Week 9 - Hemodynamic Stability: Vasopressors & Inotropes Flashcards
What is the goal of anesthesia related to hemodynamics?
Maintain organ and tissue perfusion (flow) and avoid hypertensive crisis
What factors influence PO2 at the inspired gas level (PIO2) in the oxygen cascade? How can the CRNA control/alter these?
Inspired Oxygen Concentration (FiO2) – CRNA sets level
Barometric Pressure (Pb) – Hyperbaric Chamber?
What factors influence PO2 at the alveolar gas level (PAO2) in the oxygen cascade? How can the CRNA control/alter these?
Alveolar Ventilation – ventilation strategies (adequate tidal volume, pressure, PEEP, CPAP)
Oxygen Consumption – decrease shivering, avoid hyperthermia, increase anesthetic depth
What factors influence PO2 at the arterial blood level (PaO2) in the oxygen cascade? How can the CRNA control/alter these?
Scatter of V/Q ratios
Venous admixture (Qs/Qt: pulmonary shunt fraction) – ventilation perfusion (decrease shunt and dead space)
What factors influence PO2 at the cell PO2 level in the oxygen cascade? How can the CRNA control/alter these?
Blood Flow – Q = P/R; R = n8L/r^4
Hemoglobin Concentration – oxyhemoglobin dissociation, maintain normal acid-base balance, normothermia, 2,3-DPG
What cardiac and peripheral vascular factors affect tissue blood flow? (2)
Local vascular resistance
Mean aortic pressure
What cardiac and peripheral vascular factors affect mean aortic pressure? (2)
Cardiac Output
Total peripheral resistance
What is stroke volume? What affects each component of SV?
End-Diastolic Volume minus End-Systolic Volume
- EDV: filling pressure (preload) and compliance
- ESV: afterload and contractility
How do neurohumoral factors influence blood pressure?
- Renal Na+ and H2O handling –> affects blood volume
- Venous Compliance –> affects preload
- Inotropy –> affects stroke volume
- Heart Rate –> affects cardiac output
- SVR –> affects MAP
What are the hemodynamic effects of volatile anesthetics?
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)
What is the effect of volatiles on the baroreceptor reflex?
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
What effects does nitrous oxide have on hemodynamics?
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)
How do Propofol, etomidate, and ketamine affect BP and HR?
Propofol = decrease BP and HR
Etomidate = no change in BP and HR (possible slight decrease in BP)
Ketamine = increase BP and HR
What are the heart rate caused hypotension etiologies in anesthesia?
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
What are the preload caused hypotension etiologies in anesthesia?
- Inadequate intravascular volume
- Excessive surgical bleeding
- Excessive vasodilation
- Pericardial tamponade
- Pneumothorax
- Embolus
- Tricuspid, pulmonary, or mitral stenosis
- Hypoproteinemia
What are the afterload caused hypotension etiologies in anesthesia?
Low SVR:
- drug induced vasodilation
- anaphylaxis
- sepsis
- anemia
- hepatic failure/AV malformations
- neurogenic
Mechanical Obstruction:
- hypertrophic obstructive cardiomyopathy
- systolic anterior motion of mitral valve
What are the contractility caused hypotension etiologies in anesthesia?
- Non ischemic cardiomyopathy
- Myocardial ischemia
- LV infarction
- RV infarction
- Valvular dysfunction
- Volatile anesthetics
How do volatile anesthetics affect the auto-regulation of blood flow?
They get rid of auto-regulation so you need to be diligent on maintaining BP
How low is too low for hypotension? What is a safe BP?
~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
What types of patients should not be subjected to hypotension?
- 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
Blood pressure decreases ___ mmHg for every ___ cm height above the point of measurement.
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
What are the step to hemostatic control of blood pressure?
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
What are the intrinsic factors that control blood pressure? What can we do to help these?
Frank-Starling Mechanism (Stroke Volume) – we can maintain optimum preload
SA and AV node (Heart Rate and A/V synchronization) – we can administer antiarrythmics
What reflexes control blood pressure? What can we do to help these?
