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
Advantages of PDE III inhibitors ( Milrinone, enoximone)
by Decrease metabolism of cAMP- reinforce effects of dobutamine
Can be useful in patients with b blockers.
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
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.
Levosimendan disadvantage
long half life (days) limiting practicality of its use in acute shock states
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.
Four phases in the treatment of shock
Salvage
Optimization
Stabilization
De-escalation
Four phases in the treatment of shock
Salvage
Obtain a minimal acceptable blood pressure- perform life saving measures
Four phases in the treatment of shock
Optimization
Provide adequate oxygen availability - optimize CO, SVO2, lactate
Four phases in the treatment of shock
Stabilization
Provide organ support- minimize complications
Four phases in the treatment of shock
De-escalation
Wean from vasoactive agents- achieve a negative fluid balance.
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
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.
TTO of anaphylactic shock (a form of distributive shock):
IV epinephrine
Tto of hemorrhagic shock
blood transfusions
Tto pulmonary embolism
systemic thrombolytics
Tto cardiogenic shock:
inotropes and sometimes mechanical support (e.g., intra-aortic balloon pump)
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.
Vasopressors
NE mechanism of action, indications
a1 >>b1> b2
Indicated in shock ( distributive, cardiogenic, mixed)
FIRST LINE VASOPRESSOR IN SHOCK
NE side effects
arrhythmias, peripheral ( digital) ischemia
NE effect on SVR and CO
Increases both
Phenylephrine (Neosynephrine) MOA and indications
a1
increases SVR
distributive shock
useful in tachyarrhythmias
Phenylephrine EA
reflex tachycardia and severe peripheral and visceral vasoconstriction
Vasopressin MOA and indications in shock
V1,V2
Increases SVR
Add to NE in septic shock
Vasopressin SE
arrhythmias, cardiac ischemia, peripheral and splachnic vasoconstriction
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
Epinephrine EA
Ventricular arrhythmias, cardiac ischemia
Dopamine MOA and clinical indications
D1 >> B1>A1>B2
Immediate precursor of NE
increases CO, mild increase SVR
iNDICATIONS: Bradycardia, shock ( cardiogenic, distributive)
Dopamine SE
ventricular arrhythmia, cardiac ischemia, tissue ischemia or gangrene
Dobutamine MOA and clinical indication
B1>>B2>A1
Increases HR
USED IN CARDIOGENIC SHOCK
IS AN INOTROPE, CAN CAUSE HYPOTENSION
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.
B2 adrenergic receptor stimulator
Vasodiation - increased Ca2+ uptake by the Sarcoplasmic reticulum
a1 adrenergic receptors stimulation
smooth muscle contraction and increase in SVR
Stimulation of D1 and D2 dopaminergic receptors in kidney and splachnic vasculature-
renal and mesenteric vasodilation
Monroe Kellie Doctrine
cranial compartment is not compressible. When the volume increases too much, usually at volumes greater than 100-120mL the intracranial pressure begins to rise
Equation of Cerebral Perfusion pressure and targets in ICP
CPP =MAP- ICP
When ICP increases cerebral perfusion will decrease
<4 years 50
4-10 years. 60
>9 years 70
CSF functions
- Absorb shock to CNS
- Cushions CNS from bony surroundings
- Helps circulate nutrients and waste
Normal ICP value
5-15 mmHg ( or 7-20 cm of H2O)
Differential diagnosis in ICP
- Space occupying lesions
- Diffuse cerebral edema
- Hydrocephalus
- Miscellaneous
Causes of space occupying lesions that can cause increased ICP
Intracranial bleeding: intraparenchymal, subdural,epidural
Tumor
