Exam 2 (Everything but Renal)

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What is shock?

A life-threatening medical condition that results from inadequate tissue perfusion.

  • It is not a disease itself, but rather the possible consequences of many diseases.

  • It is a systemic response to an illness/injury that leads to a cascade of events with a potentially fatal outcome.

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Regulatory Mechanisms in Shock (image)

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Pathophysiology of Shock (image)

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What are the Stages of Shock?

  • Initial Insult

  • Compensatory Stage—compensation

  • Progressive Stage—decompensation

  • Irreversible Stage—refractory (unresponsive to treatment)

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Initial Insult: What are potential sources of shock?

  • Infection

  • Trauma

  • Blood loss

  • Dehydration

  • Hyperthermia

  • Allergic reaction

  • Poisoning

  • SCI

  • MI

  • Burns

Each of these can lead to decreased cardiac output of blood circulation and begin the cascade toward a shock state.

<ul><li><p>Infection</p></li><li><p>Trauma</p></li><li><p>Blood loss</p></li><li><p>Dehydration</p></li><li><p>Hyperthermia</p></li><li><p>Allergic reaction</p></li><li><p>Poisoning</p></li><li><p>SCI</p></li><li><p>MI</p></li><li><p>Burns</p></li></ul><p>Each of these can lead to decreased cardiac output of blood circulation and begin the cascade toward a shock state.</p><p></p>
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Compensatory Stage—Systemic Actions: What does the body do?

  • Tries to increase supply to meet demand

  • Sympathetic nervous system activated

  • Renin-Angiotensin-Aldosterone (RAA) system activated

  • Glucocorticoids released

  • Blood flow decreases to non-vital organs

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Compensatory Stage: Clinical Manifestations

  • Relatively normal BP

  • Tachycardia

  • Tachypnea

  • Decreased PaCO2

  • Diaphoresis

  • Cool or clammy skin (except in certain distributive shocks)

  • Decreased UOP

  • Hypoactive bowel sounds

  • Increased serum glucose

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What are the 3 ways compensation is measured?

  1. Mentation

  2. Blood Pressure

  3. Pulse Oxygenation

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Progressive Stage—Systemic Actions: What does the body do?

  • Overworked heart can’t meet body’s requirements, becomes ischemic and fails.

  • Microcirculation regulation fails, leading to widespread capillary permeability.

  • Prolonged tissue hypoxia leads to acidosis and cellular dysfunction.

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Progressive Stage: Clinical Manifestations

  • Hypotension (this is a late sign!)*

  • Tachycardia/tachypnea

  • Pulmonary edema/crackles

  • Multiple Organ Dysfunction Syndrome (MODS)**

  • Altered mental status

  • AKI (oliguria/anuria)

  • GI ischemia (ulcers/bloody diarrhea)

  • Abnormal hemostasis (increased clotting times, bruises/petechiae)

*Low B/P indicates prolonged tissue ischemia and poor prognosis. We must intervene before this develops.

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Multiple Organ Dysfunction Syndrome (MODS)

Changes in other systems besides the initial area…

  • Respiratory P/F ratio < 250 w/o pneumonia, or < 200 w/ pneumonia

  • MAP < 65 mmHg, SBP < 90 mmHg, or SBP decrease > 40 from baseline

  • Creatinine > 2 mg/Dl

  • UOP < 0.5 mL/kg/hr in 6 hours or < 400 mL in 24 hours.

  • Bilirubin > 2 mg/dL

  • Platelets <100,000/mm3

  • INR > 1.5 or aPTT > 60 secs

  • Lactate > 2 mmol/L

<p>Changes in other systems besides the initial area…</p><ul><li><p>Respiratory P/F ratio &lt; 250 w/o pneumonia, or &lt; 200 w/ pneumonia</p></li></ul><ul><li><p>MAP &lt; 65 mmHg, SBP &lt; 90 mmHg, or SBP decrease &gt; 40 from baseline</p></li><li><p>Creatinine &gt; 2 mg/Dl</p></li><li><p><u>UOP &lt; 0.5 mL/kg/hr in 6 hours or &lt; 400 mL in 24 hours</u>.</p></li><li><p>Bilirubin &gt; 2 mg/dL</p></li><li><p>Platelets &lt;100,000/mm3</p></li><li><p>INR &gt; 1.5 or aPTT &gt; 60 secs</p></li><li><p>Lactate &gt; 2 mmol/L</p></li></ul><p></p>
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Irreversible Stage—Systemic Actions: What does the body do?

  • MODS progresses to total organ failure

  • Liver and kidneys fail, leading to significant metabolic acidosis

  • BP stays low despite treatment

  • Survival is unlikely

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Irreversible Stage: Clinical Manifestations

  • Significantly diminished cardiac output

  • Pale, cyanotic, or yellowish skin

  • Anuria

  • Disseminated Intravascular Coagulation (DIC)

  • Coma

  • Death

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Disseminated Intravascular Coagulation (DIC)

Definition: 

  • Inappropriate coagulation occurs within the blood vessels

  • Endothelial damage triggers clotting cascade and widespread clot formation

  • Systemic over-consumption of clotting factors

  • Clotting factors get used up and patient develops uncontrollable bleeding

Causes:

  • Not fully understood, but it’s most often associated with sepsis, severe infections, trauma, cancer, and obstetric complications.

