In cardiogenic shock, the overwhelming majority of cases are caused by an abrupt depression and/or loss of contractility (intrinsic performance) of the heart irrespective of loading conditions with a subsequent significant fall in SV/CO [1, 2, 5, 37].

This occurs most often due to a critical loss of contractile tissue/mass [37] secondary to acute myocardial infarction [17–19, 24], resulting in acute loss of total pump force [39] and altered diastolic properties (diminished relaxation and compliance) [5, 37, 39]. Hence, in CS both systolic and diastolic function are considerably failing [40, 41]. Traditionally, CS is seen as a mechanical problem [37] with corresponding neurohormonal (namely enhanced sympathetic discharge and activation of the renin-angiotensin-aldosterone-system, RAAS) activation and response [40, 42]; this paradigm is summarized in the diagram (see Fig. 3.1).

Severe myocardial dysfunction, as in the case of CS, leads directly to both decreased SV and an increase in LVEDP [37, 40, 41]. Subsequently, the marked reduction in SV causes hypotension [37] and systemic hypoperfusion [37], compromising the coronary perfusion, causing myocardial ischaemia or aggravating existing myocardial ischaemia [5, 40, 42, 43] leading to progressive impairment of myocardial function [5, 40, 42, 43]. Furthermore, as depicted by the diagram by Antman [42] (see Fig. 3.1), in response to the considerable impairment of the cardiac contractility [16, 37, 43, 44], a compensatory systemic vasoconstriction [37, 40, 42–44] secondary to neuroendocrine [37, 43–45], in particular sympathetic activation [37, 40, 42–44], occurs. The neurohormonal—mediated systemic vasoconstriction exerts additional substantially adverse loading conditions (enhanced pre- and afterload) [42–44, 46] onto the already compromised myocardial function. Vasoconstriction, of course, includes the venous system and it is particularly the splanchnic venous constriction which directly provokes, due to considerable fluid redistribution, acute cardiac volume loading [47–49]. However, it is namely the increase in afterload due to arterial vasoconstriction which has substantial detrimental effects as the left ventricle is highly afterload-sensitive [43, 44, 46, 50]. Renal sodium and water retention (attributed to non-osmotic arginine vasopressin effects and to the actions of the activated RAAS) aggravates the overfilling by fluid accumulation [45, 51] and thus contributes, in the presence of already elevated filling pressures, to the precipitation of pulmonary congestion or even pulmonary edema [52].

However, obviously a severely diminished contractility alone does not precipitate CS [53–55]:

LV-EF is found to be on average 30% in patients with CS and thus lies absolutely within the range many stable post-AMI patients display [5, 56, 57]. Furthermore, LV-EF stays the same 2–3 weeks after CS when functional circulatory conditions are markedly, if not completely, different [58]. Even patients with low normal EF and without severe mitral regurgitation may present or develop CS in the acute setting [59]. Furthermore, several studies on cardiogenic shock [5, 54, 60–63] have revealed a fundamentally different hemodynamic profile than expected and previously established: Although the contractility is severely impaired with a marked fall in SV and a compromised diastolic function, the peripheral systemic resistance is often only marginally to moderately elevated (see Fig. 3.2 by Cotter [62]).

Moreover, this “inappropriate” vasoconstriction (inappropriate low systemic vascular resistance) in relation to the severity of the myocardial depression, and the consecutive circulatory implications, first and foremost hypoperfusion, is found in the majority of patients [62–65]. Thus, CS affects the integral circulatory system [55, 66] and has to be considered to be a systemic rather than a solely cardiac disorder [67–69]. Indeed, the considerable myocardial dysfunction initiates CS development [55] at which the primarily underlying myocardial dysfunction directly leads to both, reduced SV (and thus diminished CO) resulting in global tissue and cellular hypoperfusion and thus oxygen and nutrient undersupply [70–74], and to elevated filling pressures [64, 75]. The latter potentially provokes pulmonary congestion/edema [37, 40, 76]. Consecutively, compensatory, mainly neurohormonal, response is launched [37, 40, 42, 55], intending to stabilize preferentially cardio-circulatory and cerebral functions by diverting the blood flow to “vital” organs via several complex and interconnected neuroendocrine pathways [49, 55]. Accordingly, CS obviously is a systemic affliction and an integrative malfunction of the circulatory system applies [55, 66, 68].

