Pathophysiology and management of cardiogenic shock

Journal of Clinical Medicine

The pathophysiology of cardiogenic shock (CS) varies depending on its etiology, which may lead to different hemodynamic profiles (HP) and may help tailor therapy. We aimed to assess the HP of CS patients according to their etiologies of acute myocardial infarction (AMI) and acute decompensated chronic heart failure (ADCHF). We included patients admitted for CS secondary to ADCHF and AMI. HP were measured before the administration of any inotrope or vasopressor. Systemic Vascular Resistances index (SVRi), Cardiac Index (CI), and Cardiac Power Index (CPI) were measured by trans-thoracic Doppler echocardiography on admission. Among 37 CS patients, 28 had CS secondary to ADCHF or AMI and were prospectively included. The two groups were similar in terms of demographic data and shock severity criteria. AMI CS was associated with lower SVRi compared to CS related to ADCHF: 2010 (interquartile range (IQR): 1895–2277) vs. 2622 (2264–2993) dynes-s·cm−5·m−2 (p = 0.002). A trend toward a higher...

The Journal of Surgical Research, 1992

Narayana Medical Journal

Shock is defined as circulatory insufficiency that creates an imbalance between tissue oxygen supply and oxygen demand. The result of shock is global tissue hypoperfusion and is associated with a decreased venous oxygen content and metabolic acidosis (lactic acidosis). (4) Pathophysiology (4) Shock is classified into four categories by etiology: (1) Hypovolemic (caused by inadequate circulating volume), (2) Cardiogenic (caused by inadequate cardiac pump function),

Circulation Research, 1962

AVe studied 2-t adult mongrel dogs (20 to 25 Kg.), anesthetized with morphine (3 ing./.Kg 1 .) and 0.25 nil./Kg. of a combination of equal volumes of Dial-uretliane solution (100 and 400 ing./ ml., respectively) and of pentobarbital sodium (60 mg./ml.).

Research in Experimental Medicine, 1996

The end-systolic pressure-volume relation (ESPVR) is accepted as a load-independent measure of cardiac contractility. Potential curvilinearity of the ESPVR, dependency on coronary perfusion pressure (CPP) and sensitivity to the type of loading intervention might limit its use in hemorrhagic shock. This study compared ESPVRs obtained by caval and aortic occlusion under physiological loading conditions at baseline with those obtained during hemorrhagic shock (mean arterial pressure 45 mmHg). The left ventricular (LV) pressure (tip manometer) and volume (conductance catheter) were measured in ten anesthetized pigs. ESPVRs were fitted to linear and quadratic models. Within end-systolic pressure (Pes) ranges obtained under baseline conditions, ESPVR displayed only minimal curvilinearity (second-order coefficient a<0.007) and could be accurately described by a linear model. However, nonlinearity of ESPVRs obtained over wider load ranges is suggested by negative volume axis intercepts of the linear model. Steeper ESPVR with aortic than with caval occlusion (2.28_+0.22 vs 3.41_+0.51 mmHg/ml, ns) could not be proven owing to the large interindividual variance of ESPVR slopes with both loading interventions. During shock the Pes range obtained by caval occlusion decreased to very low levels (from 49_+2 to 34_+1 mmHg), ESPVR did not adequately fit either of the two models (mean R<0.66), and critical reduction of CPP induced negative ESPVR slope in four of ten experiments. In contrast, aortic occlusion at shock resulted in linear ESPVR (R = 0.927_+0.029), Pes ranges (92-+3 to 58_+4 mmHg) comparable to the ones obtained by caval occlusion at control (113_+5 to 73_+6 mmHg), and steeper ESPVR than at control (3.41_+0.51 to 7.38_+1.0 mmHg/ml, P<0.05). Interpretation of the increased ESPVR slope obtained with aortic occlusion as due to increased contractility in shock is, however, complicated by different Pes ranges. It is concluded

Journal of Clinical Investigation, 1971

The effect of intra-aortic counterpulsation (IACP, 22-94 hr) on hemodynamics and cardiac energetics was evaluated in 10 patients in shock after acute myocardial infarction. The data clearly indicate that IACP improves myocardial oxygenation, enhances peripheral perfusion, and probably improves myocardial contractility in the severely diseased heart. Before treatment, decreases in cardiac index (mean value, 1.22 liter/min per m 2), systolic ejection rate (67 ml/sec), and time-tension index per minute (1280 mm Hg•sec/min) were observed. Systemic vascular resistance varied widely. Low coronary blood flow (68 ml/min per 100 g) was associated with increased myocardial oxygen extraction (79%), low coronary sinus oxygen tension (20 mm Hg), and abnormal myocardial lactate-pyruvate metabolism. During 4-6 hr of IACP, systolic pressure and left ventricular outflow resistance decreased by 18% and 24%, respectively, while cardiac index improved by 38%. Diastolic arterial pressure rose 98%. Increase in coronary blood flow from an average of 68 to 91 ml/100 g per min (P < 0.001) was significantly correlated with rise in mean arterial pressure (r = 0.685). This correlation was best expressed in a third-order curve, which intercepts the point of no flow at a mean aortic pressure of 30 mm Hg. The flow-pressure curve is relatively flat above 65-70 mm Hg, but becomes steeper as mean aortic pressure falls below this point. Myocardial oxygen consumption remained essentially unchanged […]

Journal of Surgical Research, 1976

Chest, 2019

Scientific statements and publications have recommended the use of vasoconstrictors as the first-line pharmacologic choice for most cases of cardiogenic shock (CS), without the abundance of strong clinical evidence. One challenge of guidelines is that the way recommendations are stated can potentially lead to oversimplification of complex situations. Except for acute coronary syndrome with CS, in which maintenance of coronary perfusion pressure seems logical prior to revascularization, physiologic consequences of increasing afterload by use of vasoconstrictors should be analyzed. Changing the CS conceptual frame, emphasizing inflammation and other vasodilating consequences of prolonged CS, mixes causes and consequences. Moreover, the considerable interpatient differences regarding the initial cause of CS and subsequent consequences on both macro-and microcirculation, argue for a dynamic, step-by-step, personalized therapeutic strategy. In CS, vasoconstrictors should be used only after a reasoning process, a review of other possible options, and then should be titrated to reach a reasonable pressure target, while checking cardiac output and organ perfusion.

