Patrick McQuillan

The Ohio State University, Columbus, OH, United States

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Publications (19)52.95 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: A reliable screening test for Coronary Artery Disease (CAD) in liver transplant (LT) candidates with end stage liver disease is essential because a high percentage of perioperative mortality and morbidity is CAD-related. In this study the effectiveness of Myocardial Perfusion Imaging (MPI) for identification of significant CAD in LT candidates was evaluated. Records of 244 patients meeting criteria for MPI were evaluated: 74 met inclusion criteria; 40 had a positive MPI and cardiology follow-up; 27 had a negative MPI and underwent LT; and 7 had a negative MPI and then had coronary angiography or a significant cardiac event. A selective MPI interpretation strategy was established where MPI-positive patients were divided into high, intermediate, and low CAD-risk groups. The overall incidence of CAD in this study population was 5.1% and our strategy resulted in PPV 20%, NPV 94%, sensitivity 80%, and specificity 50% for categorizing CAD risk. When applied only to the subset of patients categorized as high CAD-risk, the strategy was more effective, with PPV 67%, NPV 97%, sensitivity 80%, and specificity 94%. We determined that renal dysfunction was an independent predictive factor for CAD (p<0.0001, Odds Ratio=8.1), and grades of coronary occlusion correlated significantly with chronic renal dysfunction (p=0.0079).This article is protected by copyright. All rights reserved.
    Clinical Transplantation 01/2015; · 1.49 Impact Factor
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    ABSTRACT: In this report, we describe a case of posterior reversible encephalopathy syndrome in a female patient after deceased donor liver transplantation. She developed posterior reversible encephalopathy syndrome on postoperative day 3 and did not improve despite adjustments in immunosuppressive therapy. The patient had symptoms of severe brain edema requiring maximal therapy, which included cooling, mannitol, 3% saline, and a pentobarbital infusion. Attempts to lighten the level of sedation failed because of recurring intractable seizure activity. Reductions in therapeutic support were ultimately successful after 62 days of continuous pentobarbital therapy. The patient awoke neurologically intact and was discharged to a rehabilitation center in good condition.
    A & A case reports. 12/2014; 3(11):149-52.
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    ABSTRACT: Cardiac ischemia and angina pectoris are commonly experienced during exertion in a cold environment. In the current study we tested the hypotheses that oropharyngeal afferent blockade (i.e., local anesthesia of the upper airway with lidocaine) as well as systemic beta-adrenergic receptor blockade (i.e., intravenous propranolol) would improve the balance between myocardial oxygen supply and demand in response to the combined stimulus of cold air inhalation (-15 to -30° C) and isometric handgrip exercise (Cold + Grip). Young healthy subjects underwent Cold + Grip following lidocaine, propranolol, and control (no drug). Heart rate (HR), blood pressure, and coronary blood flow velocity (CBV, from Doppler echocardiography) were measured continuously. Rate pressure product (RPP) was calculated and changes from baseline were compared between treatments. The change in RPP at the end of Cold + Grip was not different between lidocaine (2441 ± 376) and control conditions (3159 ± 626); CBV responses were also not different between treatments. With propranolol, the HR (8 ± 1 versus 14 ± 3 bpm) and RPP responses to Cold + Grip were significantly attenuated. However, at peak exercise propranolol also resulted in a smaller ΔCBV (1.4 ± 0.8 versus 5.3 ± 1.4 cm/sec, P=0.035) such that the relationship between coronary flow and cardiac metabolism was impaired under propranolol (0.43 ± 0.37 versus 2.1 ± 0.63 au). These data suggest that cold air breathing and isometric exercise significantly influence efferent control of coronary blood flow. Additionally, beta-adrenergic vasodilation may play a significant role in coronary regulation during exercise.