In fact, CS is a so–called central shock characterized by scarce peripheral and organ perfusion attributed to substantial pump failure and therefore organ derangement right from the onset of the disorder [77]. The “unexpected and surprising” hemodynamic profile predominantly featuring inappropriately and functionally insufficient vasoconstriction in the presence of a, by all means, “comparably” not too bad LV-EF of around 30% (however remember, EF is a coupling indicator and is inversely related to afterload [78–81], therefore an EF of 30% in the presence of low SVR as in CS is absolutely not comparable with an EF of 30% in the presence of normal or high SVR as in stable heart failure patients!) is consistent with and reflects the systemic inflammatory response (SIR) applying in CS [5, 12, 54, 55, 61, 65]: Hypoperfusion, a hallmark of CS [55], restauration of blood pressure by neuro-endocrine activation as well ischemia and reperfusion precipitate a systemic inflammatory response [5, 49, 55, 82] and thus are coining a clinical-hemodynamic picture quite similar to that in sepsis [65].

Namely the ischemia—reperfusion conditions are associated with the generation and the release of vasodilative acting mediators [83–85]: First and foremost high concentrations of NO and peroxy-nitrites (mediators with vasodilative effects) offset and counteract the neurohormonal mediated compensatory vasoconstriction, and, in fact, lead to an inappropriate circulatory response with potentially net vasodilation [5, 9, 62–64, 83, 84]. Indeed, elevated plasma levels of inflammatory markers and cytokines including TNF alpha and IL-6, indicating activated systemic inflammatory cascades, are demonstrated in CS [55, 61, 86, 87], while procalcitonin concentrations stay low reflecting the absence of a microbial infection underlying this setting [86]. Kohsaka [65] detected high levels of inducible NO-synthetase (iNOS) subsequent to the release of inflammatory mediators in patients with acute myocardial infarction. In fact, substantial evidence suggests that high levels of iNOS are expressed, attributed to the inflammatory response arising in the setting of AMI which is attended by and intrinsically tied to ischemia-reperfusion issues [83, 84]. This implies inadequate high levels of NO, potentially contributing to vasodilation, and of peroxynitrite, the latter with not only vasodilative [88] but also cardiotoxic and negative inotropic effects [82]. Elevated iNOS levels are per se associated with myocardial dysfunction [89, 90]. Raised, high levels of iNOS and NO are found after trauma and as a result of exposure of cells, particularly endothelial cells and cardiomyocytes, to inflammatory mediators, inducing the cells to express iNOS in unphysiological high ranges [84]. This has been specifically observed in experimental models of AMI and subsequent reperfusion [85]. Cytokine levels are reported to even increase after reperfusion following PCI applied in the setting of AMI [83]. Unphysiologically high levels of NO and iNOS and the subsequent generation of NO-derived species like peroxynitrite are reported to exhibit several deleterious effects: (a) to directly inhibit myocardial contractility, (b) to display pro-inflammatory effects, (c) to induce systemic vasodilation (d) to suppress mitochondrial respiration in non-ischemic myocardium, (e) to reduce catecholamine responsivity [54, 91–93], and (f) to mediate myocardial stunning [54]. iNOS induced NO production is found to be particularly deleterious during ischemia-reperfusion episodes [91, 92]. Accordingly, the effect of the compensatory released vasoconstrictive mediators (catecholamines, angiotensin II, endothelin-1) attaining intermittent stabilization and/or even improvement of coronary and peripheral perfusion [82] will be markedly attenuated and may be even off-reverted by the vasodilative effects of those agents generated in general in the setting of systemic inflammation but specifically in the wake of ischemia-reperfusion issues associated with AMI [67, 82]. This particularly occurs if the hemodynamic alterations and the compensatory response persist [82] and Rudiger strongly recommends to reverse CS within hours [66]].

As such, CS is also a result of the mismatch arising from substantially impaired myocardial performance and disproportionate, inadequate peripheral vascular dilation [63, 64].

Nontheless, additional “infectieous” features may trigger and aggravate the inflammatory cascades: Disrupted intestinal mucosal barrier function due to gut hypoperfusion may allow for translocation of bacteria or bacterial material like toxins [49, 82]. In the shock trial, 18% of all patients with CS were suspected of suffering from sepsis, and indeed, of those 18%, 74% had positive blood cultures (that means, in total about 14% of all CS patients showed a bacterial infection/bacterial-associated inflammation) [65] which, in turn, fuels the inflammatory cascades.

