Nursing Field Notes / Cardio · Pathophysiology Course
Cardiogenic Shock 🫀
The PUMP is broken — CARDIOgenic = CARDIAC fails
NG-196Cardio · ShockADHD-friendly visual edition
The heart fails to pump blood out of the heart and to the body — like in a heart attack where heart muscle DIES, or a heart failure exacerbation. The tank is full. The pipes are fine. The motor quit. That is why this is the only shock with a HIGH preload — and the only one you must not flood with fluid.
📉 Watch the BP trendEach set of vitals is lower than the last while the HR climbs. That trend is the diagnosis.
🎈 JVD + cracklesBlood backs up behind a failing pump: distended neck veins, wet lungs, S3, frothy pink sputum.
🧊💧 COLD & WETThe classic profile. Cold = low output. Wet = congestion. Do not bolus fluid.
🧨
CAUSE
STEP 1 · THE MOTOR QUIT
Something destroyed, stunned or disorganized the muscle — and the same volume that used to move forward now backs up.
🫀 Forward failure and backward failure — from one dead wall
One failing ventricle produces both problems at once — that is why the cardiogenic patient is hypotensive AND fluid-overloaded at the same time, a combination no other shock produces.
🧠 “Cold in front, wet behind.” In front of the pump: nothing gets delivered (cold skin, low BP, no urine). Behind the pump: everything piles up (JVD, crackles, S3).
🚨 What breaks the pump
💔 Myocardial infarction — the #1 cause. Heart tissue dies and stops contracting (classically a large anterior/LV infarct)
💊 Overdose of beta-blockers or calcium channel blockers
🧠 “MI, muscle, rhythm, valve.” Four ways a pump quits: the muscle dies, the muscle is tired, the rhythm is chaos, or a part falls off.
🔬 Mechanism: the death spiral
💔 Heart muscle dies or fails
▼
📉 Stroke volume ↓ → cardiac output ↓
▼
🩸 BP falls → coronary arteries get less blood too
▼
💔 More muscle becomes ischemic
▼
🌀 Output falls further — the loop feeds itself
Meanwhile the SNS raises HR and SVR to defend the BP — which raises myocardial oxygen demand on a heart that already can't get oxygen. Compensation makes it worse.
🧠 “The heart steals from itself.” Coronary arteries fill during diastole from aortic pressure. When BP falls, the pump's own supply line is the first thing cut off.
🔎
CLUES
STEP 2 · READ THE TREND
One set of vitals means nothing. Four sets in a row, each worse than the last — that's cardiogenic shock announcing itself.
⭐ The exhibit question: just look at the blood pressure
Classic stem — a client with an MI confirmed by elevated troponin. Which complication should the nurse report? Open the exhibit and the blood pressure goes lower and lower while the pulse and respirations climb.
🧠 “Down, down, down.” If the exhibit gives you a column of blood pressures and each is lower than the one above it after an MI, the answer is cardiogenic shock — nothing else in that stem produces a steady downhill BP.
🧠 High wedge + low index = cardiogenic. "Wedge" (PAWP) is a window onto the left atrium — high wedge means the left ventricle isn't emptying.
🧊💧 The COLD & WET quadrant — where cardiogenic shock lives
🧠 “Cold & Wet = Cardiogenic.” Both C-words. Cold skin (no forward flow) plus wet lungs (backward congestion) is the fingerprint that separates this from every other shock.
📊 Where cardiogenic sits among the shocks
Type
Preload (CVP/PAWP)
CO
SVR
Skin
Hypovolemic
↓↓
↓
↑
Cold, clammy, pale
Cardiogenic ⬅️
↑↑
↓↓
↑
Cold, clammy, mottled
Septic — warm / early
↓
↑
↓↓
WARM, flushed, dry
Septic — cold / late
↓
↓
↑
Cold, clammy, mottled
Neurogenic
↓
↓
↓↓
WARM, dry, pink + BRADYcardia
Anaphylactic
↓
↓
↓↓
WARM, flushed + hives / swelling
Cardiogenic is the only row with an UP arrow in the preload column.
🧠 Same cold skin, opposite neck. Hypovolemic = flat neck veins. Cardiogenic = distended. That single finding tells you whether to give fluid or withhold it.
