Chapter 30 — Cardiogenic Shock and Mechanical Complications of Infarction

📚 Guideline basis

SCAI SHOCK stage classification (Baran DA, et al. 2019; Naidu SS, et al. 2022 update); 2023 ESC guidelines for acute coronary syndromes; AHA scientific statements on cardiogenic shock; 2025 ESC/EACTS valvular heart disease guidelines for the acute valvular complications; ASE 2015 chamber quantification (17-segment model).

Pathophysiology & Mechanisms

Cardiogenic shock is a low-output state with end-organ hypoperfusion caused by primary cardiac failure. Two vicious cycles operate simultaneously.

The mechanical cycle. Reduced contractility lowers stroke volume and systemic pressure; reduced coronary perfusion pressure worsens ischaemia; ischaemia further reduces contractility. Compensatory vasoconstriction raises afterload, which reduces stroke volume further. Rising LVEDP raises subendocardial wall stress and compresses subendocardial vessels, closing the loop.

The inflammatory cycle. Extensive myocardial injury triggers a systemic inflammatory response with iNOS induction, nitric oxide-mediated vasodilatation, and capillary leak. This is why up to a third of cardiogenic shock patients are vasodilated rather than vasoconstricted, why SVR is an unreliable classifier, and why the physiology often looks mixed.

SCAI SHOCK stages and their echocardiographic correlates

Stage	Clinical	Typical echocardiographic findings
A — At risk	Normal perfusion, no shock	Large regional wall motion abnormality or reduced EF with preserved SVI
B — Beginning	Hypotension or tachycardia, no hypoperfusion	Low-normal SVI, rising E/e′, mild RV involvement
C — Classic	Hypoperfusion requiring intervention	SVI < 35 mL/m², low LVOT VTI, elevated E/e′, B-lines, dilated IVC
D — Deteriorating	Failing to respond to initial escalation	Falling VTI despite inotropes, worsening MR, rising PASP, RV dysfunction appearing
E — Extremis	Circulatory collapse, refractory arrest	Minimal contraction, minimal or absent aortic valve opening, near-absent VTI

The staging is clinical; echocardiography contributes the mechanism and the trend. Serial LVOT VTI is the single most useful monitored variable in this population.

Diagnostic Synthesis

Regional wall motion and the 17-segment model

Segmental analysis in the parasternal short axis (basal, mid, apical levels) and the three apical views maps to coronary territories:

Territory	Segments
LAD	Anterior and anteroseptal walls at basal and mid levels; all apical segments; apical cap
RCA	Inferior and inferoseptal walls at basal and mid levels; inferior apical segment
Circumflex	Anterolateral and inferolateral walls at basal and mid levels; lateral apical segment

Grade each segment: normal, hypokinetic, akinetic, dyskinetic, aneurysmal.

RWMA does not equal infarction. It occurs in myocarditis, stress cardiomyopathy, sepsis, post-arrest stunning, and after cardiac surgery, and it can be simulated by left bundle branch block, ventricular pacing and post-pericardiotomy septal motion. A pattern that crosses coronary territories (particularly circumferential apical akinesis with preserved basal function) points to stress cardiomyopathy rather than a single-vessel event.

Right ventricular infarction — the management inversion

Occurs in a substantial proportion of inferior STEMIs (proximal RCA occlusion). Findings: RV dilatation and hypokinesis with a normal or hyperdynamic LV lateral wall, inferior LV wall motion abnormality, dilated IVC, elevated RA pressure, and frequently tricuspid regurgitation.

The management inverts the usual RV failure rules:

Do	Avoid
Volume loading — the RV infarct is preload-dependent, and this is the one RV failure state where fluid reliably helps	Nitrates and diuretics — precipitate profound hypotension
Maintain AV synchrony; pace atrially or dual-chamber if needed	Ventricular pacing alone
Cardiovert new atrial fibrillation early	Delay in reperfusion
Inotrope if fluid alone is insufficient	Excessive volume — beyond a point the dilating RV shifts the septum and lowers LV output

Note that this exception applies to ischaemic RV failure with a preload-deficient right ventricle, not to the pressure-overloaded RV of ARDS or pulmonary embolism, where volume is harmful (Chapters 9, 32, 33).

Mechanical complications

Typically 2–7 days after infarction, and the reason every post-infarct patient with new haemodynamic deterioration needs an urgent echocardiogram.

Complication	Echocardiographic signature	Clinical clue
Ventricular septal rupture	Colour Doppler flow across the septum with a high-velocity systolic jet (LV-to-RV gradient); RV volume overload; Qp/Qs > 1.5; apical after LAD, basal-inferior after RCA occlusion	New harsh pansystolic murmur with thrill; step-up in oxygen saturation
Papillary muscle rupture	Mobile echodensity attached to chordae prolapsing into the LA; flail leaflet; massive eccentric MR; posteromedial in ~75–80% (single blood supply); hyperdynamic LV with low forward output	Flash pulmonary oedema, often after a small inferior infarct; murmur may be soft
Free wall rupture	Pericardial effusion with echodense clot, chamber collapse, electromechanical dissociation	Sudden collapse; PEA arrest
Pseudoaneurysm	Contained rupture — a narrow neck relative to the cavity, with to-and-fro colour flow through it	Distinguishing from a true aneurysm (wide neck, myocardium in the wall) is the key call
LV thrombus	Echodense mass in an akinetic or aneurysmal apex, distinct from the endocardium, seen in two planes; contrast improves detection	Anterior infarct; embolic risk
Dynamic LVOT obstruction	Hyperdynamic basal segments with apical akinesis, SAM, dagger-shaped LVOT envelope, posteriorly directed MR	Hypotension worsening with inotropes (Chapter 28)
Acute severe MR from tethering	Type IIIb, no structural lesion, dynamic	Worsens with ischaemia and hypertension

The pattern to recognise: new murmur plus new deterioration 2–7 days post-infarct requires immediate imaging and, for VSD or papillary muscle rupture, immediate surgical referral. Medical stabilisation is a bridge measured in hours.