Moreover, systemic inflammation is further reported to stiffen large, elastic arteries like the aorta while simultaneously the medium-sized and small peripheral vessels dilate [94]. Large artery stiffening arises most likely due to altered NO bioavailability as acute inflammation is shown to impair normal endothelial performance and reduces NO bio-availability, possibly through the cytokine cascade [95–98]. Arterial stiffening is recognized to increase the vascular load imposed on the left ventricle [99, 100] and to directly affect ventricular arterial coupling [101]. However, as reduced wave reflections (pulsatile load) due to peripheral vascular dilatation are noticed and total peripheral resistance is measured lower under these inflammatory conditions [94], net LV afterload may not increase. Reduced peripheral resistance (resulting from peripheral vasodilation) and concomitantly blunted wave reflections will diminish the afterload. However, in total, LV afterload is supposed to increase in inflammatory conditions since (1) peripheral vascular resistance is generally only mild to moderately reduced in CS [62], (2) the changes in vascular resistance precipitate just minor changes on ventricular wall stress (which reflects “true” afterload) [102], and (3) central vascular stiffening directly alters ventricular–arterial coupling (uncoupling) [101]. This suggestion is supported by the fact that peripheral vascular resistance is not really seen by the heart [78]. Unfortunately, studies systematically evaluating this issue are missing. Increased pulse wave velocities and a raised augmentation index as demonstrated in SIRS [94], are independently associated with systolic and diastolic dysfunction [103–105] and hence inflammation, in fact, impacts on disease course and is markedly involved in CS pathobiology.

SIRS may result in further troublesome hemodynamic effects contributing to CS disorder: CS, as the other shock types, features and suffers from microcirculatory dysfunction being part of the pathobiology [106]. Increasing heart failure severity is associated with NO imbalance and endothelial dysfunction (ED) [107, 108]. Low peripheral resistance predisposes patients to endothelial damage [65], and inflammatory agents like TNF alpha induce endothelial dysfunction [109]. Hypoxic/ischemic injury affiliated with hypo- and/or malperfusion is demonstrated to insult endothelial cells causing ED [110–113]. Hence, as the vascular endothelium takes a crucial role in regulating and is central to functions of microcirculation [114, 115], there is no doubt that microhemodynamics are altered in AHFS, particularly in severe AHF and CS [108, 116–118]. ED is meanwhile a widely recognized and an acknowledged feature in circulatory shock pathobiology [119, 120], where the endothelial cells are ascertained to be both target but also contributor to the disease development and progression [112, 121]. Indeed, endothelial cells are considered to take a central and crucial role in the pathophysiology and pathogenesis of acute and chronic heart failure [122–125].

Furthermore, since autoregulation is a hallmark and a critical issue in the physiology of microcirculation [108, 113, 114], a compromised autoregulation (which inevitably ensues in case of hypoperfusion and hypotension [126, 127]) contributes to, and is part of, the microcirculatory alterations found in CS [39].

Microcirculatory alterations display as their most deleterious impact heterogenous blood flows [108, 128], a hallmark of shock [108, 129], and as such generate hypoxic and non-hypoxic areas in close vicinity, called dysoxic tissue regions [130, 131]. Heterogenous microvascular perfusion has been demonstrated in patients with CS [108]. Heterogenous perfusion is associated with disturbed oxygen extraction [70] and thus may lead to further cellular injury [132] in the heart as well as in distant organs [68, 108, 114, 119, 133].

Noteworthy for therapeutic management, in contrary to septic shock, where at least in advanced disease states micro- and macrocirculation are dissociated (which means that a successfully recuscitated macrocirculation will not subsequently translate into an improved or even normalized microcirculation [134, 135]), a close correlation between macro- and microcirculation seems to exist in cardiogenic shock states and thus microcirculatory alteration will usually improve when marcocirculation can be restored [136, 137].

As such, altered microcirculation has to be seen as an essential element in the pathobiology of shock states [77, 108] and the aberrations are basically referred to as a loss of regulation of the peripheral vasomotor tone, associated with endothelial cell dysfunction [138], eliciting heterogenous and maldistributed blood flows creating dysoxic tissue regions [72, 139].