  • Never the primary issue/disease; occurs in response to another disease process or injury.

<p><span><strong>Definition:&nbsp;</strong></span></p><ul><li><p><span>Inappropriate coagulation occurs within the blood vessels</span></p></li><li><p><span>Endothelial damage triggers clotting cascade and widespread clot formation</span></p></li><li><p><span>Systemic over-consumption of clotting factors</span></p></li><li><p><span>Clotting factors get used up and patient develops uncontrollable bleeding</span></p></li></ul><p style="text-align: left"><span><strong>Causes:</strong></span></p><ul><li><p><span>Not fully understood, but it’s most often associated with sepsis, severe infections, trauma, cancer, and obstetric complications.</span></p></li><li><p><span>Never the primary issue/disease; occurs in response to another disease process or injury.</span></p></li></ul><p></p>
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Some assessment findings on a patient with DIC

  • Blood leaking from around their IV sites

  • Bloody noses occurring often

  • Gums bleeding very easily

  • Pink tinges in their urine

  • Dark tarry stools

  • Petechiae, ecchymosis, bruising

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Clinical Findings in Shock (image)

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Shock in General: Initial S/Sx

  • Tachycardia

  • Tachypnea/shortness of breath

  • Decreased blood pressure

  • Delayed capillary refill

  • Pale, cyanotic, cool, or clammy skin

  • Decreased urine output

  • Weakness/lethargy

  • Dizziness/lightheadedness

  • Altered level of consciousness

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What are the 4 types of Shock?

  1. Hypovolemic

  2. Cardiogenic

  3. Obstructive

  4. Distributive

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Hypovolemic Shock

Decreased intravascular volume due to fluid loss.

<p><span>Decreased intravascular volume due to fluid loss. </span></p>
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Hypovolemic Shock: Causes

  • External bleeding (trauma)

  • Internal bleeding (GI or bleeding disorders)

  • Burns

  • Diarrhea/vomiting

  • Dehydration

  • Diuresis (such as via hemodialysis)

  • Diabetes insipidus

<ul><li><p>External bleeding (trauma)</p></li><li><p>Internal bleeding (GI or bleeding disorders)</p></li><li><p>Burns</p></li><li><p>Diarrhea/vomiting</p></li><li><p>Dehydration</p></li><li><p>Diuresis (such as via hemodialysis)</p></li><li><p>Diabetes insipidus</p></li></ul><p></p>
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poor skin turgor; thirst

In addition to the common signs and symptoms of shock, a patient in hypovolemic shock may exhibit ____ ____ ______ and ______.

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Hypovolemic Shock: Primary Treatment Goals

  • Find the source and stop it! (#1)

  • Replace lost intravascular volume.

  • Redistribute fluid volume.

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Cardiogenic Shock: Causes

  • Myocardial infarction (#1)

  • Heart failure

  • Dysrhythmias

  • Coronary artery disease

  • Cardiomegaly

  • Myocarditis

  • Cardiac valve disorders

  • Drug toxicity

<ul><li><p><mark data-color="yellow" style="background-color: yellow; color: inherit">Myocardial infarction (#1)</mark></p></li><li><p>Heart failure</p></li><li><p>Dysrhythmias</p></li><li><p>Coronary artery disease</p></li><li><p>Cardiomegaly </p></li><li><p>Myocarditis</p></li><li><p>Cardiac valve disorders</p></li><li><p>Drug toxicity </p></li></ul><p></p>
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Cardiogenic Shock

Impairment or failure of the myocardium

<p><span>Impairment or failure of the myocardium</span></p>
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crackles in lungs; chest pain

In addition to the common signs and symptoms of shock, a patient in cardiogenic shock may exhibit _______ __ _____ and _____ ____.

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Cardiogenic Shock: Primary Treatment Goals

  • Restore tissue perfusion (including to the heart itself)

  • Improve cardiac contractility

  • Manage other organ dysfunction

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Obstructive Shock

Inability of the heart to fill properly

<p><span>Inability of the heart to fill properly</span></p>
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Obstructive Shock: Causes

  • Pneumothorax

  • Cardiac Tamponade

  • Pulmonary embolism

  • Pulmonary hypertension

  • Aortic dissection

  • Restrictive cardiomyopathy

  • Tumors

  • Sickle Cell Disease

<ul><li><p>Pneumothorax</p></li><li><p>Cardiac Tamponade</p></li><li><p>Pulmonary embolism </p></li><li><p>Pulmonary hypertension</p></li><li><p>Aortic dissection</p></li><li><p>Restrictive cardiomyopathy</p></li><li><p>Tumors</p></li><li><p>Sickle Cell Disease</p></li></ul><p></p>
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  • Chest or abdominal pain

  • Distended jugular veins

  • Muffled heat sounds (in cardiac tamponade)

  • Unequal peripheral pulses (in aortic dissection)

In addition to the common signs and symptoms of shock, a patient in obstructive shock may exhibit:

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Obstructive Shock: Primary Treatment Goal

Remove the obstruction!

