Final · Week 13 · Standalone study page
M13 · Shock & MODS
This page keeps all of the original course information, while reducing the decision to one module: perfusion failure, shock patterns and organ support.
▸M13Shock & MODSWeek 13
💡 The one idea
Shock is not low blood pressure — it is inadequate tissue perfusion. Blood pressure is the last thing to fall, because compensation holds it up until it cannot.
By the time BP drops, the patient has been in shock for a while.
📈 The stages, and what fails at each
The earliest reliable signs are a rising heart rate and restlessness — not hypotension. Restlessness is cerebral hypoxia and it is frequently the first thing the nurse notices.
| Type | Problem | Skin | First treatment |
|---|---|---|---|
| Hypovolemic | Not enough volume | Cold, clammy | Fluids / blood |
| Cardiogenic | Pump failure | Cold, clammy | Inotropes — fluids may worsen it |
| Septic | Vasodilation + leak | Warm, flushed early | Cultures, then antibiotics + fluids |
| Anaphylactic | Massive histamine release | Warm, flushed, hives | Epinephrine IM |
| Neurogenic | Lost sympathetic tone | Warm, dry, bradycardic | Fluids, vasopressors |
🚨 The two exceptions worth memorizing
Neurogenic shock is the only shock with a SLOW heart rate. Every other type is tachycardic. Seen after spinal cord injury above T6.
Cardiogenic shock is the one where fluids can kill. The pump is already failing; more volume floods the lungs.
✅ Sepsis — the hour-one bundle
- Measure lactate — it is the tissue-perfusion marker
- Blood cultures BEFORE antibiotics
- Broad-spectrum antibiotics within 1 hour
- 30 mL/kg crystalloid for hypotension or lactate ≥ 4
- Vasopressors if still hypotensive — norepinephrine first line
Cultures come before antibiotics - but never delay antibiotics beyond an hour to get them.
⭐ High-yield — what the exam actually asks
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- Four stages: initial (cellular damage, normal vitals), compensatory (tachycardia is the earliest response, then vasoconstriction), progressive (fluids, antibiotics, pressors, intubation), refractory (irreversible → MODS → death).
- MAP is the perfusion indicator, goal
>65. Do not panic at an SBP in the 80s–90s if the MAP is adequate. Lactate goal≤2; lactate >2 with suspected infection means septic shock. - Confusion and altered mental status are LATE signs, not early ones.
- Hypovolemic: 15–30% volume loss (~1 L). H&H high = fluid loss and hemoconcentration; H&H low = active bleeding. Fix the cause + fluids; blood products if bleeding.
- Cardiogenic: pump failure, most often MI. Fluids are not the treatment — cardiac management is. MONA (morphine, oxygen, nitroglycerin SL
q5 min ×3max, aspirin ~324 mgnot 81 mg); definitive treatment is cath with stent, or CABG. BNP normal<200; serial troponins.
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- Sepsis bundle — order matters, all within the first hour: labs including lactate → blood cultures BEFORE antibiotics (2 sets / 4 bottles; with a central line, draw one peripherally and one from the line) → antibiotics before fluids → IV fluids → vasopressors only if fluids fail, targeting MAP
≥65. - SIRS needs 2 of 4: temp
>38.3°Cor<36°C, HR>90, RR>20, WBC>12,000or<4,000or>10%bands. Meeting criteria is not automatically sepsis. - Monitor response with serial lactate (should trend down) and MAP. Do not repeat blood cultures immediately — they take ~3 days. UTI is the most common sepsis source, especially in older adults. LR is now favored over NS.
- Neurogenic: hypotension + bradycardia, the opposite of every other shock. Anaphylactic: epinephrine first, then oxygen, then fluids — fluids are not the priority. Obstructive: relieve the obstruction (needle decompression for tension pneumothorax; pericardiocentesis at the 5th intercostal space for tamponade — Beck's triad = muffled heart sounds, JVD, hypotension).
- Norepinephrine is the first-line pressor. Central line, titrate to MAP. Phentolamine reverses extravasation; prolonged use causes digital necrosis. Use IO access if no line can be placed fast enough.
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- Modified Trendelenburg (legs elevated) shifts ~
300 mLback to the heart and tests fluid responsiveness. VSq15 min. - MODS = the original failing organ plus 2 more (3 total). Mortality exceeds
60%once 4+ organs are involved. - Intubation: preoxygenate 100%, sedate before you paralyze, and keep sedation going afterward. Confirm with bilateral breath sounds and symmetric chest rise, then ETCO2 (yellow/green = trachea, purple = esophagus → pull and retry), with CXR as the gold standard.
🎧 From the LSC exam-prep recording
What the faculty actually said in the review session for this week — their numbers, their worked calculations, their priority rulings. On an exam, this beats the textbook.