In conclusion, the systemic inflammatory reaction contributes substantially to the pathogenesis and the course of CS [52, 54, 55, 61, 65, 82]: The mismatch between marked myocardial depression caused by loss of contractile mass [24, 37, 40, 54], ischemia-reperfusion injury [42, 49, 65, 82–85], cardiodepressent substances [82, 89, 90, 109], and the inappropriate vasodilation may result in CS [63, 64]. Incipient CS leads to profound, persistent, and refractory vasodilatation and hypotension [1, 54, 83, 84] and to the development of MODS/MOF [5, 54, 61] with its deleterious outcome, if not treated adequately and in time [54, 55, 66].

Hence, the pathogenesis of CS is largely determined by

the latter with inherent vasodilatory properties, thereby altering macro- but also microcirculatory hemodynamics [52, 54, 55, 61, 65, 82, 86, 87, 108]. The ‘only’ marginal to moderate, disproportionate increase in peripheral resistance (SVR/SVRI) has gained pathognomonic meaning for CS: The relatively low SVR/SVRI is essentially caused by the vasodilative mediators (largely NO, peroxynitrite), which are generated in the context of the inflammatory reaction and the ischemic-reperfusion issues that apply in the setting of CS complicating AMI. This vasodilative capability basically offsets the vasoconstrictive effects (mainly) launched by the neurohormonal-based compensatory mechanisms precipitated in response to the loss of pump function [54, 60–62, 65].

It has to be noted that a small group of patients in the SHOCK registry and trial [5, 27, 28] were clinically normotensive, or only mildly hypotensive, but still diagnosed as cardiogenic shock: They were systemically hypoperfused with low CO and elevated left ventricular filling pressures but with an “elevated” SVR and therefore able to maintain a reasonable blood pressure [9]. These patients should have been classified as being in a pre-shock state [3], where the systemic inflammatory response is not (yet) significantly active/activated.

There is quite a wide range of intensity and impact of the inflammatory response reported, afflicting some patients severely and some more marginally, as such, the violence of SIRS decisively impacts on the malady course [54, 140, 141].

Hochman [54] suggested a new cardiogenic shock paradigm, having integrated the newer pathophysiological aspects [61, 62, 65, 82] within the older existing concepts [42], as depicted in Fig. 3.3.

Myocardial perfusion is compromised by hypotension [5, 43] and may induce ischaemia or exacerbate existing ischemia [37]. The decreased coronary perfusion pressure (especially in multi-vessel coronary disease [40]) secondary to the decrease in MAP, caused by the poor cardiac performance/contractility and vasodilatation, may lead to a critically low BP [5, 40, 42, 61]. Critical hypoperfusion itself aggravates the myocardial perfusion deficit [142], exacerbating the myocardial ischemia and implementing a vicious cycle leading to a more and more severely ischemic myocardium [40, 42]. This is seen even in shock states not initially caused by impaired myocardial contractility [1, 2], but when the blood pressure is so low that the perfusion of the end-organs [1, 13] (especially the heart [13, 143–145]) becomes critically dependent on the hemodynamics [5, 40, 145].

The compensatory neuroendocrine response may also contribute to this deleterious development, thus showing to be maladaptive: Initial vasoconstriction and fluid retention increase pre- and afterload, thereby enhance ventricular wall stress and consecutively myocardial oxygen demand, as does the tachycardia often resulting from the catecholamine release within the compensatory features [52, 55, 146].

Accordingly, “ischemia causes myocardial dysfunction which, in turn worsens ischema” [37]. Topalian [52] expresses this as “ischemia begets ischemia” and Hollenberg [37] strongly advises against the incidence of a vicious cycle arising consisting of ischemia, deterioration of myocardial function, and shock.

The compliance, a diastolic property, of the left ventricle will be reduced by myocardial ischemia, and subsequently the LVEDP will rise [147–151], as will the pulmonary capillary pressure, putting the patient at risk of developing pulmonary congestion / edema [76, 149–152]. Additionally, LV end-diastolic filling increases in situations of severely impaired systolic LV-function in order to maintain SV (via Frank-Starling- mechanism) [37, 40, 153]; this will augment the LVEDP further, putting the patients at even higher risk of pulmonary congestion/oedema [40, 76] and further ischemia [37, 40].

Thus, both, altered systolic and diastolic properties contribute to the increase in LVEDP [40, 76].

However, LVEDP reflects the compliance of the left ventricle [153], and abnormally high LVEDPs indicate enhanced LV-stiffness [154]. Since the compliance of the heart chambers is demonstrated to continuously vary, particularly in critically ill patients [155, 156], but even in healthy persons [157], changes in LVEDP may not correlate with changes in left ventricular filling volume at all. As such, some patients with CS will definitely show normal or even low filling pressures [9, 158, 159]. Hence, caution is advised in interpretation of LVEDPs as the value, and even changes, may not correctly indicate LV- preload and intravascular volume conditions [156, 157, 160]. Anyway, essentially and typically, LVEDP is elevated and CO low in CS [40].

