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accs > kettering section g: pathology > Flashcards

kettering section g: pathology Flashcards

1
Q

Respiratory care for Guillain Barre patient

A
  • Closely monitor Vt, VC, NIF should intubation/mechanical ventilation be indicated
  • Oxygen therapy for hypoxemia
  • Hyperinflation therapy (IS/SMI, IPPB)
  • Pulmonary hygiene
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2
Q

Disease-modifying treatment for Guillian-Barre

A
  • Either plasma exchange or intravenous immune globulin (IVIG)
  • Not recommended to do both plasma exchange and IVIG
  • Do not use glucocorticoids
    (UTD)
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3
Q

What findings would be typical in primary assessment of Guillian-Barre patient?

A
  • Febrile illness in last 1-4 weeks, often viral in nature
  • Acute weakness, especially in the legs
  • Shallow breathing
  • Diminished breath sounds
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4
Q

What findings would be typical in secondary assessment of Guillian-Barre patient?

A
  • PFTs: Decreased Vt, FVC, NIF
  • ABG: acute ventilatory failure with hypoxemia; watch for PaCO2 > 45 mmHg
  • Lumbar puncture: high protein level in CSF
  • Electromyography: abnormal
  • Nerve conduction studies: abnormal (Kettering, UTD, CMARD)
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5
Q

What stressors can provoke clinical manifestations of myasthenia gravis?

A
  • Emotional upset
  • Physical stress
  • Exposure to extreme temperature changes
  • Pregnancy
  • Febrile illness
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6
Q

What primary assessment findings would be typical for myasthenia gravis exacerbation?

A
  • Gradual onset of weakness
  • Previous admissions for MG
  • Weakness improves with rest
  • Ptosis
  • Diplopia
  • Dysphagia
  • Shallow breathing
  • Diminished
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7
Q

What secondary assessment findings would be typical for myasthenia gravis?

A
  • Decreasing Vt, VC, NIF
  • Acute ventilatory failure with hypoxemia watch for PaCO2 > 45 mmHg
  • Reduced Vt, FVC
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8
Q

What test is given to assess myasthenia gravis?

A

Tensilon test

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9
Q

How is the tensilon test interpreted?

A

If Vt, VC, NIF, and weakness improve with Tensilon: Myasthenic crisis.
If Vt, VC, NIF, and weakness worsen with Tensilon: Cholinergic crisis.

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10
Q

Maintenance drugs for myasthenia gravis

A

Prostigmine (Neostigmine)

Pyridostigmine (Mestinon, Regonol)

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11
Q

What class of drugs is indicated for myasthenia gravis?

A

anticholinesterase therapy

cholinesterase inhibitors

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12
Q

What medication should be given for myasthenia gravis patient caught in a cholinergic crisis?

A

Atropine will relieve the symptoms of a cholinergic crisis.

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13
Q

What psychiatric morbidity is common after critical illness?

A

Depression
Anxiety
Post-traumatic stress disorder

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14
Q

What percentage of ARDS survivors will experience chronic cognitive impairment?

A

70-78%

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15
Q

What percentage of ICU survivors will experience chronic cognitive impairment?

A

25-78%

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16
Q

Generally define “cognitive ability.”

A

The way a person experiences and thinks about the world.

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17
Q

What capacities could be impaired in a person with cognitive impairment?

A 
Intelligence
Attention
Learning
Memory
Language
Visual/spatial skills
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18
Q

What elements of executive function could be impaired in a patient with cognitive impairment?

A 
Reasoning
Decision making
Planning
Problem solving
Working memory
Sequencing
Control
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19
Q

Define delirium.

A

An acute behavioral disturbance characterized by

  • Acute confusion
  • Inattention
  • Disorganized thinking
  • Fluctuating mental status
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20
Q

Name subtypes of delirium.

A
  • Hypoactive or quiet delirium
  • Hyperactive delirium
  • -though delirium is dynamic and can fluctuate between hypo- and hyperactive types
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21
Q

Describe hypoactive delirium.

A

Reduced mental & physical activity

Inattention

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22
Q

Describe hyperactive delerium

A

Agitation
Combativeness
At risk for self-extubation, pulling lines, falling

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23
Q

Is ICU delirium a permanent state?

A

Kettering: No, ICU delirium is temporary

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24
Q

The immunosuppression of HIV can lead to what categories of conditions?

A
  • Opportunistic infections (such as pneumonias)
  • Secondary neoplasms
  • Neurologic manifestations
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25
Q

What opportunistic pulmonary infections can plague people with HIV?

A
  • Pneumocystis carini/jiroveci
  • Toxoplasmosis
  • Candidiasis (esophageal, tracheal, pulmonary
  • Mycobacteriosis (atypical TB)
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26
Q

Name populations at risk for HIV.

A
  • Homosexual/bisexual men
  • IV drug abusers
  • Recipients of blood transfusion (e.g., patients with hemophilia)
  • Imprisoned people
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27
Q

Name the three phases in which systemic immune complex diseases develop.

A
  1. Formation of antigen-antibody complexes in circulation.
  2. Deposition of immune complexes in various tissues.
  3. Inflammatory reactions in various sites throughout the body.
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28
Q

What results from the 3 phases of systemic immune complex disease development?

A

Vasoconstriction and edema

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29
Q

What happens during transplant organ rejection?

A

An immunological reaction causing hypersensitivity response of the host to the donor organ.

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30
Q

How do burns affect the cardiovascular system?

