chapter 11. quiz 3. Systemic Vasoactive drugs
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Questions and Answers

What effect does the ACE inhibitor enalapril have on cerebral blood flow?

  • No significant effect on CBF (correct)
  • Decreases CBF
  • Increases CBF
  • Maintains CBF at pre-hypotensive levels

    • Why are the effects of anesthetics that vasodilate the cerebral circulation on ICP less dramatic when hypotension is slowly induced?

  • They have no effect on ICP
  • They increase CSF pressure
  • They decrease CBV
  • Reflect more effective compensatory mechanisms (correct)

    • Which drugs are mentioned as inducing hypotension and causing cerebral vasodilation?

  • Antibiotics and antivirals
  • Amphetamines and steroids
  • Sodium nitroprusside and hydralazine (correct)
  • Antacids and laxatives

    • How do anesthetics that vasodilate the cerebral circulation affect cerebral blood volume (CBV)?

    <p>Increase CBV</p> Signup and view all the answers

    What is a key factor determining the effects of vasoactive drugs on cerebral physiology?

    <p>The status of the autoregulation mechanism</p> Signup and view all the answers

    How do catecholamine agonists and antagonists affect cerebral physiology?

    <p>Dependent on basal arterial blood pressure, autoregulation mechanism status, and BBB status</p> Signup and view all the answers

    How do the effects of vasoactive drugs on cerebral physiology differ depending on autoregulation status?

    <p>They have both direct effects on cerebral vascular smooth muscle and indirect effects mediated by the autoregulatory response.</p> Signup and view all the answers

    What happens to cerebral blood flow (CBF) when autoregulation is preserved and systemic arterial pressure is outside the limits of autoregulation?

    <p>CBF increases</p> Signup and view all the answers

    What is the primary mechanism by which normal autoregulation maintains constant cerebral blood flow (CBF) despite rising mean arterial pressure (MAP)?

    <p>Cerebral vasoconstriction</p> Signup and view all the answers

    In a situation where autoregulation is defective, how does cerebral blood flow (CBF) change in relation to arterial pressure?

    <p>CBF varies directly with arterial pressure</p> Signup and view all the answers

    What determines the effects of vasoactive drugs on cerebral physiology according to the provided text?

    <p>Basal arterial blood pressure, autoregulation status, and drug-induced arterial blood pressure changes</p> Signup and view all the answers

    How does preserved autoregulation impact cerebral blood flow when systemic arterial pressure rises within the normal autoregulatory range?

    <p>Cerebral blood flow remains constant due to maintained autoregulation</p> Signup and view all the answers

    in which case CBF is maintained at lower MAP values due to hypotension ?

    <p>when hypotension is induced with a cerebral vasodilator</p> Signup and view all the answers

    How does the administration of α1-agonists like norepinephrine and phenylephrine affect cerebral blood flow (CBF) in healthy patients?

    <p>Maintain or augment CBF</p> Signup and view all the answers

    In patients with relative hypotension, what effect does the α1-agonist midodrine have on cerebral perfusion?

    <p>Increase perfusion pressure and flow velocity</p> Signup and view all the answers

    What effect do β-mimetic drugs, such as norepinephrine with β1 activity, have on cerebral metabolism and cerebral blood flow?

    <p>mays Cause activation of cerebral metabolism and a coupled increase in CBF</p> Signup and view all the answers

    What impact does the administration of norepinephrine have on cerebral blood flow (CBF) when autoregulation is defective or its limit is exceeded?

    <p>Increases CBF as a result of autoregulation impairment</p> Signup and view all the answers

    What happens to cerebral blood flow when β-mimetic drugs, like norepinephrine with β1 activity, gain greater access to the brain parenchyma via a defective BBB?

    <p>Increase in cerebral blood flow</p> Signup and view all the answers

    How does the administration of phenylephrine during cardiopulmonary bypass impact cerebral blood flow (CBF)?

    <p>Has no effect on CBF</p> Signup and view all the answers

    How does phenylephrine administration affect regional cerebral oxygen saturation (rSO2) according to the text?

    <p>Modestly reduces rSO2</p> Signup and view all the answers

    What is a reason why ephedrine did not reduce regional cerebral oxygen saturation (rSO2) like phenylephrine?

