Cardiovascular I Flashcards

1
Q

CNS Neurotransmitters

A

Epi, NE, dopa, serotonin, GABA, ACh

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2
Q

Agonists

Natural Catecholamines

A

Epi, NE, dopa

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3
Q

Agonists

Synthetic Catecholamines

A

Isoproterenol & dobutamine

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4
Q

α

Receptor Potency

A

NE > epi > Isoproterenol

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5
Q

β

Receptor Potency

A

Isoproterenol > epi > NE

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6
Q

α1 Receptors Location

A

Post-synaptic

Locations: CV (heart), vasculature, glands, & gut

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7
Q

α1 Receptors MOA

A

Activation causes vasoconstriction & GI tract relaxation

Eye - iris (radial muscle) contraction → pupil dilation (mydriasis)

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8
Q

α2 Receptors Location

A

Pre-synaptic AND post-synaptic

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9
Q

α2 Pre-Synaptic

A

1° location pre-synaptic
Location: CV (coronaries), peripheral vascular smooth muscle, & brain
Activation causes NE release inhibition & inhibits sympathetic outflow → vasodilation
↓BP ↓HR → inhibit CNS activity

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10
Q

α2 Post-Synaptic

A

Location: CNS & coronaries

Activation causes constriction, sedation, & analgesia

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11
Q

β1 Location

A

ONE HEART

Cardiac muscle (myocardium), SA node, ventricular conduction system, coronaries, & kidney

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12
Q

β1 MOA

A

Activation causes ↑inotropy, chronotropy, myocardial conduction velocity, coronary relaxation, & renin release

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13
Q

β2 Location

A

TWO LUNGS

Vascular, bronchial & uterine smooth muscle, skin smooth muscle, myocardium, coronaries, kidneys, & GI tract

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14
Q

β2 MOA

A

Vasodilation, bronchodilation, uterine relaxation, gluconeogenesis (↑glucose), glycogenolysis (breaks down glycogen → glucose), insulin release, K+ uptake (cellular)

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15
Q

Ephedrine MOA

A

Direct & indirect (NT release) α/β

→ vasoconstriction ↑HR ↑inotropy

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16
Q

Phenylephrine (Neo-synephrine) MOA

A

Direct α vasoconstriction → reflex bradycardia

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17
Q

What determines blood pressure?

A
BP = CO x SVR
CO = (HR x SV)
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18
Q

What factors influence SV?

A

Contractility

Preload - venous tone & intravascular volume

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19
Q

How do β blockers & Ca2+ channel blockers ↓BP?

A

↓HR & contractility

BP = HR x SV x SVR

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20
Q

What drugs impact venous tone & therefore preload?

A

α1 agonists
α blockers
Angiotensin converting enzyme inhibitors ACEi -pril
Angiotensin II receptor blockers ARBs -sartan
Direct vasodilator - Nitroprusside

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21
Q

How do diuretics, ACEi, & ARBs influence BP?

A

Renin-angiotensin-aldosterone

Na+ & H2O retention/excretion → PRELOAD

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22
Q

What drugs directly innervate SVR?

A

α1 antagonists

α2 agonists

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23
Q

What drugs influence circulating regulators that determine SVR?

A

α1 antagonists
α1 agonists
ACEi & ARBs

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24
Q

What drugs influence local SVR regulators? How?

