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
Q

α Adrenergic Receptors

A

GPCR
Ligands - NE, epi, dopa (↑doses)

α1 → excitatory ↑Ca2+ → smooth muscle contraction
α2 → inhibitory ↓CAMP ↓NE release

26
Q

β Adrenergic Receptors

A

β1, β2, β3

GPCRs

27
Q

1st line HTN treatment

A

Thiazide diuretic

UNLESS diabetes or CKD

28
Q

α Antagonists

A

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
Q

Phentolamine

A

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
Q

Phentolamine Dose

A

HTN emergency 30-70 mcg/kg

SQ extravasation 2.5-5 mg

31
Q

Phenoxybenzamine

A
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
Q

Prazosin

A

Selective α1 antagonist
Tachycardia less common
Dilates arterioles & and veins

33
Q

Prazosin Uses

A

PO preop BP control in pheochromocytoma patients
Essential HTN combined w/ thiazides
↓afterload in heart failure
Raynaud phenomenon - vasodilation ↑peripheral blood flow

34
Q

Yohimbine

A

Selective α2 antagonist
Less common
↑NE release from the post-synaptic neuron

Used to treat orthostatic HoTN & impotence

35
Q

Selective α1a Antagonists

A

Terazosin & Tamsulosin
Long-acting
Effective prostate smooth muscle relaxation to ease micturition
Most common SE → orthostatic HoTN

36
Q

β Blocker Effects

A

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
Q

What is chronic β blocker use associated with?

A

Receptor UPregulation

Sudden d/c → exaggerated SNS response

38
Q

Non-Selective β Blockers

A

Propranolol
Nadalol
Timolol
Pindolol

39
Q

Cardioselective β1 Blockers

A
Metoprolol
Atenolol
Acebutolol
Betaxolol
Esmolol
40
Q

β Blocker SE

A
↓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
Q

What is the β blocker prototype?

A

Propranolol

Non-selective β antagonist

42
Q

Metoprolol (Lopressor)

A
β1 selective antagonist
PO 50-400mg
IV 1-15mg
Hepatic metabolism
Elim 1/2 time 3-4 hours
43
Q

What is the most selective β1 antagonist?

A

Atenolol

- Least CNS effects

44
Q

Atenolol

A

Selective β1 antagonist
No hepatic metabolism
Renal excretion (increased elim 1/2 time in patients w/ renal disease)
PO only

45
Q

Esmolol (Breviblock)

A
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
Q

Labetalol

A

Combined non-selective α AND β antagonist
β&raquo_space;> 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
Q

α2 Agonists

A

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
Q

Considerations with Clonidine administration

A

↓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
Q

α2 Agonist SE

A
Bradycardia
Sedation
Xerostomia (dry mouth)
Impaired concentration
Nightmares
Depression
Vertigo
Extrapyramidal symptoms
Male lactation
50
Q

Vasopressin

A

Antidiuretic hormone (ADH)

51
Q

Vasopressin

Production & Storage

A

Produced in the hypothalamus

Stored in the posterior pituitary

52
Q

Vasopressin MOA

A

Potent vasoconstrictor

Dilates renal afferent, pulmonary, and cerebral arterioles

53
Q

Vasopressin Receptors

A

V1 - vasoconstriction
V2 - H2O reabsorption in the renal collecting ducts
V3 - located in the CNS & modulate corticotrophin secretion

54
Q

Vasopressin Uses

A
Post cardiopulmonary bypass shock
Refractory HoTN
Reduce bleeding in von Willebrand
DI antidiuresis
Treat enuresis (involuntary urination or wetting the bed)
55
Q

Vasopressin Dose

Bolus

A

1-2 units

Dilute 20 units in 20mL

56
Q

Vasopressin Dose

Infusion

A

0.03-0.04 units/min

Max dose 0.1 unit/min

57
Q

Vasopressin Onset

A

1-5 minutes

58
Q

Vasopressin Peak

A

5 minutes

59
Q

Vasopressin DOA

A

10-30 minutes

60
Q

Vasopressin Complications

A

> 0.04 units/min
GI ischemia d/t potent vasoconstriction at the mesenteric artery
↓CO
Skin or digital necrosis