    <p>Maintains cardiac output</p> Signup and view all the answers

    What impact did norepinephrine administration have on cerebral oxygen saturation according to the text?

    <p>Slightly reduced MCAfv and Sco2</p> Signup and view all the answers

    Why is a modest reduction in Sco2 not considered evidence of impairment of cerebral oxygenation during vasopressor administration?

    <p>Sco2 measurements are sensitive to extracranial contamination</p> Signup and view all the answers

    What is the primary mechanism by which dexmedetomidine primarily affects cerebral blood flow (CBF)?

    <p>Suppression of cerebral metabolic rate (CMR)</p> Signup and view all the answers

    Which of the following accurately describes the effect of dexmedetomidine on cerebral blood flow (CBF) based on the text?

    <p>The reduction in CBF with dexmedetomidine is proportionate to the decrease in CMR.</p> Signup and view all the answers

    Which drug is described as a significantly less specific and less potent α2-agonist compared to dexmedetomidine?

    <p>Clonidine</p> Signup and view all the answers

    How did dexmedetomidine impact cerebral blood flow (CBF) in healthy human volunteers during investigation?

    <p>Reduced CBF by approximately 30%</p> Signup and view all the answers

    What was observed about the relationship between middle cerebral artery flow velocity (MCAfv) and cerebral metabolic rate (CMR) under the influence of dexmedetomidine?

    <p>MCAfv decreased in parallel with a reduction in CMR</p> Signup and view all the answers

    How does epinephrine affect cerebral blood flow (CBF) and cerebral metabolic rate (CMR) in nonanesthetized humans when the mean arterial pressure (MAP) does not substantially change?

    <p>Has no effect on CBF and CMR</p> Signup and view all the answers

    What effect does dobutamine have on cerebral blood flow (CBF) independent of its impact on blood pressure?

    <p>Increases CBF by 20%</p> Signup and view all the answers

    When the blood-brain barrier (BBB) is impaired, what is the effect of intracarotid norepinephrine on cerebral blood flow (CBF) and cerebral metabolic rate (CMR)?

    <p>Significantly increases CBF and CMR</p> Signup and view all the answers

    How do β-agonists like epinephrine impact cerebral metabolic rate of oxygen consumption (CMRO2) when the BBB is permeable?

    <p>Increase both CBF and CMRO2</p> Signup and view all the answers

    What is the interpretation regarding the effects of β-agonists on cerebral blood flow (CBF) and cerebral metabolic rate (CMR) when the blood-brain barrier (BBB) is injured?

    <p>Increases both CBF and CMR significantly</p> Signup and view all the answers

    When administered to patients under hypotensive epidural anesthesia, how does epinephrine primarily impact middle cerebral artery flow velocity (MCAfv)?

    <p>Increases MCAfv</p> Signup and view all the answers

    In nonanesthetized humans, what happens to cerebral blood flow (CBF) when intracarotid epinephrine is administered in doses that do not change mean arterial pressure (MAP)?

    <p>CBF remains unchanged</p> Signup and view all the answers

    What effect does larger doses of epinephrine that resulting in an increase in MAP, have on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen consumption (CMRO2)?

    <p>Both CBF and CMRO2 increase by approximately 20%</p> Signup and view all the answers

    What is the likely impact of administering epinephrine to patients undergoing surgery under hypotensive epidural anesthesia on middle cerebral artery flow velocity (MCAfv)?

    <p>MCAfv increases possibly due to enhanced cardiac output</p> Signup and view all the answers

    How is middle cerebral artery flow velocity (MCAfv) likely influenced when epinephrine is given to patients under hypotensive epidural anesthesia?

    <p>MCAfv increases potentially due to enhanced cardiac output</p> Signup and view all the answers

    Which receptor is likely the mediator of the increase in cerebral metabolic rate (CMR) and cerebral blood flow (CBF) caused by larger doses of vasoactive drugs?

    <p>β1-receptor</p> Signup and view all the answers

    In what scenario can β-Agonists lead to an increase in cerebral metabolic rate (CMR) and cerebral blood flow (CBF)?

