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Yr 4 - ACC > Inotropes & Vasopressors > Flashcards

Inotropes & Vasopressors Flashcards

1
Q

What are inotropes?

A

Agents that increase myocardial contractility (inotropy).

E.g. adrenaline, dobutamine, isoprenaline, ephedrine

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2
Q

What are vasopressors?

A

Agents that cause vasoconstriction leading to increased systemic and/or pulmonary vascular resistance.

E.g. noradrenaline, vasopressin, metaraminol, vasopressin, methylene blue

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3
Q

What are inodilators?

A

Agents with inotropic effects that also cause vasodilation leading to decreased systemic and/or pulmonary vascular resistance (SVR, PVR).

E.g. milrinone, levosimendan

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4
Q

What is adrenaline?

A

A sympathomimetic amine with both alpha and beta adrenergic stimulating properties.

Beta > alpha

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5
Q

What are the 2 key indications for adrenaline?

A

1) anaphylaxis

2) cardiac arrest

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6
Q

ALS adrenaline dose in anaphylaxis?

A

0.5ml 1:1000 IM

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7
Q

ALS adrenaline dose in cardiac arrest?

A

10ml 1:10,000 IV

or

1ml of 1:1000 IV

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8
Q

Where is adrenaline produced from?

A

Adrenal medulla

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9
Q

What makes up the adrenal gland?

A

1) outer cortex

2) inner medulla

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10
Q

What 2 hormones is the outer adrenal cortex responsible for secreting?

A

Cortisol & aldosterone

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11
Q

What 2 hormones is the inner adrenal medulla responsible for secreting?

A

Adrenaline & noradrenaline

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12
Q

Action & effects of adrenaline?

A

Acts on both alpha and beta receptors:

1) Increases both heart rate and contractility (b1)

2) Acts on β 2 receptors in skeletal muscle vessels, causing vasodilation

3) Causes vasoconstriction in the skin & kidneys (causes a narrow pulse pressure)

4) Increases cardiac output and total peripheral resistance

5) inhibits insulin secretion by the pancreas (α adrenergic)

6) stimulates glucagon secretion in the pancreas (β adrenergic)

7) stimulates glycogenolysis in the liver and muscle (α adrenergic)

8) stimulates glycolysis in muscle (α adrenergic)

9) stimulates ACTH

10) stimulates lipolysis by adipose tissue (β adrenergic receptors)

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13
Q

What is phentolamine?

A

a non-selective alpha-adrenoceptor antagonist.

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14
Q

Indications for phentolamine?

A

1) reverse vasoconstrictive effects of adrenaline e.g. in digital ischaemia (think local anaesthetic)

2) hypertensive crisis e.g. interaction of MAOIs with tyramine foods, pheochromocytoma

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15
Q

Effect of adrenaline on the pancreas?

A

1) Inhibits insulin secretion (action on α adrenergic receptors)

2) Stimulates glucagon secretion (action on β adrenergic receptors)

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16
Q

Effect of adrenaline on blood glucose?

A

Raises blood glucose by:

1) inhibiting insulin
2) stimulating glucagon release
3) stimulates glycogenolysis in the liver and muscle
4) stimulates glycolysis in muscle
5) stimulates ACTH
6) stimulates lipolysis by adipose tissue

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17
Q

How does adrenaline affect ACTH?

A

Increases ACTH (which then increases cortisol)

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18
Q

How can adrenaline affect potassium?

A

Causes hypokalaemia

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19
Q

2 key indications for noradrenaline?

A

1) Acute hypotension

2) On-going treatment of acute hypotension

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20
Q

What is vasopressin?

A

An endogenous hormone with a direct antidiuretic effect on the kidney.

Also known as antidiuretic hormone (ADH).

21
Q

Where is ADH made/released?

A

Made in the hypothalamus.

Released from the posterior pituitary.

22
Q

Give 3 physiological changes that trigger ADH release

A

1) an increase in plasma osmolarity (detected by osmoreceptors in the hypothalamus)

2) a reduction in blood volume

3) an increase in the levels of angiotensin II

23
Q

Role of ADH/vasopressin in dehydration?

A

ADH increases water reabsorption by binding to V2 receptors, subsequently anchoring water channels (aquaporins to the apical membrane of cells in the collecting duct and DCT of the kidney.