A
  • Increased capillary permeability & fluid loss result in hypovolemia.
  • Loss of fluids decreases preload and cardiac output.
  • After 24-48 hours, inflammatory mediators influence cardiac contraction and relaxation.
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31
Q

How should the myocardial depression of burn injury be treated?

A

Fluids

Inotropic agents

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32
Q

What challenges complicate blood pressure monitoring in burn patients?

A
  • Post-burn edema decreases accuracy of cuff blood pressure

* Vasoconstriction from catecholamine release decreases accuracy of arterial blood pressure

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33
Q

Signs and symptoms of cyanide poisoning.

A 
Lethargy
Nausea
Headache
Weakness
Coma
Decreased Ca-vO2
Severe metabolic acidosis
Unresponsiveness to fluids or oxygen
ST elevation possible on EKG
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34
Q

Treatment for cyanide poisoning

A
  • 100% oxygen (Kettering)
  • Inhaled amyl nitrate pearls Kettering)
  • Hydroxocobalamine (Cyanokit)
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35
Q

The asphyxiant gases and hypoxic environments of house fires.

A
  • FiO2 < 0.21
  • Carbon monoxide
  • Cyanide
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36
Q

Fire environment insults to pulmonary system

A

Inflammation
Acid-base imbalance
Airway injury
Chest wall constriction

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37
Q

Watch for these pulmonary problems in smoke inhalation

A
  • Transient pulmonary hypertension
  • Decreased lung compliance
  • Hypoxia
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38
Q

Infections of burn wounds may have what pulmonary consequence?

A

ARDS

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39
Q

Why might burn injury patients be extubated early?

A

To avoid VAP and tracheal stenosis.

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40
Q

What percentage of burn patients suffer from smoke inhalation injury?

A

10-30%

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41
Q

How should upper airway edema in the burn patient be treated?

A

With standard therapy–

  • cool aerosol
  • oxygen
  • racemic epinephrine
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42
Q

What intervention can be considered for severe inhalation injury?

A

Intrapulmonary percussive ventilation (IPV)

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43
Q

What clinical events common to burn patients might lead to early renal failure?

A
  • -Delayed resuscitation
  • -Hypotension
  • -Rhabdomyolysis (especially with electrical burns)
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44
Q

What developments in burn patients may lead to late renal failure?

A
  • Sepsis
  • Toxic medications
  • Pre-existing conditions
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45
Q

Early responses to renal failure in burn patients.

A
  • Fluid resuscitation
  • Monitor I/Os
  • Monitor lines for sepsis
  • Monitor for pneumonia
  • Monitor for urinary tract infections
  • -Some patient may eventually require dialysis
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46
Q

Measures for GI system in burn patients.

A
  • -Watch for ileus, common in patients with burns > 20% TBSA

- -Start early feeding, oral or enteral

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47
Q

What endocrine system changes can be anticipated in burn patients?

A
  • -Hypothalamus secretes antidiuretic hormone to increase fluid retention
  • -Adrenocorticotropic hormones release aldosterone & glucocorticoid cortisol
  • -Neurotransmitters adrenaline & noradrenaline released.
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48
Q

Burn patients suffer these hematopoietic system effects relevant to respiratory care.

A

Decreased RBCs, Hgb, Hct. with resulting decreased oxygen carrying capacity.

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49
Q

Anticipate these alternations to the immune system in burn patients.

A
  • -Risk of infection that rises in direct relation to size of burn
  • -Loss of barrier function in burned skin, allowing pathogens passage to the body
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50
Q

Kettering guides to ventilating bariatric patients.

A
  • Key Vt to IBW rather than actual weight
  • Set Vts at 6-8 mL/kg IBW for lung protection
  • Use PEEP to offset chest weight
    (monitor for decreased venous return/cardiac output/BP)
  • Avoid common problem of pt/ventilator asynchrony (use spontaneous modes of ventilation; PS may be useful)
  • Elevate head of bed to prevent aspiration & VAP
  • Consider early extubation to NPPV or CPAP
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51
Q

What features, in obese patients, correlate with difficult intubation?

A
  • Large or bull neck

* Mallampati score >= 3

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52
Q

Take these actions if snoring with daytime somnolence and/or apneic periods are observed in obese patient.

A
  • Evaluate with sleep study at discharge
  • Provide CPAP or BPAP post-operatively
  • Use a simple evaluation tool such as the Epworth Sleepiness Scale
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53
Q

Common risks for obese patients

A
  • Aspiration
  • Inadequate ventilation via BVM
  • Difficult intubation
  • Hypoxemia secondary to apnea
  • Atelectasis
  • Hemodynamic instability
  • DVT and pulmonary embolism
  • Post-op respiratory dysfunction
  • Delayed recovery from surgery
  • Decreased ability to respond to stress (fr HTN to hyperglycemia)
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54
Q

What is the connection between obesity and rhabdomyolysis?

A
  • The two often connected
  • Also called “Pressure-induced myoglobinuria”
  • Caused by excessive pressure on tissue from body weight
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55
Q

How does one watch for rhabdomyolysis in the obese patient?

A
  • Watch for dark or brown urine
  • Watch for acute renal failure
  • Monitor CPK
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56
Q

How does one treat rhabdomyolysis in the obese patient?

A

Treat aggressively with fluids.

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57
Q

What medical conditions are associated with OSA in the obese?

A
  • Obesity Hypoventilation Syndrome (OHS)
  • Pickwickian Syndrome
  • Compensated respiratory acidosis
  • Cor pulmonale
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58
Q

Circulatory conditions common preoperatively in obese patients?

A

Systemic HTN

Pulmonary HTN

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59
Q

How is “obesity” defined?

