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Anesthesia Pharm > Week 9 - Hemodynamic Stability: Vasopressors & Inotropes > Flashcards

Week 9 - Hemodynamic Stability: Vasopressors & Inotropes Flashcards

1
Q

What is the goal of anesthesia related to hemodynamics?

A

Maintain organ and tissue perfusion (flow) and avoid hypertensive crisis

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2
Q

What factors influence PO2 at the inspired gas level (PIO2) in the oxygen cascade? How can the CRNA control/alter these?

A

Inspired Oxygen Concentration (FiO2) – CRNA sets level

Barometric Pressure (Pb) – Hyperbaric Chamber?

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3
Q

What factors influence PO2 at the alveolar gas level (PAO2) in the oxygen cascade? How can the CRNA control/alter these?

A

Alveolar Ventilation – ventilation strategies (adequate tidal volume, pressure, PEEP, CPAP)

Oxygen Consumption – decrease shivering, avoid hyperthermia, increase anesthetic depth

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4
Q

What factors influence PO2 at the arterial blood level (PaO2) in the oxygen cascade? How can the CRNA control/alter these?

A

Scatter of V/Q ratios

Venous admixture (Qs/Qt: pulmonary shunt fraction) – ventilation perfusion (decrease shunt and dead space)

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5
Q

What factors influence PO2 at the cell PO2 level in the oxygen cascade? How can the CRNA control/alter these?

A

Blood Flow – Q = P/R; R = n8L/r^4

Hemoglobin Concentration – oxyhemoglobin dissociation, maintain normal acid-base balance, normothermia, 2,3-DPG

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6
Q

What cardiac and peripheral vascular factors affect tissue blood flow? (2)

A

Local vascular resistance

Mean aortic pressure

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7
Q

What cardiac and peripheral vascular factors affect mean aortic pressure? (2)

A

Cardiac Output

Total peripheral resistance

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8
Q

What is stroke volume? What affects each component of SV?

A

End-Diastolic Volume minus End-Systolic Volume

  • EDV: filling pressure (preload) and compliance
  • ESV: afterload and contractility
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9
Q

How do neurohumoral factors influence blood pressure?

A
  • Renal Na+ and H2O handling –> affects blood volume
  • Venous Compliance –> affects preload
  • Inotropy –> affects stroke volume
  • Heart Rate –> affects cardiac output
  • SVR –> affects MAP
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10
Q

What are the hemodynamic effects of volatile anesthetics?

A

Produce dose dependent arterial hypotension:

  • decreased LV afterload = decreased SVR and decreased wall tension
  • decreased myocardial contractility = negative inotrope (cardioprotective)
  • left ventricular-arterial coupling = negative dromotrope (decreased conduction speed of AV node)
  • depression of SA node = negative chronotropic (Des exception, tachy w/ rapid increase in dose)
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11
Q

What is the effect of volatiles on the baroreceptor reflex?

A

Depress baroreceptor reflex control of arterial pressure to varying degrees

  • more so with older volatiles – ISO has the least effect
  • CO is more easily maintained as baroreceptor reflex compensates for decreased SVR and contractility
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12
Q

What effects does nitrous oxide have on hemodynamics?

A

Causes direct negative inotropic effects

Doesn’t substantially affect LV diastolic function

Produces modest increase in pulm and systemic arterial pressure via a sympathomimetic effect (decreases contractility but maintains BP)

*actions are dependent to some degree on the baseline anesthetic (N2O doesn’t alter sympathetic vasoconstrictor-induced maintenance of arterial pressure - reason for relative stability of hemodynamics during N2O anesthesia)

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13
Q

How do Propofol, etomidate, and ketamine affect BP and HR?

A

Propofol = decrease BP and HR

Etomidate = no change in BP and HR (possible slight decrease in BP)

Ketamine = increase BP and HR

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14
Q

What are the heart rate caused hypotension etiologies in anesthesia?

A

Low HR causes of HoTN:
-volatile agents, opioids, beta blockers, Ca+ channel blockers, digitalis, AChE inhibitors, intrinsic conduction defects, excess vagal tone

High HR causes of HoTN:
-A-fib, A-flutter, V-tach

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15
Q

What are the preload caused hypotension etiologies in anesthesia?