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- Their four buckets: distributive = too much vasodilation · hypovolemic = not enough volume · cardiogenic = the pump · obstructive = something blocking or squeezing the pump.
- Universal numbers: urine output minimum
30 mL/hr, adult blood volume ~5 L. Stages run compensated → decompensated (metabolic acidosis, rising creatinine) → irreversible. - Hypovolemic case: BP 78/50, HR 132, RR 28, UO 10 mL/hr, Hgb
8.2, Hct25%. Underlying-cause treatment is rapid isotonic crystalloid — not pressors, not oxygen. - Cardiogenic case: troponin I
2.9(normal <0.03), BNP157(normal <100), crackles, SpO2 88% on 4 L, UO 15 mL/hr. To improve cardiac output the answer is inotropes. No big fluid boluses, and no nitroglycerin while hypotensive — 80 becomes 60. - Obstructive / tamponade: Beck's triad — JVD, hypotension, muffled heart sounds. Definitive answer is pericardiocentesis; they note BP can jump from 78/50 to 140/80 in minutes.
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- Neurogenic: C5 injury, BP 74/42, HR 48 — the one shock that does not produce tachycardia (vagus intact, sympathetic chain lost), warm skin, cap refill under 2 seconds, low temp. Treat with norepinephrine. High-dose corticosteroids are never used in spinal cord injury — dismiss that option on sight. Neurogenic shock (hemodynamic) and spinal shock (motor/sensory) are separate and can coexist.
- SIRS vs septic shock as they drew it: the SIRS case had BP 110/68, WBC 18,000, lactate
1.8. Septic shock requires SBP under 90 and lactate over 2, with 4 as the key marker, plus a vasopressor need. Their progression case: BP 78/46, HR 132, cap refill over 4 s, UO 100 mL in 8 hours, lactate4.2. - MODS = at least two major organ systems failing. Confusion (neuro), oliguria and rising creatinine (renal), high bilirubin and enzymes (hepatic), low platelets and DIC.
- After a 2 L bolus in sepsis, monitor for pulmonary edema, respiratory distress, DIC, and hyperglycemia from stress glycogenolysis — not hypoglycemia, not hypernatremia.
- Deterioration ABG: PaO2
58, PaCO280, pH7.31→ intubate. Cranking a nasal cannula to 15 L/min is not an answer.
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- Post-intubation bow tie: early complications = hypotension and VAP · immediate actions = new vital signs and repeat ABG · effectiveness = PaO2 above 80 and MAP at or above 65. Temperature and WBC are data points, not effectiveness indicators.
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- What shock actually is: hypotension and hypoperfusion of the vital organs — not an emotional state. The body abandons everything except heart, lungs and brain.
- The hypovolemic picture they gave: BP 78/50, HR 132, RR 28, pale and diaphoretic, black tarry stools, and urine output of 10 mL in an hour.
- A urine output of ten mL/hr is the kidney refusing to let go of a single drop because the body is in serious trouble — well under the
30 mL/hrfloor. - Hypovolemic: the tank is empty. Volume first — crystalloid, then blood if it is a hemorrhage. Vasopressors do not fill an empty tank, and squeezing an empty circuit makes the perfusion worse.
- Cardiogenic: the pump has failed. Improve contractility (dobutamine) and reduce afterload — but vasodilators only if the pressure can tolerate them, which is why the question kept asking which cardiogenic client gets them.
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- Obstructive: something is physically blocking flow — cardiac tamponade, tension pneumothorax, massive PE. The treatment is to relieve the obstruction: pericardiocentesis, needle decompression, thrombolysis. More fluid does not fix a blockage.
- Distributive and septic: the tank has got bigger, not emptier. Fluids first, then norepinephrine. Lactate and cultures before antibiotics, and antibiotics inside the first hour.
- Urine output is the earliest organ marker in every type of shock. It falls before the blood pressure tells you anything useful.
- Why a diuretic is the wrong answer in shock: the problem is not too much fluid, it is not enough perfusion. A diuretic takes away what little volume she has.
- MODS is the end point — organ after organ failing because perfusion was not restored in time. That is what all of this is trying to prevent.
⚠️ Exam traps
- Warm flushed skin with bounding pulses points to septic or anaphylactic, never cardiogenic (which is cold and clammy).
- JVD with muffled heart sounds is obstructive tamponade, not cardiogenic — even though it involves the heart.
- No shock type increases urine output. Rising output means the treatment is working.
- Bradycardia + hypotension = neurogenic. Bradycardia + hypertension is not shock at all — think ICP.
