Chapter 321 - Approach to the Patient with Critical Illness Flashcards

1
Q

Critical care physicians often must redirect the goals of care from resuscitation and cure to comfort when the resolution of an underlying illness is not possible.
True or False?

A

True.

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2
Q

Severity-of-illness scoring systems are usefull tools to assess individual patient outcomes.
True or False?

A

False.
“Although these scoring systems have been validated as tools to assess populations of critically ill patients, their utility in predicting individual patient outcomes is not clear.”

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3
Q

Name the main usefulness of severity-of-illness (SOI) scoring systems. How were these scales obtained?

A

“SOI scoring systems are important for defining populations of critically ill patients. Such systematic scoring allows effective comparison of groups of patients enrolled in clinical trials. In verifying a purported benefit of therapy, investigators must be confident that different groups involved in a clinical trial have similar illness severities. SOI scores are also useful in guiding hospital administative policies, directing the allocation of resources such as nursing and ancillary care and assisting in assessments of quality of ICU care over time.”

“All existing SOI scoring systems are derived from patients who have already been admited to the ICU.”

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4
Q

Which Severity-of-Illness Scoring system is most commonly used in intensive unit cares in North America?

A

APACHE II.

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5
Q

Name the variables measured for APACHE II score calculation.

A

“Age, type of ICU admission (after elective surgery vs nonsurgical or after emergency surgery), chronic health problems, and 12 physiologic variables (the worst values for each in the first 24 h after ICU admission) are used to derive a score).”

The 12 physiologic variables include: rectal temperature, mean blood pressure, heart rate, respiratory rate, arterial pH, oxygenation, serum sodium, serum potassium, serum creatinine, hematocrit, white blood cell count and Glasgow Coma Score.

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6
Q

Which year was SAPS 3 developped?

A

2005

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7
Q

Name the differences between SAPS and APACHE.

A

“The SAPS II score, used more frequently in Europe than in the United States, was derived in a manner similar to the APACHE score. This score is not disease specific but rather incorporates these underlying disease variables: AIDS, metastatic cancer, and hematologic malignancy.”

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8
Q

There is no shock without hypotension.

True or False?

A

False.

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9
Q

How does one clinically differentiate diminished from increased cardiac output?

A

“Clinical evidence of dimished cardiac output includes a narrow pulse pressure - a marker that correlates with stroke volume - and cool extremities with delayed capillary refill. Signs of increased cardiac output include a widened pulse pressure (particularly with a reduced diastolic pressure), warm extremities with bounding pulses, and rapid capillary refill.”

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10
Q

How do you define shock and which clinical signs would you look for if you suspect that a patient might have a shock diagnosis?

A

“shock, a common condition necessitating ICU admission or occurring in the course of critical care, is defined by the presence of multisystem end-organ hypoperfusion. Clinical indicators include reduced mean arterial pressure (MAP), tachycardia, tachypnea, cool skin and extremities, acute altered mental status, and oliguria.”

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11
Q

Since mean arterial pressure is a product of cardiac output and systemic vascular resistance (SVR), if you find clinical signs of reduced cardiac output and hypotension, what might one infer as the cause of hypotension?

A

Reduced SVR.

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12
Q

Which of the following is the best predictor of fluid responsiveness: (A) static measurement of right atrial pressure; (B) change in right atrial pressure with spontaneous respiration.

A

B.

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13
Q

Patients with hypovolemic shock may also manifest larger changes in pulse pressure as a function of respiration during mechanical ventilation.
True or False?

A

True.

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14
Q

Which signs would you expect to find in a hypotensive patient with cardiac dysfunction?

A

“A hypotensive patient with increased intravascular volume and cardiac dysfunction may have an S3 and/or S4 gallops on examination, increased jugular venous pressure, extremity edema, and crackles on lung auscultation.”

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15
Q

In a patient with cardiogenic shock suspicion, which imagiologic signs would you expect to find on x-ray and electrocardiography?

A

“The chest x-ray may show cardiomegaly, widening of the vascular pedicle, Kerley B lines, and pulmonary edema. Chest pain and electrocardiographic changes consistent with ischemia may be note.”

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16
Q

What is the most common cause of high-cardiac-output hypotension?

A

Sepsis.

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17
Q

Name causes of high-cardiac-output hypotension other than sepsis.

A

“Other causes include liver failure, severe pancreatitis, burns and other trauma that elicit the systemic inflammatory response syndrome (SIRS), anaphylaxis, thyrotoxicosis, and peripheral arteriovenous shunts.”

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18
Q

Shock has only one category as its cause.

True or False?

A

False.

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19
Q

Which are the main categories of shock?