1) When someone becomes dehydrated, the osmolarity of the extracellular fluid increases

2) ADH released from posterior pituitary

3) Water is reabsorbed at an increased rate at the level of the kidney

4) This acts to increase the intravascular fluid volume.

5) This increases BP through an increase in venous pressure, thereby boosting venous return to the heart, and increasing cardiac output.

24
Q

Role of ADH in haemorrhagic shock?

A

ADH also acts as a vasoconstrictor targeting V1 receptors on vascular smooth muscle at high concentrations.

25
Q

What is renin?

A

A hormone released from granular cells in the juxtaglomerular apparatus.

26
Q

What is renin released in response to?

A

1) increased concentration of salt in the blood

2) reduction in renal blood flow

3) stimulation from the sympathetic nervous system acting on beta-1 receptors.

27
Q

Describe the renin-angiotensin-aldosterone system (RAAS)

A

1) Renin released from granular cells in the juxtaglomerular apparatus in the kidneys

2) Renin converts angiotensinogen (a protein synthesised by the liver) into angiotensinogen I

2) Angiotensinogen I is subsequently converted by angiotensinogen-converting enzyme (ACE) into angiotensin II.

3) Angiotensin II causes vasoconstriction in the systemic circulation and the renal microvasculature, preferentially constricting the efferent arteriole.

4) Angiotensin II activates aldosterone, which increases salt reabsorption

5) Angiotensin II also causes increase in plasma volume through stimulation of ADH

28
Q

Where is ACE primarily found?

A

In the lungs

29
Q

Role of ACE in the lungs?

A

Rids the body of a vasodilator called bradykinin, causing further vasoconstriction.

30
Q

Where does aldosterone act?

A

Aldosterone acts on the principal cells found in the DCT and collecting duct of the nephron, increasing Na+ reabsorption while simultaneously increasing K+ secretion into the tubules.

31
Q

Effect of aldosterone on Na+ and K+?

A

Increases Na+ reabsorption

Increases K+ secretion into the tubules

32
Q

Indications for vasopressors?

A

1) Variceal haemorrhage: terlipressin causes constriction of the splanchnic vessels

2) Septic shock (cardiac arrest)

33
Q

Role of vasopressors?

A

Increase BP by causing contraction of smooth muscle in arteries.

This results in an increase in systemic vascular resistance.

34
Q

Role of inotropes?

A

Increase contractibility of heart

35
Q

define stroke volume

A

The volume of blood pumped out of the heart with each beat

36
Q

What is found on x axis of Frank Starling curve?

A

Ventricular end diastolic volume (mmHg)

37
Q

What is found on y axis of Frank Starling curve?

A

Stroke volume (ml)

38
Q

What does the Frank Starling law state?

A

The force or tension developed in a muscle fiber depends on the extent to which the fiber is stretched.

In the heart, increasing ventricular end-diastolic volume (preload) increases strength of ventricular contraction during systole (stroke volume).

This is true up until a certain point when sarcomeres in the heart can become overstretched, and the stroke volume begins to fall.

39
Q

Define preload

A

The amount of sarcomere stretch experienced by cardiomyocytes at the end of ventricular filling during diastole.

Preload is directly related to ventricular filling.

40
Q

Impact of positive inotropes on Frank Starling curve? (e.g. digoxin)

A

Moves curve UPWARDS i.e. increases strength of contraction and therefore stroke volume.

41
Q

Impact of negative inotropes on Frank Starling curve? (e.g. beta blockers)

A

Moves curve DOWNWARDS i.e. decreases strength of contraction and therefore stroke volume.

42
Q

Why are inotropes & vasopressors normally only given in ICU?

A

1) Short half life - need to be given as infusion

2) Require constant invasive monitoring e.g. arterial line for BP

3) Best delivered via a central line

43
Q

Give 3 examples of positive inotropes

A

1) Dobutamine

2) Dopamine

3) Adrenaline

44
Q

What is a key side effect of inotropes?

A

Myocardial ischaemia - as they increase how hard a heart contracts which increases its oxygen demand.

45
Q

Give 4 examples of vasopressors

A

1) Noradrenaline

2) Metaraminol

3) Phenylepherine

4) Adrenaline

46
Q

Give 2 key adverse effects of vasopressors

A

1) Can cause increased work on heart, due to constriction of arteries and increased afterload

2) Can contribute to hypertensive episodes

47
Q

Is adrenaline a vasopressor or inotrope?

A

Both

48
Q
A

Yr 4 - ACC (73 decks)

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