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Distributive Shock

Loss of sympathetic vasomotor tone/ “maldistribution of blood flow”

  • is marked by systemic vasodilation that leads to increased capillary permeability and decreased blood flow to the brain, heart, and kidneys, causing damage to vital organs.

<p>Loss of sympathetic vasomotor tone/ “maldistribution of blood flow”</p><ul><li><p>is marked by systemic vasodilation that leads to increased capillary permeability and decreased blood flow to the brain, heart, and kidneys, causing damage to vital organs.</p></li></ul><p></p>
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Distributive Shock: Causes

  • Sepsis (#1)

  • Neurological dysfunction

  • Spinal cord injury (SCI)

  • Anaphylaxis

  • Hypersensitivity reaction

  • Effects of medication

<ul><li><p><mark data-color="yellow" style="background-color: yellow; color: inherit">Sepsis (#1)</mark></p></li><li><p>Neurological dysfunction</p></li><li><p>Spinal cord injury (SCI)</p></li><li><p>Anaphylaxis</p></li><li><p>Hypersensitivity reaction</p></li><li><p>Effects of medication </p></li></ul><p></p>
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  • Warm or flushed skin

    • Blood sits/hangs out in vessels longer than normal due to the widespread vasodilation…

  • Other symptoms depend on the type of distributive shock the patient is experiencing

In addition to the common signs and symptoms of shock, a patient in distributive shock may exhibit:

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Distributive Shock: Primary Treatment Goals

  • Restore sympathetic tone

  • Reverse the cause

  • Support BP, pulse, and respirations

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Types of Distributive Shock

  • Neurogenic Shock

  • Anaphylactic Shock

  • Septic Shock

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Neurogenic Shock

Is a life-threatening condition in which the central nervous system becomes damaged, leading to loss of vascular tone, widespread vasodilation, and dangerously low blood pressure.

  • Pathophysiology:

    • Damage to the sympathetic nervous system allows the parasympathetic system to take over unopposed, often leading to bradycardia and worsening cardiac output.

    • Intravascular volume remain the same, but vasodilation and bradycardia combine to create hypoxic state.

  • Causes:

    • Spinal cord injury (SCI) is the most common cause, but other causes can include:

      • Spinal anesthesia

      • Autoimmune disorders, such as Guillain-Barre Syndrome or Transverse Myelitis

      • Severe stroke

      • Meningitis

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Anaphylactic Shock

Is a life-threatening condition in which the body’s immune system overreacts to an allergen, causing rashes, hives, itching, edema, and if left untreated, severe hypotension and airway obstruction.

  • Pathophysiology:

    • Allergens bind to IgE, which triggers a massive release of histamine from mast cells and basophils. Histamine then causes widespread vasodilation and capillary permeability, leading to hypotension and loss of intravascular fluid.

    • Histamines, along with prostaglandins and leukotrienes, cause smooth muscle contraction in the airways, limiting ventilation.

  • Causes:

    • Can be caused by any numbers of potential allergens, differing from person to person.

      • Medications (antibiotics, NSAIDs, contrast dye, ACE inhibitors)

      • Foods (nuts, fruits, shellfish, milk)

      • Insect stings (bees, wasps, hornets)

      • Latex

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General Treatment of Shock: Early Identification

  • ABCs

  • Assess and report subtle changes:

    • LOC, UOP, skin tone, cap refill

  • Vital Signs:

    • HR, RR, BP, MAP, Temp, SpO2

  • Note and report concerning lab trends

  • Initiate timely treatment

  • Correct precipitating event

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General Treatment of Shock: Establish Adequate Tissue Perfusion

  • Promote adequate cardiac output:

    • Restore intravascular volume (fluid replacement)

    • Restore vasomotor tone (vasoactive medications)

  • Ensure adequate oxygenation

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General Treatment of Shock: Restore Normal Cell Function

  • Establish proper acid-base balance

  • Provide nutritional support

  • Use of antacids, PPIs, or H2 antagonists to prevent GI injury

  • Short-term, mild hyperglycemia may be acceptable (140-180)—Permissive hyperglycemia

    • We don’t want them in a hypoglycemic state because their body needs enough glucose to recover from this shock state.

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General Treatment of Shock: Monitor Labs

  • Lactate levels

  • Complete metabolic panel (CMP)—for electrolyte balances

  • Complete blood count (CBC)—for blood cell counts, including WBCs and platelets

  • Blood cultures (if an infection is suspected)

  • Base deficit and anion gap

  • ABGs

  • Signs of MODs**

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General Treatment of Shock: Monitor Hemodynamics

  • Blood pressure:

    • MAP is generally the guiding factor (desired > 65 mmHg)

  • Continuous monitoring (VS/ECG)

  • Other measurements as warranted (PP, CVP, etc.)

