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EDAIC Online course (BCSAC 2021) > Cardiovascular physiology & pharmacology > Flashcards

Cardiovascular physiology & pharmacology Flashcards

1
Q

Cardiac AP?

A
  1. Phase (0) = Rapid depolarization - opening of fast sodium channels
  2. Phase (1) = Sodium channels close and potassium channels open
  3. Phase (2) = Plateau - open L-type calcium channel. Slow repolarization
  4. Phase (3) = Rapid repolarization - L-type calcium channels close and potassium efllux occurs
  5. Phase (4) = Sodium / potassium pumps restore the ionic gradients. Slow loss of potassium
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2
Q

Absolute refractory period ?

A
  1. Plateau phase / Phase (2)

2. Another AP cannot be generated

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3
Q

Relative refractory period?

A

Occurs between phases 3 & 4

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4
Q

Pacemaker AP?

A
  1. SA nodes have PM potential
  2. This is dependent on the leakage of sodium into the cell in phase (4)
  3. Threshold potential is at -40 mV
  4. Phase (3) = Repolarization. Calcium channels close and potassium channels open with efflux of potassium
  5. Phase (4) hyperpolarization occurs and potassium efflux stops - Threshoold potential is reached
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5
Q

CVP curve ?

A

A = Atrial contraction

C = Tricuspid valve elevation into RA

X = Downward movement of contracting RV

V = Back pressure from blood filling the RA

Y = Tricuspid valve open is ventricular diastole

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6
Q

Pathologies of A-wave - CVP?

A
  1. Absent in AF
  2. Large wave if atrium has hypertrophy
  3. Tricuspid stenosis = Cannon A-waves
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7
Q

Pathologies of V-waves - CVP?

A
  1. Giant V-waves are cause by tricuspid incompetence / regurgitation
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8
Q

Factors affecting stroke volume?

A
  1. Preload
  2. Contractility
  3. Afterload
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9
Q

Preload ?

A
  1. Represented by venous return

2. Depends on blood volume, posture and venous tone

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10
Q

Afterload represented by?

A
  1. Peripheral vascular resistance
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11
Q

Blood pressure regulation?

A
  1. Short-term

2. Long-term

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12
Q

Short-term Blood pressure regulation?

A

Mediated by;

  1. Arterial baroreceptors
  2. Cardiac baroreceptors
  3. Vasomotor centre in the brainstem
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13
Q

Long-term Blood pressure regulation?

A
  1. Neuronal
  2. Hormonal
  3. Renin angiotensin aldolsterone system
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14
Q

Frank-starling relationship?

A

The force of contraction of cardica muscle is proportional to it’s initial fibre length

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15
Q

Increased End Diastolic Volume?

A

There is increase in stroke volume due to increased forceful contraction

LVEDV may be used as preload

There is increased cardiac output

Not favourable in heart failure

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16
Q

Frank starling curve? Right and downward shift ?

A
  1. Heart failure
  2. Beta-blockers
  3. Hypoxia
  4. Acidosis
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17
Q

Frank starling curve? Left and upwards shift ?

A
  1. Inotropes
  2. Sympathetic stimulation

Improvement in contractility

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18
Q

Venous return?

A

Components include;

VR = MSFP - RAP / Rven x 80

MSFP = Mean systemic filling pressure

RAP = Right atrial pressure

Rven = Venous resistance

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19
Q

Determinants of venous return?

A
  1. Presence of pressure gradient along the vessel
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20
Q

Abscence of venous return?

A

Occurs when RAP = MSFP then no pressure gradient exists and thus VR = 0

This will occur at RAP of 7 mmHg

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21
Q

Flow / venous return increases?

A
  1. With reduction in RAP

2. Reduction of resistance in the venous system increases the venous return and cardiac output

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22
Q

Baroreceptors?