A

BMI >= 30 kg/m2

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60
Q

Supportive treatment for Guillien-Barré:

A
  • Manage initially in the ICU because patients are at risk of neuromuscular respiratory failure and severe autonomic dysfunction.
  • Monitor VC and NIF while weakness is progressing should mechanical ventilation be indicated.
  • Monitor heart rhythms and blood pressure against development of arrhythmias–sinus tachycardia most common problem.
  • Daily auscultation for bowel silence and development of adynamic ileus.
  • Manage pain primarily with gabapentin or carbamazepine.
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61
Q

What is apheresis?

A

The general technique of extracorporeal blood purification whereby one constituent is removed (by centrifugation or membrane filtration) and the remainder is returned to the patient. (LITFL)

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62
Q

What is plasmapheresis?

A

A subset of apheresis– blood purification technique designed for removal of large molecular weight substances from the plasma; the plasma is removed by centrifigation or membrane filtration and is replaced with “cleaned” autologous plasma or by donor plasma or by another replacement colloid solution (“plasma exchange”). (LITFL)

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63
Q

Considering post-injury resuscitation for orthopedic trauma, what constitutes the acute period?

A

12-24 hours

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64
Q

Resuscitation goals following orthopedic trauma should be concerned with what principles?

A
  • Optimizing tissue perfusion
  • Ensuring normothermia
  • Restoring coagulation
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65
Q

What is the goal-directed therapy for post-injury resuscitation in orthopedic trauma?

A
  • Hemoglobin > 10 g/dL
  • Cardiac index > 3.8 L/min/m2
  • Oxygen delivery DO2 > 500mL/min/m2
  • Temperature > 35ºC
  • Base excess: ≥ -6
  • Normal coagulation indices
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66
Q

Patient recovering from orthopedic trauma has ongoing need for pressers. What condition should the clinician consider?

A

Adrenal insufficiency.

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67
Q

What areas are most at risk in blunt trauma injuries?

A
  • Liver
  • Spleen
  • Pancreas
  • Mesenteric arteries
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68
Q

How should blunt trauma injuries to abdominal organs be assessed?

A

With ultrasound and/or peritoneal lavage.

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69
Q

Considerations for abdominal aortic injuries in trauma.

A
  • They present primarily with signs/symptoms of hypotension
  • They can be diagnosed with ultrasound
  • They may be life-threatening
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70
Q

In instances of facial trauma, what is the highest priority?

A

Managing the airway
—use chin-lift/jaw thrust to open airway
—prepare for emergent tracheostomy/cricothyrotomy

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71
Q

What conditions in facial trauma indicate intubation?

A
  • Glasgow Coma Scale <9
  • Sustained seizure
  • Unstable midface trauma
  • Direct injury to airway
  • Aspiration risk
  • Oxygenation problems
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72
Q

What does ORIF stand for?

A

Open Reduction Internal Fixation

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73
Q

Why does orthopedic trauma require vigilance?

A
  • Missed fractures cause significant morbidity & mortality
  • Unrecognized ischemia or compartment syndrome may result in amputation
  • Unrecognized ischemia can produce life-threatening rhabdomyolysis and resulting electrolyte imbalance
  • Fracture hematoma can cause SIRS and multiple organ failure
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74
Q

How does fat embolism syndrome from long bone fractures present?

A

Classic triad:

  • -hypoxemia (Kettering: ARDS)
  • -neurological abnormalities
  • -characteristic red-brown petechial rash
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75
Q

Prolonged post-op care for orthopedic trauma may result in what lethal triad that can leave a patient dead in 24 hours?

A
  • Acidosis
  • Coagulopathy
  • Hypothermia
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76
Q

Kettering’s points for spinal cord injury, respiratory failure, and intubation

A
  • Elect early intubation
  • Consider hypoxia and hypercapnea to be late signs of respiratory failure
  • Intubate if VC < 10mL/kg
  • Intubate if NIF < -20 cmH2O
  • Note that NPPV is contraindicated
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77
Q

What are the most common causes of death in patients with spinal cord injury?

A
  • Pneumonia
  • Septicemia
  • Pulmonary embolism
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78
Q

Two key features of shock due to neurological causes

A
  • Loss of peripheral vasoconstriction

* Loss of cardiac compensation

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79
Q

Treatment for shock due to neurological problems

A
  • Volume resuscitation
  • Vasoactive medications: norepinephrine, dopamine, & phenylephrine
  • Methylprednisolone within 8 hours of injury for > 23 hours (may increase rate of respiratory complications)
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80
Q

How does Kettering say to clear cervical spine?

A
  • Normal flexion/extension films

* Normal MRI within 48 hours

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81
Q

Secondary injuries from spinal cord injury–those beyond injury from cord compression.

A 
Systemic and vascular insults—
• Hypotension
• Electrolyte imbalance
• Edema
• Excitotoxicity
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82
Q

Kettering’s definition of trauma

A

Any bodily injury caused by any kind of accident—motor vehicle crash, etc.

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83
Q

What circumstances typically give rise to decelerating trauma?

A

MVC

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84
Q

What are the initial tasks of trauma care?

A
  • Secure airway—assume injury to cervical spine and full stomach
  • Support ventilation and oxygenation
  • Support circulation and perfusion
  • Goal-directed therapy to the end points of C.I., DO2, SvO2
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85
Q

Emergent treatment for tension pneumothorax

A
  • 14-16 gauge IV catheter inserted into 2nd or 3rd intercostal space in the mid-clavicular line
  • Follow with chest tube insertion
  • Give fluids to maintain cardiac output
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86
Q

Emergent treatment for flail chest.