A

Hypovolemic, cardiogenic and high-cardiac-output with decreased systemic vascular resistance (high-output hypotension).

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20
Q

Septic and cardiogenic shock may have survival improvement if early resuscitation is conducted.
True or False?

A

True.
“The goal of early resuscitation is to reestablish adequate tissue perfusion and thus to prevent or minimize end-organ injury.”

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21
Q

Name the causes of acute hypoxemic respiratory failure.

A

“Acute hypoxemic respiratory failure may occur in patients with cardiogenic shock and pulmonary edema as well as in those who are in septic shock with pneumonia or acute respiratory distress syndrome (ARDS).”

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22
Q

What kind of pH disturbance would you expect to find in a patient with shock?

A

Acute metabolic (often lactic) acidosis.

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23
Q

Explain the pathophysiollogy for increased ventilatory load and consequent ventilatory failure in patients with cardiogenic shock.

A

Cardiogenic shock may lead to pulmonary edema and incrased ventilatory load. Shock with hypoperfusion (of any cause) may also include decreased vascularization of respiratory muscles and consequent lactic acid production.
“Lactic acid production from inefficient respiratory muscle activity presents an additional ventilatory load.”

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24
Q

The percentage of cardiac output dedicated to respiratory muscles may increasetenfold or more in shock patients.
True or False?

A

True.

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25
Q

What are the indicators of respiratory distress?

A

“Patients demonstrate respiratory distress by an inability to speak full sentences, accessory use of respiratory muscles, paradoxical abdominal muscle activity, extreme tachypnea (>40 breaths/min), and decrasing respiratory rate despite an increasing drive to breathe.”

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26
Q

Mechanical ventilation reduces median arterial pressure (MAP).
True or False?
Argue your answer.

A

True.
“ With the institution of mechanical ventilation for shock, further declines in MAP are frequently seen. The reasons include impeded venous return from positive-pressure ventilation, reduced endogenous catecholamine secretion once the stress associated with respiratory failure abates, and the actions of drugs used to facilitate endotracheal intubation (e.g., propofol, opiates).”

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27
Q

Name two major goals of mechanical ventilation.

A

“Mechanical ventilation may relieve the work of breathing and allow redistribution of a limited cardiac output to other vital organs.”

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28
Q

How many patients might need mechanical ventilatory support in UCI?

A

≥75% in some UCIs.

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29
Q

What are the causes of alveolar flooding?

A

Pulmonary edema, pneumonia or alveolar hemorrhage.

30
Q

Is there any other name for Acute Respiratory Distress Syndrome (ARDS)? How do you define this syndrome?

A

“Low-pressure pulmonary edema”.
“This syndrome is defined by acute onset (equal or less than 1 week) of bilateral opacities on chest imaging that are not fully explained fully explained by cardiac failure or fluid overload and of shunt physiology requiring positive end-expiratory pressure (PEEP).”

31
Q

Name causes for type I respiratory failure.

A

“Type I respiratory failure occurs in clinical settings such as sepsis, gastric aspiration, pneumonia, near-drowning, multiple blood transfusions, and pancreatitis.”

32
Q

What is the mortality for Acute Respiratory Distress Syndrome?

A

Close to 30% (it was traditionally very high - 50-70%).

33
Q

How do you explain ventilator-induced “volutrauma”?

A

“For many years, physiciains have suspected that mechanical ventilation of patients with Acute Respiratory Distress Syndrome may propagate lung injury. Cyclical collapse and reopening of alveoli may be partly responsible for this adverse effect.”

“Animal studies have suggested that stretching and overdistention of injured alveoli during mechanical ventilation can further injure the lung.”

34
Q

What is the best strategy for mechanical ventilation and fluid administration in patients with Acute Respiratory Distress Syndrome (ARDS)?

A

“[A] study showed a dramatic reduction in mortality rate in the low-tidal volume group [6mL/Kg of ideal body weight] from that in the high-tidal-volume group [12mL/Kg] (31% versus 39,8%). In addition, a “fluid-conservative” management strategy (maintaining a low central venous pressure [CVP] or pulmonary capillary wedge pressure [PCWP]) is associated with fewer days of mechanical ventilation than a “fluid-liberal” strategy (maintaining a relatively high CVP or PCWP) in ARDS.”

35
Q

What are the causes of type II respiratory failure?

A

“this type of respiratory failure is a consequence of alveolar hypoventilation and results from the inability to eliminate carbon dioxide effectively. Mechanisms are categorized by impaired central nervous system (CNS) drive to breathe, impaired strenght with failure of neuromuscular function in the respiratory system, and increased load(s) on the respiratory system.”

36
Q

Name causes of dimished CNS drive.

