Effect of lactic acidosis on canine hemodynamics and left ventricular function

Area of Science:

• Physiology
• Cardiovascular Research
• Acid-Base Balance

Background:

• Hypoperfusion states can lead to lactic acidosis, creating a cycle where acidemia further impairs cardiac output.
• The detrimental effects of lactic acidosis on cardiac output are hypothesized to stem from either direct myocardial depression or impaired venous return/right ventricular dysfunction.

Purpose of the Study:

• To investigate the mechanisms underlying reduced cardiac output during progressive lactic acidosis.
• To differentiate between myocardial depression and altered venous return as causes of decreased cardiac output in this condition.

Main Methods:

• Utilized anesthetized, mechanically ventilated dogs.
• Infused 0.5 N lactic acid to induce progressive acidemia.
• Measured left ventricular pressure-volume relationships using ultrasonic crystals and a catheter-tipped transducer.
• Monitored cardiac output, stroke volume, systemic arterial pressure, pulmonary artery pressure, and right atrial pressure.

Main Results:

• Lactic acidosis significantly reduced cardiac output, stroke volume, and mean systemic arterial pressure.
• Mean pulmonary artery pressure and right atrial pressure increased significantly during acidemia.
• Stroke volume reduction was attributed to depressed left ventricular contractility (decreased maximum dP/dt and Emax), without changes in left ventricular end-diastolic volume.
• Pulmonary hypertension occurred, potentially masking expected responses to myocardial depression.

Conclusions:

• Progressive lactic acidosis in dogs impairs cardiac output primarily through direct depression of left ventricular contractility.
• Reduced venous return or hypovolemia were not the main drivers of decreased cardiac output in this model.
• Acidemia-induced pulmonary hypertension may influence the overall cardiovascular response.