A
  • Stabilize chest wall

* Consider mechanical ventilation

87
Q

Emergent treatment flail chest or sucking chest wound.

A
  • Insert chest tube
  • Endotracheal intubation
  • Cover sucking chest wound to seal opening
88
Q

Classically, how is cardiac tamponade/hemopericardium said to present present clinically ?

A

By Beck’s Triad:
• Hypotension
• Jugular venous distention
• Muffled heart sounds

Note that pulses paradoxes may be present.

89
Q

Treatment for cardiac tamponade

A
  • Pericardiocentesis
  • Subxiphoid pericardial window preferred
  • Thoracotomy in ED
  • Note that decompression only buys time
  • Avoid positive pressure ventilation to minimize effects on venous return
90
Q

What preparation does Kettering recommend to meet the fluid requirements of an incoming trauma patient?

A
  • Prepare to place two large-bore IV lines (for blood products)
  • Commercial warming equipment
  • Simple IV pressure bags
  • Colloid, crystalloid, & blood products
91
Q

Why are pressure bags required for IV lines?

A
  • To increase transfusion pressure

* To increase transfusion volume

92
Q

Name the leading crystalloids

A
  • Normal saline

* Lactated Ringer’s

93
Q

How much crystalloid is required to replace blood?

A
  • 3L crystalloid required to replace 1L of lost blood
  • Crystalloid equilibrates in interstitial and intercellular spaces
  • Crystalloid, however, lacks the oxygen delivery power of RBCs
94
Q

How do subdural hematomas form?

A
  • May occur during a decelerating injury

* Results from sheering of veins between brain and venous sinuses

95
Q

How does an SDH appear on CT scan?

A

As a crescent-shaped hyperdensity that follows the contour of the brain (also in Hess 1017)

96
Q

What kind of CT scan should we order for SDH?

A

A CT without contrast—since contrast dye can increase ICP

97
Q

What mortality is associated with SDH?

A

5-60% mortality!

98
Q

What condition is commonly associated with epidural hematoma?

A

Skull fracture

99
Q

How do patients with epidural hematoma present?

A

Awake and alert—then then become comatose

100
Q

What mortality is associated with epidural hematoma?

A

With surgical evacuation, mortality comes down to 5-10%

101
Q

What conditions form the TBI family?

A
  • SDH
  • Epidural hematoma
  • Cerebral contusion
  • Intraventricular hemorrhage
  • Subarachnoid hemorrhage
  • Diffuse axonal injury
102
Q

How should ICP, MAP and CPP be managed, according to Kettering?

A

—Maintain ICP no higher than 20-26
—Maintain mean arterial pressure > 90 mmHg
—Maintain cerebral perfusion pressure (CPP) > 60 mmHg

103
Q

For the TBI patient—stabilize critical life functions and place cervical spine in precautions—and then assess—

A
  • Level of consciousness (ability to speak, follow commands, vision and pupillary response)
  • Perform ice water caloric reflex test
  • Assess Glasgow Coma Scale
104
Q

What might the ice water caloric reflex test reveal?

A

May indicate brainstem injury.

105
Q

What is malignant hyperthermia?

A

A rapidly increasing temperature caused by uncontrolled skeletal muscle metabolism leading to rhabdomyolysis and death

106
Q

Name anesthesia reversal agents for neuromuscular blocking agents.

A

Anticholinesterase (neostigmine, edrophonium, pyridostigmine)
Anticholinergic (atropine, glycopyrrolate)

107
Q

What med is the old-school treatment for post-op delerium? What kind of drug is it? What side effects does it have and not have?

A

Haloperidol
Which is an antipsychotic with minimal hypotensive effects
With the potential side effect of Torsades de Pointes

108
Q

What consequences follow from uncontrolled pain the the post-op patient?

A

Sympathetic nervous stimulation

  • -elevates catecholamine levels
  • -tachycardia
  • -hypertension
  • -increased SVR
  • -increased myocardial O2 consumption
109
Q

What consequences follow from upper abdominal and thoracic pain in post-op patients?

A
  • -Inability to breathe deeply
  • -Inability to cough
  • -Development of atelectasis
  • -Retained secretions
  • -Hypoxemia
  • -Pneumonia
110
Q

Name causes of hypoxemia post-operatively.

A
  • Residual anesthesia or muscle relaxant
  • Upper airway obstruction due to decreased level of consciousness
  • Pulmonary Edema
  • Cardiac ischemia
111
Q

Name causes of post-operative pulmonary edema.

A
  • Heart failure
  • ARDS
  • Aspiration
  • Infection
  • Trauma
  • Transfusion reaction
  • Neurogenic pulmonary edema from head injury/trauma
112
Q

What is negative pressure pulmonary edema?

A

Pulmonary edema developing after strenuous inspiratory effort against an obstructed airway

  • May develop up to 10 hours after effort
  • Occurs typically in young, vigorous adult who had laryngospasm
  • Treatment is support
113
Q

What broad changes can occur during malignant hyperthermia?

A
  • -Oxygen consumption can increase three fold

- -Blood lactate can increase 15-20 fold

114
Q

What are the signs of malignant hyperthermia?

A
  • -Skeletal muscle rigidity
  • -Tachycardia
  • -Hypertension
  • -Increased PetCO2
  • -Acidosis
  • -Arrhythmias
  • -Hyperthermia (body temperature may be >109degrees F
  • -Cyanosis
  • -Electrolyte abnormalities
  • -Increased creatinine
  • -Myoglobinuria
  • -Coagulopathy
  • -Cardiac failure
  • -Pulmonary edema
115
Q

When patient presents more than one sign of malignant hyperthermia, what further assessment is warranted?