    AJP Heart and Circulatory Physiology 05/2014; · 4.01 Impact Factor
  • S D Adhikary, A Hadzic, P M McQuillan
    BJA British Journal of Anaesthesia 11/2013; 111(5):844-845. · 4.24 Impact Factor
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    ABSTRACT: Tactile stimulation of the oropharynx (TSO) elicits the gag reflex and increases heart rate (HR) and mean arterial pressure (MAP) in anesthetized patients. However, the interaction between upper airway defense reflexes and the sympathetic nervous system has not been investigated in conscious humans. In Experiment 1, beat-by-beat measurements of HR, MAP, muscle sympathetic nerve activity (MSNA) and renal vascular resistance (RVR) were measured during TSO and tactile stimulation of the hard palate (Sham) in the supine posture. In Experiment 2, TSO was performed before and after inhalation of 4% lidocaine via nebulizer. Rate pressure product (RPP) was determined. Compared to Sham, TSO elicited the gag reflex and increased RPP (Δ36 ± 6 vs. 17 ± 5%), MSNA (Δ122 ± 39 vs 19 ± 19%) and RVR (Δ55 ± 11 vs. 4 ± 4%). This effect occurred within 1-2 cardiac cycles of TSO. The ΔMAP (12 ± 3 vs. 6 ± 1 mmHg) and the ΔHR (10 ± 3 vs. 3 ± 3 bpm) were also greater following TSO compared to Sham. Lidocaine inhalation blocked the gag reflex and attenuated increases in MAP (Δpre: 16 ± 2; Δpost: 5 ± 2 mmHg) and HR (Δpre: 12 ± 3; Δpost: 2 ± 2 bpm) in response to TSO. When mechanically stimulated, afferents in the oropharynx not only serve to protect the airway but also cause reflex increases in MSNA, RVR, MAP, and HR. An augmented sympathoexcitatory response during intubation and laryngoscopy may contribute to perioperative cardiovascular morbidity and mortality.
    Journal of Applied Physiology 04/2013; · 3.43 Impact Factor
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    ABSTRACT: We have recently shown that a saline infusion in the veins of an arterially occluded human forearm evokes a systemic response with increases in muscle sympathetic nerve activity (MSNA) and blood pressure. In this report, we examined whether this response was a reflex that was due to venous distension. Blood pressure (Finometer), heart rate, and MSNA (microneurography) were assessed in 14 young healthy subjects. In the saline trial (n = 14), 5% forearm volume normal saline was infused in an arterially occluded arm. To block afferents in the limb, 90 mg of lidocaine were added to the same volume of saline in six subjects during a separate visit. To examine whether interstitial perfusion of normal saline alone induced the responses, the same volume of albumin solution (5% concentration) was infused in 11 subjects in separate studies. Lidocaine abolished the MSNA and blood pressure responses seen with saline infusion. Moreover, compared with the saline infusion, an albumin infusion induced a larger (MSNA: Δ14.3 ± 2.7 vs. Δ8.5 ± 1.3 bursts/min, P < 0.01) and more sustained MSNA and blood pressure responses. These data suggest that venous distension activates afferent nerves and evokes a powerful systemic sympathoexcitatory reflex. We posit that the venous distension plays an important role in evoking the autonomic adjustments seen with postural stress in human subjects.
    AJP Heart and Circulatory Physiology 06/2012; 303(4):H457-63. · 4.01 Impact Factor
  • R Kapoor, S D Adhikary, C Siefring, P M McQuillan
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    ABSTRACT: Recently, ultrasound-guided saphenous nerve blocks within and distal to the adductor canal have shown success. However, a potential side effect is an unintentional block of branches of the nerve to the vastus medialis resulting in undesired motor weakness. We dissected 40 embalmed cadaver thighs to determine the course and relation of the saphenous nerve to the nerve to the vastus medialis. Measurements were taken between various landmarks, and descriptive statistics were used to present the collected data. In 72.5% of specimens, the most distal visible branch of the nerve to the vastus medialis pierced the muscle proximal to the site where the saphenous nerve crosses the anterior surface of the superficial femoral artery to become medial to the vessel. Knowledge of this anatomy may help establish a safe region in preventing motor blockade when performing saphenous nerve blocks.
    Acta Anaesthesiologica Scandinavica 03/2012; 56(3):365-7. · 2.36 Impact Factor
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    ABSTRACT: Cold storage in any of the commonly used preservation solutions is not always adequate for donation after cardiac death (DCD) liver grafts due to prolonged warm ischemic time. In this study, we used a third-generation perfluorocarbon (PFC), Oxycyte, for DCD liver graft preservation in a rat model. Twenty-eight rats (14 in each group) were used. Thirty minutes after cardiopulmonary arrest, livers were harvested and flushed with a cold and pre-oxygenated solution of either University of Wisconsin (UW) or UW + 20% PFC. After 8 h of cold preservation in either of the investigated solutions, liver graft specimens were analyzed for evidence of ischemic injury. Hemotoxylin and eosin staining (H and E), as well as immunohistochemical analysis with anti-cleaved caspase 3 antibody, was performed. Levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in the preservation solution were analyzed at 1 and 8 h during preservation. In the PFC group, the degree of cell congestion, vacuolization and necrosis were all significantly less than in the UW group (P = 0.002-0.004). The number of cells with a positive cleaved caspase 3 antibody reaction was reduced by about 50% in comparison with the UW group (P < 0.006). The AST level in the PFC group was significantly less than in the UW group after 8 h of preservation (P < 0.048). The addition of PFC to UW solution significantly decreases the degree of histologic damage in rat DCD liver grafts. This preservation strategy can be potentially helpful for organ preservation after prolonged warm ischemia.
