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ACE-Inhibitor or ARB-Induced Refractory Hypotension Treated With Vasopressin in Patients Undergoing General Anesthesia for Dentistry: Two Case Reports
Caitlin M. WatersDDS,
Kristen PelczarDMD,
Edward C. AdlesicDMD,
Paul J. SchwartzDMD, and
Joseph A. Giovannitti JrDMD
Article Category: Case Report
Volume/Issue: Volume 69: Issue 3
Online Publication Date: Oct 06, 2022
DOI: 10.2344/anpr-69-02-06
Page Range: 30 – 35

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Figure 2; Renin angiotensin pathway. Angiotensinogen is a protein synthesized in the liver and released into the blood stream. Renin, an enzyme released by the juxtaglomerular cells, converts angiotensinogen to the inactive precursor, angiotensin I. Angiotensin-converting enzyme (ACE), found primarily on vascular endothelium, converts angiotensin I to the active molecule, angiotensin II. Angiotensin II is a potent vasoconstrictor, and also stimulates aldosterone release from the adrenal cortex. This increases sodium and water reabsorption in the kidney. ACE inhibitors limit the conversion of angiotensin I to angiotensin II and therefore act as vasodilators and also diminish sodium and water retention. These same effects can be produced by angiotensin-receptor blockers (ARBs) that act as antagonists at angiotensin II receptors on target tissues.
Daniel E. Becker
Figure 2
Figure 2

Renin angiotensin pathway. Angiotensinogen is a protein synthesized in the liver and released into the blood stream. Renin, an enzyme released by the juxtaglomerular cells, converts angiotensinogen to the inactive precursor, angiotensin I. Angiotensin-converting enzyme (ACE), found primarily on vascular endothelium, converts angiotensin I to the active molecule, angiotensin II. Angiotensin II is a potent vasoconstrictor, and also stimulates aldosterone release from the adrenal cortex. This increases sodium and water reabsorption in the kidney. ACE inhibitors limit the conversion of angiotensin I to angiotensin II and therefore act as vasodilators and also diminish sodium and water retention. These same effects can be produced by angiotensin-receptor blockers (ARBs) that act as antagonists at angiotensin II receptors on target tissues.

Figure 1.; Trend of cardiovascular vitals for case 1. Vasopressin stabilized labile hypotension unresponsive to standard vasopressors in a patient who continued angiotensin receptor blocker (ARB) therapy preoperatively.
Caitlin M. Waters,
Kristen Pelczar,
Edward C. Adlesic,
Paul J. Schwartz, and
Joseph A. Giovannitti Jr
Figure 1.
Figure 1.

Trend of cardiovascular vitals for case 1. Vasopressin stabilized labile hypotension unresponsive to standard vasopressors in a patient who continued angiotensin receptor blocker (ARB) therapy preoperatively.

Figure 2.; Trend of cardiovascular vitals for case 2. Vasopressin stabilized labile hypotension unresponsive to standard vasopressors in a patient who continued angiotensin-converting enzyme inhibitor (ACEI) therapy preoperatively.
Caitlin M. Waters,
Kristen Pelczar,
Edward C. Adlesic,
Paul J. Schwartz, and
Joseph A. Giovannitti Jr
Figure 2.
Figure 2.

Trend of cardiovascular vitals for case 2. Vasopressin stabilized labile hypotension unresponsive to standard vasopressors in a patient who continued angiotensin-converting enzyme inhibitor (ACEI) therapy preoperatively.

Figure 3.; Effects of angiotensin-converting enzyme inhibitor (ACEIs) and angiotensin receptor blockers (ARBs) on vasoconstriction. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by ACEIs or ARBs inhibits hormonal regulation of blood pressure (BP), leaving only the vasopressinergic system fully functional during general anesthesia.
Caitlin M. Waters,
Kristen Pelczar,
Edward C. Adlesic,
Paul J. Schwartz, and
Joseph A. Giovannitti Jr
Figure 3.
Figure 3.

Effects of angiotensin-converting enzyme inhibitor (ACEIs) and angiotensin receptor blockers (ARBs) on vasoconstriction. Inhibition of the renin-angiotensin-aldosterone system (RAAS) by ACEIs or ARBs inhibits hormonal regulation of blood pressure (BP), leaving only the vasopressinergic system fully functional during general anesthesia.