⚠️ What it turns into — the complication for each one
The disorder cards below run definition, causes, signs, diagnostics, management and nursing. This is the part they do not have, and it is where the exam lives: so what happens if this is missed or left? One idea covers the lot: the cells are not getting oxygen. Compensation hides it early — a normal blood pressure with a rising heart rate and a falling urine output is shock, and the blood pressure is the last thing to go.
| Disorder | What it turns into |
|---|---|
| The stages of shock | Progression from compensated to progressive to irreversible shock and MODS. The danger is being reassured by a blood pressure that compensation is holding up |
| Hypovolemic shock | Acute kidney injury, ischemic bowel, MODS and cardiac arrest. Then the complications of the treatment: over-resuscitation causing pulmonary edema and ARDS, and the coagulopathy and hypothermia of massive transfusion |
| Cardiogenic shock | Pulmonary edema, dysrhythmia, cardiac arrest. The highest mortality of any shock state — and fluids, which help every other kind, make this one worse |
| Distributive shock | Refractory hypotension as the vessels stay dilated, MODS, and DIC when it is septic. In neurogenic shock, bradycardia rather than the tachycardia every other shock produces |
| Obstructive shock | Cardiac arrest unless the obstruction is relieved — needle decompression for a tension pneumothorax, pericardiocentesis for tamponade, thrombolysis or embolectomy for a massive PE. No amount of fluid or pressor fixes a mechanical block |
| Multiple organ dysfunction syndrome | Mortality climbs with every organ that fails. ARDS, acute kidney injury, hepatic failure, DIC and encephalopathy, in a sequence that feeds itself |
📈 Shock and MODS, section by section
The stages first, then the four kinds of shock by mechanism, then MODS. Work out which tank, pump, pipe or blockage has failed and the management follows. Same six sections every time.
The Stages of ShockOpenClose
🖼️ InfographicsNeurogenic Shock
Definition and Overview
Shock is not a diagnosis, it is a state: the tissues are not getting enough oxygen to do their work. Whatever the cause, it moves through four stages. Initial — cells switch to anaerobic metabolism and lactate starts to rise, with no visible signs at all. Compensatory — the body fights back and mostly succeeds. Progressive — the compensation fails. Refractory — the damage is irreversible. The whole point of the staging is that the reversible window is early, before the blood pressure falls.
Causes and Risk Factors
Anything that drops the volume, the pump, the vessel tone or the outflow. The stages themselves are driven by the sympathetic nervous system and the renin–angiotensin–aldosterone system trying to hold the pressure up, and then by the acidosis and capillary leak that follow when they cannot.
Clinical Manifestations
Compensatory: heart rate and respiratory rate up, blood pressure still normal, narrowing pulse pressure, cool pale skin, decreased bowel sounds, urine output falling, and restlessness or anxiety — the first sign, and the one most often dismissed. Progressive: hypotension, tachycardia with weak thready pulses, mottled skin, crackles, oliguria under 30 mL/hr, confusion or lethargy, metabolic acidosis. Refractory: profound hypotension unresponsive to drugs, anuria, multiple organ failure. A normal blood pressure does not mean the client is not in shock — in the compensatory stage it is normal by definition.
Assessment and Diagnostic Findings
Serial lactate is the marker of tissue oxygen debt; a rising lactate means it is getting worse whatever the blood pressure says. Continuous vital signs, mean arterial pressure — keep it above 65 mmHg — hourly urine output, level of consciousness, skin temperature and capillary refill. ABGs, CBC, electrolytes, renal and liver function, coagulation studies. Central venous pressure and central venous oxygen saturation where lines are in.
Medical Management
Find and fix the cause, and support perfusion while you do. Oxygen for everyone. Fluids for most. Vasopressors and inotropes when fluid is not enough. Correct the acidosis by fixing the perfusion, not by chasing the pH.
Nursing Management and Client Education
Trust the early signs. A client who is newly restless, tachycardic and breathing faster with a normal blood pressure is your one chance to catch this — escalate then. Large-bore IV access, oxygen, flat or with legs elevated if hypovolaemic, and keep them warm. Hourly urine output is your bedside perfusion monitor; report under 30 mL/hr. Reassess after every intervention. Explain to the family what the numbers mean, and keep explaining — this moves fast.
Hypovolemic ShockOpenClose
🖼️ InfographicsHypovolemic Shock
Definition and Overview
Shock from losing volume — there is not enough blood or fluid in the tank to fill it. Preload falls, so stroke volume and cardiac output fall with it. It is the most common shock, and generally the most fixable, because the treatment is to put the volume back.
Causes and Risk Factors
Absolute loss: hemorrhage (trauma, surgery, GI bleeding, ruptured aneurysm, postpartum), and fluid loss from vomiting, diarrhea, diuresis, diabetes insipidus or burns. Relative loss — the fluid is still in the body but not in the vessels — in ascites, peritonitis, bowel obstruction and third spacing. Signs appear once about 15% of volume is gone, and become obvious past 30%.