🪜
THE 4 STAGES
STEP 3 · STAGE IT
Same four stages as every shock — here they are with the failing-pump patient's own findings written in.
🪜 The 4 stages of shock — identical on every shock page
Stage
What's happening
What you see
I · INITIAL
Cardiac output falls just enough that cells switch to anaerobic metabolism → lactic acid builds, blood glucose rises.
Nothing. Signs & symptoms are ABSENT in this stage — only a rising lactate gives it away.
II · COMPENSATORY
The sympathetic nervous system and renin–angiotensin–aldosterone rescue the pressure: catecholamines, vasoconstriction, ADH and aldosterone hold on to salt and water.
Tachycardia · tachypnea · restless & anxious · cold clammy skin · narrowing pulse pressure · urine < 30 mL/hr. BP is still near normal.
III · PROGRESSIVE
Compensation fails. Capillaries leak, acidosis deepens, organs begin to die.
MODS — multiple organ dysfunction syndrome. The body no longer responds to fluids or vasopressors.
Unresponsive · profound hypotension · anuria · DIC · death is imminent.
🧠 “I Can't Perfuse Right” — Initial · Compensatory · Progressive · Refractory. The stage you must catch is COMPENSATORY: the cuff still looks fine, so your clues are heart rate, respiratory rate, mental status and urine output.
📈 Stage progression — cardiogenic findings on each stage
🧠 In cardiogenic shock, stage II is a set of vitals — not one. The compensatory stage looks like “BP 128/82, HR 96”. It only reveals itself when you line it up next to the last set.
🩺
CARE
STEP 4 · HELP THE PUMP
Make the heart squeeze better, make its job easier, and open the blocked artery — without drowning it in fluid.
💊 Inotropes — “more FORCEFUL beats”
Positive INOtropic = more forceful contraction → more blood comes OUT of the heart → cardiac output rises. That is exactly what a failing pump needs.
Tachycardia >100/min and dysrhythmiasNCLEX TIP; extravasation risk
Dobutamine 💊
Nearly pure beta-1 — raises contractility and cardiac output with little vasoconstriction. The inotrope of choice in modern cardiogenic-shock practice.
May lower BP (mild beta-2 dilation); tachycardia, ectopy
Digoxin 💊
“D is for DEEP contraction” — a positive inotrope that also slows the rate (negative chronotropic). Used in heart failure and rate control in AF.
Hold and reassess if apical pulse < 60; hypokalemia worsens toxicity
Norepinephrine 💊
Strong alpha-1 with some beta-1 — used to hold the MAP ≥ 65 when the patient is frankly hypotensive so the coronaries stay perfused.
SOURCE vs PRACTICE The source infographic names Dopamine and Digoxin as the inotropes — both are genuinely positive inotropes and both are fair game on an exam. In current critical-care practice, however, the acute agents are dobutamine (inotrope) and norepinephrine (pressor); digoxin has a slow onset and a narrow therapeutic window, so it is a chronic heart-failure drug rather than a shock rescue drug. Know both framings.
🧠 “D drugs make it DEEP: Dopamine · Dobutamine · Digoxin.” All three deepen the squeeze. INO = force. CHRONO = rate.Chronos means time — chronotropes change beats per minute.
💊 Digoxin safety — the part that gets tested
🫀 Take the apical pulse for a full minute before every dose — hold if under 60 and notify the provider
🧠 “Low K, high dig.” Potassium and digoxin compete for the same pump site — drop the potassium and the digoxin takes over. A patient on dig and furosemide is a toxicity question waiting to happen.
🚨 Fluids: the exception to every other shock
In hypovolemic and septic shock you fill the tank first. In cardiogenic shock the tank is already overfull — the pump just can't move it.
❌ No large fluid boluses in LV cardiogenic shock — they cause flash pulmonary edema
✅ Careful diuresis (e.g. IV furosemide) to unload the congested lungs, guided by BP
✅ Nitrates reduce preload and afterload — only if the blood pressure tolerates it
⚠️ Exception to the exception: a RIGHT ventricular infarct (with an inferior MI) presents with hypotension, JVD and CLEAR lungs — that patient needs fluid, and nitroglycerin is contraindicated
🧠 “Wet lungs = no fluid. Clear lungs + JVD = fluid.” Listen to the chest before you hang anything. The lungs decide.