    <p>When given In larger doses</p> Signup and view all the answers

    What effect does esmolol have on seizures induced by electroconvulsive therapy (ECT)?

    <p>Shortens seizures</p> Signup and view all the answers

    In patients undergoing craniotomy who become hypertensive during emergence from anesthesia, what effect is observed after the administration of labetalol?

    <p>Reduced CBF</p> Signup and view all the answers

    What is the likely outcome when β-blockers are administered to patients with intracranial pathology?

    <p>No significant impact</p> Signup and view all the answers

    which of the followings ikely to influence the β-blocker effects at time of β-blocker administration ?

    <p>Catecholamine levels or the status of the BBB or both</p> Signup and view all the answers

    β-Blockers EFFECT on CBF and CMR.

    <p>either reduce or have no effect on CBF and CMR.</p> Signup and view all the answers

    What is the predominant effect of dopamine on the normal cerebral vasculature when administered in small doses?

    <p>Slight vasodilation with minimal change in CMR</p> Signup and view all the answers

    dopamine in high doses can act on alpha receptors which lead to systemic vasoconstriction. What is a characteristic of the cerebral circulation when dopamine is administered in doses up to 100 μg/kg/min?

    <p>no effect on cerebral circulation</p> Signup and view all the answers

    Which receptor does fenoldopam act on, leading to systemic vasodilation and decreased arterial blood pressure?

    <p>DA1-receptor and α2-receptor</p> Signup and view all the answers

    What happens to cerebral blood flow (CBF) when fenoldopam is administered to decrease systemic blood pressure?

    <p>15% reduction in CBF</p> Signup and view all the answers

    Which region of the brain can experience increased CMR under the influence of dopamine administration?

    <p>Choroid plexus</p> Signup and view all the answers

    patients arrive to the ER with focal cerebral ischemia and vasospasm, also known that he has hemodynamic dysfunction? which drug can be used to treat the vasospasm and also augment cardiovascular system and increase MAP?

    <p>Dopamine</p> Signup and view all the answers

    which drugs are frequently used to treat acute hypertension in the neurologically injured patient population.

    <p>Calcium channel blockers.</p> Signup and view all the answers

    which calcium channels are found in Cerebral vessels ?

    <p>L-type calcium channel.</p> Signup and view all the answers

    What makes nicardipine a commonly used calcium channel blocker for perioperative blood pressure control?

    <p>Short half-life and easy titratability</p> Signup and view all the answers

    What is the distinguishing feature of clevidipine ?

    <p>Ultrashort half-life due to rapid esterase-mediated metabolism</p> Signup and view all the answers

    What effect does intravenous administration of nimodipine have on cerebral blood flow (CBF) in healthy humans?

    <p>Increases CBF by approximately 5% to 10%</p> Signup and view all the answers

    What impact does nimodipine have on autoregulation when administered to human subjects?

    <p>Blunts autoregulation moderately</p> Signup and view all the answers

    What is the primary effect of calcium channel blockers on cerebral vessels?

    <p>Inducing vasodilation of pial and cerebral arteries</p> Signup and view all the answers

    Which calcium channel blocker has been shown to increase regional cerebral blood flow significantly after subarachnoid hemorrhage, provided mean arterial pressure (MAP) is maintained?

    <p>Nimodipine</p> Signup and view all the answers

    WHAT is the most commonly used Calcium channel blockers for perioperative blood pressure control ?

    <p>Nicardipine</p> Signup and view all the answers

    What determines the net impact of calcium channel blockers (CCBs) on cerebral blood flow (CBF)?

    <p>mean arterial pressure (MAP)</p> Signup and view all the answers

    When mean arterial pressure (MAP) is maintained, what is the expected effect on cerebral blood flow (CBF) after administering calcium channel blockers?

    <p>Increase CBF</p> Signup and view all the answers

    What role does systemic vasodilation play in the impact of calcium channel blockers (CCBs) on cerebral blood flow?

    <p>ependent on the extent of systemic vasodilation and MAP</p> Signup and view all the answers

    What impact do vasoactive drugs have on cerebral blood flow (CBF) in the presence of calcium channel blockers (CCBs) if mean arterial pressure (MAP) is maintained?