Clinical Manifestations
Tachycardia first, then hypotension. Weak thready pulse, narrowed pulse pressure, cool clammy pale skin, delayed capillary refill, flat neck veins, thirst, tachypnoea, oliguria, and anxiety progressing to confusion. Orthostatic changes appear before resting hypotension does.
Assessment and Diagnostic Findings
Find the source of the loss — look for the obvious bleed and then for the hidden one (abdomen, pelvis, thighs, GI tract). Serial hemoglobin and hematocrit, noting that in acute hemorrhage they are normal at first because whole blood is lost. Type and crossmatch. Lactate, ABGs, electrolytes, coagulation studies. Hourly urine output, central venous pressure (low), and daily weight.
Medical Management
Stop the loss and replace the volume. Control bleeding by pressure, endoscopy or surgery. Isotonic crystalloid — normal saline or lactated Ringer's — is the first fluid, in boluses, with the response reassessed each time. Blood products for hemorrhage, with a balanced ratio in massive transfusion. Vasopressors are a late and second-line measure here; squeezing an empty tank does not help. Oxygen throughout.
Nursing Management and Client Education
Two large-bore IVs — large bore matters more than central access for speed. Warm the fluids in a large transfusion; cold fluid causes hypothermia which worsens coagulopathy. Apply direct pressure to external bleeding. Position supine, and elevate the legs (modified Trendelenburg) rather than tipping the whole bed head-down. Monitor for transfusion reaction, and for the other direction — crackles, rising respiratory rate and jugular distension mean you have overshot. Hourly urine output and strict intake and output. Keep the client warm and keep talking to them; they are frightened and the reassurance is genuine care.
Cardiogenic ShockOpenClose
🖼️ InfographicsCardiac TamponadeCardiogenic Shock
Definition and Overview
Shock because the pump has failed. The volume is there but the heart cannot move it, so cardiac output falls while pressure backs up behind the failing ventricle into the lungs. It carries the highest mortality of the shock states.
Causes and Risk Factors
Acute myocardial infarction is the leading cause, particularly a large anterior MI. Then end-stage heart failure, dysrhythmias, cardiomyopathy, myocarditis, valve failure, papillary muscle or septal rupture after MI, and cardiac surgery. Risk is higher with diabetes, prior infarction, older age and delayed reperfusion.
Clinical Manifestations
Hypotension with tachycardia and a weak thready pulse, cold clammy mottled skin, oliguria, confusion, and the distinguishing feature — signs of backward failure: crackles, dyspnea, frothy pink sputum, jugular venous distension and an S3 gallop. Chest pain if there is ongoing ischemia. Fluid boluses that help every other shock can drown this one — the lungs are already wet.
Assessment and Diagnostic Findings
12-lead ECG and serial troponins to find the infarct. Echocardiography for ejection fraction, wall motion and valve or septal rupture. Chest x-ray showing pulmonary congestion. Hemodynamic monitoring: cardiac output low, systemic vascular resistance high, and pulmonary artery wedge pressure high — that combination is what names it. ABGs, lactate, BNP, renal function, hourly urine output and continuous cardiac monitoring.
Medical Management
Restore coronary blood flow — percutaneous coronary intervention or thrombolysis for infarction, and the sooner the better. Reduce the work of the heart and improve output: inotropes (dobutamine, milrinone) to strengthen contraction, cautious vasopressors to hold the pressure, and diuretics and vasodilators to unload the ventricle once the pressure allows. Oxygen and often mechanical ventilation. Mechanical support — intra-aortic balloon pump or a ventricular assist device — when drugs are not enough.
Nursing Management and Client Education
High Fowler's position, oxygen, and absolute rest — every bit of work you save the heart counts. Continuous cardiac and hemodynamic monitoring; titrate infusions carefully and by protocol. Give fluid only as ordered and in small amounts, listening to the lungs before and after. Strict hourly intake and output and daily weight. Manage pain and anxiety, because both raise oxygen demand. Cluster care so the client can rest. Watch the femoral or radial site after PCI, and the limb distal to a balloon pump. Teach the family what the monitors mean, and be honest with them — this is a critical illness and they deserve to know.
Distributive ShockVolume is fine, the vessels are notOpenClose
Definition and Overview
Shock from the vessels dilating and leaking, so the same amount of blood no longer fills a much larger space and does not stay where it is put. Three kinds share this mechanism: septic (infection), neurogenic (loss of sympathetic tone), and anaphylactic (massive allergic mediator release). Septic shock is by far the most common shock in hospital.