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
What humoral factors control blood pressure? What can we do to help these?
Renin-Angiotensin-Aldosterone System – we can administer vasopressin
How does the baroreceptor reflex work?
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
What are the doses of vasopressin? When is it is used?
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
Explain the CNS control of the heart and blood vessels
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
What neurotransmitters and receptors are involved in BP control?
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
How are catecholamines metabolized? What are their end products?
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
Where are alpha-1 receptors located and what is the agonists effects?
Post synaptic in smooth muscle throughout the body
Agonists:
- Pupil dilation
- Bronchoconstriction
- Uterine contraction
- Vasoconstriction (Increase SVR/Afterload)
Where are alpha-2 receptors located and what occurs when they are activated?
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
What is the receptor activity and physiologic effects of epinephrine?
Alpha ++
Beta-1 ++
Beta-2 ++
- Increases: CO, HR, SVR, MAP
- No effect on peripheral vascular resistance
What is the receptor activity and physiologic effects of isoproterenol?
Beta-1 +++
Beta-2 +++
NO Alpha
- Increases: CO, HR
- Decreases: SVR, MAP
- No effect on peripheral vascular resistance
What is the receptor activity and physiologic effects of norepinephrine?
Alpha +++
Beta-1 ++
NO Beta-2
- Increases: SVR, MAP, PVR
- No effect on CO, HR
- increased contractility and increased afterload
- some reflexive bradycardia
What is the receptor activity and physiologic effects of dopamine?
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
What is the receptor activity and physiologic effects of dobutamine?
Beta-1 +++
Beta-2 +
NO Alpha
- Increases: CO, HR
- Decreases: SVR, MAP, PVR
What is the receptor activity and physiologic effects of phenylephrine?
Alpha +++
NO Beta-1 or Beta-2
- Increases: SVR, MAP, PVR
- Decreases: HR
- No effect on CO
What is the receptor activity and physiologic effects of vasopressin?
V1 and V2 receptors
- Increases: SVR, MAP
- No effect on CO, HR, PVR
What is the receptor activity and physiologic effects of ephedrine?
Alpha +
Beta-1 +
Beta-2 +
- Increases: CO, HR, SVR, MAP
- No effect on PVR
What is the use of phenylephrine in anesthesia?
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
What is the dosing of phenylephrine?
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
What is ephedrine and how does it work?
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)
What is the dosing of ephedrine?
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
When is epinephrine used in anesthesia?
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
What is the dosing of epinephrine?
- 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
How many mg of epi are in 5mL of a 1:10,000 solution?
1:10,000 = 1000mg/10,000mL = 0.1 mg/mL
5 mL x 0.1 mg/mL = 0.5 mg
What is the dosing of norepinephrine?
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
At what doses of dopamine do you get beta-1, alpha, and dopaminergic effects?
Dopaminergic: 0.5-2 mcg/kg/min
Beta-1: 2-10 mcg/kg/min
Alpha: >10 mcg/kg/min
What are the beta selective inotropes?
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
What is milrinone and its effects?
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
What vasopressor/inotrope is the drug of choice for refractory bradycardia?
Isoproterenol
- 01-0.2 mcg/kg/min
* no co-infusion with alkaline medications
What vasopressor/inotrope is the drug of choice for septic shock? What about septic shock with systolic dysfunction?
Septic Shock: norepinephrine
Septic Shock with systolic dysfunction: dopamine
*both have drug-drug interactions with MAO-Is and TCAs
What vasopressor/inotrope is the drug of choice for stress echocardiography?
Dobutamine
2-20 mcg/kg/min
*co-administration with alkaline solutions can decrease activity
What vasopressor/inotrope is the drug of choice for mild hypotension of general or regional anesthesia?
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
What vasopressor/inotrope is the drug of choice for post-cardiopulmonary bypass vasoplegia?
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
Which vasopressor or inotrope may increase MAC via direct CNS stimulation?
Ephedrine
