Shock / Sepsis / MODS CONTENT

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Last updated 5:59 PM on 9/12/26
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32 Terms

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Early s/sx of septic shock

Tachycardia, bounding pulses, BP may be normal due to compensation, warm / flushed skin, febrile, confusion, decreased urine output

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Late signs of septic shock

Tachycardia, weak/thready pulses, hypotension, cool/pale skin / necrosis, hypothermia, lethargy or coma, anuria, bleeding

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Sepsis / septic shock goal

Identify and initiate txt for patients in early sepsis within 1 hour to optimize patient outcomes

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Sepsis bundles

Evidence-based bundled interventions to foster early recognition and interventions in pts with sepsis

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Diagnostics

Indication of infection - fever / inc WBC / Changes in BP / RR / HR

-Lung consolidation-pneumonia

-Frequent or painful urination-UTI

-Severe abdominal pain-peritonitis

-Labs: CBC BMP UA UC Blood Cultures Lactate

-CT scans / MRI

-SIRS criteria

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Sepsis bundle: steps

1.Fluid resuscitation

2.Vasopressors : if fluid resuscitation didn’t achieve a MAP of 65 mm/Hg

3.Bloodwokr: serum lactation or and two sets of blood cultures ( CBC coag studies, B<P, LFTs, ABG’s)

4.Antibiotics: should be administered within 1 hour of sepsis (CULTURES SHOULD BE DONE BEFORE ABX GIVEN)

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Septic shock assessments

Neuro, VS, hemodynamic monitoring (CO), RT monitoring (lung sounds, effort, rate, SAT), urinary output, skin color and temp, cap refill, signs of bleeding

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Septic shock actions

Asepsis, mouth care q24h, O2 as orderedm food replacement as ordered, lactic acid monitoring, 2 blood cultures (different sites), vasoactive drips as ordered (norepi)

-Supportive care: nutrition, turning, DVT, strss ulcer prophylaxis, ROM, delirium management

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Sepsis / shock complications

-Stress ulcers: PPI-pantoprazole, H2 Blockers-Famotadine, Mucosal protectants-Sucralfate

-Disseminated intravascular coagulopahty: 2 phases-clotting or thrombosis and bleeding

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Anaphylaxis patho / complications

Occurs after sensitization

-Massive vasodilation that affects multiple body system

-Anaphylactic shock runs the risk of cardiovascular and respiratory failure

-High risk: asthma, chronic lung disease, medications (beta blockers / alpha adrenergic blcokers), mastocytosis

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Anaphylaxis S / Sx

-Initial: rash/urticaria, SOB / wheezing, stomach pain / nausea, facial swelling, fainting

-Anaphylaxis if untreated: hypotension / hypoxia

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Anaphylaxis medical management

REMOVE THE TRIGGER

-IM epi-can repeat 2-3x, IV epi if IM is ineffective, maximize oxygenation (100% nonrebreather / intubation)

-IV fluid-circulatory support

-Other meds (antihistamines, corticosteroids, inhaled bronchodilators)

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Neurogenic shock: decreased CO with decreased venous and arterial vasodilation

A phenomenon that occurs after a spinal cod injury

-Vascular tone is significantly decreased (inability to vasoconstriction)-vessels are relaxed and dilated. This leads to pooling of the blood, decreasing return to the heart and decreasing CO

-Unable to compensate via tachycardia which may lead to severe bradycardia

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Neurogenic shock s / sx

Warm, dry skin , flushed appearance, hypotension, bradycardia

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Neurogenic shock: medical management

Cardiovascular support (while finding the cause)

-Fluid resuscitation, vasoactive IV meds (dopamine / epi / norepi / phenylephrine), bradycardia-atropine, pacing

-Intubation and mechanical ventilation

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Pacing in neurogenic shock

A medical intervention used to manage severe bradycardia by delivering electrical impulses to the heart, improving heart rate and cardiac output

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Hemorrhagic shock: pathophysiology

Caused by insufficient perfusion of both and oxygen to the body tissues resulting in an imbalance of oxygen supply and demand