Causes and Risk Factors
Septic: any infection, most often pneumonia, urinary, abdominal or line-related, in someone older, immunosuppressed or instrumented. Neurogenic: spinal cord injury at or above T6, spinal anaesthesia, and severe pain or emotional shock. Anaphylactic: foods, drugs (penicillins, contrast, NSAIDs), insect stings and latex, in someone previously sensitised.
Clinical Manifestations
All three cause hypotension with a wide pulse pressure and low vascular resistance. What separates them: septic shock is warm, flushed and febrile with a bounding pulse early, turning cold and mottled late. Neurogenic shock is the odd one — hypotension with bradycardia, and warm dry skin below the level of injury, because the sympathetic outflow is gone and cannot raise the heart rate. Anaphylactic shock comes on within minutes with urticaria, angio-edema, stridor, wheeze and a sense of impending doom.
Assessment and Diagnostic Findings
Septic: lactate, blood cultures from two sites before antibiotics, CBC, procalcitonin, and cultures of every plausible source. Neurogenic: neurological examination, level of injury, and imaging of the spine; distinguish it from hemorrhagic shock in a trauma client, which is the real diagnostic trap. Anaphylactic: it is a clinical diagnosis — treat first, investigate later; tryptase afterwards, and referral for allergy testing. For all three: continuous vital signs, oxygenation, mental status and hourly urine output.
Medical Management
Septic: the one-hour bundle — lactate, cultures, broad-spectrum antibiotics, 30 mL/kg crystalloid — then noradrenaline as first-line vasopressor, and source control. Neurogenic: cautious fluids, vasopressors, and atropine for the bradycardia; immobilise and stabilize the spine. Anaphylactic: intramuscular adrenaline (epinephrine) into the outer thigh, immediately and repeated every 5 to 15 minutes as needed — it is the treatment, and everything else is adjunct. Then oxygen, fluids, antihistamines, corticosteroids and bronchodilators, and be ready to secure the airway.
Nursing Management and Client Education
Septic: recognize it early, draw cultures before antibiotics but never delay the antibiotic, monitor perfusion hourly, and get unnecessary lines and catheters out. Neurogenic: maintain spinal immobilisation, move the client as a unit, watch for bradycardia during suctioning, use compression devices and reposition frequently — and remember they cannot feel pressure damage happening. Anaphylactic: stop the trigger, then give adrenaline — do not send someone for antihistamines first. Keep the airway equipment and a second dose at hand, and observe for a biphasic reaction up to 12 hours later. Teach the client to carry two auto-injectors, to check expiry dates, to wear medical identification, and that every anaphylaxis goes to the emergency department even if the injector worked.
Obstructive ShockOpenClose
Definition and Overview
Shock because something outside the heart is physically blocking it from filling or emptying. The pump is fine and the volume is fine; the obstruction is mechanical, which means drugs and fluid will not fix it — relieving the obstruction will, and usually within minutes.
Causes and Risk Factors
Cardiac tamponade (pericardial fluid or blood compressing the heart), tension pneumothorax, massive pulmonary embolism, and less often constrictive pericarditis, severe pulmonary hypertension or a large abdominal mass in pregnancy. Risk follows chest trauma, cardiac surgery, central line placement, mechanical ventilation, immobility, surgery, cancer and clotting disorders.
Clinical Manifestations
Hypotension with jugular venous distension — the giveaway that the problem is obstruction rather than volume — tachycardia, dyspnea and a rising respiratory rate. Tamponade: Beck's triad of hypotension, distended neck veins and muffled heart sounds, with pulsus paradoxus. Tension pneumothorax: absent breath sounds on one side with tracheal deviation away from that side — this is decompressed at the bedside, not sent for a chest x-ray. Pulmonary embolism: sudden dyspnea, pleuritic chest pain, hypoxaemia and often a clear chest examination.
Assessment and Diagnostic Findings
Bedside echocardiography for tamponade and for right ventricular strain. Chest x-ray, but not before decompressing an obvious tension pneumothorax. CT pulmonary angiography for embolism, with D-dimer used to rule out low-risk cases. ECG (low voltage and electrical alternans in tamponade; right heart strain in PE), ABGs, troponin and BNP.
Medical Management
Relieve the obstruction. Tamponade → pericardiocentesis or a pericardial window. Tension pneumothorax → immediate needle decompression, then a chest tube. Massive pulmonary embolism → anticoagulation, and thrombolysis or embolectomy for hemodynamic collapse. Oxygen and cautious fluids to support filling in the meantime; vasopressors as a bridge only.