    Journal of Surgical Research 04/2011; 175(1):131-7. · 2.12 Impact Factor
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    ABSTRACT: The objectives of this prospective, observational study were (1) to determine whether a transplanted liver graft releases proinflammatory cytokines into the systemic circulation upon reperfusion and (2) to determine whether they contribute to any subsequent hemodynamic instability observed after graft reperfusion (if this release occurs). Blood samples from 17 consecutive patients undergoing liver transplantation were analyzed for cytokines, including tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), IL-2, IL-6, and IL-8. Blood samples were obtained from the radial artery, portal vein, and flush blood (a sample taken from a catheter placed above the infrahepatic inferior vena cava clamp). The amount of catecholamines necessary to maintain a mean arterial pressure between 65 and 75 mm Hg during graft reperfusion was compared with the level of cytokines. A statistical analysis was performed with the least squares method, Kendall's tau-b test, and regression analysis. We demonstrated that flush blood from the liver grafts contained a significant amount and variety of cytokines. Most of these were removed by graft irrigation. The concentration of TNF-α in samples obtained from flush blood at the end of liver irrigation was significantly higher than the concentration in samples obtained from the radial artery (P = 0.0067) or portal vein (P = 0.0003) before reperfusion. This correlated directly with the amount of catecholamines used to treat hemodynamic instability. Although there were increased levels of IL-1β, IL-2, and IL-8 in the flush blood, there was no statistically significant correlation between the levels of these cytokines and the amount of catecholamines used.
    Liver Transplantation 03/2011; 17(3):324-30. · 3.79 Impact Factor
  • Jian Cui, Patrick McQuillan, Lawrence I Sinoway
    CIRCULATION; 01/2011
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    ABSTRACT: Refractory hypotension is a frequent event during reperfusion of a liver graft. Measures that help maintain hemodynamic stability include correction of electrolytes and acid-base abnormalities as well as administration of fluid and/or catecholamines. Vasoplegic syndrome represents the most severe form of hemodynamic instability. Management of this condition is very difficult due primarily to the inadequate response to even very high doses of catecholamines. A 60-year-old patient presented for liver transplantation due to end stage liver disease. After an initially uneventful hepatic phase, the patient developed excessive tachycardia and refractory hypotension during cross-clamping of the vena cava. The situation rapidly deteriorated despite administration of fluid and extremely high doses of norepinephrine and vasopressin. A transesophageal echocardiogram (TEE) performed at that time failed to demonstrate any cardiac dysfunction or signs of pulmonary emboli. Subsequent blood cultures and imaging studies did not confirm any signs of sepsis. Further investigation revealed an increased preoperative level of cyclic guanosine monophosphate (cGMP). cGMP is the second messenger for nitric oxide, and is responsible for relaxation of vascular smooth muscle with subsequent vasodilatation. This finding suggests a release of nitric oxide in the systemic circulation which could have been a potential cause for vasoplegic shock. Release of nitric oxide in the systemic circulation can be a potential cause of vasoplegic syndrome. Future investigation will demonstrate whether a patient's preoperative cGMP plasma level can be a potential predictor of intraoperative hemodynamic instability.
    Medical science monitor: international medical journal of experimental and clinical research 09/2010; 16(9):CS114-7. · 1.22 Impact Factor
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    ABSTRACT: We present a case of severe hyperammonemia with subsequent brain herniation in an adult man after renal transplantation. After successful surgery and an initially uneventful postoperative course, the patient developed significant mental status changes associated with seizure activity. His condition rapidly deteriorated, requiring mechanical ventilation and cardiovascular support. Laboratory studies at that time demonstrated an increased serum ammonia level without evidence of liver or kidney dysfunction. Further investigation revealed an increased orotic acid level in the urine, suggesting a urea cycle disorder (UCD). Despite aggressive therapy, the patient's condition continued to deteriorate. Magnetic resonance imaging demonstrated severe brain edema with no cerebral perfusion; after consultation with the family, care was withdrawn. The combination of hyperammonemia and elevated urine orotic acid with normal liver and kidney function suggested a UCD. It is important to note that patients with a UCD may be free of symptoms for many years. Several factors are able to trigger the disease in adulthood, leading to encephalopathy and death. In this case, the patient's seizures were initially assumed to be a side effect of immunosuppressive therapy. Further diagnostic measures were only performed late in the course of the disease, which delayed the diagnosis of UCD.