A
  • Inadequate intravascular volume
  • Excessive surgical bleeding
  • Excessive vasodilation
  • Pericardial tamponade
  • Pneumothorax
  • Embolus
  • Tricuspid, pulmonary, or mitral stenosis
  • Hypoproteinemia
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16
Q

What are the afterload caused hypotension etiologies in anesthesia?

A

Low SVR:

  • drug induced vasodilation
  • anaphylaxis
  • sepsis
  • anemia
  • hepatic failure/AV malformations
  • neurogenic

Mechanical Obstruction:

  • hypertrophic obstructive cardiomyopathy
  • systolic anterior motion of mitral valve
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17
Q

What are the contractility caused hypotension etiologies in anesthesia?

A
  • Non ischemic cardiomyopathy
  • Myocardial ischemia
  • LV infarction
  • RV infarction
  • Valvular dysfunction
  • Volatile anesthetics
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18
Q

How do volatile anesthetics affect the auto-regulation of blood flow?

A

They get rid of auto-regulation so you need to be diligent on maintaining BP

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19
Q

How low is too low for hypotension? What is a safe BP?

A

~20-30% below baseline in a normal healthy patient

*safe BP = a BP equal to or higher than 2/3 of the known resting MAP

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20
Q

What types of patients should not be subjected to hypotension?

A
  • Carotid stenosis
  • Known valvular disorders,
  • Known heart failure
  • Known fixed cardiac output
  • Known severe coronary artery stenosis
  • may develop cerebral or myocardial ischemia with hypotension
  • *maintain these patients at their normal BP if possible
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21
Q

Blood pressure decreases ___ mmHg for every ___ cm height above the point of measurement.

A

Blood pressure decreases 2 mmHg for every 2.5 cm (1 inch) height above the point of measurement

  • BP within brain in sitting pt under anesthesia is about 12-16 mmHg lower than the BP measured at the upper arm
  • check for temporal pulse if pt is in this position – if pulse felt then most likely adequate perfusion of brainstem
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22
Q

What are the step to hemostatic control of blood pressure?

A

1) Stimulus: produces change in variable
2) Change detected by receptor
3) Input: info sent along afferent pathway to the control center
4) Output: info sent along efferent pathway to the effector
5) Response of effector feeds back to influence magnitude of stimulus and returns variable to homeostasis

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23
Q

What are the intrinsic factors that control blood pressure? What can we do to help these?

A

Frank-Starling Mechanism (Stroke Volume) – we can maintain optimum preload

SA and AV node (Heart Rate and A/V synchronization) – we can administer antiarrythmics

24
Q

What reflexes control blood pressure? What can we do to help these?

A

Baroreceptor – we can be aware of bradycardia with pure alpha agonsits

Chemoreceptor – we can maintain optimal O2 saturation, ETCO2, pH

Atrial Receptor (Bainbridge) – we can maintain optimum preload

25
Q

What humoral factors control blood pressure? What can we do to help these?

A

Renin-Angiotensin-Aldosterone System – we can administer vasopressin

26
Q

How does the baroreceptor reflex work?

A

A sudden increase in BP leads to decreased HR, CO, and SVR

A sudden decrease in BP leads to increased HR, CO, and SVR

*giving a pure alpha agonists, you will see a decrease in HR due to this reflex

27
Q

What are the doses of vasopressin? When is it is used?

A

Infusion Rate: 0.01 to 0.04 units/min

Bolus: 1-2 units

One 40 unit dose may be substituted for either 1st or 2nd dose of epi in cardiac arrest

T1/2 = 10-20 minutes

*Consider in refractory HoTN (shock, hemorrhage) and patients who are on ACE inhibitors

28
Q

Explain the CNS control of the heart and blood vessels

A

Change in blood pressure is sensed by the carotid and aortic baroreceptors — signal is sent to the medullary CV control center — Parasympathetic neurons send signal to the SA node; Sympathetic neurons send signals to the SA node, ventricles, arterioles, and veins

29
Q

What neurotransmitters and receptors are involved in BP control?