Nursing Management and Client Education
Recognize the pattern — shock plus distended neck veins — and escalate immediately, because the fix is a procedure and it is time-critical. Have the pericardiocentesis or chest tube tray ready. After a chest tube, monitor the drainage, the water seal and for subcutaneous emphysema. On anticoagulation, watch for bleeding, teach a soft toothbrush and an electric razor, and go through the interactions and the follow-up bloods. Prevention is the part nursing owns: early mobilisation, compression devices and prophylactic anticoagulation prevent the embolism in the first place. Teach clients after discharge to report sudden breathlessness or chest pain rather than waiting to see if it passes.
Multiple Organ Dysfunction SyndromeOpenClose
Definition and Overview
The failure of two or more organ systems in someone whose body can no longer keep its own internal balance without help. It is the end of the road for prolonged shock and severe sepsis: the inflammatory response that was meant to be protective becomes systemic, the microcirculation clots and leaks, and organs fail one after another. Mortality rises steeply with each system involved.
Causes and Risk Factors
Sepsis and septic shock are the commonest precursors. Then any prolonged shock, major trauma, extensive burns, pancreatitis, massive transfusion, and prolonged surgery. Age, malnutrition, immunosuppression, chronic organ disease and delayed resuscitation all worsen the odds.
Clinical Manifestations
It follows a fairly consistent order. Lungs first — acute respiratory distress syndrome, with refractory hypoxaemia and bilateral infiltrates. Then kidneys (rising creatinine, falling urine output), liver (jaundice, rising bilirubin and enzymes), gut (ileus, bleeding, translocating bacteria), coagulation (falling platelets, DIC with simultaneous clotting and bleeding), heart (falling output, needing pressors) and brain (encephalopathy). Hyperglycaemia and profound catabolism throughout.
Assessment and Diagnostic Findings
Trend everything, because the diagnosis lives in the trend: ABGs and the PaO2/FiO2 ratio, creatinine and hourly urine output, bilirubin and liver enzymes, platelet count, PT/INR, fibrinogen and D-dimer, lactate, glucose, and the level of consciousness. Continuous hemodynamic monitoring and daily weight. Cultures repeatedly, hunting for an unresolved source.
Medical Management
There is no specific treatment — the management is to support every failing system while removing the cause. Source control and antibiotics. Lung-protective mechanical ventilation with low tidal volumes. Renal replacement therapy. Transfusion and factor replacement for DIC. Glucose control, early enteral nutrition, and stress-ulcer and venous thromboembolism prophylaxis. Prevention is the real treatment: recognising and reversing shock early is what stops this happening.
Nursing Management and Client Education
Meticulous, unglamorous care is what changes outcomes here: hand hygiene, head of bed at 30 degrees, oral care, early mobilisation, turning, line and catheter care, and getting devices out as soon as they are not needed. Track and report every trend — you will see the next organ start to fail before the numbers are dramatic. Strict intake and output and daily weight. Nutrition early, enterally if the gut works at all. Talk to the family honestly and often, involve palliative care alongside active treatment rather than instead of it, and support goals-of-care conversations — for many clients this becomes the decision that matters most, and they should not face it unprepared.
🧠 Mind maps 1
One per disorder, built from the structure of your ATI chapter.
🎯 Who gets it
- Cardiogenic shock stems from MI (especially anterior wall), heart failure, cardiomyopathy, or valve failure.
- Older adults face higher cardiogenic shock risk from MI and cardiomyopathy.
- Hypovolemic shock follows major fluid loss (vomiting, diarrhea) or blood loss (trauma, burns, DKA).
- Older adults dehydrate easily from even small fluid losses, especially with diuretics.
👀 What you see
- Findings can include chest pain, lethargy, and somnolence.
- Restlessness, anxiousness, and dyspnea are common shock findings.
- Diaphoresis, thirst, and muscle weakness can also occur.
- Nausea and vomiting are common findings across shock types.
🧪 What confirms it
- ABGs show metabolic acidosis with a low pH and low PaO2 in shock.
- PaCO2 first drops from hyperventilation, then rises with respiratory failure.
- Blood lactic acid rises due to anaerobic metabolism.
- Blood glucose levels can climb from stress-induced hypermetabolism during shock.
🩺 What you do
- Maintain MAP at least
65 mm Hgto ensure adequate organ perfusion. - Report urine output below
0.5 mL/kg/hr; monitor it hourly. - Use a 100% non-rebreather mask for high-flow O2; COPD clients start at
2 L/minnasal cannula. - Position the client supine with legs elevated (Trendelenburg) to treat hypotension.
💊 Drugs
- Milrinone and dobutamine strengthen cardiac contraction and increase cardiac output.
Read left to right: who gets it → what you see → what confirms it → what you do → what goes wrong. Cover a column and rebuild it out loud.
🎥 Lecture recordings 4
Tap a card to open that recording in Google Drive. The same list lives in the lecture library.
