decrease mortality
Decrease the amount of FIO2 needed
Improves oxygenation
No haemodynamic complication

44
Q

Advantages of negative pressure ventilator

A

Decreased risk for pnuemonia
Decreased need for sedation
Less decrease in cardiac output
Cheaper than positive pressure ventilation
Comfortable for patient
Easy to wean patient

45
Q

Disadvantages for negative pressure ventilation

A

Difficulty to suction pt
Inability to generate high intrapulmonary pressures
Limited access to the pt body
Contraindicated where you cannot maintain upper airway
Pressure sores

46
Q

Indications for mechanical ventilation

A

PaO2 less than 60mmHg
Inability to clear secretions independently
Increasing exhaustion of respiratory muscles
Increased confusion and inability to protect airway
Loss of bulbar function
Life threatening disorder of another system
Elective preoperative ventilation
Therapeutic hyperventilation
GCS of 8 or lower with TBI
CNS depression
Burns above 50% BSA OR 40% with inhalation injury

47
Q

Signs of Tracheal tube obstruction

A

Patient anxiety
Use of the accessory muscles and possible nasal flaring
Dismissed breathe sounds on auscultation
High PIP and low tidal volume readings

48
Q

What is the purpose of hemodynamic monitoring ?

A

To determine the patient’s efficacy of cardiac function and to determine their fluid replacement needs

49
Q

What are the associated complications associated with Swann-Ganz Catheter

A

Invasive monitoring (pulmonary artery catheter)
Pulmonary infarction
Perforation Of the pulmonary artery
Ballon can rapture leading to pulmonary embolism
Catheter kink and intra cardiac knotting
Pneumothorax

50
Q

What’s to remember with cardiac function index

A

Normal (4.5-6.5l/min)
If less than norm pt may not tolerate techniques increasing demand of myocardium

51
Q

What to remember with pulmonary occlusion pressure (PAOP)

A

Normal 6-12 mmHg
If low pt may not be able to tolate positive pressure techniques (MHI, VHI or upright sitting)

52
Q

What to remember with systemic vascular resistance (SVR)

A

Normal (700-1600 dyn/s cm3)
If low pt may not tolerate positive pressure interventions

53
Q

What is hypoxia

A

Inadequate deliver of oxygen to body tissues (PaO2 less than 60mmHg)

54
Q

List the pathophysiology Basis of hypoxemia

A

V/Q mismatch
Hypoventilation
Diffusion limitation

55
Q

List the different types of hypoxemia

A

Anaemic hypoxemia
Stagnant hypoxemia
Histotoxic hypoxemia
Hypoxic hypoxemia

56
Q

Clinical features of hypoxemia

A

Restlessness
Confusion
Sweating
Tachycardia
Hypertension
Cyanosis

57
Q

Worsening neurological signs of hypoxemia

A

Blurred vision
Tunnel vision
Loss of coordination
Impaired judgement
Convulsions

58
Q

Long-term effects of hypoxemia

A

Pulmonary hypertension
Death
Cardiac arrthymias
Tissue damage and organ dysfunction

59
Q

What is non-invasive ventilation

A

Delivery of mechanical ventilation to the longs with techniques that do not involve the endotracheal airway

60
Q

Aims of non-invasive ventilation

A

Improve gas exchange
Optimize lung volumes
Reduce WOB

61
Q

List non-invasive ventilation

A

Negative pressure vent
Abdominal displacement vent
Positive pressure vent
Diaphragm pace (stimulate phrenic nerve)
Glassopharyngeal breathing

62
Q

Explain how does the negative pressure vent works

A

It’s works by delivery pressure below the atmospheric pressure increasing transpulmonary pressure to increase and the atmospheric pressure in the mouth to inflate the alveolar

Exhalation is passive

63
Q

Explain how does the abdominal vent work

A

Patient relies on the displacement of the abdominal visceral organ encourage motion of the diaphragm and ventilation

64
Q

Explain how does the positive pressure vent work

A

Delivering of increased pressure of gas (above atmospheric pressure) to the airways causing alveolar distensing pressure therefore inflating the lungs

65
Q

What is CiPAP

A

continous positive airway pressure
During both inhalation and Exhalation

66
Q

Benefits of CPAP

A

Constant p during inhalation and Exhalation increased FRC
opens collapsed alveolar
Less intrapulmonary shunting occurs
Improved oxygenation

67
Q

What is BiPAP ?

A

Cycles between 2 different positive pressures

68
Q

List the 2 different kinds of BiPAP

A

Inspiratory PAP
Expiratory PAP

69
Q

List the short term goal of NIPPV

A

Reduce work of breathing
Improve or stabilize gas exchange
Optimize pt comfort
Good patient ventilator synchrony
Minimize risk
Avoid intubation where possible

70
Q

List long term goal of NIPPV

A

Improve sleep duration quality
Enhance functional status
Prolong survival

71
Q

List the 3 stages of shock

A

Preshock
Frank shock
Refractory shock

72
Q

List the types of shock?

A

Cardiogenic shock
Hypovolaemic shock
Neurogenic shock
Septic shock

73
Q

List the classification of ICU acquired Weakness

A

Critical illness polyneuropathy (CIP)
Critical illness myopathy (CIM)
Critical illness neuromyopathy (CINM)

74
Q

Name the problems that critically I’ll patients often present with

A

Increased WOB
decreased lung volume and lung compliance
Decreased mucociliary clearance and secretion retention
Decreased gas exchange
Weakness of extremely and resp muscles

75
Q

Complications following OHS

A

post operative pulmonary complications
Cardiovascular instability
Sternal complications
Stroke
Hemorrhage
Myocardial ischemia

76
Q

List the risk factors for sternal complications (Pre-screen)

A

Smoking
Diabetes
Obesity
COPD
large chest circumference
Females with large breasts

77
Q

List pathophysiological basis of hypoxemia

A

VQ mismatch
Hypoventilation
Diffusion limitation

78
Q

List the different types of hypoxaemia

A

Anaemic hypoxemia
Stagnant hypoxemia
Histotoxic hypoxemia
Hypoxic hypoxemia

PHYSIO 4th yr (3 decks)

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