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General Treatment of Shock: Provide Psychosocial Support

  • Provide emotional support and help reduce anxiety

  • Communication with the patient and family members, including education about condition

  • Care plan may include end-of-life issues and/or grief counseling

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General Treatment of Shock: Provide Advanced Supportive Care as Needed

May include intubation, ventilation, dialysis, etc.

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General: Fluid Replacement

  • Fluid Challenge: 500 to 1,000 mL bolus of isotonic crystalloid

    • One-time bolus to see how the patient does…

  • Aggressive Fluid Resuscitation: 30 mL/kg (using IDEAL body weight)

    • Long continuous bolus

  • Crystalloids for IV treatment of shock: (they’re more acidic!)

    • 0.9% saline (Normal Saline Solution)—super cheap!

    • Lactated Ringer’s (closely mirrors regular blood plasma)—more $$

*Rule of Thumb: The best fluid is the fluid that’s readily available!

<ul><li><p><strong>Fluid Challenge</strong>: 500 to 1,000 mL bolus of isotonic crystalloid</p><ul><li><p>One-time bolus to see how the patient does…</p></li></ul></li><li><p><strong>Aggressive Fluid Resuscitation</strong>: <mark data-color="yellow" style="background-color: yellow; color: inherit">30 mL/kg (using IDEAL body weight)</mark></p><ul><li><p>Long continuous bolus</p></li></ul></li><li><p><strong>Crystalloids for IV treatment of shock</strong>: (they’re more acidic!)</p><ul><li><p>0.9% saline (Normal Saline Solution)—super cheap!</p></li><li><p>Lactated Ringer’s (closely mirrors regular blood plasma)—more $$</p></li></ul></li></ul><p><strong>*Rule of Thumb</strong>: The best fluid is the fluid that’s readily available!</p><p></p>
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Why isn’t D5W included on the list for IV fluid treatment for shock?

  • D5W sitting in the bag is isotonic. The second it enters your body it’s not isotonic anymore because your body grabs onto the dextrose and uses it → converts it into sugar, and you’re just left with water, which is hypotonic.

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General: Fluid Replacement (Alternative or Adjunctive)

The following solutions can be use in special cases of shock, especially when isotonic crystalloids are not available or sufficient. However, they are NOT first-line therapies.

  • Hypertonic solution for IV fluid treatment of shock:

    • 3% Sodium Chloride (HSS)

      • Can only be administered once or else you’re going to give them hypernatremia.

      • Good for patients who have edema, increased ICP

  • Colloids for IV fluid treatment of shock:

    • Albumin—large protein molecule

    • Dextran—large sugar molecule

**essentially pulling more fluids back into the vasculature

<p>The following solutions can be use in special cases of shock, especially when isotonic crystalloids are not available or sufficient. However, they are<span style="color: red"><strong> NOT </strong></span><strong>first-line therapies.</strong></p><ul><li><p><strong>Hypertonic solution for IV fluid treatment of shock</strong>:</p><ul><li><p>3% Sodium Chloride (HSS)</p><ul><li><p>Can only be administered once  or else you’re going to give them hypernatremia.</p></li><li><p>Good for patients who have edema, increased ICP</p></li></ul></li></ul></li><li><p><strong>Colloids for IV fluid treatment of shock</strong>:</p><ul><li><p>Albumin—large protein molecule</p></li><li><p>Dextran—large sugar molecule </p></li></ul></li></ul><p>**essentially pulling more fluids back into the vasculature </p>
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Fluid Replacement in Shock (image)

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Complications of Fluid Replacement

Fluid administration can be a double-edged sword, both helpful and harmful. Close monitoring is essential to patient safety!

  • We need to avoid under resuscitating and over resuscitating.

  • Insufficient fluid replacement = higher incidence of morbidity and mortality due to lack of tissue perfusion.

  • Excessive fluid administration = higher incidence of morbidity and mortality due to multiple side effects:

    • Acute Lung Injury (ALI)

      • It’s basically pulmonary edema because a bunch of fluid is dumped into the patient and the fluid goes the wrong way (alveoli instead of blood vasculature)-this is why a fluid challenge is done!

    • Abdominal Compartment Syndrome (ACS) and/or Intra-abdominal hypertension (IAH)

      • similar to ascites

    • Multiple Organ Dysfunction Syndrome (MODS)

    • Hypothermia* (fluid = room temp 72F; patient = 98.6F)

    • Acidosis*

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General: Vasoactive Medications

  • These medications are used when fluid therapy alone does not maintain MAP.

  • Dosages are often based on patient weight and titrated to patient response (mcg/min or mcg/kg/min)

  • Continuous monitoring is a must!

  • These medications should be administered in a central line to avoid extravasation and tissue necrosis.

    • The meds can be started in a peripheral, but eventually need to be moved to central asap.