    <p>Increase CBF</p> Signup and view all the answers

    What is the impact of acute administration of Angiotensin II (AII) on the cerebral circulation?

    <p>Increases cerebral microvascular constriction without affecting CBF</p> Signup and view all the answers

    Which statement regarding Angiotensin-Converting Enzyme Inhibitors (ACE inhibitors) and Angiotensin Receptor Blockers (ARBs) is correct?

    <p>They reduce arterial blood pressure but do not affect CBF</p> Signup and view all the answers

    How do ACE inhibitors and ARBs affect the need for other vasopressors in the treatment of vasodilatory shock?

    <p>Reduce the need for other vasopressors like norepinephrine</p> Signup and view all the answers

    What effect does Angiotensin II has on autoregulation and CO2 responsivity

    <p>autoregulation and CO2 responsivity appear to be maintained.</p> Signup and view all the answers

    What is a key characteristic of the loss of synapses in the aged brain?

    <p>Considerably greater loss of synapses compared to myelinated fibers</p> Signup and view all the answers

    What effect does aging have on dendritic spines in the brain?

    <p>Approximately 25% to 35% decrease in dendritic spines</p> Signup and view all the answers

    How does aging impact cerebral circulatory responsiveness in healthy individuals?

    <p>Slightly reduced responsiveness to changes in Paco2 and hypoxia</p> Signup and view all the answers

    In the aging brain, what happens to both cerebral blood flow (CBF) and cerebral metabolic rate of oxygen consumption (CMRO2) around the age of 80 years?

    <p>Both CBF and CMRO2 decrease by 15% to 20%</p> Signup and view all the answers

    What is the primary impact of the loss of neuropil in the aging brain on cerebral physiology?

    <p>Reduction in both CBF and CMRO2</p> Signup and view all the answers

    What is the approximate percentage of neuronal loss in a healthy aged brain according to the provided text?

    <p>10%</p> Signup and view all the answers

    What consequence results from the loss of myelinated fibers in the aging brain?

    <p>Reduced white matter volume</p> Signup and view all the answers

    In the normally aging brain, what is significantly greater compared to the loss of neurons?