    Transplantation Proceedings 06/2010; 42(5):1982-5. · 0.95 Impact Factor
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    ABSTRACT: Obstructive sleep apnea (OSA) is associated with increased sympathetic nerve activity, endothelial dysfunction, and premature cardiovascular disease. To determine whether hypoxia is associated with impaired skeletal muscle vasodilation, we compared femoral artery blood flow (ultrasound) and muscle sympathetic nerve activity (peroneal microneurography) during exposure to acute systemic hypoxia (fraction of inspired oxygen 0.1) in awake patients with OSA (n=10) and controls (n=8). To assess the role of elevated sympathetic nerve activity, in a separate group of patients with OSA (n=10) and controls (n=10) we measured brachial artery blood flow during hypoxia before and after regional alpha-adrenergic block with phentolamine. Despite elevated sympathetic activity, in OSA the vascular responses to hypoxia in the leg did not differ significantly from those in controls [P=not significant (NS)]. Following regional phentolamine, in both groups the hypoxia-induced increase in brachial blood flow was markedly enhanced (OSA pre vs. post, 84+/-13 vs. 201+/-34 ml/min, P<0.002; controls pre vs. post 62+/-8 vs. 140+/-26 ml/min, P<0.01). At end hypoxia after phentolamine, the increase of brachial blood flow above baseline was similar (OSA vs. controls +61+/-16 vs. +48+/-6%; P=NS). We conclude that despite high sympathetic vasoconstrictor tone and prominent sympathetic responses to acute hypoxia, hypoxia-induced limb vasodilation is preserved in OSA.
    Journal of Applied Physiology 03/2010; 108(5):1234-40. · 3.43 Impact Factor
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    ABSTRACT: Animal studies have shown that the increased intravenous pressure stimulates the group III and IV muscle afferent fibres, and in turn induce cardiovascular responses. However, this pathway of autonomic regulation has not been examined in humans. The aim of this study was to examine the hypothesis that infusion of saline into the venous circulation of an arterially occluded vascular bed evokes sympathetic activation in healthy individuals. Blood pressure, heart rate, and muscle sympathetic nerve activity (MSNA) responses were assessed in 19 young healthy subjects during local infusion of 40 ml saline into a forearm vein in the circulatory arrested condition. From baseline (11.8 +/- 1.2 bursts min(-1)), MSNA increased significantly during the saline infusion (22.5 +/- 2.6 bursts min(-1), P < 0.001). Blood pressure also increased significantly during the saline infusion. Three control trials were performed during separate visits. The results from the control trial show that the observed MSNA and blood pressure responses were not due to muscle ischaemia. The present data show that saline infusion into the venous circulation of an arterially occluded vascular bed induces sympathetic activation and an increase in blood pressure. We speculate that the infusion under such conditions stimulates the afferent endings near the vessels, and evokes the sympathetic activation.
    The Journal of Physiology 07/2009; 587(Pt 14):3619-28. · 4.38 Impact Factor
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    ABSTRACT: During exercise, muscle mechanoreflex-mediated sympathoexcitation evokes renal vasoconstriction. Animal studies suggest that prostaglandins generated within the contracting muscle sensitize muscle mechanoreflexes. Thus we hypothesized that local prostaglandin blockade would attenuate renal vasoconstriction during ischemic muscle stretch. Eleven healthy subjects performed static handgrip before and after local prostaglandin blockade (6 mg ketorolac tromethamine infused into the exercising forearm) via Bier block. Renal blood flow velocity (RBV; Duplex Ultrasound), mean arterial pressure (MAP; Finapres), and heart rate (HR; ECG) were obtained during handgrip, post-handgrip muscle ischemia (PHGMI) followed by PHGMI with passive forearm muscle stretch (PHGMI + stretch). Renal vascular resistance (RVR, calculated as MAP/RBV) was increased from baseline during all paradigms except during PHGMI + stretch after the ketorolac Bier block trial where RVR did not change from baseline. Before Bier block, RVR rose more during PHGMI + stretch than during PHGMI alone (P < .01). Similar results were found after a saline Bier block trial (Delta53 +/- 13% vs. Delta35 +/- 10%; P < 0.01). However, after ketorolac Bier block, RVR was not greater during PHGMI + stretch than during PHGMI alone [Delta39 +/- 8% vs. Delta40 +/- 12%; P = not significant (NS)]. HR and MAP responses were similar during PHGMI and PHGMI + stretch (P = NS). Passive muscle stretch during ischemia augments renal vasoconstriction, suggesting that ischemia sensitizes mechanically sensitive afferents. Inhibition of prostaglandin synthesis eliminates this mechanoreceptor sensitization-mediated constrictor responses. Thus mechanoreceptor sensitization in humans is linked to the production of prostaglandins.