<ul><li><p>These medications are <strong>used when fluid therapy alone does not maintain MAP</strong>.</p></li><li><p>Dosages are often based on patient weight and titrated to patient response <mark data-color="yellow" style="background-color: yellow; color: inherit">(mcg/min or mcg/kg/min)</mark></p></li><li><p>Continuous monitoring is a must!</p></li><li><p><span style="color: red"><strong>These medications should be administered in a central line to avoid extravasation and tissue necrosis</strong></span>.</p><ul><li><p>The meds can be started in a peripheral, but eventually need to be moved to central asap.</p></li></ul></li></ul><p></p>
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Select Vasoactive Agents Used in Treating Shock (image)

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General: Nutritional Therapy

Catabolic process body breaks down lean muscle, so nutritional support is key.

  • Enteral nutrition (via the GI tract) is preferred, but parenteral nutrition (via central line) can be given if the patient has GI impairment.

    • Caloric intake may start off slowly due to fragile state of body (~12.5 kCal/kg), but as the body recovers, caloric intake is slowly increased to ~20-25 kCal/kg.

      • low → up

    • Protein intake is important—Shock patients should receive roughly 1.3 g/kg/day rather than the usual recommendation of 0.8 g/kg/day.

      • up → down

    • Nutrition includes carbohydrate (dextrose), amino acids, lipids, electrolytes, vitamins, trace elements (zinc, copper, manganese, selenium, etc.), and water. ← (TPN)

  • Administration of protective meds (antacids, H2 blockers, PPIs) are also important to prevent peptic ulcer formation.

<p><strong>Catabolic process body breaks down lean muscle, so nutritional support is key.</strong></p><ul><li><p>Enteral nutrition (via the GI tract) is preferred, but parenteral nutrition (via central line) can be given if the patient has GI impairment.</p><ul><li><p><strong>Caloric intake may start off slowly </strong>due to fragile state of body (~12.5 kCal/kg), but as the body recovers, <strong>caloric intake is slowly increase</strong>d to ~20-25 kCal/kg.</p><ul><li><p>low → up</p></li></ul></li><li><p>Protein intake is important—Shock patients should receive roughly 1.3 g/kg/day rather than the usual recommendation of 0.8 g/kg/day.</p><ul><li><p>up → down</p></li></ul></li><li><p>Nutrition includes carbohydrate (dextrose), amino acids, lipids, electrolytes, vitamins, trace elements (zinc, copper, manganese, selenium, etc.), and water. ← (TPN)</p></li></ul></li><li><p>Administration of protective meds (antacids, H2 blockers, PPIs) are also important to prevent peptic ulcer formation.</p></li></ul><p></p>
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Hypovolemic Shock: Potential Treatment Strategies

  • Surgical intervention to control bleeding (#1)

  • IV fluid resuscitation with isotonic crystalloids

  • Blood transfusion (generally if Hgb < 7 g/dL)*—varies by institution

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Hypovolemic Shock Treatment: Blood Transfusions

  • Indicated in episodes of significant blood loss (Hgb < 7 g/dL).

  • Generally administered over 2 to 4 hours, unless its emergent, where it is given as rapidly as possible (use large gauge IV).

    • Time permitting, patient’s blood should be typed and crossmatched.

    • In an emergency, type O negative blood may be used.

  • Blood products may include whole blood, PRBCs, FFP, and platelets:

    • Rule of thumb: 1 unit of PRBCs should raise Hgb by 1 g/dL.

    • Severity of blood loss dictates how much the patient receives.

    • Massive transfusion protocol (MTPs) utilize varying ratios of PRBCs, FFP, and platelets (ex. 4:2:1, 2:1:1, or 1:1:1)

  • Monitor for transfusion reactions*:

    • Vital signs (including temperature)

    • SOB, increased WOB, adventitious lung sounds

    • Altered mental status

    • Hives/rash, flushing, back pain (wheezing)

**Should any undesirable symptoms occur, the first thing to do is stop the infusion!

<ul><li><p>Indicated in episodes of significant blood loss (Hgb <u>&lt;</u> 7 g/dL).</p></li><li><p><strong>Generally administered over 2 to 4 hours, unless its emergent, where it is given as rapidly as possible (use large gauge IV).</strong></p><ul><li><p>Time permitting, patient’s blood should be <u>typed and crossmatched</u>.</p></li><li><p>In an emergency, type O negative blood may be used.</p></li></ul></li><li><p><strong>Blood products may include whole blood, PRBCs, FFP, and platelets</strong>:</p><ul><li><p><strong><mark data-color="yellow" style="background-color: yellow; color: inherit">Rule of thumb</mark></strong><mark data-color="yellow" style="background-color: yellow; color: inherit">: 1 unit of PRBCs should raise Hgb by 1 g/dL</mark>.</p></li><li><p>Severity of blood loss dictates how much the patient receives.</p></li><li><p>Massive transfusion protocol (MTPs) utilize varying ratios of PRBCs, FFP, and platelets (ex. 4:2:1, 2:1:1, or 1:1:1)</p></li></ul></li><li><p><strong>Monitor for transfusion reactions*</strong>:</p><ul><li><p>Vital signs (including temperature)</p></li><li><p>SOB, increased WOB, adventitious lung sounds</p></li><li><p>Altered mental status</p></li><li><p>Hives/rash, flushing, back pain (wheezing)</p></li></ul></li></ul><p>**Should any undesirable symptoms occur, the first thing to do is stop the infusion!</p><p></p>
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Cardiogenic Shock: Potential Treatment Strategies