Sharing the interventricular septum and being enclosed by “one” (the) pericardium, interactions between left and right ventricle occur [161–164]. As such, RV function may be affected by a dysfunctional LV, and may contribute to CS [55].

Foremost, the increased left-sided filling pressures being transmitted back, precipitating pulmonary hypertension [165, 166], acutely afterload the RV [152, 165–170]. Consecutively, as the right ventricle can poorly tolerate and adapt to pressure loading [171, 172], an immediate dilatation of the right chamber (with an increase in RVEDV) occurs in order to compensate for the elevated load imposed on RV [172–174]. Concomitantly with that increase in RV filling volume (RVEDV), both RVEDP (increase due to (a) the rise in filling volume [174, 175] and due to (b) pericardial constraint following the rule of constant total cardiac volume [161, 163, 176, 177]) and LVEDP increase (pericardial constraint associated with diastolic ventricular interdependence [178–181]). Attributed to the stronger impact of the pericardial constraint on the thin-walled right heart, the rise of RVEDP is disproportionally higher than the rise of LVEDP [178, 179]. RV-dilatation and the marked increase in RVEDP may result in deleterious consequences, since, due to diastolic ventricular interdependence [178–180, 182], the shift of the IVS towards the cavity of the left ventricle will impair the net space for LV filling volume, (further) compromising LV–SV and LV performance [163, 182–185]. Moreover, up to 40% (Diamino allocates up to 66% of RV pressure generation and up to 80% of the RV flow to LV contraction/LV assistance [186]) of RV contractility force, due to anatomical arrangement of myofibres [182], is generated by LV-contraction, referred to as systolic ventricular interdependence [164, 187, 188]. Therefore, an impaired LV contraction may markedly affect RV systolic performance and reduce RV-SV, subsequently supplying the LV with an even more inappropriately low filling volume [189, 190]: Thus, only a sufficient RV pump ensures appropriate LV preload and consecutively guarantees LV output [191, 192], hence prevents (further) LV pump failure—a series effect as the two ventricles are arranged in a row [191–193].

Moreover, RV may be involved in the ischemic process, although a predominant RV—infarction and associated shock is a rare event: In only 5% of patients predominant RV—infarctions are reported [194], however, acute RV myocardial involvement is complicating 50% of all inferior AMIs [195]. As such, if ischemia involves the RV, any additional threat (e.g. RV afterloading) may cause fatal consequences.

The haemodynamic alterations and the severity of circulatory compromise in predominantly RV- AMI are determined by the damage to the RV itself (extent of RV ischaemia and the subsequent RV-dysfunction), the ventricular interaction (mediated by the septum and by the restraining pericardium [196] affecting the LV-function), and the involvement of the LV in the ischemic injury [194]. Since RV contractility considerably depends on systolic LV-function, particularly on the contraction of the helical fibres of the IVS [197–199], a loss of systolic LV support (e.g. due to LV infarction—the perfusion of the IVS may be provided to a considerable amount by a big right coronary artery!) may result in deleterious hemodynamic consequences [197–201] and early onset of hypotension and shock [202].

Accordingly, a predominant RV-infarction, or a relevant ischemic involvement of the right ventricle in LV-AMI requires special attention and a sophisticated therapeutic approach: The traditional and common practice of aggressive volume loading [55, 163] may be erroneous and disastrous, as volume loading in the presence of elevated RVEDPs and/or a dilated RV (and thus relevant pericardial constraint) may, due to DVI, further impede LV-filling and hence markedly diminish LV-SV [163, 177, 179, 183, 184]. In addition to the altered LV-geometry following the septal shift towards the left chamber cavity, LV systolic function is affected as well [203]. Thus, fluid application may end up in full-blown circulatory failure [55]—thus, in contrary, volume unloading is necessary and the appropriate way!

In the vast majority the diagnosis of CS is established by clinical signs of hypoperfusion, ischemic chest pain, enzymatic analysis and ECG [37, 49, 55, 225, 226]. A normal ECG virtually excludes the possibility of CS caused by myocardial infarction [40]. In addition, an echocardiogram is absolutely essential in the initial assessment of all patients suffering from (cardiogenic) shock [3, 37, 227–229] and should be performed as early as possible.