    AJP Heart and Circulatory Physiology 06/2008; 294(5):H2184-90. · 4.01 Impact Factor
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    ABSTRACT: The extent to which sympathetic nerve activity restrains metabolic vasodilation in skeletal muscle remains unclear. We determined forearm blood flow (FBF; ultrasound/Doppler) and vascular conductance (FVC) responses to 10 min of ischemia [reactive hyperemic blood flow (RHBF)] and 10 min of systemic hypoxia (inspired O(2) fraction = 0.1) before and after regional sympathetic blockade with the alpha-receptor antagonist phentolamine via Bier block in healthy humans. In a control group, we performed sham Bier block with saline. Consistent with alpha- receptor inhibition, post-phentolamine, basal FVC (FBF/mean arterial pressure) increased (pre vs. post: 0.42 +/- 0.05 vs. 1.03 +/- 0.21 units; P < 0.01; n = 12) but did not change in the saline controls (pre vs. post: 0.56 +/- 0.14 vs. 0.53 +/- 0.08 units; P = not significant; n = 5). Post-phentolamine, total RHBF (over 3 min) increased substantially (pre vs. post: 628 +/- 75 vs. 826 +/- 92 ml/min; P < 0.01) but did not change in the controls (pre vs. post: 618 +/- 66 vs. 661 +/- 35 ml/min; P = not significant). In all conditions, compared with peak RHBF, peak skin reactive hyperemia was markedly delayed. Furthermore, post-phentolamine (pre vs. post: 0.43 +/- 0.06 vs. 1.16 +/- 0.17 units; P < 0.01; n = 8) but not post-saline (pre vs. post: 0.93 +/- 0.16 vs. 0.87 +/- 0.19 ml/min; P = not significant; n = 5), the FVC response to hypoxia (arterial O(2) saturation = 77 +/- 1%) was markedly enhanced. These data suggest that sympathetic vasoconstrictor nerve activity markedly restrains skeletal muscle vasodilation induced by local (forearm ischemia) and systemic (hypoxia) vasodilator stimuli.
    AJP Heart and Circulatory Physiology 10/2007; 293(4):H2289-95. · 4.01 Impact Factor
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    ABSTRACT: Animal studies suggest that prostaglandins in skeletal muscles stimulate afferents and contribute to the exercise pressor reflex. However, human data regarding a role for prostaglandins in this reflex are varied, in part because of systemic effects of pharmacological agents used to block prostaglandin synthesis. We hypothesized that local blockade of prostaglandin synthesis in exercising muscles could attenuate muscle sympathetic nerve activity (MSNA) responses to fatiguing exercise. Blood pressure (Finapres), heart rate, and MSNA (microneurography) were assessed in 12 young healthy subjects during static handgrip and postexercise muscle ischemia (PEMI) before and after local infusion of 6 mg of ketorolac tromethamine in saline via Bier block (regional intravenous anesthesia). In the second experiment (n = 10), the same amount of saline was infused via the Bier block. Ketorolac Bier block decreased the prostaglandins synthesis to approximately 33% of the baseline. After ketorolac Bier block, the increases in MSNA from the baseline during the fatiguing handgrip was significantly lower than that before the Bier block (before ketorolac: Delta502 +/- 111; post ketorolac: Delta348 +/- 62%, P = 0.016). Moreover, the increase in total MSNA during PEMI after ketorolac was significantly lower than that before the Bier block (P = 0.014). Saline Bier block had no similar effect. The observations indicate that blockade of prostaglandin synthesis attenuates MSNA responses seen during fatiguing handgrip and suggest that prostaglandins contribute to the exercise pressor reflex.
    AJP Heart and Circulatory Physiology 10/2007; 293(3):H1861-8. · 4.01 Impact Factor
  • The FASEB Journal 01/2007; 21:613-8. · 5.48 Impact Factor
  • CIRCULATION; 01/2006