Critical Care Flashcards

(70 cards)

1
Q

Sepsis definition

A

life-threatening organ dysfunction caused by a dysregulated host response to infection

Organ dysfunction defined by the SOFA score

New definition eliminates SIRS because of the poor sensitivity and specificity of these criteria.

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2
Q

SOFA score?

A

range, 0–24 with higher scores indicating more severe illness) ≥2 points from baseline.

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3
Q

SOFA score what does it measure?

A

Neuro- GCS- 15 Resp- PaO2/FiO2 >=400 CV- MAP/vasopressors requirement- >=70 Liver- Bilirrubin <1.2 Renal- Creatinine or urine output- Cr <1.2 Coagulation - platelets > 150

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4
Q

SOFA score

A
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5
Q

quick SOFA

A

Patient in ICU

alteration in mental status

systolic blood pressure ≤100 mm Hg

respiratory rate ≥22/min

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6
Q

Septic Shock definition

A

development of shock (circulatory failure that causes inadequate cellular oxygen utilization) from sepsis (as defined above).

Patients with septic shock have persistent hypotension despite volume resuscitation and require vasopressors to maintain a mean arterial pressure >70 mm Hg. Hospital mortality associated with septic shock is ≥40%

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7
Q

Treatment Septic Shock

A

1.Early antibiotic therapy:each hour of delay in delivery of appropriate antibiotics increased mortality by about 7%.

Antibiotics should be targeted to the organisms most likely to cause infection in the suspected organ system; if the source of infection is not yet known, empiric broad-spectrum antibiotics are indicated.

2. Volume resuscitation:

Crystalloids, including IV normal saline or lactated Ringer’s solution, are the fluids of choice for resuscitation of severe sepsis and septic shock.

Initial fluid challenge should be at a minimum of 30 cc/kg of crystalloids (~2L for a 70 kg adult) for patients with sepsis-induced hypoperfusion.

3. Vasopressors:

Vasopressors should be initiated if a patient is not responsive to fluid resuscitation.

The safest way to deliver vasopressors is through central venous access (internal jugular, subclavian, femoral catheter, or peripherally inserted central cannula).

Surviving Sepsis Campaign guidelines recommend norepinephrine as the first-choice vasopressor in septic shock.

Other treatments: Many therapies that have been used in the treatment of septic shock are no longer part of clinical practice because high-quality trials have not shown benefit (and have sometimes shown harm). Examples include hydrocortisone (benefit disproven in septic shock in the CORTICUS trial and more recently in severe sepsis in the HYPRESS trial) and activated protein C (initially promising in PROWESS but later disappointing in PROWESS-SHOCK).

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8
Q

Shock definition

A

circulatory failure that causes inadequate cellular oxygen utilization associated with the presence of the following:

  • systemic arterial hypotension
  • clinical signs of tissue hypoperfusion (cool and clammy skin, low urine output, altered mental status)
  • increased serum lactate level
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9
Q

MAP formula

A

Mean arterial pressure = cardiac output (CO) x systemic vascular resistance (SVR)

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10
Q

Causes of Shock

A

Mean arterial pressure = cardiac output (CO) x systemic vascular resistance (SVR); therefore, shock can be due to a decrease in SVR, CO, or both.

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11
Q

Examples distributive shock

A

Sepsis, Anaphylaxis

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12
Q

Examples Hypovolemic shock

A

Hemorrhage, internal fluid lossess( third spacing) and external fluid loss ( GI )

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13
Q

Examples obstructive shock

A

Pulmonary embolism, cardiac tamponade, tension pneumothorax

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14
Q

Examples cardiogenic shock

A

Acute MI

Advanced valvular disease

End-stage cardiomyopathy

Myocarditis

Cardiac Arrhythmias

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15
Q

Hypotension

A

Usually SBP < 90 or MAP < 70

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16
Q

Tissue Hypoperfusion ( “ 3 windows of the body “)

A
  1. Cutaneus: skin is cold and clammy, with vasoconstriction and cyanosis- findings are most evident at low-flow states
  2. renal ( urine output < 0.5 ml/kg/hr)
  3. Neurologic ( altered mental state, typically includes obtundation, disorientation and confusion )
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17
Q

Hyperlactemia values

A

normal lactate is ~ 1mmol per liter

hyperlactemia > 1.5 mmol/lt

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18
Q

What do hypovolemia, cardiogenic and obstructive shock have in common that differentiate them from distributive shock?