A

Parasympathetic (Vagus Nerve): ACh acts on muscarinic receptors in the heart and vessels

Sympathetic:

  • Adrenergic – norepi acts on alpha receptors in the vessels and beta receptors in the heart
  • Cholinergic – ACh acts on muscarinic receptors in sweat glands and vessels
  • Dopaminergic – dopamine acts on dopamine1 receptors in renal vessels

Adrenal: epi and norepi act on alpha receptors in the vessels and beta receptors in the heart

30
Q

How are catecholamines metabolized? What are their end products?

A

Metabolized by COMT and MAO

  • Dopamine end product = HVA (homovanillic acid)
  • Norepi end product = normetanephrine –> VMA (vanillylmandelic acid)
  • Epi end product = metanephrine –> VMA (vanillylmandelic acid)

*HVA & VMA are conjugated in the liver and excreted in the urine

31
Q

Where are alpha-1 receptors located and what is the agonists effects?

A

Post synaptic in smooth muscle throughout the body

Agonists:

  • Pupil dilation
  • Bronchoconstriction
  • Uterine contraction
  • Vasoconstriction (Increase SVR/Afterload)
32
Q

Where are alpha-2 receptors located and what occurs when they are activated?

A

Pre-synaptic nerve terminals – negative feedback loop that inhibits Norepi release
*Activation inhibits cAMP levels which decreases Ca++ entry into the neuronal terminal and limits the release of norepi

Activation:

  • sedation in CNS
  • reduced sympathetic outflow and peripheral vasodilation
33
Q

What is the receptor activity and physiologic effects of epinephrine?

A

Alpha ++
Beta-1 ++
Beta-2 ++

  • Increases: CO, HR, SVR, MAP
  • No effect on peripheral vascular resistance
34
Q

What is the receptor activity and physiologic effects of isoproterenol?

A

Beta-1 +++
Beta-2 +++
NO Alpha

  • Increases: CO, HR
  • Decreases: SVR, MAP
  • No effect on peripheral vascular resistance
35
Q

What is the receptor activity and physiologic effects of norepinephrine?

A

Alpha +++
Beta-1 ++
NO Beta-2

  • Increases: SVR, MAP, PVR
  • No effect on CO, HR
  • increased contractility and increased afterload
  • some reflexive bradycardia
36
Q

What is the receptor activity and physiologic effects of dopamine?

A

Alpha ++
Beta-1 ++
DA1 and DA2 ++
NO Beta-2

  • Increases: CO, HR, SVR, MAP
  • No effect on PVR
  • lower doses activate DA1 receptors causing vasodilation
  • larger doses activates alpha receptors causing vasoconstriction
  • activation of DA2 receptors inhibit release of norepi from storage granules
37
Q

What is the receptor activity and physiologic effects of dobutamine?

A

Beta-1 +++
Beta-2 +
NO Alpha

  • Increases: CO, HR
  • Decreases: SVR, MAP, PVR
38
Q

What is the receptor activity and physiologic effects of phenylephrine?

A

Alpha +++
NO Beta-1 or Beta-2

  • Increases: SVR, MAP, PVR
  • Decreases: HR
  • No effect on CO
39
Q

What is the receptor activity and physiologic effects of vasopressin?

A

V1 and V2 receptors

  • Increases: SVR, MAP
  • No effect on CO, HR, PVR
40
Q

What is the receptor activity and physiologic effects of ephedrine?

A

Alpha +
Beta-1 +
Beta-2 +

  • Increases: CO, HR, SVR, MAP
  • No effect on PVR
41
Q

What is the use of phenylephrine in anesthesia?

A

Dose dependent vasoconstrictor used to increase BP due to vasodilator effects of anesthesia agents

*non-catecholamine with predominately alpha-1 agonist activity

  • Reflex bradycardia
  • Can cause pulmonary HTN
42
Q

What is the dosing of phenylephrine?

A

Bolus: 50-100 mcg (0.5-1.0 mcg/kg)
*Duration: short, approx 15 min

Infusion: 0.25 to 1.0 mcg/kg/min (increased pressure but may impede renal blood flow)

*Available in 10 mg/mL vial and MUST be diluted for use – usually 100 mcg/mL

43
Q

What is ephedrine and how does it work?