A
  1. Mechanoreceptors
  2. Respond to stretch
  3. Temrinal myelinated nerve endings located within the vessel walls and cardiac chambers
  4. Their AP / firing rate is altered in response to changes in BP
  5. Create a negative feedback mechanism
  6. Located in the carotid sinus and aortic arch wall
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23
Q

Classification of Baroreceptors?

A

High pressure baroreceptors: Carotid sinus and aortic arch

Low pressure barorreceptors; Chambers of the heart, large systemic veins and pulmonary beds.

24
Q

Baroreceptor reflex? See picture diagram

A
  1. Increased BP
  2. Baroreceptor discharge impulses in carotid and aortic vessels
  3. Along vagus and glossopharyngeal nerves to the brainstem
  4. Discharge along the nerves increases with increase in BP with reduction in sympathetic outflow and increase in parasympathetic flow
  5. Thus reduction in blood pressure
25
Q

Immediate response to blood loss?

A
  1. Baroreceptor reflex activation
  2. Reduced parasympathetic activity
  3. Increased sympathetic activity
  4. Increase contractility, tachycardia and increased SVR
  5. Redistribution of CO from the skin, muscle and viscera to the brain and heart
26
Q

Immediate response to blood loss? Neurohumoral

A
  1. Increased ADH secretion from posterior hypophysis

2. Increased adrenal release of NA, A and cortisol via sympathetic nervous system

27
Q

Aldosterone?

A

Increases sodium and water at the distal convoluted tubule

28
Q

Uses of Valsalva maneuver?

A
  1. Used to assess autonomic function

2. Termination of SVT

29
Q

Phases of valsalva maneuver? (4 phases)

A
  1. Increased thoracoabdominal pressure. Transient increase of venous return. increased BP and lowering HR
  2. Sustained rise in thoracic pressure reduces venous return. Fall in BP with restoration by compensatory tachycardia
  3. Pressure release and further fall in BP. HR remains elevated
  4. BP is restored with reflex bradycardia
30
Q

Valsalva maneuver and autonomic dysfunction?

A
  1. Persistent fall in BP following +ve intrathoracic pressure
  2. No relfex tachycardia
  3. On release of pressure, overshoot of BP does not occur.

Hence impaired baroreceptor reflex

31
Q

Read haemodynamic changes in ?

A
  1. Exercise
  2. Pregnancy
  3. Children
  4. Post-heart transplant
32
Q

Sympathomimetics - Adrenergic agonists? See picture

A
  1. Adrenoreceptors or dopamine receptors
  2. Basic structure is benzine ring with amine side chains (catechol)
  3. Naturally occuring or synthetic agents
33
Q

Adrenaline?

A
  1. Dose dependent
  2. Low doses B1 - Increased CO & coronary dilation. Decrease in peripheral vascular resistance. Splanchnic vasodilation
  3. High dose Alpha 1 - Rise in SVR
34
Q

Noradrenaline ?

A
  1. Low doses - Tachycardia

2. High doses relfex bradycardia and splanchnic vasoconstriction

35
Q

Read - Vaughan William classification of antiarrhythmic drugs

A

See picture

36
Q

Amiodarone ?

A
  1. Poorly absorbed from the gut - Bioavailability 50-70%
  2. About 95% protein bound
  3. Large vD 70 L/kg
  4. Excreted by lacrimal gland, skin and billiary tract
  5. Weak class I, II and IV action
  6. Blocks potassium channels and slows repolarization - Increasing duration of AP
  7. Increases the effective refractory period
  8. Half-life - 20 to 100 days
  9. 5mg/kg loading dose and 15mg/kg over 24 hours
37
Q

Structured responses?

A
  1. Indications
  2. Contraindications
  3. Side effects
38
Q

Indications for Amiodarone?

A
  1. SVT

2. WPW syndrome

39
Q

Side effects of Amiodarone?