All NUR 258 recordings →🖼️ Infographics & deep dives 5
One page per kind of shock, plus the overview. Read the overview first.
📋 Active Learning Templates 1
One per disorder. Every row is filled from that section of the ATI chapter — print it, cover the right, rebuild it.
📋 Shock6 parts
Filled from ATI chapter 38, row by row from that chapter’s own sections — 12 of 12 rows have content.
2 rows came from outside your ATI chapter — 1 cite a source, 1 are built from this page’s own notes. Each one is labeled.
🧭 What it isAlterations in Health (Diagnosis) · Health Promotion & Disease Prevention
Alterations in Health (Diagnosis)
- Shock is inadequate tissue perfusion that can progress to organ failure; maintaining MAP at least
65 mm Hgpreserves perfusion. Four types—cardiogenic, hypovolemic, obstructive, distributive—move through initial, compensatory, progressive, and refractory stages.
Health Promotion & Disease Prevention
- Reduce cardiogenic shock risk with exercise, healthy diet, stress reduction, and not smoking.
- Stay well hydrated during exercise or hot weather to prevent hypovolemic shock.
- Seek care early for illness, trauma, dehydration, or bleeding signs.
- Know dehydration signs: thirst, low urine output, and dizziness.
- Wear seatbelts and helmets; use caution around dangerous equipment or activities.
- Seek early care for infection signs: redness, swelling, drainage, fever, urinary burning.
👀 How it shows upAssessment — Risk Factors · Assessment — Expected Findings
Assessment — Risk Factors
- Cardiogenic shock stems from MI (especially anterior wall), heart failure, cardiomyopathy, or valve failure.
- Older adults face higher cardiogenic shock risk from MI and cardiomyopathy.
- Hypovolemic shock follows major fluid loss (vomiting, diarrhea) or blood loss (trauma, burns, DKA).
- Older adults dehydrate easily from even small fluid losses, especially with diuretics.
- Obstructive shock follows blocked blood flow: PE, tamponade, tension pneumothorax, aortic dissection.
- Neurogenic shock, a distributive type, follows loss of sympathetic tone from head or spinal trauma.
- Septic shock is most often caused by gram-negative bacteria.
- Sepsis affects
1.7 millionU.S. adults yearly with over250,000deaths.
Assessment — Expected Findings
- Findings can include chest pain, lethargy, and somnolence.
- Restlessness, anxiousness, and dyspnea are common shock findings.
- Diaphoresis, thirst, and muscle weakness can also occur.
- Nausea and vomiting are common findings across shock types.
🧪 How it is confirmedLaboratory Tests · Diagnostic Procedures
Laboratory Tests
- ABGs show metabolic acidosis with a low pH and low PaO2 in shock.
- PaCO2 first drops from hyperventilation, then rises with respiratory failure.
- Blood lactic acid rises due to anaerobic metabolism.
- Blood glucose levels can climb from stress-induced hypermetabolism during shock.
- Cardiac enzymes rise with cardiac ischemia or infarction.
Diagnostic Procedures
- An arterial line allows continuous BP monitoring and blood draws for ABGs.
- A pulmonary artery catheter measures CVP, PA pressures, and cardiac output to guide care.
🩺 What you doNursing Care · Medications · Therapeutic Procedures
Nursing Care
- Maintain MAP at least
65 mm Hgto ensure adequate organ perfusion. - Report urine output below
0.5 mL/kg/hr; monitor it hourly. - Use a 100% non-rebreather mask for high-flow O2; COPD clients start at
2 L/minnasal cannula. - Position the client supine with legs elevated (Trendelenburg) to treat hypotension.
- Alert the provider and rapid response team right away if status changes.
- Titrate IV drips using CVP, PA pressures, cardiac output, and pulse pressure.
- Dopamine is dose-dependent: low doses boost kidney perfusion, high doses cause vasoconstriction.
- Give vasopressors through a central line; extravasation can cause tissue necrosis.
- In hypovolemic shock, replace fluid volume before starting vasopressor medications.
Medications
- Milrinone and dobutamine strengthen cardiac contraction and increase cardiac output.
Therapeutic Procedures
- Needle decompression or a chest tube relieves tension-pneumothorax pressure on the heart and vessels.
- Surgery may correct the underlying cause of shock: bleeding ulcer, wound, artery, or vein.
- Before surgery, secure the airway, give oxygen, and stabilize with fluids or medications.
- After surgery, track BP, ECG, PA pressures, cardiac output, CVP, and urine output.
- Check the surgical site for bleeding and monitor the CBC after the procedure.
- Monitor airway, breath sounds, and ABGs to confirm adequate oxygenation after surgery.
💬 Around the patientClient Education · Interprofessional Care
Client Education
From this module — built from the notes above on this page, not a section of the ATI chapter.