  • Thrombolytics, PCI, Stents, or CABG (for coronary artery occlusion)

  • Medications (for dysrhythmias or electrolyte imbalances)

  • Mechanical assistive devices (IABP, Impella, LVAD, or ECMO)

  • Use fluids with extreme caution.

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Obstructive Shock: Potential Treatment Strategies

  • Fibrinolytics and DOACs (for PE)

  • Surgical intervention (for PE, tumors, aortic dissection, or splenic sequestration)

  • Needle decompression/chest tube (for pneumothorax)

  • Pericardiocentesis (for cardiac tamponade)

  • Medications (HTN meds for restricted cardiomyopathy or PH)

  • Use fluids with extreme caution

    • It’s not a volume problem. The fluids are being obstructed/backed up and adding more fluids can back it up even more, so be cautious!

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Distributive Shock: Neurogenic Shock—Potential Treatment Strategies

  • Spinal stabilization and surgery

  • Atropine (for bradycardia)

  • DVT or VTE prophylaxis (LMWH)

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Distributive Shock: Anaphylactic Shock—Potential Treatment Strategies

  • Remove causative agent

  • Medications (IM epinephrine 1:1000, B2 agonists, antihistamines, corticosteroids)

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Hemodynamic Monitoring

The use of technology to provide quantitative information about a patient’s vascular capacity, fluid volume, pump effectiveness, and tissue perfusion.

  • Gives us insights into the patient’s preload, after load, and/or SVR.

  • Used to guide their plan of care.

<p>The use of technology to provide quantitative information about a patient’s vascular capacity, fluid volume, pump effectiveness, and tissue perfusion.</p><ul><li><p>Gives us insights into the patient’s preload, after load, and/or SVR.</p></li><li><p>Used to guide their plan of care.</p></li></ul><p></p>
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Volumes, Pressures, & Saturations: Cardiac Output

  • CO = Stroke volume (SV) x heart rate (HR)

  • Normal range = 4-8 L/min

  • Stroke volume is determined via echocardiography

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Volumes, Pressures, & Saturations: Blood Pressure (BP)

Systolic blood pressure (SBP):

  • Normal range = 100-140 mmHg

Diastolic blood pressure (DBP):

  • Normal range = 60-90 mmHg

Usually measured via NIBP cuff readings, but arterial lines are most accurate.

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Pulse Pressure (PP)

  • PP = SBP - DBP

  • Normal range = 40-60 mmHg

  • Wide pulse pressure (< 60 mmHg) usually indicates arteriosclerosis, atherosclerosis, or aortic regurgitation.

  • *Narrow pulse pressure (< 40 mmHg) can be an indicator of shock from decreased CO or increased SVR.*

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Mean Arterial Pressure (MAP)

  • MAP = DBP + 1/3(SBP - DBP)***

  • Normal range = 70-100 mmHg

  • Most accurate estimate of organ perfusion

  • MAP below 65 mmHg in adults is associated with multi-organ failure

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Volumes, Pressures, & Saturations: Saturation of Peripheral Oxygen (SpO2) and Saturation of Arterial Oxygen (SaO2)

Normal range = 95-100%

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Volumes, Pressures, & Saturations: Central Venous Oxygen Saturation (ScvO2)

Normal range = 70-80%

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Volumes, Pressures, & Saturations: End-Tidal Carbon Dioxide (EtCO2) and Arterial Pressure of Carbon Dioxide (PaCO2)

Normal range = 35-45 mmHg

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Volumes, Pressures, & Saturations: Urine Output (UOP)

Normal range = > 0.5 mL/kg/hr

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Volumes, Pressures, & Saturations: Central Venus Pressure (CVP)

  • Normal range = 8-12 mmHg

  • Used to estimate right arterial pressure and overall fluid status

    • Less than = dehydration or decreased fluid volume; Higher than = fluid overload

  • If used to evaluate fluid needs, also consider BP, UOP, and HR

Ex: if giving a lot of fluids and its at a 4, fluids might be elsewhere → should probably listen to the lungs! (ALI)

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Volumes, Pressures, & Saturations: Pulmonary Artery Pressure (PAP)

  • Normal range = mPAP of 12-20 mmHg

  • Used to estimate right ventricular function and assess for pulmonary hypertension (PH)

    • right side of the heart → lungs

    • How well is the right side of the heart doing its job?