Figure 4.; Mechanism of vasopressinergic vs adrenergic vasoconstriction. Vasopressin (V1) receptor activation by vasopressin produces short-term vasoconstriction that increases vascular resistance and mean arterial pressure (MAP).14 V1 receptor agonists are effective in patients with severe hypotension and renin-angiotensin-aldosterone system (RAAS) blockade when conventional adrenergic treatment fails.15
Caitlin M. Waters,
Kristen Pelczar,
Edward C. Adlesic,
Paul J. Schwartz, and
Joseph A. Giovannitti Jr
Figure 4.
Figure 4.

Mechanism of vasopressinergic vs adrenergic vasoconstriction. Vasopressin (V1) receptor activation by vasopressin produces short-term vasoconstriction that increases vascular resistance and mean arterial pressure (MAP).14 V1 receptor agonists are effective in patients with severe hypotension and renin-angiotensin-aldosterone system (RAAS) blockade when conventional adrenergic treatment fails.15

Cardiovascular Drugs: Implications for Dental Practice Part 1 — Cardiotonics, Diuretics, and Vasodilators
Daniel E. BeckerDDS
Article Category: Research Article
Volume/Issue: Volume 54: Issue 4
Online Publication Date: Jan 01, 2007
DOI: 10.2344/0003-3006(2007)54[178:CDIFDP]2.0.CO;2
Page Range: 178 – 186

an endogenous vasoconstrictor that also promotes release of aldosterone, leading to sodium and water retention ( Figure 2 ). The angiotensin-converting enzyme (ACE) inhibitors block the formation of angiotensin II and thereby promote vasodilation and limit excessive retention of sodium and water. Enthusiasm for this drug class is understandable considering the role of arterial resistance and sodium retention in the pathogenesis of essential hypertension and congestive heart failure. 1 , 3 , 7 One is cautioned not to regard ACE inhibitors as diuretics; they do not

Changes in Blood Pressure During Induction of Anesthesia and Oral and Maxillofacial Surgery by Type and Timing of Discontinuation of Antihypertensive Drugs
Yoshihiro MomotaDDS, PhD,
Kazuhiro KanedaDDS, PhD,
Kumiko ArishiroMD, PhD,
Naotaka KishimotoDDS,
Seiji KanouDDS, and
Junichiro KotaniDDS, PhD
Article Category: Research Article
Volume/Issue: Volume 57: Issue 1
Online Publication Date: Jan 01, 2010
DOI: 10.2344/0003-3006-57.1.13
Page Range: 13 – 17

January 2003 to December 2005. Patients were classified into the following 5 groups by type of antihypertensive regimen described in their medical record: angiotensin receptor blockers (ARB) as monotherapy; calcium channel blockers (CCBs) as monotherapy; β-blockers as monotherapy; combination of ARB and CCBs; and combinations of CCBs, angiotensin converting enzyme (ACE) inhibitors, α-blockers, and β-blockers ( Table 1 ). After excluding patients receiving β-blockers as monotherapy because of the small number of patients in this category, comparisons among the remaining

Anesthetic Management of the Hypertensive Patient: Part I
Russell YanceyDDS
Article Category: Research Article
Volume/Issue: Volume 65: Issue 2
Online Publication Date: Jan 01, 2018
DOI: 10.2344/anpr-65-02-12
Page Range: 131 – 138

powerful feedback system for long-term control of arterial pressure and volume homeostasis. 11 The RAAS is stimulated by reduced cardiac output, decreased renal perfusion, hypovolemia, and decreased sodium intake. The stimulation of the RAAS traditionally begins with angiotensinogen, which is generated by the liver and cleaved by renin, released from the juxtaglomerular cells in the kidneys, in response to hypotension or decreased renal perfusion pressure, to form angiotensin I. Angiotensin I is further cleaved by angiotensin-converting enzyme (ACE) produced primarily

Confirmed Transmission of Hepatitis C in an Oral Surgery Office
Joel M. WeaverDDS, PhD
Article Category: Other
Volume/Issue: Volume 61: Issue 3
Online Publication Date: Jan 01, 2014
DOI: 10.2344/0003-3006-61.3.93
Page Range: 93 – 94

standard of care advanced, I have now witnessed two “game-changing” events that have forever changed how dental practices should be run. The first involved a dentist, David Acer, who in the late 1980s somehow infected 6 patients with HIV in his practice. However, only local anesthesia was used in those cases. That served as a wake-up call for dentistry, and the use of gloves in dentistry markedly increased after that event. The second major event is the one reported here. Although the use of rusty dental instruments could have been the cause of the HCV transmission, your