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Regulation of Body Function > Inotropic Drugs (Dawes) > Flashcards

Inotropic Drugs (Dawes) Flashcards

1
Q

What do Inotropic and Vasopressor Drugs do?

A

Both drugs result in increased BP (alpha and beta agonists) with very narrow therapeutic window.

  • Inotropic drugs i_ncrease force of contraction._
  • Vasopressor drugs increases vascular tone.
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2
Q

Define Inotropes

A

Inotrope is changing the force of (cardiac) muscle contraction. It can be positive or negative.

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3
Q

Define Shock

A

Shock is characterized by inadequate organ perfusion to meet the tissue’s oxygen demand, leading to organ dysfunction.

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4
Q

What are the categories of Shock

A
  • Hypovolemic (e.g. haemorrhage, dehydration)
  • Cardiogenic (e.g. heart failure)
  • Distributive (most common) (e.g. sepsis, anaphylaxis)
    • Severe, overwhelming infection causes profound vasodilatation due to release of corticoids, cytokines etc.
    • This leads to poor perfusion to organs (septic shock)
  • Obstructive (e.g. cardiac tamponade, pulmonary embolism)
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5
Q

What are the features of Shock?

A
  • Hypotension/hypovolemia
  • LV impairment
  • Changes in vascular resistance
  • Poor renal/peripheral perfusion
  • Confused/sedated
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6
Q

What are the goals of Shock resucitation?

A
  • Restore blood pressure (ensure patient is euvolemic, maximise CO, measure centrally via intra-aortic balloon pump)
  • Normalize systemic perfusion (inotropes and vasopressors, benefits outweighs risks in emergency revascularisation and initial medical stabilisation)
  • Preserve organ function (renal perfusion)
  • Treat underlying cause (antibiotics; relieve tamponade)
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7
Q

What is cardiogenic shock?

What is it characterized by?

A

Cardiogenic shock has multiple causes

  • Ischaemic
  • Valve dysfunction
  • Acute VSD (ventricular septal defect)

It is characterized by high systemic resistance (sympathetic activity) and low cardiac output.

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8
Q

In cardiogenic shock it is important to…….

Why?

A

In impaired ventricular function, it is important to ensure that patient is euvolemic (normal body fluid) (maximises CO), because having fluid overload or underload can further impair ventricular output.

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9
Q

What are the mechanism of action of inotropoic agents?

A

Inotropic agents augments contractility, after preload established, thus improving cardiac output

Rationale is that increased cardiac output improves global perfusion

Risk includes tachycardia and increased myocardial oxygen consumption (risk of exacerbating myocardial ischemia)

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10
Q

Vasopressors/inotropic agents are __________________ (receptors)

A

Vasopressors/inotropic agents are alpha and beta adrenoceptor agonists.

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11
Q

Name some examples of Vassopressors/inotropic drugs

A
  • They include norepinephrine, epinephrine, dobutamine, dopamine.
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12
Q

Whether drug acts preferentially as a vasopressor or a positive inotrope depends on…………..

A
  • Whether drug acts preferentially as a vasopressor or a positive inotrope depends on their potency as alpha or beta agonist.
    • Majority of a agonists are vasopressors
    • Majority of b agonists are positive inotropes/chronotropes
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13
Q

Adrenergic receptors include…

What do they do?

A

Adrenergic receptors include:

  • Alpha 1 on mostly vascular smooth muscle
  • Alpha 2 on mostly presynaptic
  • Beta 1 on mostly heart
  • Beta 2 on respiratory and uterine smooth muscle
  • Beta 3 on mostly adipocytes
  • (Dopamine)
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14
Q

Compare between B-1 and A-1 receptors int he adrengergic system

Give an example of each

A

Beta-1 Receptors

Dobutamine is b1 agonist

  • b1 receptors mostly in heart
  • Increase contractility (positive inotrope)
  • Increase heart rate (positive chronotrope)

Alpha-1 Receptors

Norepinephrine is a1 agonist

  • a1 receptors mostly in blood vessels
  • Increase tone/resistance (vasopressor)
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15
Q

Describe Norepinephrine

A

Norepinephrine (Noradrenaline)

Norepinephrine is first-choice vasopressor.

  • It is potent a-adrenergic agonist (vasoconstriction)
  • It has minimal b1 adrenergic agonism (minimal inotropic, chronotropic effect)
    • Uptake 1 mechanism
      • Pre-synaptic mechanism of rapid norepinephrine uptake, therefore short half-life of norepinephrine

It increases peripheral resistance and increases systolic/diastolic BP

Its route via continuous intravenous infusion with dose of 1-100ug/min

  • Start with low dose, titrate dosage according to BP
  • Monitoring effects to reduce side effects such as coronary vasoconstriction
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16
Q

Decribe Epinephrine (adrenaline)

A

Epinephrine has mixed a and b adrenergic effects

  • Can cause both v_asoconstriction and vasodilatation (_depends on adrenoceptor density in that organ),
    • net effect of ­increasing BP
  • It is _potent inotrope and chronotrop_e (used in cardiac arrest situations)
    • Uptake 2 mechanism
      • Post-synaptic mechanism of fast epinephrine uptake, therefore short half-life

It i_ncreases myocardial oxygen consumption_ particularly in coronary heart disease

Its route via continuou_s intravenous infusion_ with dose 1-10ug/min.

17
Q

What is Epinephrine used in?