A
  • -Draw ABG
  • -Draw central venous blood gas
  • -Evaluate for respiratory acidosis and hyperkalemia
116
Q

How should malignant hyperthermia be treated?

A
  • Discontinue anesthetics (to stop the triggering agent)
  • Hyperventilate with 100% oxygen (to compensate for acidosis)
  • Dantrolene sodium (for muscle relaxation)
  • Sodium bicarbonate (for severe acidosis)
  • Apply ice, cold fluids, cooling blanket, heat exchanger (to control fever)
  • Monitor intake/output
117
Q

How does dantrolene sodium work?

A

Dantrolene sodium is a postsynaptic muscle relaxant that lessens excitation-contraction coupling in muscle cells. It inhibits the release of Ca2+ ions from sarcoplasmic reticulum stores by antagonizing ryanodine receptors. (W)

118
Q

How is diagnosis of cystic fibrosis secured?

A
  • -Sweat chloride test
  • -Chloride level > 60mEq/L positive for CF
  • -Two positive tests required to confirm diagnosis
  • -In-utero genetic testing now available
119
Q

Which organs are affected by CF?

A
  • Lungs
  • Pancreas
  • Liver
  • GI tract
120
Q

What digestive problems plague people with CF?

A
  • Hypoproteinemia & malnutrition (from lack of digestive enzymes)
  • Diabetes 1 or 2 (can be caused by pancreatic problems
121
Q

What about the noses of patients with CF?

A
  • Sinus infections and nasal polyps common

* Nasal intubation may be contraindicated

122
Q

Name common bacteria behind cystic fibrosis pneumonia.

A 
●Pseudomonas aeruginosa
●Staphylococcus aureus (methicillin-sensitive or methicillin-resistant species)
●Burkholderia cepacia complex
●Nontypeable Haemophilus influenzae
●Stenotrophomonas maltophilia
●Achromobacter species
●Nontuberculous mycobacteria
(UTD)
123
Q

Common secondary pulmonary problem for patients with cystic fibrosis.

A

Bronchiectasis.

124
Q

Why are patients with cystic fibrosis so thin?

A
  • GI tract lacks digestive enzymes
  • Hypoproteinemia
  • Malnutrition
125
Q

Why do people with cystic fibrosis get diabetes?

A

Because of problems with pancreas.

126
Q

How might PE appear on EKG?

A

Anterior t-wave inversion.

127
Q

Should you order a CXR for PE?

A
  • Not helpful for PE.

* May r/o other processes.

128
Q

How might CXR suggest PE?

A
  • Abrupt cutoff of pulmonary artery
  • Focal oligemia (localized engorged vessels)
  • Distention of proximal portion of pulmonary artery
  • -Classic “wedge-shaped infiltrate” is rarely seen
129
Q

What is the imaging of choice for PE?

A

Spiral CT with contrast dye

130
Q

What test is helpful for PE for a hemodynamically unstable patient?

A

Echocardiogram–can help differentiate PE from non-PE events.

131
Q

What echocardiogram findings are suggestive of PE?

A
  • Right-sided thrombi
  • Right ventricular dilation
  • Hypokinesis
  • Tricuspid regurgitation
  • Paradoxical shift of ventricular septum
132
Q

Name the hemodynamic changes in pulmonary embolism.

A
  • Increased PVR
  • Increased right heart afterload
  • Increased PAP
  • Increased MPAP
  • Decreased left-heart preload
133
Q

How does PE cause hypoxia?

A
  • Increased alveolar deadspace
  • V/Q mismatch
  • Right to left shunting
  • Decreased mixed venous oxygen saturation (with cardiogenic shock)
134
Q

How can DVT be detected?

A
  • Lower limb venography

* Compression ultrasound in ICU

135
Q

Why does DVT pose a problem?

A
  • DVT often goes undiagnosed

* Risk following major surgery or trauma in absence of prophylaxis

136
Q

Common causes of DVT.

A
  • -Blood clot that has migrated from another location

- -Fatty embolism following traumatic long-bone fracture

137
Q

What happens when mechanical ventilation is initiated in the patient with pulmonary hypertension?

A
  • RV afterload increases
  • RV preload decreases
  • PEEP–increases PAP and PVR
  • Permissive hypercapnea–increases PAP and PVR
138
Q

How should hemodynamically unstable pulmonary hypertension be treated?

A

Vasopressors–

  • Dobutamine reduces PVR and increases cardiac output
  • Also increases shunting and may decrease oxygenation
139
Q

Name the prostacyclins–generic and commercial names

A
  • Epoprostenol (Flolan)
  • Treprostinil (Tyvaso)
  • Iloprost (Ventavis)
140
Q

Medications for pulmonary hypertension

A
  • Prostacyclins
  • Inhaled nitric oxide
  • Oral pulmonary vasodilators
141
Q

Name a common oral pulmonary vasodilator that can be used for pulmonary hypertension.

A

Sildenafil (Viagra, Revatio)

142
Q

Any problem with pulmonary arterial hypertension with Afib or AV block?

A
  • Can reduce cardiac output

* Should be treated

143
Q

Why is fluid management in the setting of pulmonary arterial hypertension challenging?

A
  • Hypovolemia results in decreased preload and cardiac output (right ventricle is preload dependent)
  • Hypervolemia can exacerbate right ventricular overload (decreases left ventricular filling which decreases cardiac output)
144
Q

How is supplemental oxygen rationalized for pulmonary arterial hypertension?