A

“drug overdose, brainstem injury, sleep-disordered breathing, and severe hypothyroidism.”

37
Q

Name causes of hypoventilation categorized as neuromuscular.

A

“Reduced strenght can be due to impaired neuromuscular transmission (e.g., myasthenia gravis, Guillain-Barré syndrome, amyotrophic lateral sclerosis) or respiratory muscle weakness (e.g., myopathy, electrolyte derangements, fatigue).”

38
Q

Noninvasive positive-pressure ventilation has been shown to be beneficial in treating patients with exacerbations of chronic obstructive pulmonary disease.
True or False?

A

True.

39
Q

Which caues might contraindicate noninvasive positive-pressure ventilation?

A

Hemodynamic instability, inability to protect the airway, respiratory arrest.

40
Q

What is the relantionship between type IIII respiratory failure and noninvasive positive-pressure ventilation?

A

“Noninvasive positive-pressure ventilation may also be used to reverse regional atelectasis.”

41
Q

How does one define type III respiratory failure?

A

“This form of respiratory failure results from lung atelectasis. Because atelectasis occurs so commonly in the perioperative period, this form is also called perioperative respiratory failure.”

42
Q

40% of cardiac output might be distributed to the respiratory muscles in shock patients.
True or False?

A

True.

43
Q

Which mechanically ventilated patients should undergo a daily spontaneous breathing trial?

A

“If oxygenation is stable (i.e., PaO2/FiO2 [partial pressure of oxygen/fraction of inspired oxygen] >200 and PEEP equal or less than 5cmH2O), cough and airway reflexes are intact, and no vasopressor agents or sedatives are being administered, the patient has passed the screening test and should undergo a spontaneous breathing trial.”

44
Q

What is a spontaneous breathing trial?

A

“This trial consists of a period of breathing through the endotracheal tube without ventilator support (both continuous positive airway pressure (CPAP) of 5cmH2O and an open T-piece breathing system can be used) for 30-120 min.”

45
Q

When should one stop a spontaneous breathing trial?

A

“The spontaneous breathing trial is declared a failure and stopped if any of the following occur: (1) respiratory rate >35/min for >5min, (2) O2 saturation 140/min or a 20% increase or decrease from baseline, (4) systolic blood pressure less than 90mmHg or >180mmHg or (5) incrased anxiety or diaphoresis.”

46
Q

What is the valure of f/VT (respiratory rate to tidal volume in liters ratio) that is indicative for extubation?

A

Less than 105.

47
Q

Although careful approaches to mechanically ventilated patients and extubations indications, how many patients might have respiratory distress afterwards?

A

10%.

48
Q

What is the mainstay for pain control in ventilated pain? Other than pain, is there any indication for sedation in these patients?

A

“Opiates are the mainstay of therapy for pain control in mechanically ventilated patients. After adequate pain control has been ensured, additional indications for sedation include anxiolysis; treatment of subjective dyspnea; psychosis; facilitation of nursing care; reduction of autonomic hyperactivity, which may precipitate myocardial ischemia; and reduction of total O2 consumption (VO2).”

49
Q

In Acute Respiratory Distress Syndrome neuromuscular blocking agents are occasionally needed even if sedation is optimized.
True or False?

A

True.

although more frequent in ARDS, this applies to any sedation optmization with profound ventilator dyssynchrony

50
Q

Which agents might be responsible for postparalytic syndrome?

A

Neuromuscular blocking agents.

51
Q

Why is it that sedative-induced amnesia is mandatory when one uses neuromuscular blocking agents?

A

This is due to the fact that the latter agents do not

52
Q

Sedative-induced amnesia is mandatory for all patients undergoing intubation and mechanical ventilation.
True or False?

A

False.
“Outside the setting of pharmacologic paralysis, few data support the idea that amnesia is mandatory in all patients who require intubation and mechanical ventilation.”

53
Q

Name examples of sedatives that might be used to induce amnesia.

A

“Amnesia can be achieved reliably with benzodiazepines such as lorazepam and midazolam as well as the IV anesthetic agent propofol.”

54
Q

Since sedatives might accumulate, especially in patients with hepatic and/or renal function impairment, how can one reduce their dosage overtime, with better major outcomes?

A

“A nursing protocol-driven approach to sedation of mechanically ventilated patients or daily interruption of sedative infusions paired with daily spontaneous breathing traials have been shown to prevent excessive drug accumulation and shorten the duration of both mechanical ventilation and ICU stay.”

55
Q

How does one define multiorgan system failure? Name some of the main causes.