Critical Care Nursing Clinics of North America, 2014

In health, functional components of the microcirculation provide oxygen and nutrients and remove waste products from the tissue beds of the body's organs. Shock states overwhelmingly stress functional capacity of the microcirculation, resulting in microcirculatory failure. In septic shock, there is abundant evidence that inflammatory mediators cause or contribute to hemodynamic instability. In nonseptic shock states, the microcirculation is better able to compensate for alterations in vascular resistance, cardiac output (CO), and blood pressure. Autoregulation at the arteriolar level and the endothelium and erythrocyte at the cellular level maintain oxygen diffusion gradients sufficient to support aerobic metabolism. In comparison with septic shock, hypovolemic and cardiogenic shock states are not challenged with the additional burden of infection and its consequential effects on the microcirculation. Global hemodynamic and oxygen delivery (D : O 2) parameters are appropriate for assessing, monitoring, and guiding therapy in hypovolemic and cardiogenic shock but, alone, are inadequate for septic shock.

Circulation Research, 1970

The contributions of metabolic acidosis, coronary perfusion pressure (CPP) and adrenergic support to left ventricular performance during hemorrhagic shock at aortic pressure (AP) of 30 ± 5 mm Hg were evaluated in cats in which AP, cardiac output (CO), and heart rate (HR) were controlled, and arterial pH, Po 2 and Pco 2 were continuously monitored. After 2 hours of shock, the stroke volume (SV), ejected at end-diastolic pressure of 10 cm H 2 O (SV 10 ), was irreversibly reduced to 46 ± 4% (P &lt; .001) of initial values (arterial pH 6.93 ± .05). In control animals SV 10 after 2 hours was 86 ± 6% (pH 7.32 ± .07). Eight animals were subject to shock, but their CPP was held at 100 mm Hg. These showed no difference in SV 10 from controls after 2 hours, although the pH had fallen to 6.90 ± .05. Reduction of CPP in these animals without correction of pH resulted in a rapid fall of SV 10 . In 10 animals subjected to shock for 2 hours, the arterial pH was maintained near 7.40 by infusion of ...

Journal of emergency and critical care medicine, 2021

Current Problems in Cardiology, 2009

Financial support by the Netherlands Heart Foundation for the publication of this thesis is gratefully acknowledged (Het verschijnen van dit proefschrift werd mede mogelijk gemaakt door steun van de Nederlandse Hartstichting).

Chest, 2019

Scientific statements and publications have recommended the use of vasoconstrictors as the first-line pharmacologic choice for most cases of cardiogenic shock (CS), without the abundance of strong clinical evidence. One challenge of guidelines is that the way recommendations are stated can potentially lead to oversimplification of complex situations. Except for acute coronary syndrome with CS, in which maintenance of coronary perfusion pressure seems logical prior to revascularization, physiologic consequences of increasing afterload by use of vasoconstrictors should be analyzed. Changing the CS conceptual frame, emphasizing inflammation and other vasodilating consequences of prolonged CS, mixes causes and consequences. Moreover, the considerable interpatient differences regarding the initial cause of CS and subsequent consequences on both macro-and microcirculation, argue for a dynamic, step-by-step, personalized therapeutic strategy. In CS, vasoconstrictors should be used only after a reasoning process, a review of other possible options, and then should be titrated to reach a reasonable pressure target, while checking cardiac output and organ perfusion.

Brazilian Journal of Medical and Biological Research, 2008

We evaluated the recovery of cardiovascular function after transient cardiogenic shock. Cardiac tamponade was performed for 1 h and post-shock data were collected in 5 domestic large white female pigs (43 ± 5 kg) for 6 h. The control group (N = 5) was observed for 6 h after 1 h of resting. During 1 h of cardiac tamponade, experimental animals evolved a low perfusion status with a higher lactate level (8.0 ± 2.2 vs 1.9 ± 0.9 mEq/L), lower standard base excess (-7.3 ± 3.3 vs 2.0 ± 0.9 mEq/L), lower urinary output (0.9 ± 0.9 vs 3.0 ± 1.4 mL·kg -1 ·h -1 ), lower mixed venous saturation, higher ileum partial pressure of CO 2 -end tidal CO 2 (EtCO 2 ) gap and a lower cardiac index than the control group. Throughout the 6-h recovery phase after cardiac tamponade, tamponade animals developed significant tachycardia with preserved cardiac index, resulting in a lower left ventricular stroke work, suggesting possible myocardial dysfunction. Vascular dysfunction was present with persistent systemic hypotension as well as persistent pulmonary hypertension. In contrast, oliguria, hyperlactatemia and metabolic acidosis were corrected by the 6th hour. The inflammatory characteristics were an elevated core temperature and increased plasma levels of interleukin-6 in the tamponade group compared to the control group. We conclude that cardiovascular recovery after a transient and severe low flow systemic state was incomplete. Vascular dysfunction persisted up to 6 h after release of tamponade. These inflammatory characteristics may also indicate that inflammatory activation is a possible pathway involved in the pathogenesis of cardiogenic shock.