A

The first 3 have low cardiac output hence inadequate oxygen transport.

In distributive shock the main deficit lies in perophery, with decreased SVR and altered oxygen extraction. They have high CO.

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19
Q

Initial approach to the patient in shock

A
  • monitoring of arterial BP
  • Blood sampling
  • Central venous catheter for infusion of fluids and vasoactive agents and to guide fluid therapy
  • MNEMONIC VIP:
    1. Ventilate ( O2 administration)
    2. Infuse ( fluid resuscitation)
    3. Pump ( admistration of vasoactive agents)
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20
Q

Ventilatory support in shock

A

Immediate O2 delivery to prevent pulmonary HTN.

Pulse oximetry is often unreliable as a result of peripheral vasoconstriction - so to evaluate O2 requirements require blood gas monitoring

Endotracheal intubation: all patients with severe dyspnea, hypoxemia, or persistent or worsening acidemia ( ph<7.30)

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21
Q

Advantages of Invasive mechanical ventilation in shock

A

Reduce O2 demand of respiratory muscles

decrease LV afterload by increasing intrathoracic pressure

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22
Q

Abrupt decrease in arterial pressure after initiation of invascive mechanical ventilation strongly suggests?

A

hypovolemia and a decrease in venous return

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23
Q

Aim of fluid resuscitation in shock

A

improve microvascular blood flow and increase cardiac output.

  • ideal is that CO becomes preload-independent

Even in patients with cardiogenic shock- since acute edema can result in a decrease in the effective intravascular volume

Close monitoring of fluid to avoid risk of edema and its unwanted consequences.