-Causes: blood loss (trauma / internal bleeding / aneurysms), fluid loss (vomiting, diarrhea, excessive urination or burns), third spacing

-A subunit of hypovolemic shock that directly refers to blood loss

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Hypovolemic shock: s / sx

-Compensatory: normal BP, tachy, restless/confusion, pale / cool / clammy, weak pulses, hyperventilation, hypoactive bowel sounds

-Progressive: Lethargy, hypotension, anuria, cool / cyanotic skin, weak / absent pulses, dysrhythmias

-Refractory: coma, severe hypotension, ischemic and necrotic cold extremities, renal / hepatic failure

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Hypovolemic shock: medical management

Assess and stabilize airway

-Rapid fluid resuscitation: non-hemorrhagic: warm crystalloids (NS/LR), hemorrhagic: packed red blood cells or fresh frozen plasma / platelets

-Identify cause of bleeding and control / stop

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Hypovolemic shock: nursing management

Assessments

-ActionsL 100% nonrebreather mask, prepare for intubation, insert large-bore IV line, fluid replacement as ordered

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Pathophysiology: cardiogenic shock

Circulatory failure and hypoperfuson caused by cardiac dysfunction leading to myocardial ischemia

-inadequate pumping ability of the heart / decreased cardiac output and poor tissue perfusion

-Pump failure

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Compensation of cardioghenic shock

Decreased blood pressure, elevated HR to compensate

-Increase in catecholamines causing vasoconstriction

-Activation of RAAS system causing retention of Na and free fluid (trying to correct decreased CO)

-Blood shunting to brain and vital organs, causing increase in myocardial wok and increased O2 demand

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Potential causes of cardiogenic shock

MI , severe valvular dysfunction, severe HF, cardiac tamponade, ventricular hypertrophy, cardiomyopathy, dysrhythmias, tension pneumothorax, blunt cardiac injury, pulmonary HTN

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Cardiogenic shock: s/sx

Chest pain, diaphoresis, N / V, hypotension, decreased LOC / urine output, weal pulses, pale / cool skin, decreased bowel sounds, SOB / crackles

-As it worsens: profound hypotension and brady / organ failure

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Cardiogenic shock medical management

12-lead EKG & cardiac enzymes (rules out MI)

-CX-r/o tension pneumothorax, tamponade, confirm presence of PE

-Stabilize oxygenation: 100% O2 non-rebreather, intubation and ventilation

-Drug therapy- increase CO / BP:

Vasopressors (BP)-dopamine/norepinephrine

Inotropes (contractility)-subtractive / dopamine

Intra-aortic Baltic (drug heart pump-temp) / ventricular assist device (helps heart pump-perm)

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Obstructive shock pathophysiology

Occurs when blood flow is blocked and circulation to the major organs is disrupted

-PE, pulmonary htn, tension pneumothorax, mechanical ventilation with high PEEP, aortic dissection, pericardial tamponade, pericardial effusion, cardiac mass

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Initial stage of shock

Too little oxygen in the blood to feed organs, body switches from aerobic to americium metabolism

-Increased lactic acid

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Compensatory stage of shock

Aldosterone released to maintain BP

-Vasoconstriction to shunt blood to vital organs

-Increased HR

-Sympathetic nervous system releases catecholamines to compensate for low oxygen

(Step two)

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Progressive stage of shock

Oliguria, altered LOC, pallor / cool clammy skin, electrolyte imbalance, hypotension

(Stage three)

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Refractory stage of shock

Irreversible cellular and organ failure

-Impending death

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Overall basics of shock txt and therapies

Txt is focused supportive care

-IV fluids, ventilation, hemodynamic monitoring, IV antibiotics, norepinephrine IV for MAP, blood and blood products, mechanical circulatory support, nutrition, hemodynamic monitoring

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Cardiogenic shock on the kidneys relation

Heart’s inability → kidneys taking it as a sign that there’s low BP → kidneys release renin to start the cascade

-This backfires because this leads to fluid overload since the heart cannot handle more fluid / increases workload