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Volumes, Pressures, & Saturations: Pulmonary Artery Wedge Pressure (PAWP)

  • Normal range = mPAWP of 6-12 mmHg

  • Used to estimate left atrial pressure (left atrium)

  • Decreased in hypovolemic and distributive shock**

    • The left side of the heart has less blood in it

  • Elevated in cardiogenic shock***

    • The heart can’t pump it out (blood is pooling)

  • Increased or decreased in obstructive shock depending on the cause**

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Examples of Invasive Hemodynamic Monitoring Equipment

  • Central Venous Pressure Monitoring

  • Pulmonary Artery Pressure Monitoring (Swan-Ganz catheter)

<ul><li><p>Central Venous Pressure Monitoring </p></li><li><p>Pulmonary Artery Pressure Monitoring (Swan-Ganz catheter) </p></li></ul><p></p>
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Sepsis: Prevalence and Vulnerable Populations

Each year in the U.S.:

  • 1.7 million Americans develop sepsis

  • Roughly 350,000 die from sepsis

  • 1 in 3 patients who die in the hospital has sepsis

The most vulnerable people are:

  • Older adults

  • Infants

  • Pregnant women

  • Those with chronic conditions

  • Immunocompromised patients

<p><strong>Each year in the U.S.</strong>:</p><ul><li><p>1.7 million Americans develop sepsis</p></li><li><p>Roughly 350,000 die from sepsis</p></li><li><p>1 in 3 patients who die in the hospital has sepsis</p></li></ul><p><strong>The most vulnerable people are</strong>:</p><ul><li><p>Older adults</p></li><li><p>Infants</p></li><li><p>Pregnant women</p></li><li><p>Those with chronic conditions</p></li><li><p>Immunocompromised patients </p></li></ul><p></p>
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A form of distributive shock that is caused by a cascade of events:

  • Initiation of immune system

  • Inflammatory products activated

  • Vasodilation and blood vessel permeability (decreased SVR)

  • Impaired oxygen exchange

  • Trigged coagulation products

  • Developments of organ failure, ARDS, DIC

Sepsis is …

<p>Sepsis is …</p>
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What are the most common HAIs?

  • Catheter Associated Urinary Tract Infection (CAUTI)

  • Central Line Associated Blood Stream Infection (CLABSI)

  • Ventilator Associated Pneumonia (VAP)

  • Surgical Site Infection (SSI)

  • Clostridium Difficile Infection (CDI)

<ul><li><p>Catheter Associated Urinary Tract Infection (CAUTI)</p></li><li><p>Central Line Associated Blood Stream Infection (CLABSI)</p></li><li><p>Ventilator Associated Pneumonia (VAP)</p></li><li><p>Surgical Site Infection (SSI)</p></li><li><p>Clostridium Difficile Infection (CDI) </p></li></ul><p></p>
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Sepsis: Patient Assessment

  • Septic patients can present in different ways.

  • A thorough assessment is key.

  • Make sure to pay attention to labs!

<ul><li><p>Septic patients can present in different ways.</p></li><li><p>A thorough assessment is key.</p></li><li><p>Make sure to pay attention to labs!</p></li></ul><p></p>
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Systemic Inflammatory Response Syndrome (SIRS)

SIRS criteria consists of:

  • Heart rate > 90 bpm

  • Respiratory rate > 20 rpm

  • Temperature > 38.8 C (100.9 F) or < 36.0 C (96.8 F)

  • WBC > 12,000/mm3 or < 4,000/mm3 or > 10% bands

  • Altered Mental Status

  • Glucose > 140 mg/dL in absence of diabetes

**2 or more and you’re positive for SIRS, but not everyone who is positive for SIRS is septic.

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SIRS: What are bands?

They are immature WBCs.

Ex: someone’s WBCs went from 5,000 to 9,000—which is WNL, but if their bands are 17%, that means that their body had to ramp up production of WBCs because they have an acute infection.

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source of infection; 2

A patient needs to already have a ______ __ _________ along with _ or more of the SIRS Criteria to be considered to have sepsis.

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Not everyone who is positive for SIRS is septic. What are some examples?

  • A patient having an asthma exacerbation.

  • A patient experiencing a panic attack.

  • A patient suffering from heat exhaustion.

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bacteremia

The biggest source of sepsis is __________.

<p>The biggest source of sepsis is __________.</p>
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Sepsis: Nursing Responsibilities

  • Recognize early

  • Treat promptly:

    • Follow the Sepsis Bundle**

    • Fluid Replacement

    • Pharmacologic

  • Astute ongoing assessment

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The Surviving Sepsis Campaign (SSC)

Was launched in 2002 as a collaborative initiative of the European Society of Intensive Care Medium (ESICM), the International Sepsis Forum (ISF), and the Society of Critical Care Medicine (SCCM). It is updated every 4 years.

~Sepsis Bundle

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Sepsis Nursing Responsibilities Soap Box

  • Monitor your patient for trends and report significant changes!

    • Do not just wait for a parameter to cross a predetermined threshold.

Nursing is about anticipation and preemptive action; addressing potential problems before they become actual problems.