- Explain what is happening in plain words — shock is frightening and the explanation is usually skipped.
- Teach the early signs to survivors and families: restlessness and anxiety, cool clammy skin, thirst, and a rising heart rate before the blood pressure falls.
- Blood pressure falls late. Waiting for it is waiting too long.
- For those at risk — adrenal insufficiency, severe allergy, immunosuppression — teach the specific emergency plan and carry the kit.
- After recovery: expect fatigue and cognitive fog for weeks, and know the signs of a returning infection.
Interprofessional Care
- Respiratory therapy manages ventilator settings, chest physiotherapy, suctioning, and inhaled medications.
⚠️ What goes wrongComplications
Complications
Not in your ATI chapter — filled from StatPearls, 2023.
- Delayed recognition or treatment of shock can lead to irreversible changes, including multiorgan failure and death.
- Untreated shock progresses through worsening stages, ending in irreversible organ dysfunction and multiorgan failure.
- Septic shock carries an estimated mortality rate of about 40 to 50 percent.
- Cardiogenic shock carries an even higher estimated mortality rate of about 50 to 75 percent.
- Hypovolemic and obstructive shock generally have much lower mortality and respond better to prompt treatment than septic or cardiogenic shock.
StatPearls (NCBI Bookshelf) · Shock · open the source →
📝 Notes & key concepts
The lines from this module that carry a number, a dose or an absolute rule — the ones that decide questions. Everything else is on the cards above.
- MAP is the perfusion indicator, goal
>65. Do not panic at an SBP in the 80s–90s if the MAP is adequate. Lactate goal≤2; lactate >2 with suspected infection means septic shock. - Hypovolemic: 15–30% volume loss (~1 L). H&H high = fluid loss and hemoconcentration; H&H low = active bleeding. Fix the cause + fluids; blood products if bleeding.
- Cardiogenic: pump failure, most often MI. Fluids are not the treatment — cardiac management is. MONA (morphine, oxygen, nitroglycerin SL
q5 min ×3max, aspirin ~324 mgnot 81 mg); definitive treatment is cath with stent, or CABG. BNP normal<200; serial troponins. - Sepsis bundle — order matters, all within the first hour: labs including lactate → blood cultures BEFORE antibiotics (2 sets / 4 bottles; with a central line, draw one peripherally and one from the line) → antibiotics before fluids → IV fluids → vasopressors only if fluids fail, targeting MAP
≥65. - SIRS needs 2 of 4: temp
>38.3°Cor<36°C, HR>90, RR>20, WBC>12,000or<4,000or>10%bands. Meeting criteria is not automatically sepsis. - Monitor response with serial lactate (should trend down) and MAP. Do not repeat blood cultures immediately — they take ~3 days. UTI is the most common sepsis source, especially in older adults. LR is now favored over NS.
- Neurogenic: hypotension + bradycardia, the opposite of every other shock. Anaphylactic: epinephrine first, then oxygen, then fluids — fluids are not the priority. Obstructive: relieve the obstruction (needle decompression for tension pneumothorax; pericardiocentesis at the 5th intercostal space for tamponade — Beck's triad = muffled heart sounds, JVD, hypotension).
- Norepinephrine is the first-line pressor. Central line, titrate to MAP. Phentolamine reverses extravasation; prolonged use causes digital necrosis. Use IO access if no line can be placed fast enough.
- Modified Trendelenburg (legs elevated) shifts ~
300 mLback to the heart and tests fluid responsiveness. VSq15 min. - MODS = the original failing organ plus 2 more (3 total). Mortality exceeds
60%once 4+ organs are involved. - Intubation: preoxygenate 100%, sedate before you paralyze, and keep sedation going afterward. Confirm with bilateral breath sounds and symmetric chest rise, then ETCO2 (yellow/green = trachea, purple = esophagus → pull and retry), with CXR as the gold standard.
- Universal numbers: urine output minimum
30 mL/hr, adult blood volume ~5 L. Stages run compensated → decompensated (metabolic acidosis, rising creatinine) → irreversible. - Hypovolemic case: BP 78/50, HR 132, RR 28, UO 10 mL/hr, Hgb
8.2, Hct25%. Underlying-cause treatment is rapid isotonic crystalloid — not pressors, not oxygen. - Cardiogenic case: troponin I
2.9(normal <0.03), BNP157(normal <100), crackles, SpO2 88% on 4 L, UO 15 mL/hr. To improve cardiac output the answer is inotropes. No big fluid boluses, and no nitroglycerin while hypotensive — 80 becomes 60.
🎯 Module quiz
Questions for this module. They also feed the Mega Quiz.
Nothing here yet — drop it in when you have it