A

“Multiorgan system failure, which is commonly associated with critical illness, is defined by the simultaneous presence of physiologic dysfunction and/or failure of two or more organs. Typically, this syndrome occurs in the setting of severe sepsis, shock of any kind, severe inflammatory conditions such as pancreatitis, and trauma.”

56
Q

After admission to an ICU (Intensive Care Unit), when is it usual that a patient might die - earlier or later in ICU stay?

A

“it is uncommon for critically ill patients to die in the initial stages of resuscitation. Instead, many patients succumb to critical illness later in the ICU stay, after the initial presenting problem has been stabilized.”

57
Q

Name the three principles that apply to any definition of multiorgan system failure.

A

“Although there is debate regarding specific definitions of organ failure, several general principles governing the syndrome of multiorgan system failure apply. First, organ failure, no matter how it is defined, must persist beyond 24 h. Second, mortality risk increases with the accrual of failing organs. Third, the prognosis worsnes with increased duration of organ failure.”

58
Q

What is the “gold-standard” for respiratory gas exchange testing?

A

Arterial blood-gas analysis.

59
Q

How does a pulse oximetry work? Explain what its physical properties.

A

“pulse oximetry takes advantage of differences in the absorptive properties of oxygenated and deoxygenated hemoglobin. At wavelenghts of 660 nm, oxyhemoglobin reflects light more effectively than does deoxyhemoglobin, whereas the reverse is true in the infrared spectrum (940 nm). A pulse oximeter passes both wavelenghts of light through a perfused digit such as a finger, and the relative intensity of light transmission at these two wavelenghts is recorded. From this information, the relative percentage of oxyhemoglobin is derived. Since arterial pulsations produce phasic changes in the intensity of transmitted light, the pulse oximeter is designed to detect only light of alternating intensity. This feature allows distinction of arterial and venous blood O2 saturations.”

60
Q

Plateau pressure is only affected by respiratory system compliance and not by airway resistance.
True or False?

A

True.

61
Q

In controlled-volume mechanical ventilation, how is it that airway resitance is calculated?

A

“during volume-controlled ventilation, the difference between the peak (airway resistance + respiratory system compliance) and plateau (respiratory system aompliance only) airway pressures provides a quantitative assessment of airway resistance.”

62
Q

In controlled-volume mechanical ventilation, how is it that respiratory compliance is measured?

A

“The compliance of the respiratory system is defined by the change in pressure of the respiratory system per unit change in volume.”

63
Q

What is the usual gradient between peak and plateau airway pressures during mechanical ventilation?

A

> 15cmH2O at a respiratory flow of 1L/sec.

64
Q

Give examples of reduced respiratory compliance, either to due to disease of the chest wall or lungs.

A

“Pathophysiologic processes such as pleural effusions, pneumothorax, and increased abdominal girth all reduce chest wall compliance. Lung compliance may be reduced by pneumonia, pulmonary edema, intersticial lung disease, or auto-PEEP.”

65
Q

If one suspects isolated disease that leads to dimished respiratory compliance, how would you expect to find the gradient between peak and plateau airway pressures?

A

Normal.

66
Q

Explain the auto-PEEP phenomenon.

A

“Auto-PEEP occurs when there is insuficcient time for emptying of alveoli before the next inspiratory cycle. Since the alveoli have not decompressed completely, alveolar pressure remains positive at the end of exhalation (functional residual capacity). Thuis phenomenon results most commonly from critical narrowing of distal airways in disease processes such as asthma and COPD.”

67
Q

Why is it that oxygen delivery (QO2) in a normal adult is 1058mL O2 per minute?

A

QO2 = 50dL/min x (1,39 x 15g/dL [hemoglobin concentration] x 1,0 [hemoglobin % saturation] + 0,0031 x 100 [PaO2]) = 50dL/min (cardiac output) x 21,6 mL O2 per dL blood (CaO2) = 1058 mL O2 per min

68
Q

What is the content of O2 in mixed venous blood (with at least 75% saturation)?

A

15,76mL/dL.

69
Q

Name causes for increased VO2.

A

Fever, agitation, shivering and thyrotoxicosis.

70
Q

Pulmonary artery catheterization is a useful monitoring tool that decreases morbidity and mortality.
True or False?

A

False.
“[The pulmonary artery catheter] has never been validated as a tool associated with reduction in morbidity and mortality rates. Indeed, despite numerous prospective studies, mortality or morbidity rate benefits associated with use of the pulmonary artery catheter have never been reported in any setting.”

71
Q

Pulmonary artery catheterization is mandatory in most critically ill patients.
True or False?

A

False.

72
Q

What is the dynamic value of central venous pressure that may predict increased cardiac output after IV fluid administration in patients with septic shock?

A

Decrease of >1mmHg during inspiration in a spontaneously breathing patient.