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24
Q
A
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25
Fluid-challenge goal
Determine a patients actual response to fluids while limiting the risks of Adverse Effects
26
Fluid challenge technique ( 4 elements)
1. Type of fluid- crystalloids first line - well tolerated and cheap - Use of albumin to crrect severe hypoalbuminemia in some pts 2. Rate of fluid administration: 300-500ml of fluid during a period of 20-30 min. 3. Define objective of fluid challenge: 1. increase in Systemic arterial pressure, decrease HR, or increase urine output 4. Safety: the major risk is pulmonary edema= so define a limit of CVP to prevent fluid overload.
27
First line vasopressors in shock - and why
Adrenergic agonists - rapid onset of action , high potency , short half life allows easy dose adjustment NE usually first line
28
Why pure apha blockers are not preferred as vasopressors ( ie. phenylephrine)?
Because besides increasing vascular tone and blood pressure ( desirable in shock) they d**ecrease cardiac output** and i**mpair tissue blood flow** ( especially in hepatosplachnic region )
29
Norepinephrine
alpha adrenergic properties and modest b blockers- help maintint CO. Increases MAP with little change HR or CO.
30
Norepinephrine dose
0.1-2 mcg/kg/min
31
Dopamine MOA
Predominantly B adrenergic effects ( increase HR and contractility) at lower doses and alpha adrenergic effects at higher doses but its effects are relatively weak NOT A FIRST LINE TTO IN SHOCK
32
Epinephrine
predominantly B adrenergic effects at low doses, with alpha adrenergic at higher doses. Increased rate of arrythmia and decrease in splachnic blood flow, latate levels NO benefit of epinephrine over Epinephrine in septic shock SECOND LINE
33
Vasopressin deficiency in shock?
Can develop in patients with very hyperkinetic forms of distributive shock ad the administration of low dose vasopressin may result in substantial increases in arterial pressure. -- should not be given at doses higher than 0.04 U per minute and should be administered only in patients with high level of CO.
34
First line inotrope in shock? when is it used?
Dobutamine - to increase CO regardless of whether NE is also being given.
35
Dobutamine MOA
predominantly B adrenergic properties, less likely to induce tachycardia than isoproterenol. limited effects on arterial pressure
36
Milrinone and enoximone MOA
PDE III - Combine inotropic and vasodilating properties
37
Advantages of PDE III inhibitors ( Milrinone, enoximone)
by Decrease metabolism of cAMP- reinforce effects of dobutamine Can be useful in patients with b blockers.
38
PDE III inhibitors disadvantages
not recommended in patients with hypotension very long half-lifes ( 4-6 hrs) - preventing the minute to minute adjustment Prefered to be given in short term infusions of small doses rather than continuous infusions
39
Levosimendan MOA
binds to cardiac troponin C and increases calcium sensitivity of myocites. Acts as vasodilator by opening ATP- sensitive potassium channels in vascular smooth muscle.
40
Levosimendan disadvantage
long half life (days) limiting practicality of its use in acute shock states
41
Goals of hemodynamic support
Arterial pressure 65-70mmHg is a good initial goal but levels should be adjusted to restore tissue perfusion -assessed by mental status, skin appearance and urine output.
42
Four phases in the treatment of shock
Salvage Optimization Stabilization De-escalation
43
Four phases in the treatment of shock Salvage
Obtain a minimal acceptable blood pressure- perform life saving measures
44
Four phases in the treatment of shock Optimization
Provide adequate oxygen availability - optimize CO, SVO2, lactate
45
Four phases in the treatment of shock Stabilization
Provide organ support- minimize complications
46
Four phases in the treatment of shock De-escalation
Wean from vasoactive agents- achieve a negative fluid balance.
47
In low-flow states mechanism of hyperlactatemia vs. distibutive shock
In low-flow states- tissue hypoxia with development of anaerobic metabolism Distributive shock- may also involve increased glycolysis and inhibition of pyruvate dehydrogenase In both cases -altered clearance can be fue to impaired liver function
48
Hyperlactatemia
In patients with shock and a blood lactate level of more than 3 mmol per liter, Jansen et al.24 found that targeting a decrease of at least 20% in the blood lactate level over a 2-hour period seemed to be associated with reduced in-hospital mortality.
49
TTO of anaphylactic shock (a form of distributive shock):
IV epinephrine
50
Tto of hemorrhagic shock
blood transfusions
51
Tto pulmonary embolism
systemic thrombolytics
52
Tto cardiogenic shock:
inotropes and sometimes mechanical support (e.g., intra-aortic balloon pump)
53
Principles of vasopressors in shock
Patients with distributive, hypovolemic, and obstructive shock should **be given IV fluid resuscitation prior to initiation of vasopressors**. Typically, **vasopressors are titrated to a mean arterial pressure of 65 mm Hg,** although decreasing lactate level and improving urine output are reassuring signs of adequate organ perfusion. Inotropes may be **indicated in the treatment of cardiogenic shock from primary pump failure.**
54
Vasopressors
55
NE mechanism of action, indications
a1 \>\>b1\> b2 Indicated in shock ( distributive, cardiogenic, mixed) FIRST LINE VASOPRESSOR IN SHOCK
56
NE side effects
arrhythmias, peripheral ( digital) ischemia
57
NE effect on SVR and CO
Increases both
58
Phenylephrine (Neosynephrine) MOA and indications
a1 increases SVR **distributive shock** **useful in tachyarrhythmias**
59
Phenylephrine EA
reflex tachycardia and severe peripheral and visceral vasoconstriction
60
Vasopressin MOA and indications in shock
V1,V2 Increases SVR Add to NE in septic shock
61
Vasopressin SE
arrhythmias, cardiac ischemia, peripheral and splachnic vasoconstriction
62
Epinephrine MOA, indications
a1\>b1\> b2 increases HR, SVR, CO Indications: shock ( anaphylactic, cardiogenic, distributive) cardiac arrest and bronchospasm FIRST LINE TTO FOR ANAPHYLAXIS AND CARDIAC ARREST
63
Epinephrine EA
Ventricular arrhythmias, cardiac ischemia
64
Dopamine MOA and clinical indications
D1 \>\> B1\>A1\>B2 Immediate precursor of NE increases CO, mild increase SVR iNDICATIONS: Bradycardia, shock ( cardiogenic, distributive)
65
Dopamine SE
ventricular arrhythmia, cardiac ischemia, tissue ischemia or gangrene
66
Dobutamine MOA and clinical indication
B1\>\>B2\>A1 Increases HR USED IN CARDIOGENIC SHOCK IS AN INOTROPE, CAN CAUSE HYPOTENSION
67
B1 adrenergic receptor stimulation
**myocardial contraction** through Ca2+ mediated facilitation of actin-myosin complex binding with troponin C and enhance chronicity through Ca2+ channel activation.
68
B2 adrenergic receptor stimulator
Vasodiation - increased Ca2+ uptake by the Sarcoplasmic reticulum
69
a1 adrenergic receptors stimulation
smooth muscle contraction and increase in SVR
70
Stimulation of D1 and D2 dopaminergic receptors in kidney and splachnic vasculature-
renal and mesenteric vasodilation