Critical Care Flashcards
Sepsis definition
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.
SOFA score?
range, 0–24 with higher scores indicating more severe illness) ≥2 points from baseline.
SOFA score what does it measure?
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
SOFA score
quick SOFA
Patient in ICU
alteration in mental status
systolic blood pressure ≤100 mm Hg
respiratory rate ≥22/min
Septic Shock definition
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%
Treatment Septic Shock
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).
Shock definition
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
MAP formula
Mean arterial pressure = cardiac output (CO) x systemic vascular resistance (SVR)
Causes of Shock
Mean arterial pressure = cardiac output (CO) x systemic vascular resistance (SVR); therefore, shock can be due to a decrease in SVR, CO, or both.
Examples distributive shock
Sepsis, Anaphylaxis
Examples Hypovolemic shock
Hemorrhage, internal fluid lossess( third spacing) and external fluid loss ( GI )
Examples obstructive shock
Pulmonary embolism, cardiac tamponade, tension pneumothorax
Examples cardiogenic shock
Acute MI
Advanced valvular disease
End-stage cardiomyopathy
Myocarditis
Cardiac Arrhythmias
Hypotension
Usually SBP < 90 or MAP < 70
Tissue Hypoperfusion ( “ 3 windows of the body “)
- Cutaneus: skin is cold and clammy, with vasoconstriction and cyanosis- findings are most evident at low-flow states
- renal ( urine output < 0.5 ml/kg/hr)
- Neurologic ( altered mental state, typically includes obtundation, disorientation and confusion )
Hyperlactemia values
normal lactate is ~ 1mmol per liter
hyperlactemia > 1.5 mmol/lt
What do hypovolemia, cardiogenic and obstructive shock have in common that differentiate them from distributive shock?
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.
Initial approach to the patient in shock
- 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)
Ventilatory support in shock
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)
Advantages of Invasive mechanical ventilation in shock
Reduce O2 demand of respiratory muscles
decrease LV afterload by increasing intrathoracic pressure
Abrupt decrease in arterial pressure after initiation of invascive mechanical ventilation strongly suggests?
hypovolemia and a decrease in venous return
Aim of fluid resuscitation in shock
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.
Fluid-challenge goal
Determine a patients actual response to fluids while limiting the risks of Adverse Effects
Fluid challenge technique ( 4 elements)
- Type of fluid- crystalloids first line - well tolerated and cheap
- Use of albumin to crrect severe hypoalbuminemia in some pts - Rate of fluid administration: 300-500ml of fluid during a period of 20-30 min.
- Define objective of fluid challenge: 1. increase in Systemic arterial pressure, decrease HR, or increase urine output
- Safety: the major risk is pulmonary edema= so define a limit of CVP to prevent fluid overload.
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
Why pure apha blockers are not preferred as vasopressors ( ie. phenylephrine)?
Because besides increasing vascular tone and blood pressure ( desirable in shock) they decrease cardiac output and impair tissue blood flow ( especially in hepatosplachnic region )
Norepinephrine
alpha adrenergic properties and modest b blockers- help maintint CO.
Increases MAP with little change HR or CO.
Norepinephrine dose
0.1-2 mcg/kg/min
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
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
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.
First line inotrope in shock? when is it used?
Dobutamine - to increase CO regardless of whether NE is also being given.
Dobutamine MOA
predominantly B adrenergic properties, less likely to induce tachycardia than isoproterenol.
limited effects on arterial pressure
Milrinone and enoximone MOA
PDE III - Combine inotropic and vasodilating properties
Vasopressors
