SPE 2: sepsis and septic shock Flashcards
what are the 4 types of shock
1) cardiogenic
2) hypovolemic
3) distributive
4) obstructive
cardiogenic shock
results from poor pumping function or circulatory overload
-decrease CO, increase SVR, increase PCWP
hypovolemic shock
results from poor fluid intake or excessive fluid loss (sweating, diarrhea, vomiting, hemorrhage, etc…)
-decrease CO, increase SVR, decrease PCWP
distributive shock
results from vasodilation leading to low SVR
a. Ex: Sepsis, Anaphylaxis, Hepatic failure, neurogenic shock (autonomic dysfunction from
traumatic brain injury, spinal cord injury, etc…)
- septic and anaphylactic: increase CO, decrease SVR, decrease PCWP
- neurogenic: decrease CO,decrease SVR, decrease PCWP
obstructive shock
– results mostly from extracardiac causes of heart failure
a. Ex: Cardiac tamponade, pulmonary embolism, tension pneumothorax, constrictive
pericarditis, etc…
-decrease CO, increase SVR, PCWP variable
sepsis
is broadly defined as life-threatening organ dysfunction caused by a dysregulated host response to an infection
how do you classify organ dysfunction
is defined by a qSOFA score or SOFA score >2
what is qSOFA
“quick Sequential Organ Failure Assessment”
-ADVANTAGE: can be completed at bedside with no need for labs
criteria:
-resp rate >22
-altered mentation
-systolic blood pressure <100mmHG
what is SOFA
“Sequential Organ Failure Assessment”
-Needs laboratory data to complete
criteria
- respiration (PaO2/FIo2)
- coagulation (platelets)
- Liver (bilirubin)
- cardiovascular (administration of vasopressors with type and dose rate of infusion)
- CNS (glasgow coma scale)
- Renal (creatinine and urine output)
what is the prognosis of sepsis
inpatient mortality >10%
what is septic shock
is broadly defined as a subset of septic patients in which circulatory and cellular
metabolism abnormalities are profound and substantially increase the risk of hospital
mortality (>40%)
clinically
= sepsis with persisting hypotension and requiring vasopressors to maintain MAP>65 mmHg and having a serum lactate > 2 mmol/L despite adequate volume resuscitation
signs and sx of septic shock
- Hypotension
- Tachycardia
- Altered mental status
- Oliguria
signs and sx of sepsis
-Temperature: > 38 °C or < 36°C
-Heart rate: > 90
-Tachypnea: respiratory rate > 20
-Leukocytosis (WBC > 12,000) or leukopenia (WBC < 4000)
-Signs of end-organ perfusion:
-Early sepsis has warm extremities from vasodilation (compared to cardiogenic shock
which has cool extremities)
-If Septic shock develops, extremities can become cool from redirection of blood to core
organs
-Skin mottling in septic shock
-CNS: Altered mental status
-Kidney: Oliguria or anuria
-Bowel: Absent bowel sounds or ileus are often signs
of end-organ hypoperfusion
lab testing for sepsis
-Complete metabolic panel (CMP)
-assesses for acute liver injury, acute kidney injury (AKI), electrolytes, etc…
-Complete blood count (CBC) with differential
-assesses for leukocytosis/leukopenia, anemia, and thrombocytopenia
-PT (INR), PTT, Fibrinogen, D-dimer, peripheral blood smear
-assesses for DIC (see below in complications of sepsis)
-Arterial blood gas (ABG)
-assesses for hypoxemia and possible ARDS (from PaO2:FiO2 ratio)
-Serum lactate
-assesses for signs of poor organ perfusion
-Plasma procalcitonin
-elevated procalcitonin levels are associated with bacterial infections and sepsis
-unfortunately, its exact role in diagnosis and management of sepsis has not clearly
been defined and thus it is not routinely checked in many centers
-has been proposed as a tool to determine duration of antibiotics (particularly in
community-acquired pneumonia)
-Identify source of infection (depends on patient):
-consider obtaining urinalysis with microscopy, urine culture, blood cultures (peripheral
and through any lines), sputum cultures, stool cultures, lumbar puncture with
CSF analysis, paracentesis with ascites analysis and culture, wound cultures,
chest-ray, etc…
complication of sepsis: DIC (about)
-Characterized by abnormal activation of the coagulation cascade and formation of
microthrombi throughout the microcirculation leading to organ dysfunction and
consumption of platelets, fibrin, and coagulation factors which ultimately results in
hemorrhage as well
-Thus, it is a hematologic disorder characterized by clotting and bleeding
-It can be secondary to sepsis, malignancy, trauma, preeclampsia (and other obstetric
complications), and many other diseases
what do labs reveal in DIC
- Thrombocytopenia
- Elevated PT and PTT levels
- Elevated D-dimer and fibrin degradation products (FDPs)
- Decreased fibrinogen levels
- Abnormal peripheral blood smear (Schistocytes and helmet cells present)
what can DIC result in?
-Can result in acute kidney injury (AKI), acute hepatic injury, acute lung injury, neurologic
complications, and adrenal failure (Waterhouse-Friderischen syndrome), etc…
what is the list of complications of sepsis?
