Concepts in the Pharmacologic and Nonpharmacologic Support of Cardiovascular Function in Critically Ill Surgical Patients

Sibbald, William J.; Calvin, James E.; Holliday, Ronald L.; Driedger, Albert A.

doi:10.1016/s0039-6109(16)42991-9

Cited by 40 publications

(6 citation statements)

References 58 publications

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“…The main mechanism used by tissues to preserve aerobic metabolism during low‐flow states is increased oxygen extraction. As oxygen delivery decreases, a point is reached (critical DO 2 ) at which oxygen extraction cannot be further increased in order to support adequate tissue oxygenation and aerobic metabolism 6,39,40 . At this point, anaerobic metabolism ensues, and lactate is produced.…”

Section: Causes Of Lactic Acidosismentioning

confidence: 99%

“…An increase in cardiac output can partially compensate for decreased blood oxygen content from anemia or hypoxemia. Compensation for hypoperfusion that is a result of hypovolemia or inadequate cardiac output is more difficult because no acute mechanism exists to effectively increase oxygen content 40 . A combination of hypoperfusion and decreased blood oxygen content can further complicate situations.…”

Section: Causes Of Lactic Acidosismentioning

confidence: 99%

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Lactate: physiology and clinical utility

Allen

Holm

2008

J Vet Emergen Crit Care

138

113

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Objective: To review the physiology of lactate production and metabolism, the causes of lactic acidosis, and the current applications of lactate monitoring in humans and animals. Data sources: Human and veterinary studies. Summary: Lactate production is the result of anaerobic metabolism. Tissue hypoxia due to hypoperfusion is the most common cause of lactic acidosis. Studies in critically ill humans have shown that serial lactate monitoring can be used to assess the severity of illness and response to therapy. Several veterinary studies have also shown lactate as a useful tool to assess severity of illness. Conclusions: Lactate measurement in critically ill veterinary patients is practical and can provide information to assess severity of illness. Further veterinary studies are needed to establish the value of serial lactate measurements for prognostic and therapeutic purposes. Information regarding lactate measurement in cats is limited, and further studies are warranted.

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Section: Causes Of Lactic Acidosismentioning

confidence: 99%

Section: Causes Of Lactic Acidosismentioning

confidence: 99%

Lactate: physiology and clinical utility

Allen

Holm

2008

J Vet Emergen Crit Care

138

113

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“…RVEDV must also increase to maintain right ventricular stroke volume and cardiac output [3]. Increases in RVEDV can occur by increasing circulatory blood volume or by increasing peripheral vascular resistance [4]. Transmural pressure may increase secondary to increases in left ventricular filling, as in acute left ventricular failure, or by increases in PVR.…”

Section: Pulmonary Vascular Resistance and Ventricular Performancementioning

confidence: 99%

“…This augmented filling of the right ventricle (RV) may result in a transient shift of the intraventricular septum from its neutral position into the left ventricle, particularly when PVR is abnormally high. If the RV dilates, left ventricular diastolic compliance will be reduced, decreasing left ventricular end diastolic volume (LVEDV), but not left ventricular end diastolic pressure (LVEDP) [4]. This process may explain the ventilation-induced changes in arterial pulse pressure characteristic of pulsus paradoxus [5].…”

Section: Diastolic Ventricular Interactionmentioning

confidence: 99%

Hemodynamic Consequences of Heart-Lung Interactions

Steingrub

Tidswell

Higgins

2003

J Intensive Care Med

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The management of critically ill patients requires a fundamental understanding of cardiopulmonary interactions associated with mechanical ventilation. The hemodynamic changes due to ventilation are a result of changes in lung volume and intrathoracic pressure (ITP) and can occur during spontaneous or positive pressure ventilation despite constant tidal volumes. Pulmonary vascular resistance (PVR) and mechanical heart-lung interactions play prominent roles in determining the hemodynamic response to mechanical ventilation. Lung inflation alters PVR and right ventricular wall tension and, at high lung volume, mechanically limits cardiac volumes. The authors will consider the mechanisms of the effects of ITP on the pulmonary arterial and venous branches. These effects will aid in understanding the complex interactions between ventilation and right and left ventricular pressures and volumes, as well as the influence of lung inflation pressure on ventricular interdependence.

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“…For RV stroke volume, and thus cardiac output, to remain constant, RV end-diastolic volume must increase further (25,29). This can be accompIished by increasing either the circulating blood volume (fluid retention or intravascular volume infusion) or the peripheral vasomotor tone (30). Transmural Ppa may increase during ventilation because of an increase in either LV filling pressure, as in acute LV dysfunction, or pulmonary vascular resistance.…”

Section: Pulmonary Vascular Resistancementioning

confidence: 99%

Cardiovascular Effects of Ventilatory Support and Withdrawal

Pinsky

1994

Anesthesia & Analgesia

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rtificial ventilation by the application of intermittent positive airway pressure and the ad-A dition of supplemental inspired 0, represents the mainstay of support in patients with respiratory failure. However, positive-pressure ventilation results in complex cardiovascular interactions that may alter blood flow in unexpected ways, thus potentially modulating 0, delivery to the body independent of its effects on arterial 0, content. The primary function of the cardiovascular-respiratory system is to deliver adequate amounts of 0, to meet the metabolic demands of the body. Oxygen delivery is equal to the product of arterial 0, content and cardiac output. Thus, if either decreases far enough, 0, delivery to the tissues will become compromised. The treatment of critically ill patients requires an understanding of cardiopulmonary interactions associated with both mechanical ventilation and the use of positive end-expiratory pressure (PEEP). Clinically, hemodynamic instability or a change associated with artificial ventilation usually occurs when ventilatory support is either added or withdrawn, rather than when ventilatory support is constant. The goal of this review is to clarify how cardiovascular function is altered by starting or stopping various ventilatory maneuvers.Clinically relevant heart-lung interactions can be conveniently grouped into four basic concepts. These concepts can be considered separately, but they often coexist in the same clinical situation. They are: a) ventilation is exercise, requiring increased organ blood flow and oxygen consumption; b) inspiration increases lung volume above end-expiratory values; c) spontaneous inspiration decreases pleural pressure; and d) positive-pressure ventilation increases pleural pressure.

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Concepts in the Pharmacologic and Nonpharmacologic Support of Cardiovascular Function in Critically Ill Surgical Patients

Cited by 40 publications

References 58 publications

Lactate: physiology and clinical utility

Lactate: physiology and clinical utility

Hemodynamic Consequences of Heart-Lung Interactions

Cardiovascular Effects of Ventilatory Support and Withdrawal

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