A

Epinephrine is used in treatment of anaphylaxis and symptomatic treatment of anaphylactic shock (Epi-Pen IMI):

  • Activates both a and b receptors
  • Potent vasopressor
  • BP increase
  • Dilates bronchi
18
Q

Describe Dobutamine

A

Dobutamine is b1 agonist.

  • It is potent inotrope, variable chronotrope
  • Half-life of ~2 minutes, IV dose 5-20ug/kg/min
  • Hepatic metabolism (glucuronide)
  • Caution in hypotension (inadequate volume) may precipitate tachycardia or worsen hypotension
19
Q

Describe the role of Dopamine

A

Dopamine is metabolic precursor of norepinephrine.

It has short half-life (both uptake 1 and 2 mechanisms).

  • Low dose (0.5-2ug/kg/min) is dopaminergic (increase renal blood flow) via D1 receptors
  • Moderate dose (2-10ug/kg/min) has b-effects (positive inotropy and chronotropy)
  • High dose (>10ug/kg/min) has a-effects (vasopressor)
20
Q

What are the vasopressor side effects?

A

Patients in shock already have high sympathetic drive

It causes vasoconstriction (a agonism), hence risk of rschaemia (cardiac, limb, gut, cerebrovascular)

It has increased cardiac work (a and b agonism), hence can lead to cardiac ischaemia and arrhythmias

21
Q

Describe the role of Amrinone/Milrinone

A

Amrinone/milrinone are phosphodiesterase III inhibitor:

  • Vasodilation
  • Positive inotrope (cardiac smooth muscle)
  • Increase cAMP, so activates protein kinase
    • Increases Ca2+ flux in myocardium
    • Ca2+ uptake into SR in vessels

Most often added with dobutamine as a second agent, need ITU environment and IV administration.

  • Dobutamine increases ATP -> cAMP
  • Phosphodiesterase III inhibitors increases cAMP -> AMP
22
Q

Describe the Levosimendan drugs

A

Levosimendan is a new calcium sensitizer (emerging role in treatment of shock). It requires IV administration.

  • It enhances troponin sensitivity to Ca2+
  • Increases inotropy

Side effects include arrhythmias, increased mortality

23
Q

Name a drug that is COMMONLY used for cardiac contractility

A

Digoxin

24
Q

What are the indicators for Digoxin?

A

Digoxin indications include atrial fibrillation (rate control)

  • Slows HR but also increases inotropy
  • Improves cardiac work
  • Treatment for acute/chronic heart failure

There is no effect on mortality, improves symptoms, reduces need for hospital admissions.

25
Q

Describe how you would give digoxin

A

Digoxin has long half-life, so requires loading dose (if initiate with normal dose, take 2-5 half-lives to achieve therapeutic effect)

  • Loading dose (long half-life) up to 1.5mg over 36hr (oral or IV)
  • Maintenance dose of 0.0625-0.25mg per day (dependent on renal function due to renal elimination, caution with CKD)
26
Q

Describe the mechanism of action of Digoxin

A

Increasing Inotropy

  • Inhibition of Na+/K+ ATPase -> increased [Na+]i
    • Increased [Na+]i is sensed by Na+/Ca2+ exchanger -? extrude Na+ and intrude Ca2+ -> increased [Ca]i
    • Therefore, it i_ncreases contractility_
  • Digoxin effect is more prominent in hypokalaemia since potassium competes with digoxin at Na+/K+ ATPase

Decreasing Chronotropy

  • Augments vagal tone at AV node
  • Slows AV conduction
  • Slows ventricular rate
27
Q

What are the clinical uses of digoxin

A

Digoxin Clinical Use

Clinical uses (ED, HDU) include:

  • Acute congestive heart failure with fast atrial fibrillation (not useful in chronic CCF?)
  • _AF rate control (_3rd line drug)
    • 1st line is beta-blockers, 2nd line calcium channel blockers (diltiazem)
    • Often need synergy between two of three drugs
28
Q

What are the side effects of digoxin?

A

Cardiac Toxicity

  • V_arious arrhythmias_
    • Bigeminy, NSVT, VT
    • 2nd or 3rd degree heart block
  • Changes in ECG (­increased PR, decreased QT, change P, change T, change ST)

Non-Cardiac Toxicity

  • Nausea/vomiting/anorexia/diarrhoea
  • Abdominal pains
  • Fatigue
  • Visual complaints
  • Muscular weakness
  • Dizziness
  • Dreams
29
Q

What are some Digoxin Interactions?

A

Metabolic

Metabolic interactions include include decreased K+ and decreased Mg2+

  • Increases digoxin effects and side effects
  • Care with use with diuretics

Drugs

Drug interactions include quinidine, amiodarone, verapamil, diltiazem, erythromycin, cyclosporin

  • Increases plasma levels of digoxin
  • Inhibit P-glycoprotein, which increase digoxin toxicity
30
Q

Describe the P-Glycoprotein drugs

A

P-glycoprotein (PGP) is multi-drug transporter. PGP protects against digoxin toxicity by….

  • Decreasing GI absorption
  • Increasing biliary excretion
  • Increasing renal excretion
  • Decreasing CNS access
31
Q

(Conclusions)

A
  • Shock is proportional to high mortality
  • Monitored on ITU, HDU, CCU
  • Treatment tailored for individual (treat underlying cause)
  • α and b agonists used to maintain BP and perfusion
  • (different) Digoxin useful in acute CCF complicated with AF

Regulation of Body Function (36 decks)

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