A
  • Hypoxemic pulmonary vasoconstriction may contribute to elevated PAP
  • Such vasoconstriction may result in small, but significant increase in PVR and decrease in cardiac output
145
Q

How does pulmonary arterial hypertension appear in pulmonary artery catheter values?

A
  • MPAP > 25 mmHg
  • PCWP > 15 mmHg (indicates pulmonary venous hypertension)
  • PAP elevated above 25/8 mmHg normal
  • Increased PVR
146
Q

What pulmonary arterial catheter test can be used to assess pulmonary arterial hypertension?

A 
Vasodilator Response Testing (K)
Vasoreactivity test (UTD)
147
Q

How is Vasoreactivity Test administered?

A
  • -Administer a short-acting vasodilator: (iNO, epoprostenol, adenosine, iloprost)
  • -Watch for MPAP to decrease by 10 mmHg and to a value <= 40mmHg (with increased/unchanged CO and minimally reduced or unchanged systemic BP)
  • -Patients positive for test can get a trial of long-tem CCB therapy
  • -Patients with negative test should be given alternative medication; CCBs in these patients my be harmful. (UTD)
148
Q

How is echocardiography useful in assessing pulmonary arterial hypertension?

A
  • -Can non-invasively estimate PAP
  • -Assesses right and left ventricular function
  • -Evaluates valvular disease (tricuspid and mitral)
149
Q

Are any lab studies useful for evaluated pulmonary arterial hypertension?

A

BNP may be useful, but it can be elevated for other reasons

150
Q

What imaging beyond chest film can be useful for assessing pulmonary arterial hypertension?

A

CT and CT angiography may be indicated for specific types of pulmonary hypertension.

151
Q

Cases of fat embolism syndrome are most commonly associated with what problems?

A

Long bone or pelvic fractures.

152
Q

Name the WHO categories of pulmonary hypertension.

A

1) Pulmonary arterial hypertension (idiopathic origins plus others)
2) PH 2/2 left heart disease
3) PH d/t chronic lung disease or hypoxemia
4) PH d/t pulmonary artery obstructions
5) PH d/t multifactorial mechanisms

153
Q

What conditions give rise to group 1 pulmonary hypertension?

A
  • Idiopathic and heritable conditions
  • Drugs and toxins
  • Connective tissue diseases
  • HIV
  • Portal hypertension
  • Congenital heart disease
  • Schistosomiasis
    etc. !
154
Q

Name some of the conditions that can lead to group 5 pulmonary hypertension

A
  • Sickle cell disease
  • Sarcoidosis
  • CKD
155
Q

CTEPH =

A

Chronic thromboembolic pulmonary hypertension

156
Q

Left heart disease that may contribute to pulmonary hypertension (Kettering)

A
  • Acute myocardial infarction
  • Cardiac valvular disease (mitral valve stenosis or regurgitation)
  • Severe diastolic dysfunction
  • Cardiomyopathy
157
Q

Pulmonary hypertension effects on the heart (Kettering)

A
  • Increased PVR increase right ventricular afterload
  • Decreased right ventricular stroke volume decreases CO
  • Right ventricular end diastolic pressure increases
  • Interventricular septum shift, resulting in decreased cardiac output
158
Q

Define acute hypertension (Kettering)

A

A marked increase in blood pressure associated with organ damage

159
Q

What blood pressure reading defines acute hypertension?

A

> 180/110 mmHg

160
Q

Name several causal areas for acute hypertension.

A
  • Neurologic cause (acute stroke)
  • Perioperative cause (seen especially in neurosurgical and caradiovascular surgery patients)
  • Cardiovascular cause (acute heart failure and chronic hypertension)
161
Q

Medication for acute hypertension (K)

A
  • “Nitroprusside is initial treatment”
  • -rapid onset, short duration, inexpensive and efficacious
  • -cyanide toxicity a potential complication
  • Nitroglycerine
  • Labetolol (beta blocker, commonly administered by IV)
  • Esmolol (beta blocker–with duration of action only 10-20 minutes)
  • Nicardipine (calcium channel blocker)
162
Q

What is cardiac tamponade?

A

Pericardial effusion that causes hemodynamic compromise

163
Q

According to UTD, what are the physical findings of cardiac tamponade?

A
  • Beck’s triad (hypotension, JVD, muffled heart sounds) –in minority of cases
  • Sinus tachycardia
  • Hypotension
  • Elevated jugular venous pressure
  • Pulsus paradoxus
  • Pericardial rub (in patients with cardiac tamponade due to inflammatory pericarditis) (UTD 20200508)
164
Q

With what modality is cardiac tamponade best evaluated?

A

Echocardiography can identify pericardial effusion and assess its hemodynamic significance. (UTD 20200508)

165
Q

How does one treat cardiac tamponade?

A
  • Aggressive fluid resuscitation
  • Inotropic support with dobutamine, dopamine, isoproterenol, norepinephrine
  • Percutaneous periardiocentesis is primary approach
  • Pericardial window done surgically (K)
166
Q

What is the treatment for pericardial disease?

A

Such anti-inflammatory drugs as–

  • NSAIDs
  • Indomethacin
  • Ibuprofen
  • Systemic corticosteroids
167
Q

Differential diagnosis of life-threatening acute pericarditis

A
  • Acute coronary syndrome
  • Pulmonary embolism
  • Aortic dissection
  • Pericardial tamponade
168
Q

One way to narrow the life-threats on the differential for life-threatening acute pericarditis–

A

Chest CT can rule out pulmonary embolism and aortic dissection

169
Q

With what modality is pericardial disease best diagnosed?