  • If a patient’s SBP was 130, but now is 95, that’s concerning. If their potassium was 3.8, but now it’s 5.0, that’s concerning. If a patient’s WBC was 5.2, but now it’s 10.2, that’s concerning.

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Sepsis Progression

  • Infection

  • Sepsis (Compensatory)

  • Severe Sepsis (Progressive)

  • Septic Shock (Irreversible)

  • Death or Recovery

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Sepsis: Infection Stage

Initial Insult

Infectious Source

  • Pneumonia

  • UTI Wounds

  • Gastrointestinal

  • Cellulitis

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Sepsis: Sepsis Stage

Compensatory Stage

2 SIRS Criteria

  • Temperature

  • Heart rate

  • Respiratory rate

  • WBC

  • AMS

  • Hyperglycemia

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Sepsis: Severe Sepsis Stage

Progressive Stage

Organ Dysfunction

  • Bilirubin

  • Platelets

  • Hypotension

  • AKI

  • Respiratory failure

  • INR/PTT

  • Lactic acidosis

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Sepsis: Septic Shock Stage

Irreversible Stage

Presence of either:

  • Lactic acidosis

  • Persistent hypotension

*DIC most likely present

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Severe Sepsis: Signs of Organ Dysfunction

  • Respiratory P/F ratio < 250 w/o pneumonia, or < 200 w/ pneumonia

  • MAP < 65 mmHg, SBP < 90 mmHg, or SBP decrease > 40 from baseline

  • Creatinine > 2 mg/Dl

  • UOP < 0.5 mL/kg/hr in 6 hours or < 400 mL in 24 hours.

  • Bilirubin > 2 mg/dL

  • Platelets <100,000/mm3

  • INR > 1.5 or aPTT > 60 secs

  • Lactate > 2 mmol/L

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The Role of Lactate

  • Lactate is an indicator of global tissue hypoxia.

  • Increased lactate levels are associated with increased morbidity and mortality.

  • Lactate levels are used to guide resuscitation efforts.

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persistent hypotension; lactic acidosis

Septic shock is classified by __________ ___________ and/or ______ ________ (lactate > 4 mmol/L)

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Sepsis 1-Hour Bundle

Our Priorities:

  1. Obtain lactate level

  2. Obtain blood cultures x2 (from two different sites, aerobic + anaerobic—so technically 4)

  3. Administer fluids

  4. Administer broad spectrum antibiotics

  5. Administer vasopressors if needed

  6. Constantly reassess

<p><strong>Our Priorities</strong>:</p><ol><li><p>Obtain lactate level</p></li><li><p>Obtain blood cultures x2 (from two different sites, aerobic + anaerobic—so technically 4)</p></li><li><p>Administer fluids</p></li><li><p>Administer broad spectrum antibiotics</p></li><li><p>Administer vasopressors if needed</p></li><li><p>Constantly reassess</p></li></ol><p></p>
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Sepsis: Broad Spectrum Antibiotics

  • Multiple antibiotics can be used; check for compatibility.

  • Delay in antibiotic administration is linked to increased mortality.

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Administer IM, PO, or IO

If you can’t get IV access on your patient for broad spectrum antibiotics…

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Broad Spectrum Antibiotics Compatibility

Incompatible medications can do many things when mixed:

  • Antagonizing (nullifying) effects

  • Precipitation (crystallization)

  • Consistency changes

  • Gas production, all of which are harmful to our patients!

Always check for compatibility within your documentation software. When in doubt, call the pharmacist!

<p><strong>Incompatible medications can do many things when mixed</strong>: </p><ul><li><p>Antagonizing (nullifying) effects</p></li><li><p>Precipitation (crystallization)</p></li><li><p>Consistency changes</p></li><li><p>Gas production, all of which are harmful to our patients! </p></li></ul><p></p><p><em>Always check for compatibility within your documentation software. When in doubt, call the pharmacist!</em></p>
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Sepsis: Fluid Resuscitation

30 cc/kg of isotonic crystalloid solution

  • Normal Saline

  • Lactated Ringers

Calculation should be made using Ideal Body Weight (IBW)

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FALSE! A history of heart failure does not exempt a patient from receiving a fluid bolus! Careful monitoring is required!

T/F: A history of heart failure exempts a patient from receiving a fluid bolus because it’s too dangerous.

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Sepsis: Persistent Hypotension and Vasopressors

IF:

  • BP is measured every 15 minutes post-fluids, so…

  • Two consecutive low BP readings indicates persistent hypotension…

THEN:

  • Vasopressors should be started without delay!

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Norepinephrine (Levophed)

What is our first-line vasopressor in septic shock?

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Persistent Hypotension and Vasopressors: Norepinephrine Dose + Receptor

Dose: 0.1-0.5 mcg/kg/min, titrate to effect

Receptor: a1 & b1

<p><strong>Dose</strong>: 0.1-0.5 mcg/kg/min, titrate to effect</p><p><strong>Receptor</strong>: a1 &amp; b1</p>