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Ketamine’s effects develop out of changes in the brain’s glutamate neurotransmitter levels. Glutamate chemical levels work to maintain a normal level of activity between the brain’s cells. This process enables the brain and body to communicate with one another on a continuous basis. Ketamine’s ability to interfere with cardiovascular functions does come with considerable risks, one of which being cardiac arrest. We would like to express our gratitude to the patient for allowing us to share her clinical history in this case report.

• ECGs were obtained prior to sedation and during the sedation approximately one minute after administration of ketamine.
• So ketamine misapplication is not only a drug abuse problem, but could also cause long-term disruption of the cardiovascular system.
• The extra work done by the heart eventually starts to damage the cells and tissues that make up the heart muscle.
• Collagen volume fraction (CVF) in each field was assessed by the digital medical image analysis system.
• The cardiovascular stimulation-inhibition balance of ketamine may be altered by severe critical illness, and the doses of any induction agent should be significantly reduced in critically ill patients.

Adverse effects

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Figure 6.

• Growing evidence suggests that long-term abuse of ketamine does harm the heart and increases the risk of sudden death.
• This can cause an increase in oxygen consumption, as well, that could attribute to observed cardiac effects, specifically in patients with underlying cardiac disease 4-6.
• However, as ketamine relies on a secondary sympathomimetic effect for its cardiovascular stability, cardiovascular and hemodynamic compromise may occur in patients who are catecholamine depleted.
• ECGs were reviewed for any ischemic changes from the baseline to post-ketamine ECG, with the two ECGs directly compared to one another.

Ketamine’s clinical and antidepressant effects can be influenced by co-administration of other drugs, though these interactions are variable and not yet fully understood. A 28-year-old female with a history of ketamine use disorder with multiple genitourinary complications presented with progressive bilateral lower extremity oedema that started 3 months prior. She also reported shortness of breath, orthopnoea, chronic cough, and decreased exercise tolerance. She reported using ketamine twice weekly along with smoking half a pack of cigarettes daily.

Respiratory System Ketamine is a potent bronchodilator suitable for anesthetizing patients at high risk for bronchospasm. Contraindications And PrecautionsKetamine is contraindicated in patients for whom a significant elevation of blood pressure would constitute a serious hazard , such as those with uncontrolled hypertension, aneurysm, thyrotoxicosis, or a history of stroke. Monitor patients with increased intracranial pressure in a setting with frequent neurologic assessments.

Figure 3. Baseline ECG on Second Visit.

After 15–25 min, they recovered completely without any treatment, but looked tired. These reactions lasted for 1–3 min after injection, and full recovery required 15–25 min. With chronic ketamine abuse, one or more of the above symptoms can escalate to the point where cardiac arrest occurs. Due to its hemodynamic stability, ketamine is a commonly used anesthetic agent for sedation during small procedures in the critical care unit.

Given their relative hemodynamic stability, ketamine and etomidate are commonly chosen anesthetic agents for sedation during the endotracheal intubation of critically ill patients. As the use of etomidate has come into question particularly in patients with sepsis, due to its effect of adrenal suppression, there has been a shift in practice with more reliance on ketamine. However, as ketamine relies on a secondary sympathomimetic effect for its cardiovascular stability, cardiovascular and hemodynamic compromise may occur in patients who are catecholamine depleted.

Ketamine Effects on Heart Function

Masson’s trichrome staining was performed exactly according to the manufacturer’s protocols (Maxin Biotechnology, Fuzhou, China). Five horizontal fields randomly selected in each slice were analysed under a light microscope, excluding blood vessels and perivascular interstitial cells. Collagen volume fraction (CVF) in each field was assessed by the digital medical image analysis system. Drug and molecular target nomenclature conforms to the British Journal of Pharmacology’s Guide to Receptors and Channels (Alexander et al., 2011).

In this study, changes in NF-κB expression showed a similar trend to those of PARP-1. In looking at the incidence of new changes suggestive of myocardial ischemia apparent on ECG immediately following administration of ketamine, it is interesting that an occurrence rate of almost 10% was shown in this study with such a small sample size. It is also notable that all of the patients who experienced ischemia were females.

PARP is a protein involved with a series of cellular processes including DNA repair and programmed cell death, cardiac hypertrophy and fibrosis. We observed that after chronic treatment with ketamine, PARP-1 expression was significantly elevated, suggesting its role in ketamine-induced apoptosis and fibrosis. AIF is involved in a caspase-independent pathway of apoptosis by translocating to the nucleus and causing large-scale DNA fragmentation and chromatin condensation. Translocation of AIF from mitochondria to the nucleus is required for PARP-1-mediated cell death (Kang et al., 2004).

The mechanism of action is primarily due to antagonism of N-methyl-D-aspartate (NMDA receptors) in the central nervous system. Ketamine can produce nystagmus with pupillary dilation, salivation, lacrimation, and spontaneous limb movements with increased muscle tone through indirect sympathomimetic activity. Cardiovascular System Ketamine increases blood pressure, heart rate, and cardiac output. Cardiovascular effects of ketamine are indirect and believed to be mediated by inhibition of both central and peripheral catecholamine reuptake. Elevation of blood pressure reaches a maximum within a few minutes of injection and usually returns to preanesthetic values within 15 minutes. In the majority of cases, the systolic and diastolic blood pressure peaks from 10% to 50% above preanesthetic levels shortly after induction of anesthesia, but the elevation can be higher or longer in individual cases.

Links to NCBI Databases

The total number of TUNEL-positive cells per field was calculated by digital medical image analysis system. The study took place at an academic medical center with a level-one trauma designation that serves as a regional referral center for orthopedic injuries and other specialty care. Ketamine’s ability to interfere with glutamate production naturally disrupts the brain’s electrical activity. Considering how nerve impulses rely on a stable level of electrical activity to function normally, this level of interference hampers the brain’s ability to communicate with the cardiovascular system.

One minute was chosen as evaluation time, given the onset of intravenous ketamine being estimated at 30 seconds. ECGs were only obtained for the purpose of the study and were not standard of care at this institution for patients undergoing a procedural sedation. ECGs were obtained on Mortara ELI 350 and ELI 380 machines (Mortara Instrument Inc., Milwaukee, WI). ECGs were reviewed by the physician performing the sedation during acute care for any abnormal findings. Due to the real-time interpretation, any abnormal ECG findings does ketamine cause cardiac arrest were addressed during the ED visit with any necessary follow-up evaluations ordered. For study analysis, ECGs were reviewed by a board-certified emergency medicine physician and a board-certified cardiologist.

Thus, a single dose of ketamine produced decreases in cardiac and pulmonary performance and in peripheral oxygen transport in this group of patients. It is proposed that in severely ill patients, preoperative stress may alter the usual physiologic responses to ketamine administration, and adverse effects may predominate. Ketamine, therefore, should be used with caution for induction of anesthesia in critically ill and in acutely traumatized patients until additional studies and further information on cardiovascular responses to ketamine are available.