A

Echocardiography

170
Q

How would pericardial disease appear on CXR?

A
  • Might appear as normal CXR

* Might show an enlarged cardiac silhouette

171
Q

How would pericardial disease appear on EKG?

A
  • Would not appear on EKG
172
Q

From where can the inflammation at the, uh, heart of pericardial disease arise?

A

It can be a systemic problem

It can be an isolated problem

173
Q

What principles should guide treatment for heart valve problems in the ICU?

A
  • Give antibiotic prophylaxis for endocarditis
  • Maintain ventilation and oxygenation
  • Treat associated cardiac arrhythmias
174
Q

How should ventilation and oxygenation be maintained for patients with heart valve problems in the ICU?

A
  • Increase FiO2 to treat hypoxemia because fever and increased work of breathing increases oxygen demands
  • Manage hypercapnea with NPPV and/or invasive ventilation
175
Q

Name major causes of pericardial effusion.

A
  • Acute pericarditis (viral, bacterial, tuberculosis, or idiopathic in origin)
  • Autoimmune disease
  • Postmyocardial infarction or cardiac surgery
  • Sharp or blunt chest trauma (including cardiac interventional or diagnostic procedure)
  • Malignancy (particularly metastatic spread of noncardiac primary tumors)
  • Renal failure with uremia
  • Myxedema
  • Aortic dissection extending into pericardium
  • Selected drugs
    (UTD)
176
Q

When does someone have a pericardial effusion?

A

When the accumulated fluid in the pericardial sac exceeds the small amount that is normally present. (UTD)

177
Q

Name the major clinical manifestations of acute pericarditis (UTD).

A
  • Chest pain (typically sharp and pleuritic–improved by sitting up and leaning forward)
  • Pericardial friction rub (a superficial scratchy and squeaking sound best heard with the diaphragm of the stethescope over the left sternal border)
  • Electrocardiogram changes (new widespread ST elevation or PR depression)
  • Pericardial effusion
    (UTD)
178
Q

Name three categories of valvular heart disease in ICU patients.

A
  • Acute onset: first episode of symptomatic disease
  • Exacerbation: flare-up of pre-existing valve disease
  • Concomitant: caused by other critical illness
179
Q

Name consequences of mitral valve failure common in ICU patients.

A
  • Decreased cardiac output with tissue hypoperfusion
  • Pulmonary hypertension with pulmonary edema
  • Right heart failure from severe pulmonary hypertension
180
Q

What life-threats arise from cardiac valvular disease?

A
  • CHF requiring immediate stabilization
  • Shock
  • Respiratory failure (K)
181
Q

Describe invasive monitoring required for cardiac valvular disease.

A
  • Peripheral arterial line: for systemic blood pressure
  • Pulmonary arterial line: for cardiac filling pressures, cardiac output, mixed venous oxygen saturation, for calculation of left ventricular stroke volume, SVR, PVR
182
Q

Per K, what tests should be ordered for cardiac valvular disease?

A
  • EKG
  • CXR (to find pulmonary hypertension, pulmonary edema, pleural effusions)
  • Echocardiography (transthoracic echocardiogram (TTE) preferred; transesophageal echocardiogram (TEE) (K)
183
Q

Name three broad categories of causation for right heart failure.

A
  • Increased pressure load (increased PVR, afterload)
  • Increased volume load (increased preload)
  • Decreased contractility
184
Q

What conditions increase RV afterload in ways that lead to right heart failure?

A
  • Pulmonary embolism
  • Pulmonary disease (hypoxic pulmonary vasoconstriction, destruction of vascular bed, interstitial lung disease, neuromuscular chest wall restriction)
  • Primary pulmonary hypertension
  • Left ventricular failure
  • ARDS
  • Positive pressure ventilation
185
Q

Name conditions that increase preload in ways that lead to right heart failure.

A
  • Atrial septal defect
  • Ventricular septal defect
  • Tricuspid valve insufficiency (K)
186
Q

What condition could reduce contractility and lead to right heart failure?

A

Myocardial ischemia including hypotension and chest trauma.

187
Q

Kettering on ventilator weaning of COPD patient.

A
  • RSBI may not be the best indicator
  • Initiate spontaneous breathing trial with pressure support
  • Extubate as soon as possible to NPPV
188
Q

Why does K say to extubate COPDers as soon as possible to NPPV?

A
  • Decreases risk of VAP
  • Has been shown to reduce ventilator length of stay
  • Has been shown to reduce mortality
189
Q

What does K say about adjusting Itime on ventilator for AECOPD?

A
  • Increased Raw requires longer Itime
  • Increased Itime may decrease Etime and lead to hyperinflation
  • Ideal ITime optimizes delivery of tidal volume without air trapping
190
Q

What does K recommend for ventilator humidification for AECOPD?

A

Avoid HMEs because they can increase Raw

191
Q

When does K say antibiotics are indicated fo AECOPD?

A

When signs of infection are present:
—Fever and chills
—Cough productive of secretions that have changed color
—Elevated white blood cell count (>10,000/mm3)

192
Q

What antibiotics does K have in mind for AECOPD?

A
  • Penicillin/penicillinase (e.g. amoxicillin/clavulanate[Augmentin])
  • Quinolone (levofloxacin, gatifloxacin, moxifloxacin)
  • Cephalosporin with a macrolide (i.e., ceftriaxone plus clarithromycin)
193
Q

What bugs are most likely behind AECOPD?