A
  • Endothelin antagonists
  • Nitroprusside
  • ACEi
  • ARBs
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25
α Adrenergic Receptors
GPCR Ligands - NE, epi, dopa (↑doses) α1 → excitatory ↑Ca2+ → smooth muscle contraction α2 → inhibitory ↓CAMP ↓NE release
26
β Adrenergic Receptors
β1, β2, β3 | GPCRs
27
1st line HTN treatment
Thiazide diuretic | UNLESS diabetes or CKD
28
α Antagonists
Non-selective - Phentolamine - Phenoxybenzamine α1 selective ↓SVR/BP → postural HoTN common SE - Prazosin α2 selective ↑NE release → tachycardia d/t cardiac β stimulation - Yohimbine
29
Phentolamine
Non-selective α antagonist ↓SVR → vasodilation ↓BP Reflex mediated ↑HR/CO Intraop HTN emergency - Pheo manipulation - Autonomic hyperreflexia (spinal cord injury) SQ to prevent tissue necrosis associated with sympathomimetic agents extravasation
30
Phentolamine Dose
HTN emergency 30-70 mcg/kg | SQ extravasation 2.5-5 mg
31
Phenoxybenzamine
``` Non-selective α antagonist Binds covalently α1 > α2 ↓SVR → vasodilation Pro-drug Onset 1 hours Elim 1/2 time 24 hours ``` PO preop BP control in pheochromocytoma patients 0.5-1 mg/kg Start 1-2 weeks prior to OR
32
Prazosin
Selective α1 antagonist Tachycardia less common Dilates arterioles & and veins
33
Prazosin Uses
PO preop BP control in pheochromocytoma patients Essential HTN combined w/ thiazides ↓afterload in heart failure Raynaud phenomenon - vasodilation ↑peripheral blood flow
34
Yohimbine
Selective α2 antagonist Less common ↑NE release from the post-synaptic neuron Used to treat orthostatic HoTN & impotence
35
Selective α1a Antagonists
Terazosin & Tamsulosin Long-acting Effective prostate smooth muscle relaxation to ease micturition Most common SE → orthostatic HoTN
36
β Blocker Effects
CV - bradycardia, ↓contractility/conduction velocity, & improve MVO2 supply/demand balance Blood vessels - skeletal muscle vasoconstriction ↑peripheral vascular disease Airway - bronchoconstriction & bronchospasm (asthma & COPD patients) JG cells - ↓renin release ↓volume → indirect ↓BP Pancreas - ↓insulin release at β2 & mask β1 hypoglycemia S/S
37
What is chronic β blocker use associated with?
Receptor UPregulation | Sudden d/c → exaggerated SNS response
38
Non-Selective β Blockers
Propranolol Nadalol Timolol Pindolol
39
Cardioselective β1 Blockers
``` Metoprolol Atenolol Acebutolol Betaxolol Esmolol ```
40
β Blocker SE
``` ↓HR/contractility/BP PVD exacerbation d/t β2 vasodilation blocked Airway resistance → bronchospasm Altered carbohydrate & fat metabolism → masks hypoglycemia ↑HR Inhibit K+ uptake into skeletal muscles Fatigue & lethargy N/V/D ↓IOP d/t ↓aqueous humor production ↓HDLs ↑CAD risk (mechanism unknown) ```
41
What is the β blocker prototype?
Propranolol | Non-selective β antagonist
42
Metoprolol (Lopressor)
``` β1 selective antagonist PO 50-400mg IV 1-15mg Hepatic metabolism Elim 1/2 time 3-4 hours ```
43
What is the most selective β1 antagonist?
Atenolol | - Least CNS effects
44
Atenolol
Selective β1 antagonist No hepatic metabolism Renal excretion (increased elim 1/2 time in patients w/ renal disease) PO only
45
Esmolol (Breviblock)
``` Selective β1 antagonist ONLY IV Onset 60 seconds Elim 1/2 time 9 minutes Rapid plasma esterase hydrolysis Poor lipid solubility (does not cross blood-brain barrier or placenta) ```
46
Labetalol
Combined non-selective α AND β antagonist β >>> α ↓BP & attenuates reflex tachycardia (β2 blockade) CO unaffected Onset (max effect) 5-10 minutes after IV admin Dose 0.1-0.5 mg/kg (2.5-5 mg) Glucuronic acid conjugation & renal excretion unchanged Elim 1/2 time 5-8 hours prolonged w/ hepatic disease
47
α2 Agonists
Clonidine & Precedex MOA: ↓sympathetic outflow from vasomotor centers in the brainstem Used to treat HTN, induce sedation, ↓anesthetic requirements, improve periop hemodynamics, & analgesia PO, transdermal patch, or IV 50/50 hepatic metabolism & renal excretion
48
Considerations with Clonidine administration
↓HR & peripheral vascular resistance → ↓CO & BP *Wean off to prevent rebound HTN w/ abrupt cessation Withdrawal syndrome occurs w/ doses > 1.2 mg/day Occurs 18 hours after acute dc Lasts 48-72 hours Treatment - rectal or transdermal Clonidine
49
α2 Agonist SE
``` Bradycardia Sedation Xerostomia (dry mouth) Impaired concentration Nightmares Depression Vertigo Extrapyramidal symptoms Male lactation ```
50
Vasopressin
Antidiuretic hormone (ADH)
51
Vasopressin | Production & Storage
Produced in the hypothalamus | Stored in the posterior pituitary
52
Vasopressin MOA
Potent vasoconstrictor | Dilates renal afferent, pulmonary, and cerebral arterioles
53
Vasopressin Receptors
V1 - vasoconstriction V2 - H2O reabsorption in the renal collecting ducts V3 - located in the CNS & modulate corticotrophin secretion
54
Vasopressin Uses
``` Post cardiopulmonary bypass shock Refractory HoTN Reduce bleeding in von Willebrand DI antidiuresis Treat enuresis (involuntary urination or wetting the bed) ```
55
Vasopressin Dose | Bolus
1-2 units | Dilute 20 units in 20mL
56
Vasopressin Dose | Infusion
0.03-0.04 units/min | Max dose 0.1 unit/min
57
Vasopressin Onset
1-5 minutes
58
Vasopressin Peak
5 minutes
59
Vasopressin DOA
10-30 minutes
60
Vasopressin Complications
> 0.04 units/min GI ischemia d/t potent vasoconstriction at the mesenteric artery ↓CO Skin or digital necrosis