A
  1. Pulmonary fibrosis - After a year of treatment (15%)
  2. Cirrhosis, hepatitis and jaundice
  3. Corneal deposits
  4. Ataxia, dizziness, depression, nightmares
  5. Thyroid dysfunction - Inhibits convertion of T4 to T3
  6. Cutaneous hypersensitivity - Blue grey discolouration of skin
40
Q

Contraindications of Amiodarone ? - Part II exam

A
  1. Heart block - Wihtout pacemakers
41
Q

Digoxin?

A
  1. Inhibits Na/K pump
  2. Increases intracellular sodium and decreased potassium
  3. Increased influx of calcium in exchange for sodium and thus increased contractility
  4. increases refractory period of AV node
  5. Decreases ventricular refractory period
  6. Acts indirectly by enhancing the release of acetylcholine at the cardiac muscarinic receptors
  7. Excreted unchanged in urine
  8. > 2.5mcg/L is toxic
42
Q

Indications of Digoxin?

A
  1. A.fib & A.flutter

2. Heart failure

43
Q

Side effects of dixogin toxicity?

A
  1. Visual disturbance - Orange tone
  2. GI disturbances
  3. Downsloping ST depression
44
Q

Treatment of Digoxin toxicity?

A
  1. Correct hypokalaemia

2. Ventricular arrhythmias - Phenytoin & lidocaine

45
Q

Classification of antihypertensive drugs? - Based on site of action

A
  1. Centrally acting - Clonidine, Methyldopa
  2. Action on heart - Beta-blockers - Atenolol
  3. Vasodilators - ACE inhibitors, Angiotensin antagonists (losartan), CCB (Nifedipine), Alpha blockers (Prazosin), Nitric oxide formation ( Sodium nitropruside, GTN), Ganglion blockers (Trimethaphan)
  4. Kidney - Diuretics
46
Q

Sodium nitroprusside ?

A
  1. Unstable in solution and needs protection from light
  2. Compensatory tachycardia and rebound HTN
  3. Increased ICP
  4. Loss of HPV
  5. Cyanide toxicity when > 8mcg.kg.min
47
Q

Cyanide toxicity ?

A
  1. Each molecule of SNP undergoes non-enzymatic degradation in RBC
  2. About 5 cyanide ions are produced
  3. Cyanide ions metabolised to thiocyanate in the liver and excreted in urine
48
Q

Mx of cyanide toxicity ?

A
  1. Chelating agents - Dicobalt edetate
  2. Sodium thiosulphate - Converts cyanide to thiocyanide
  3. Sodium nitrite - Converts Hb to methemoglobin which acts as a buffer to the cyanide
  4. Use of B12
49
Q

Beta-blockers ?

A
  1. Competitive antagonists at beta-adreno receptors
  2. Reduces cardiac output , lowering BP
  3. reset baroreceptor activity
  4. Inhibition of renin-angiotensin system
  5. Presynaptic inhibition of noradrenaline release
50
Q

Classification of beta blockers?

A

See pictures

51
Q

Indications for use of beta-blockers?

A
  1. Chronic HTN
  2. IHD
  3. Atenuation of laryngoscopy
  4. Anxiety
  5. Thyrotoxicosis
  6. Pheochromocytoma
52
Q

Contraindication for beta blockers?

A
  1. Cardiac failure
  2. B1 contraindicated in patients with symptomatic bradycardia
  3. AV block
  4. Non-selective used with caution in asthmatic patients
53
Q

Side-effects of beta blockers?

A
  1. Bronchospasm
  2. Cardiac failure
  3. Heart block
  4. Mask signs of hypoglycaemia
  5. Worsen PVD
  6. Depression and sleep disturbances
54
Q

Classification of diuretics ?

A
  1. Acetazolamide
  2. Osmotic diuretics (Mannitol)
  3. Loop diuretics (Furosemide)
  4. Thiazide diuretics
  5. Potassium sparing diuretics
55
Q

Mannitol?

A
  1. Freely filtered at the glomerulus
  2. Not reabsorbed in the tubules
  3. Increases the osmolarity of the filtrate
  4. Urinary volume is increased by osmotic effect

EDAIC Online course (BCSAC 2021) (35 decks)

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