⚙️ Mechanical support & fixing the cause
The real cure for MI-related cardiogenic shock is opening the artery — emergency cardiac catheterization with PCI (or CABG). Everything else is a bridge to that.
🎈 IABP — intra-aortic balloon pump, as drawn above
🔩 Impella / VAD — pumps that take over ventricular work
🫁 ECMO — bypasses heart and lungs entirely in the sickest patients
🩺 Treat the rhythm — cardiovert/defibrillate, pace a bradycardia
🧠 “IN with diastole, OUT with systole.” The balloon does the opposite of the heart: it fills when the heart relaxes (feeding the coronaries) and empties when the heart squeezes (lightening the load).
🐝 Also on this source card: ANAPHYLACTIC shock
A severe allergic reaction — bee sting, peanut, shellfish, latex, penicillin, contrast dye. Mast cells dump histamine, vessels dilate everywhere, capillaries leak, and the airway swells shut. It is a distributive (pipe) shock, not a pump problem.
🚨 What you see
✅ What you do
Hives/urticaria · flushing · angiedema of lips & tongue · stridor · wheezing · throat tightness · hypotension · tachycardia · GI cramping/vomiting · sense of impending doom
1. EPINEPHRINE — intramuscular, anterolateral thigh (vastus lateralis), immediately 2. Remove/stop the trigger · call for help 3. Airway & high-flow oxygen — intubate early if stridor 4. IV isotonic fluids for the vasodilation 5. Antihistamines & corticosteroids — adjuncts only 6. Bronchodilator for wheeze 7. Observe for a biphasic reaction hours later
Why epinephrine works on all of it at once:alpha-1 constricts the leaking dilated vessels (BP up, swelling down), beta-1 raises rate and force, beta-2 opens the bronchioles. EpiPen auto-injector = epinephrine = epinephrine; teach patients to carry two and to go to the ED even after the pen works.
🧠 “Epi first, everything else second.”Never delay epinephrine to give diphenhydramine or steroids — antihistamines treat the itch, epinephrine treats the dying.
📉 BP lower & lowerafter an MI with elevated troponin = cardiogenic shock
💊 INO = forceDopamine · Dobutamine · Digoxin — “D is for DEEP contraction”
🪜 I · C · P · RInitial → Compensatory → Progressive → Refractory
🎯 Cover & check — 6 rapid-fire questions
Q1: A client with an MI and elevated troponin has these vitals over 45 minutes: 140/88 → 128/82 → 104/68 → 88/58, with HR 92 → 118 and RR 24 → 32. What complication, and what do you do?
Cardiogenic shock. Alert the primary health care provider immediately — the steadily falling blood pressure with rising pulse and respirations after an MI is the classic exhibit pattern.
Q2: Which shock has an INCREASED preload, and why?
Cardiogenic. The ventricle can't eject, so volume backs up behind it — high CVP/PAWP, JVD, crackles, S3. Every other type of shock has a LOW preload.
Q3: What does "positive inotropic" mean, and which drugs on this page have it?
More forceful contraction, which increases cardiac output (more blood coming OUT of the heart). Dopamine, dobutamine and digoxin are all positive inotropes. Chronotropic = rate; dromotropic = conduction speed.
Q4: Before giving digoxin, what does the nurse check — and what stops the dose?
Apical pulse for a full minute. Hold the dose and notify the provider if it is under 60. Also check potassium — hypokalemia causes digoxin toxicity even at a normal serum level.
Q5: Why is fluid handled differently here than in hypovolemic shock?
The tank is already full — the pump is the failure. Large boluses push a congested left ventricle into flash pulmonary edema. Exception: a right ventricular infarct (hypotension + JVD + CLEAR lungs) does need volume, and nitroglycerin is contraindicated there.
Q6: When does the intra-aortic balloon inflate, and what does that accomplish?
It inflates during DIASTOLE, driving pressure backward into the coronary arteries to feed the starving myocardium, and deflates just before systole so the left ventricle ejects against less afterload.