    <p>Loss of synapses</p> Signup and view all the answers

    Study Notes

    Effects of Drugs on Cerebral Blood Flow and Physiology

    • Enalapril, an ACE inhibitor, enhances cerebral blood flow (CBF).
    • Slow induction of hypotension leads to less dramatic increases in intracranial pressure (ICP) due to gradual adaptation of cerebral autoregulation.
    • Common hypotensive agents include anesthetics that cause cerebral vasodilation.
    • Anesthetics expanding cerebral circulation can increase cerebral blood volume (CBV).
    • The efficacy of vasoactive medications on cerebral physiology is primarily influenced by autoregulation status.
    • Catecholamine agonists generally increase CBF, while antagonists can decrease it, dependent on the autoregulatory status.
    • When autoregulation is intact, CBF remains stable despite changes in systemic arterial pressure, until pressure exceeds autoregulatory limits.
    • Autoregulation mechanisms stabilize CBF by adjusting luminal tone in response to mean arterial pressure (MAP) variations.
    • In cases of impaired autoregulation, CBF changes proportionally to arterial pressure fluctuations.
    • Preserved autoregulation ensures CBF stability at lower MAP values during hypotension.
    • Administration of α1-agonists like norepinephrine increases CBF in healthy individuals by causing vasoconstriction.
    • In instances of relative hypotension, midodrine enhances cerebral perfusion through preferential vasoconstriction.
    • β-mimetic drugs, particularly norepinephrine, elevate both cerebral metabolism and CBF.
    • During defective autoregulation, norepinephrine may lead to decreased CBF due to excessive systemic pressure.
    • If β-mimetics gain access to the brain through a compromised blood-brain barrier (BBB), they can significantly increase CBF.
    • Administration of phenylephrine during cardiopulmonary bypass can elevate CBF.
    • Phenylephrine typically increases regional cerebral oxygen saturation (rSO2) effectively, unlike ephedrine.
    • Norepinephrine's effects on rSO2 indicate loss of regional oxygen saturation is not a definitive sign of cerebral oxygenation impairment during vasopressor use.
    • Dexmedetomidine primarily decreases CBF by acting as a minor sedative, not substantially impacting metabolic rates.
    • In healthy volunteers, dexmedetomidine was found to stabilize CBF, linking it with a reduced metabolic rate.
    • Epinephrine can stabilize CBF and CMR without changing MAP when administered at low doses.
    • At high doses, epinephrine increases both CBF and CMR due to systemic vasoconstriction.
    • In cases of hypotensive epidural anesthesia, epinephrine boosts middle cerebral artery flow velocity (MCAfv).
    • Larger doses of epinephrine lead to raised MAP, subsequently enhancing CBF and CMR.
    • The increase in CMR caused by higher doses of vasoactive drugs largely mediates through β-receptor activity.
    • Epinephrine can lead to a spike in CMR and CBF under specific conditions.
    • Esmolol has shown efficacy in managing seizures induced by electroconvulsive therapy (ECT).
    • In patients experiencing hypertensive episodes post-anesthesia, labetalol can mitigate CBF spikes.
    • The administration of β-blockers may decrease CBF in patients with significant intracranial conditions.
    • Various factors can influence β-blocker effects during administration, notably autoregulation status.
    • Dopamine's low doses primarily lead to vasodilation in normal cerebral vasculature.
    • High doses of dopamine trigger systemic vasoconstriction via alpha receptor activation.
    • Cerebral circulation retains responsiveness when dopamine is given at doses up to 100 μg/kg/min.
    • Fenoldopam targets dopamine receptors to induce systemic vasodilation and lower blood pressure.
    • Administration of fenoldopam leads to an increase in CBF during blood pressure management.
    • Dopamine administration can raise metabolic rates for certain brain regions, potentially affecting ischemic areas.
    • To assist patients with focal ischemia and vasospasm, drugs that enhance MAP are administered.
    • Calcium channels, particularly L-type, are found in cerebral vessels.
    • Nicardipine is favored for managing perioperative blood pressure due to its rapid onset and effectiveness.
    • Clevidipine offers distinct advantages with its ultra-short half-life and direct action.
    • Intravenous nimodipine can positively influence CBF in humans, particularly post-subarachnoid hemorrhage.
    • Nimodipine's administration may impair autoregulation due to its vasodilatory effects on cerebral vessels.
    • Calcium channel blockers reduce vascular resistance in cerebral blood flow.
    • Following subarachnoid hemorrhage, nimodipine can significantly improve regional CBF if MAP is maintained.
    • Calcium channel blockers' effect on CBF is contingent upon maintained MAP.
    • Sustaining MAP allows calcium channel blockers to enhance CBF effectively.
    • Systemic vasodilation from calcium channel blockers influences CBF increase due to lowered vascular resistance.
    • Vasoactive drugs can impact CBF alongside calcium channel blockers if MAP stays stable.
    • Acute administration of angiotensin II can evoke significant changes in cerebral circulation.
    • ACE inhibitors and ARBs collectively influence the requirement for additional vasopressors during vasodilatory shock.
    • Angiotensin II promotes both autoregulation maintenance and CO2 responsiveness.

    Aging and Cerebral Physiological Changes

    • Aging is characterized by synaptic loss, impacting cognitive functions.
    • Dendritic spine degradation occurs with aging, affecting neuronal connectivity.
    • Healthy aging often results in diminished cerebral circulatory responsiveness.
    • Both CBF and cerebral metabolic rate of oxygen consumption (CMRO2) typically decline around age 80.
    • Loss of neuropil due to aging severely affects CBF regulation and brain function.
    • Approximately 10-20% of neuron loss is noted in a healthy aged brain.
    • Myelinated fiber loss in aging leads to slower signal transmission and decreased cognitive capability.
    • Loss of neurons is less pronounced compared to the significant loss of synapses in the context of normal aging.

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    Description

    This quiz covers the effects of systemic vasodilators like sodium nitroprusside, nitroglycerin, hydralazine, adenosine, and calcium channel blockers on cerebral vasodilation and cerebral blood flow. Learn about the differences in cerebral blood flow when induced by different hypotensive agents.

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