COVID-19 Resources – Septic Shock Pathophysiology & Management -

COVID-19 Resources – Septic Shock Pathophysiology & Management

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COVID-19 Septic Shock Pathophysiology Slides

COVID-19 Septic Shock Pathophysiology Notes

COVID-19 has left us with many unanswered questions about the care and treatment for our pandemic population.

In response to the rising questions and concerns, I have decided to create some educational videos that we can refer back to related to the care and treatment of our COVID-19 patients.

Let’s get started on understanding how hemodynamics and arterial blood gas results effect our COVID-19 population.

Septic Shock Pathophysiology

When you hear the term sepsis or septic, the first thing that may come to mind is sewage such as a septic tank.

In a healthy individual, the blood is clean without infective material. In sepsis, an infection (sewage) or some other factor is causing inflammation in the bloodstream.

Sepsis = Infective material

Shock = Decreased tissue perfusion, decreased oxygenation of tissues, and low blood pressure

We begin by looking at a blood vessel.

Red blood cells within the vessel delivers oxygen to the tissues in exchange for carbon dioxide.

Infective material is introduced into the bloodstream

White Blood cells will encounter the infective material regardless if it is bacteria, viruses, or fungal infections. This infective material turns the blood vessels into septic pipes containing that sewage we discussed earlier.

The white blood cells’ job is to find the infective material and clean it up making the vessels sterile again. This process is called white blood cell activation.

This activation causes five things to occur

Step 1: call on other WBCs for help (WBC recruitment)

•The WBC want to recruit as many WBCs to the infective material to help eradicate it from the body

Step 2: Increase vessel diameter and vascular space

•Infective material is not always in the bloodstream and may be found in the interstitial tissue

•White blood cells must find a way to get into the interstitial tissue to eliminate the threat

•Performed by releasing molecules called nitrous oxide to interact with the blood vessel causing them to dilate (increasing the diameter of the blood vessel) and decrease in systemic vascular resistance (The blood and all the blood contents have more space and there is less resistance the contents are bumping up against) causing a drop in blood pressure

Step 3: WBC need to make the blood vessels leaky to get into the interstitial space

•Infective material is not always in the bloodstream and may be found in the interstitial tissue

•White blood cells must find a way to get into the interstitial tissue to eliminate the threat by causing increase vascular permeability or leaky vessels

•The inflammation and leakiness from these processes are not only happening in a localized area but is happening systemically (everyone in the body!!) due to systemic vascular vasodilation

The increase in leakiness causes fluid build up in the tissues making it very difficult for oxygen to get to the tissues it needs to perfuse. This results in the cells becoming starved for oxygen.

Increase blood vessel diameter and increase leaky vessels are what primarily cause shock

Step 4: Increased damage to blood vessels

•WBC want to destroy the infective material by releasing lytic enzymes that can damage and destroy the pathogens.

•However, due to the systemic vascular inflammation, increased vessel diameter, and leaky vessels, these lytic enzymes end up damaging blood vessels as well.

Coagulation factors (proteins that help cause clotting) are recruited due to the damage of blood vessels

When blood vessels get ruptured the body wanted to create clots to patch up the leaky spaces, so blood doesn’t continue to spill into the extravascular space

Important to remember: the leakage of blood vessels are happening everywhere!!

The coagulation factors that were deployed to help end up getting used up while trying to patch up the blood vessels. So clots start forming everywhere and some clots can break off into the bloodstream.

•Coagulation occurs in the vascular system, but the coagulation cannot keep up with the damage, so blood begins spilling out of the vessels.

Step 5: Disseminated Intravascular Coagulation (DIC)

•Characterize by systemic activation of blood coagulation leading to microvascular thrombi in various organs contributing to multiple organ dysfunction syndrome (MODS). Consumption of clotting factors and platelets in DIC can result in life-threatening hemorrhage.

•Serious complication in septic shock

Septic Shock Complications

Acute Respiratory Distress Syndrome

•Lungs are highly vascular with many blood vessels

•During septic shock, damage is happening everywhere including damage to the blood vessels in the lungs

•Oxygen is unable to be absorbed leading to respiratory distress

Cardiac Output (amount of blood your heart pumps each minute)

•Will initially increase to compensate for the decreased systemic vascular resistance

•If you increase cardiac output, then the blood pressure will remain stable

•As septic shock continues, the heart becomes damaged just as the lungs did in septic shock, leading to a drop in cardiac output and a drop in blood pressure if left untreated

Characteristics of Sepsis and Septic Shock

•Massive systemic vasodilation and hypotension

•Tachycardia; depressed contractility

•Vascular leakage leading to hypovolemia

•Compromised nutrient blood flow to organs

•Disseminated intravascular coagulation

•Abnormal blood gases and acidosis

•Respiratory distress and multiple organ failure

Septic Shock Recognition

•Early Recognition is Key!!

