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Regulation of Body Function > Inotropic vasopressor drugs - Dawes > Flashcards

Inotropic vasopressor drugs - Dawes Flashcards

1
Q

What is an inotrope

A

changes the force of cardiac muscle contractions

positive or negative

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2
Q

What is shock?

A

Inadequate oxygen perfusion to meet the tissues oxygenation demand leading to organ dysfunction

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3
Q

The types of shock

A

Hypovolemic - dehydration, haemorrhage
Cardiogenic - HF
Distributive - sepsis, anaphylaxis
Obstructive - Cardiac tamponade. PE

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4
Q

Features of patient in shock

A 
Hypotension / hypovolemia 
LV impairment 
Changes in vascular resistance 
Poor renal / peripheral perfusion 
Confused / sedated
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5
Q

Goals of shock resuscitation

A 
Restore BP 
- IV fluids
- positive inotropes 
Normalise systemic perfusion 
- postitive inotropes 
Reverse organ function 
- renal perfusion 
Treat underlying cause 
- antibiotics 
- relieve tamponade
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6
Q

Cariogenic shock,
causes?
Characterised by?

A

Ischaemia
Valve dysfunction
Actue VSD

High systemic resistance (sympathetic activity)
Low CO

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7
Q

Treatment of cardiogenic shock

A

Fluids first to improve preload
inotropes
intra aortic balloon pump

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8
Q

Inotropic agents
what
risk
rationale

A

arguments contractility, after preload established, thus improving cardiac output
rationale: increased cardiac output improves global perfusion
Risk, tachycardia and increased myocardial oxygen consumption

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9
Q

alpha and beta adrenoreceptor agonists

A

Norepinephrine
epinephrine
Dobutamine
Dopamine

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10
Q

Beta 1 agonists

A

mostly in heart
increase contractility - positive inotrope
increase heart rate - positive chronotrope
DOBUTAMINE

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11
Q

alpha 1 agonists

A

mostly in BV’s increase tone/ resistance = vasopressor

NOREPINEPHRINE

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12
Q

Alpha and beta agonists and BP

A

Beta agonists affecting the heart have very little effect on BP, whereas alpha agonists raise BP significantly

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13
Q

norepinephrine

A 
= noradrenaline 
potent alpha vasoconstrictor 
minimal beta adrenergic agonism 
minimal inotropic chronotropic effect 
Causes: increased peripheral resistance 
increased systolic/ diastolic BP 
Continuous IV infusion
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14
Q

Epinephrine

A

= adrenaline
Mixed alpha and beta adrenergic effects
can vasoconstrict and vasodilate
potent inotrope and chronotrope, used in cardiac arrest
Increases myocardial oxygen consumption particularly in coronary heart disease
continuous IV infusion

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15
Q

epinephrine for anaphylaxis

A 
activates both alpha and beta receptors 
potent vasopressor 
blood pressure increase 
dilates bronchi 
= symptomatic treatment of anaphylactic shock
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16
Q

Dobutamine

A

beta agonist - potent inotrope variable chronotrope
hepatic metabolism - glucoruonide
Caution in hypertension, inadequate volume may precipitate tachycardia or worsen hypertension
increases adenylate cyclase activity

17
Q

Dopamine

A 
metabolic precursor of norepinephrine 
at low dose 
- dopaminergic (inc renal blood flow) via D1 receptors 
Moderate dose 
- beta effects 
High dose 
- alpha effects 
* although used from time to time as an agonist, has quirky pharmacology so haven't seen much improvement in patient outcomes.
18
Q

vasopressor side effects

A

in shock sympathetic activity already high
vasoconstriction
- Ischaemia
increase cardiac work (alpha and beta agonism)
- cardiac ischaemia
- arrhythmias

19
Q

vasopressin

A

Vasopressor (VA1 receptor - VSMC)
IP3 mechanism
liver/ renal metabolism
can use when alpha agonist wont work because same effect different mechanism

20
Q

Angiotensin II

A

2017
Catecholamine resistant shock
When resistant to noradrenaline

21
Q

Amrinone / milrinone

A

Phosphodiesterase III inhibitor
- vascular / vasodilate
- cardiac smooth muscle / postitive inotrope
increase CAMP –> activates protein kinase
- myocardium = inc Ca2+ flux
- Vessels Ca2+ uptake into SR
Most often added as dobutamine as second agent
Need ITU environment
Block the breakdown of CAMP

22
Q

phosphodiesterase inhibitors - main side effects

A 
thrombocytopenia 
hypotension (vasodilation)
Arrhythmias from inc CAMP 
Increased mortality 
*are used but because of side effects need close observation therefore expensive
23
Q

What are the calcium sensitiser drugs

A

Levosimendan

Digoxin

24
Q

Levosimendan

A 
New 
I.V 
Emerging role in treatment of shock 
Calcium sensitiser 
- Enhances troponin sensitivity to Ca2+ 
- inc inotropy 
Arrhythmias increase mortality
25
Q

Digoxin

  • indications
  • why is it good to use?
A 
- atrial fibrillation: rate control 
slows HR 
improves cardiac work 
Acute / chronic HF 
- no effect on mortality 
- Improves symptoms 
- reduces hospital admissions
26
Q

Digoxin MoA

A

Normally sodium / potassium ATPase is chucking sodium out of the cell. Digoxin inhibits this therefore increasing the amount of intracellular sodium, which is picked up by the Na/Ca channel, which is activated to continue extruding sodium in exchange for inc inCa2+
But if patient has low K+, digoxin much more able to inhibit the channel therefore digoxin induced side effects

27
Q

Why is digoxin good for coronary perfusion?

A

Coronary perfusion occurs during diastole therefore by slowing heart rate inc time for diastolie = more time for coronary perfusion.
AF rate control = 3rd line digoxin
1st = beta blockers
2nd = diltiazem calcium channel blocker
You often need synergy of two of the 3 drugs to get an effect.

28
Q

Digitalis toxicity

A 
Various arrhythmias (2nd or 3rd degree heart block) 
Changes in ECG

Non cardiac

  • Nausea / vomiting / anorexia
  • Fatigue
  • Visual complaints
  • Muscular weakness
  • Abdominal pain
  • Dizziness
  • Dreams
  • Diarrhoea
29
Q

Digitalis interactions

A

Metabolic
A decrease in K+ or Mg2+ will increase the digoxin effect and side effects, care with use of diuretics
Quinidine, amiodarone, verapamil, diltiazem, erythromycin, cyclosporin.
PGP inhibitors

Regulation of Body Function (31 decks)

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