Abscess
Causes of diffuse cerebral edema that can cause increased ICP
Head trauma
diffuse axonal injury
Meningitis/Encephalitis
Hepatic encephalopathy
Reye’s Sx
Electrolyte shift
Dialysis
DKA
HTN encephalopathy
Post-anoxic brain injury
lead
uncompensated hypercapnia
Causes of hydrocephalus that can cause increased ICP
head trauma
cerebella hemorrhage/infarct
subarachnoid hemorrhage
mening/encephalitis (specially basilar)
aqueductal stenosis
hindbrain malformations
leptomeningeal metastasis
obstructing mass lesions
Miscellaneous Causes of increased ICP
craniosynostosis
venous sinus thrombosis
pseudotumor cerebri
cryoglobulinemia
iron def anemia
SLE
Drugs that Cause of increased ICP
nitrofurantoin
phenytoin
sulfonamides
tetracyclines
vit A
steroids
OCP
Types of cerebral edema and how they differ
Vasogenic, cytotoxic, hydrocephalus/intersticial
1.Vasogenic: increased permeability, location is the white matter, edema fluid is plasma infiltrate, the extracellular fluid volume is increased
Associated with tumor, abscess, infarction, lead, meningitis
2.Cytotoxic: cellular swelling, location grat and white matter, edema fluid is intracellular H20 and Na, the extracellular fluid is decreased
Associated with : decreased osmolality, ischemia,meningitis, Reye’s syndrome
- Hydrocephalus/interstitial: increased intraventricular fluid, location is periventricular matter, edema fluid is CSF, extracellular fluid increased.
Communicating vs. non communicating
Cushings triad
Hypertension,bradycardia, irregular respirations
Intracranial hypotension causes
- LP/ EVD (external ventricular drain)
- CSF leak following trauma, neurosurgery, thoracotomy (CSF.-pleural fistula)
- Dural tear
Intracranial hypotension presentation
intracranial hypotensioncauses stretch of dura and cortical veins ( pain sensitive structures)–> headache, compensatory vasodilation, and TACHYCARDIA ( Different from cushings)
Types of intracranial monitoring and purpose
Types: epidural, intraparenchymal, subarachnoid, ventricular, subdural
Goal: early detection of decompensation
- Preserve cerebral perfussion
Prevent herniation
Devices: Piezoelectric strain gauge
Fiberoptic monitoring
Pneumatic monitori
Indications for ICP monitoring
GCS 3-8
Clinical signs ( posturing, cushings triad)
Imaging consistent ( small cysterns)
Obscured neuroexamand at risk
Increased risk of ICP
Where do you insert the ICP monitoring
non dominant hemisphere - R
11 cm and 3 cm
Depth 15 mm into the cranium
Contraindications for ICP monitoring
Coagulopathy
Plt< 100,000
Plt dysfunction (aspirin)
INR> 1.3
local infection at site
Herniation syndromes
- Subfalcine: aka midline shift or cingulate hernia, mass effect with medial direction of the ipsilateral cingulate gyrus beneath the free edge of the falx cerebri
- Central herniation: Downward displacement of the brainstem , mild traction VI nerve ,if severe medullary injury and even respiratory depression
- Transtentorial, uncal:medial temporal lobe herniates inferiorly through the tentorial notch. Triad blow pupil, hemiplegia, coma
- Tonsillar herniation
Goals in ICP
- ICP < 15-20 ( lower <10-15 if skull fx/defect, higher <20-30 ifmetabolic defects)
- CPP > 50-70
- CI > 2.5-3 ( may consider pressors)
euvolemia to hypervolemia
normotension
ICP management
- Elevate head 30 degrees and midline, neck position neutral and noncompressed. ( enhance cerebral venous OUTFLOW)
- Temporal hyperventilation:Pco2 35-40 ideally
- CSF drainage: removal of CSF ideally through ventriculostomy
- Mannitol: 0.5-2 g/kg up to 300 osm
- Hypertonic Saline: 5-10 mL/kg 3% NaCL up to 145-180 meq/L. May bolus 5-10 ml/kg. and start a gtt @ 0.5-2ml/kg/hr
- Craniectomy