•Systemic Inflammatory Response Syndrome (SIRS)

•Two of the following

•Temperature > 38.3 C (100.9 F) or < 36 C (96.8 F)

•Heart Rate > 90 bpm

•RR > 20 bpm

•WBC > 12,000 or < 4,000 or >10% band forms

Step 1: “Does the patient have 2 or more SIRS?”

Step 2: “Do you suspect an infection?”

SIRS + Infection = Sepsis

Stages of Septic Shock

Stages of Septic Shock – Initial

•Decreased venous return

•Decreased stroke volume

•Decreased cardiac output

•Decreased tissue perfusion

•Most likely the only symptom at this stage is tachycardia and tachypnea

Stages of Septic Shock – Compensatory

•Tachycardia

•Cool, pale, or mottled extremities

•Agitation & Restlessness

•Normal or slightly lower blood pressure

•Decreased urine output

Stages of Septic Shock – Progressive

•Unresponsive to treatment

•Ineffective tissue perfusion leading to organ dysfunction

•Anaerobic metabolism – increased lactic acid

•Hypotension

•Tachycardia; mottled skin

•Tachypnea

•Oliguria

•Absent bowel sounds

•ABG – decreased PaO2, increased PaCO2, decreased pH, decreased HCO3

Stages of Septic Shock – Refractory

•End-organ failure – shock cannot be reversed

•Continued increased vascular permeability

•Increased cellular death

•Multiple organ dysfunction syndrome (MODS)

•Death

Multiple Organ Dysfunction in Septic Shock

Central Nervous System

•Confusion

•Altered LOC

•Psychosis

Respiratory System

•Tachypnea

•Increased oxygen needs

•Decreased P:F Ratio (ARDS)

Digestive System

•Elevated bilirubin

•Elevated LFTs

•Decreased Albumin

Cardiovascular System

Tachycardia
Hypotension

Urinary System

Decreased urine output
Increased creatinine

Hematologic System

Decreased platelets
Decreased Protein C
Increased PT/PTT

3-Hour & 6-Hour Sepsis Bundles

Early detection – 1st 3 hours

•Measure lactate level

•Obtain blood cultures prior to administration of antibiotics

•If possible – do NOT delay antibiotics

•Administer broad spectrum antibiotics within 1 hour

•Administer 30 mL/kg crystalloid for hypotension or lactate > or = 4 mmol/L

Critical Care – 1st 6 hours

•Apply vasopressor for hypotension (that does not respond to fluid resuscitation) to maintain MAP > or = 65 mm Hg

•Norepinephrine (1st choice)

•Need a central line

•Vasopressin (2nd line agent)

•For persistent hypotension after initial fluid administration, or if initial lactate was elevated, reassess volume status

•Re-measure lactate if initial was elevated – goal is to normalize it

What is a lactate?

•Blood lactate level is an important biological variable in determining the adequacy of perfusion and oxygenation

•Normal lactate level is around 1 mEq/L

•In sepsis, blood lactate levels may be raised by an increase in cellular metabolism, inhibition of pyruvate dehydrogenase, and reduced clearance

•Repeated measurements enable one to assess the efficacy of treatment

•Lactate has some prognostic utility

•Sustained (>6 h) elevated lactate portends increased mortality

•Mortality increases as lactate levels increase

•0 – 2.5 mmol/L 4.9% mortality

•2.5 – 4.0 mmol/L 9.0% mortality

•> 4.0 mmol/L 28.4% mortality

Management of Sepsis and Septic Shock

Manage Infection

•Antibiotics: Administer broad-spectrum intravenous antimicrobials for all likely pathogens within 1 hour after sepsis recognition

•Source Control: Obtain anatomic source control as rapidly as is practical

•Antibiotic stewardship: Assess patients daily for de-escalation of antimicrobials; narrow therapy based on cultures and/or clinical improvement

Manage resuscitation

•Fluids: For sepsis-induced hypoperfusion, provide 30 mL/kg of intravenous crystalloids within 3 hours with additional fluid based on frequent reassessment

•Considerations need to be made when ARDS are present

•Resuscitation target: For patients with septic shock requiring vasopressors, target a mean arterial pressure (MAP) of 65 mm Hg

•Vasopressors: Use norepinephrine as a first-choice vasopressor

Additional Medication management

•Insulin for blood sugar stability

•Corticosteroids

Mechanical ventilation in patients with sepsis-related ARDS

•Target a tidal volume of 6 mL/kg of predicted body weight