1) DIC
2) AKI
3) Acute hepatic injury
4) ARDS
ARDS
-characterized by acute and diffuse inflammatory injury to the lungs
-can be caused by multiple etiologies
-Pneumonia, aspiration of gastric contents, and sepsis account for > 85% of cases of
ARDS per recent trials
-diagnosed by onset within 7 days of initial insult, bilateral opacities on CXR or Chest CT
consistent with pulmonary edema, and by low PaO2:FiO2 ratio (Partial pressure of
arterial oxygen to the fraction of inspired oxygen)
-at least a
PaO2:FiO2 ratio < 300 mm Hg is needed for the diagnosis of ARDS
tx of sepsis: what do you need to place?
-2 large bore peripheral IVs
- Central line, typically a right internal jugular vein (RIJ) catheter
- most vasopressors must be given centrally and not through peripheral IV
- can measure CVP with transducer as well
- Arterial line
- for accurate hemodynamics and MAP to help guide fluid and vasopressor treatment
- Urinary catheter (Foley)
- also consider securing airway with endotracheal intubation
what is the goal urine output in septic pt>?
> 0.5ml/kg/hour
what are the components of the 1 Hour bundle
- Measure lactate level
- Obtain blood cultures prior to antibiotic administration
- Administer empiric broad-spectrum antibiotics
- Fluid resuscitation with IV fluids (at least 30ml/kg) for hypotensive patients or Lactate >4
-ex: 70 kg male with hypotension and sepsis would get 2100 ml of IVF bolus with
additional fluid as needed per hemodynamic status
-Crystalloid fluids (Lactated ringers, Normal Saline, etc…) are preferred over Colloid
fluids (i.e. Albumin)
-be cautious with fluid resuscitation in patients with CHF
5. Add vasopressors in adequately volume resuscitated patients to maintain mean arterial blood pressure (MAP) >65mmHG
-Norepinephrine is preferred initial vasopressor
-Vasopressin or Epinephrine can be added as the next vasopressor choice if still needed to meet MAP goal >65
-Dobutamine can be subsequently added to patients with ongoing evidence of
persistent hypoperfusion despite adequate fluid resuscitation and vasopressor
agents
what do you need to do if initial lactate is >2
- repeat lactate every few hours until normal
* lactate marker of tissue hypoperfusion
alpha-1 receptors
a. located in vascular smooth muscle
b. activations leads to vasoconstriction
beta-1 receptors
a. located mostly in the heart
b. activation increases heart rate (chronotropy) and cardiac contraction (inotropy)
beta-2 receptors
a. located in vascular and bronchial smooth muscles
b. activation leads to vasodilation and bronchodilation
dopamine receptors (D1)
a. located in renal and splanchnic (mesenteric) vascular beds
b. activation leads to vasodilation
vasopressin receptors (v1 and v2)
a. V1 receptors are located in vascular smooth muscles
i. activation leads to vasoconstriction
b. V2 receptors are located in renal collecting duct
i. activation leads to antidiuresis
chapmans point ant bronchi
intercostal space between the second and third ribs at the
sternocostal junction, bilateral
chapmans point post bronchi
midway between the spinous process and the tip of the
transverse process of T2, bilateral
chapmans point ant upper lung
intercostal space between the third and fourth ribs at the
sternocostal junction, bilateral
chapmans point post upper lung
in the space between the transverse processes of T3 and T4,
midway between the spinous process and the tip of the transverse
process, bilateral
chapmans point ant lower lung
intercostal space between the fourth and fifth ribs at the
sternocostal junction, bilateral
chapmans point post lower lung
in the space between the transverse processes of T4 and T5,
midway between the spinous process and the tip of the transverse
process, bilateral
chapmans point ant liver and gallbladder
intercostal spaces between the fifth, sixth, and seventh ribs, from the
mid-mammillary line to the sternum, right side only
chapmans point post liver and gallbladder
between the transverse processes of T5, T6, and T7, midway between
the tips of the spinous processes and the transverse processes, right side only
chapmans point ant kidney
one inch above the umbilicus, laterally on either side of the midline
chapmans point post kidney
between the transverse process of T12 and L1, midway between the
tips of the spinous processes and the transverse processes, bilateral
heart sympathetic and parasympathetic innervation
Sympathetics T1-T6
Parasympathetics Vagus Nerve (OA, AA)
lungs sympathetic and parasympathetic innervation
Sympathetics T1-T7,
Parasympathetics Vagus Nerve (OA, AA)
liver sympathetic and parasympathetic innervation
Sympathetics T5-T9,
Parasympathetics Vagus Nerve (OA, AA)
kidney sympathetic and parasympathetic innervation
Sympathetics T10-T11, Parasympathetics Vagus Nerve (OA, AA)
biomechanical model of care
OMT for SD
resp/circ model of care
- fluid status
- vent settings
- lymphatic OMT txs
neuro model of care
- PT/OT for neuro compromise
- OMT to normalize sympathetics and parasympathetics
metabolic/energetic/immune model of care
- assess ability for oral intake versus TPN
- renal/hepatic dosing of meds
- monitor ins and outs
- daily weights
behavioral model of care
-address factors leading to sepsis