Distinguishing VSD from papillary muscle rupture at the bedside: both present with a new murmur and shock. Colour Doppler across the septum settles it in seconds — and if the septum is intact, look at the mitral apparatus for a flail leaflet or a swinging mass.

Haemodynamic profiling

CPO = (MAP × CO) / 451     (watts)

Cardiac power output < 0.6 W is associated with markedly increased mortality in cardiogenic shock and is derivable entirely from echocardiography plus an arterial line.

PAPi = (PASP - PADP) / RAP

The pulmonary artery pulsatility index quantifies RV performance relative to load; low values indicate RV failure and predict the need for RV support. Echocardiographic surrogates are PASP from the TR jet, PADP from the PR end-diastolic velocity, and RAP from the IVC (with the ventilation caveat of Chapter 9). TAPSE/PASP serves the same purpose more directly.

Profile	SVI	Congestion	Interpretation
Wet and cold	Low	High (B-lines, high E/e′, dilated IVC)	Classic cardiogenic shock
Dry and cold	Low	Absent	Euvolaemic or hypovolaemic cardiogenic shock — a fluid trial may help
Wet and warm	Low-normal	High	Mixed cardiogenic/vasodilatory; inflammatory phenotype
Isolated RV	Low	High right-sided, clear lungs	RV infarct or RV failure

Therapeutic Logic

Step	Action	Echocardiographic endpoint
Reperfusion	Primary PCI is the definitive therapy; nothing below substitutes	Improving RWMA over hours to days
Restore perfusion pressure	Noradrenaline is the preferred first-line vasopressor in cardiogenic shock	MAP target achieved without a fall in VTI
Augment flow	Dobutamine or milrinone titrated to flow, not to EF	Rising LVOT VTI, rising CPO, clearing lactate
Reduce afterload where pressure permits	Vasodilator or mechanical unloading	Falling Ea, rising SV
Decongest	Diuresis or ultrafiltration	Falling E/e′, resolving B-lines, improving venous Doppler
Escalate to mechanical support	Persistent CPO < 0.6 W, rising lactate, SCAI stage D–E	Device-specific (Chapter 35)

Echocardiography for device selection

Device	Echocardiographic prerequisites	Contraindications to exclude
IABP	—	Significant aortic regurgitation; aortic dissection; severe peripheral vascular disease
Impella	Adequate LV cavity, no LV thrombus	Severe AR, LV thrombus, mechanical aortic valve, VSD (worsens shunt), severe RV failure
VA-ECMO	—	Severe AR (LV distension); aortic dissection; assess for LV distension after initiation
RV support	Low TAPSE/PASP, low PAPi, RV dilatation	—

Excluding aortic regurgitation before IABP or Impella insertion is a specific, time-critical echocardiographic responsibility.

🛑 Critical pitfall: Inserting an intra-aortic balloon pump without excluding aortic regurgitation. Diastolic augmentation drives blood retrograde into the ventricle and can be immediately fatal (Chapter 19).

🛑 Critical pitfall: Attributing new post-infarct deterioration to "pump failure" without a dedicated look for VSD and papillary muscle rupture. Both are surgically correctable and both are missed when the study is a rapid LV-function assessment.

🛑 Critical pitfall: Withholding fluid in RV infarction because "fluid is bad for the RV". Ischaemic RV infarction is preload-dependent and is the exception.

💡 Clinical pearl: Cardiac power output is computable from LVOT VTI and an arterial line, requires no catheter, and is one of the strongest haemodynamic predictors in cardiogenic shock. Report it.
💡 Clinical pearl: In the shocked post-infarct patient, put colour Doppler across the interventricular septum before doing anything else. VSD takes seconds to find and changes everything.
💡 Clinical pearl: Circumferential apical akinesis with preserved basal contraction crosses coronary territories and points to stress cardiomyopathy — which may also generate dynamic LVOT obstruction and therefore invert the inotrope decision (Chapter 38).

References

Baran DA, Grines CL, Bailey S, et al. SCAI clinical expert consensus statement on the classification of cardiogenic shock. Catheter Cardiovasc Interv 2019;94:29–37.
Naidu SS, Baran DA, Jentzer JC, et al. SCAI SHOCK stage classification expert consensus update. J Am Coll Cardiol 2022;79:933–46.
Byrne RA, Rossello X, Coughlan JJ, et al. 2023 ESC guidelines for the management of acute coronary syndromes. Eur Heart J 2023;44:3720–826.
Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults. J Am Soc Echocardiogr 2015;28:1–39.
ESC/EACTS. 2025 Guidelines for the management of valvular heart disease. Eur Heart J 2025;46:4635–.