A

Synthetic non-catecholamine – indirect and direct acting alpha and beta agonist

Works by increasing the release of NE at the synaptic junction and similar direct alpha/beta effects as epi (increase BP, HR, contractility, and CO and bronchodilator)

  • longer duration of action and less potent than epinephrine
  • direct stimulation of the CNS (may increase MAC)
44
Q

What is the dosing of ephedrine?

A

IV Bolus: 2.5-10 mg (pediatric = 0.1 mg/kg)

IM/SQ: 25-50 mg – onset = 10-20 min

Available in 1 mL vials of 50 or 25 mg/mL

  • *DILUTE for IV administration
  • Tachyphylaxis
45
Q

When is epinephrine used in anesthesia?

A

Principle treatment in anaphylaxis and cardiac arrest

Consider in severe bronchospasm (also stabilized mast cells), hypotension with bradycardia, and/or low CO

Used to prolong the effects of local anesthetics

46
Q

What is the dosing of epinephrine?

A
  1. 05 to 1.0 mg push
    * 1mg = code
    * 0.3-0.5 mg (IV/IM) = anaphylaxis

Infusion: 0.1-1.0 mcg/kg/min (1mg/250mL concentration)

*extravasation of epi at peripheral IV site may produce significant tissue ischemia

47
Q

How many mg of epi are in 5mL of a 1:10,000 solution?

A

1:10,000 = 1000mg/10,000mL = 0.1 mg/mL

5 mL x 0.1 mg/mL = 0.5 mg

48
Q

What is the dosing of norepinephrine?

A

May be bolus of 0.1 mcg/kg (short duration)

Infusion: 2-20 mcg/min (0.01-3 mcg/kg/min) – higher rates in septic shock

Comes in ampules of 4mg/mL

*MUST be diluted

49
Q

At what doses of dopamine do you get beta-1, alpha, and dopaminergic effects?

A

Dopaminergic: 0.5-2 mcg/kg/min

Beta-1: 2-10 mcg/kg/min

Alpha: >10 mcg/kg/min

50
Q

What are the beta selective inotropes?

A

Isoproterenol: potent beta-1 agonist, little effect on alpha
*positive chronotrope and inotrope

Dobutamine: initially considered as beta-1 selective but is more complicated than that

  • positive inotrope over chronotrope when compaired to isoproterenol
  • some alpha1
51
Q

What is milrinone and its effects?

A

Inodilator — phosphodiesterase type III inhibitor

Non-catecholamine inodilator

Increased CO with reduction in arterial pressure, LVED, and pulmonary vascular resistance

Drug of choice for weaning from cardiopulmonary bypass

52
Q

What vasopressor/inotrope is the drug of choice for refractory bradycardia?

A

Isoproterenol

  1. 01-0.2 mcg/kg/min
    * no co-infusion with alkaline medications
53
Q

What vasopressor/inotrope is the drug of choice for septic shock? What about septic shock with systolic dysfunction?

A

Septic Shock: norepinephrine

Septic Shock with systolic dysfunction: dopamine

*both have drug-drug interactions with MAO-Is and TCAs

54
Q

What vasopressor/inotrope is the drug of choice for stress echocardiography?

A

Dobutamine

2-20 mcg/kg/min

*co-administration with alkaline solutions can decrease activity

55
Q

What vasopressor/inotrope is the drug of choice for mild hypotension of general or regional anesthesia?

A

Phenylephrine: Bolus (50-200 mcg) or Infusion (20-200 mcg/min)

Ephedrine: Bolus (5-10 mg)

*Both have drug-drug interaction with MAO-I and TCA

56
Q

What vasopressor/inotrope is the drug of choice for post-cardiopulmonary bypass vasoplegia?

A

Vasopressin

Bolus: 0.5-2 units for mild hypotension, 20 units
Infusion: 0.1-0.4 mcg/min

*drug-drug interaction with carbamazapine, TCA, norepi, lithium, heparin

57
Q

Which vasopressor or inotrope may increase MAC via direct CNS stimulation?

A

Ephedrine

Anesthesia Pharm (18 decks)

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