The crucial aspect in the diagnosis of CS is the identification of hypoperfusion in the setting of considerable cardiac dysfunction [1, 3, 5, 37, 40]. The following signs and features are suggestive of organ/tissue hypoperfusion [3, 5, 225, 230, 231]:

CS should be considered in all patients presenting with unexplained hypotension and/or low cardiac output, unexplained impairment of mental function and unexplained pulmonary congestion [5, 13, 37]. In fact Menon [3, 9, 10] strongly recommends diagnosing CS in all patients exhibiting signs of inadequate tissue perfusion in the setting of severe cardiac dysfunction irrespective of the BP.

“CS is diagnosed after documentation of myocardial dysfunction and exclusion of alternative causes of hypotension like hypovolaemia, haemorrhage, sepsis, pulmonary embolism, tam- ponade, aortic dissection and pre-existing valvular disease” [37].

Ander [232] expresses doubts that clinical signs are sensitive enough to detect occult cardiogenic shock, particularly in patients with congestive heart failure because clinical signs may fail to diagnose inadequate oxygen delivery [233–236]; thus, the measurement of ScvO₂ and serum lactate are recommended [232, 237]:

A lactate > 2 mmol/L together with a ScvO₂ < 60% (SvO₂ < 65%) suggests occult shock [232].

64% of all patients included in the US shock register presented with hypotension, evidence of ineffective CO/hypoperfusion and pulmonary congestion [8], but 28% had evidence of peripheral hypoperfusion and hypotension and did not suffer from pulmonary congestion [8]. Thus, clear lungs may still be present even with elevated PCWP and CS [8]. This phenomenon (elevated PCWP but no clinical or radiological signs of pulmonary congestion) has been described previously [238]; it deserves emphasis because administration of large amounts of fluid will be deleterious [8, 239]. Do not treat these patients with large boluses of fluid [3, 239].

The timely identification of patients in a pre-shock [3, 10] or non-hypotensive shock [9] state is of special value to allow therapeutic intervention and prevent decline. Clinical signs of hypoperfusion (in particular cold, clammy skin and oliguria) are strongly associated with increased mortality, independent of blood pressure and other haemodynamic parameters [240]. Hypoperfusion may be a marker of impending haemodynamic collapse [9] and tachycardia in this setting (HR > 90/min) should be interpreted as a pre-shock symptom and not as a response to low cardiac output and subsequent increased sympathetic tone [3]. Take care particularly in patients with anterior AMI and keep in mind that up to 30% of patients with AMI develop cardiogenic shock late (day 5) in their disease course—and with a very poor prognosis [241].

In this situation the choice of medication should be made carefully. The use of β-blockers, in general indicated and life-saving in AMI [242, 243], may precipitate shock development in these patients [3, 12, 143, 244]. Additionally, the possible life saving compensatory activation of the renin-angiotensin system should not be counteracted by administration of ACE-inhibitors [245, 246].

A significant infarction of the right ventricle (RV-AMI) complicates 50% of all inferior myocardial infarctions [195]. On an ECG, ST-elevation in VR3 and/or VR4 (right praecordial leads) in patients with inferior ST-elevation, acute myocardial infarction is specific for RV-ischaemia due to a proximal RCA-lesion [196]. Predominantly the inferior and posterior parts of the RV are involved [194]. In this case, RV may be the crucial component in the disease process, responsible for the development for CS [178].

The recognition of this special issue is important due to a three-fold risk to develop ventricular arrhythmias and AV-nodal block [247, 248] and due to the special treatment needs: well-balanced and monitored fluid administration, fluid restriction in case of manifest RV-failure, and CS [178, 184, 249], preservation of AV-synchrony, and reduction of increased RV-afterload [250–252]. On the other hand, RV is reported to be highly resilient and may recover soon completely, possibly indicating that RV-dysfunction is probably due to stunning myocardium rather than true myocardial necrosis [253].

The LVEDP and its measurement in the definition and diagnosis of cardiogenic shock should be assessed critically; an elevated LVEDP may not be a sensitive or specific parameter with which to diagnose CS:

Thus, no reasonable correlation between LVEDV and LVEDP could ever be established [156, 157, 160] and in preference, the transmural LVEDP may be helpful to guide and monitor disease and therapeutic measures [262]. For further details see Chap. 1, paragraph 3b.