A
  • Haemophilus influenzae
  • Moraxella catarrhalis
  • Streptococcus pneumoniae
  • Pseudomonas aeruginosa
    (UTD)
194
Q

What corticosteroids does K recommend for AECOPD?

A
  • Methylprednisolone IV
  • Hydrocortisone IV
  • Prednisone PO
195
Q

What does K lead one to expect of CXR for AECOPD?

A
  • Hyperinflation/flattened diaphragms
  • Emphysematic parenchyma
  • Infiltrates or air bronchograms if pneumonia is present
196
Q

What does K say about breath sounds for AECOPD?

A
  • Fine inspiratory crackles are common
  • Expiratory or inspiratory/expiratory wheezes
  • Coarse crackles from secretions or pneumonia
  • Diminished breath sounds
197
Q

What conditions may drive COPD into exacerbation?

A
  • Upper respiratory infection (viral or bacterial)
  • Aspiration
  • Pneumonia
  • Comorbidities (CHF, cor pulmonale, diabetes)
198
Q

Name Kettering’s goals and non-invasive therapies for asthma exacerbation.

A
  • Relieve hypoxemia (HFNC for SpO2 > 90%)
  • Relieve airflow obstruction (beta agonists; anticholinergic ipratropium in ED)
  • Reduce airway inflammation (IV steroids)
  • Consider IV magnesium sulfate
  • Consider heliox via NRB
  • Consider antibiotics only if signs of bacterial infection are present
  • Consider sedatives cautiously due to potential for respiratory depresssion
199
Q

Describe Kettering’s approach to mechanical ventilation for asthma.

A
  • Use larger ETT to reduce airway resistance
  • Choose ventilator settings that minimize hyperinflation and avoid excessive airway pressure (overdistension)
  • Choose safe Vts of 4-6 mL/kg IBW
  • Set respiratory rate 12-24 bpm
  • Consider permissive hypercapnea
  • Use short Itime and longer expiratory time to minimize air trapping
  • Monitor for dynamic hyperinflation (autopeep)
  • Consider inhaled anesthetics (isoflurane or sevoflurane) with bronchodilatory effects
200
Q

Name Kettering points for CXR with asthma exacerbation.

A
  • Hyperinflation
  • Flattened diaphragms
  • Infiltrates only with infection in addition to asthma
201
Q

Describe Kettering’s steps of breath sound development in asthma exacerbation.

A
  • End-expiratory wheezing = mild symptoms
  • Expiratory wheezing throughout = increasing asthma symptoms
  • Inspiratory and expiratory wheezing = asthma crisis
  • Absent breath sounds = severe exacerbation requiring intubation & ventilation.
202
Q

How does Kettering say asthma exacerbation compromises hemodynamics?

A
  • Increased intrathoracic pressure decreases venous return and cardiac output/blood pressure
  • Pulsus paradoxus/paradoxical pulse may develop
203
Q

Kettering: Why is hyperinflation bad in asthma exacerbation?

A

It compromises the force-generating capacity of the diaphragm—

Expiration is prolonged

And still end-expiratory alveolar pressure is positive

204
Q

The three key pathologies of asthma exacerbation:

A
  • Bronchoconstriction
  • Airway inflammation
  • Production of thick secretions
205
Q

What therapies should be avoided in cardiac tamponade?

A
  • Inotropic agents: value uncertain–in theory, dobutamine might be preferred–endogenous inotropic stimulation often maximal already
  • Positive pressure ventilation: avoid if possible–positive intrathoracic pressure can further impair cardiac filling
  • With cardiac arrest and pericardial effusion, external compression offers little benefit in supplementing cardiac filling (UTD 20200508)
206
Q

What echocardiography findings accompany cardiac tamponade?

A
  • Swinging of the heart within effusion
  • Transiently reversed right atrial and right ventricular diastolic transmural pressures
  • Cardiac chamber collapse
  • Respiratory variation in volumes and flows
  • IVC plethora
207
Q

What is anasarca?

A

Edema from generalized and massive excess interstitial fluid accumulation.

208
Q

What is neurogenic pulmonary edema?

A

An increase in pulmonary interstitial and alveolar fluid that is due to an acute central nervous system injury and usually develops rapidly after the injury. (UTD accessed 20200729)

209
Q

What problems precipitate neurogenic pulmonary edema?

A
  • Epileptic seizures
  • Traumatic brain injury
  • Various forms of intracranial hemorrhage (UTD accessed 20200729)
210
Q

Define “Myelogenous”

A

Produced in the bone marrow. (Dorland’s accessed 20200729)

211
Q

Myxedema on a patient’s chart should raise what expectations?

A
  • Hypoventilation with severe hypothyroidism
  • Muscle weakness
  • Depression of respiratory drive
  • Some patients will need noninvasive or invasive ventilatory support during the initial phases of thyroid replacement (UTD accessed 20210216)
212
Q

Cheyne-Stokes respirations is commonly associated with what co-morbidities?

A
  • Cardiac disease
  • Neurologic disease
  • Sedation
  • Normal sleep
  • Acid-base disturbances
  • Prematurity
  • Altitude acclimatization (UTD accessed 202102160
213
Q

What is thrombin?

A
  • The activated form of factor II (prothrombin)

* It converts fibrinogen to fibrin (D accessed 20211109)

214
Q

How does a epidural hematoma appear on head CT?

A

“A biconvex or lenticular shape” because “clot pushes the dura mater away from the posterior wall of the skull” (Hess 1017)

accs (13 decks)

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