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NSF > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is meant by an inotrope, lusiotrope and chronotrope?

A

Chronotropes alter heart rate (positive and negative), Inotropes alter force of contraction (contractility) and lusiotropes alter diastolic relaxation.

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2
Q

By what mechanisms can positive inotropes work?

A

Sympathetic stimulation, increasing EDVV

Pharm – Enhance sympathetic activity, increase intracellular Ca2+, Increase EDVV

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3
Q

What drug groups are considered positive inotropes?

(x3 main)

A

PDE3 Inhibitors, Sympathomimetics, cardiac glycocides (digoxin), (Anticholinergics, Glucagon)

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4
Q

Outline a situation in which you would NOT want to use a positive inotropes.

A

When the patient has aortic/pulmonary stenosis – inotropes can cause further damage to vessels.

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5
Q

What is the theory of MOA of digoxin?

A

They inhibit Na/K pump in cardiac myocytes = increased intracellular Na, this reduced Ca extrusion from cell (via Na/Ca exchanger) (Because smaller gradient for Na to move into of cell), therefore more Ca moved into SR to be released during an action potential

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6
Q

What other effects can cardiac glycocides have on cardiac cells, explain?

A

Negative chronotropy, since Na+ removal from the cell is inhibited (no action potentials)

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7
Q

Which adrenoceptor can be found on cardiac myocytes?

A

Beta 1

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8
Q

Outline a situation in which sympathomimetics are used and what side effects can be predicted from their use?

A

They are sympathetic agonists. Dobutamine is used in equine anaesthesia. Their use can increase risk of automaticity and lead to tachycardia.

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9
Q

Outline how PDE3 inhibitors work.

A

PDE 3 is a cardiac specific compound. It inhibits degradation of cAMP.

  • Increased cAMP
  • PKA activation
  • phosphorylation of Ca2+ channels
  • More intracellular Ca2+ and CICR
  • Stronger contraction
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10
Q

What effects other than inotropy will PDE 3 inhibitors have?

A

Vasodilation (no myosin phosphorylation = relaxation of smooth muscle)Tachycardia

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11
Q

Name a PDE3 inhibitor used in practice. What potential side effects can it have?

A

Pimobendan - vetmedinInappetance Haemorrhage HypersalivationConstipation

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12
Q

Name the three groups of drugs that would come under the bracket of Negative Inotropes

A

Sympathetic antagonists - beta blockers

Cholinergics - Antagonise sympathetic action via M2 receptor

Calcium channel blocker - Reduce calcium influx into the cell

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13
Q

What is heart rate determined and altered by?

A

ANS

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14
Q

What is AP conduction reliant on?

A

Normal activity of Na, K and Ca channels, Normal intra and extra cellular levels of the afore mentioned ions, Correct function of intercalated discs.

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15
Q

What factors can cause abnormal cardiac rhythm?

A

Ectopic pacemakers, damaged conductive tissue, altered cardiac discs

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16
Q

Bradyarrhythmia can be treated using…

A

Positive chronotropes/ intropes, pacemakers

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17
Q

Name three bradyarrythmias.

A

AV block (1st/2nd/3rd degreeSinus sick syndromeAtrial standstill

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18
Q

What is the difference between 1st, 2nd and 3rd degree AV block?

A

1 - P-R interval is increased, caused by increased vagal tone/ ischemic damage etc2 - Some P waves are not accompanied by QRS complexes (ventricular rhythm is slower than sinus rhythm)3 - Complete block of AV node, no association between QRS and P waves. QRS are generated in the ventricle,

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19
Q

Define a supraventricular tachycardia.

A

Usually caused by reentry currents within the atria or between ventricles and atria producing high heart rates.

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20
Q

What is “sinus sick” syndrome?

A

A disturbance of SA nodal function that results in a markedly variable rhythm (cycles of bradycardia and tachycardia).

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21
Q

What is Atrial fibrillation?

A

Uncoordinated atrial depolarisation.

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22
Q

What pharmacological agents could be used to treat bradyarrhythmias?

A
  • Sympathomimetics- beta 1 agonists - also increase myocardial oxygen consumption- beta 2 agonists - +ve chrono&dromotropy
  • Anticholinergics- Atropine
  • Methylxanthines (also a bronchodilator)- Reduces hyperpolarisation
  • PDE III inhibitors- increase cAMP
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23
Q

What is the effect of a dromotrope?

A

Alters AV node conduction

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24
Q

What negative effects does tachycardia have on the body?

A

It decreases EDVV, decreasing the SV, decreasing the CO! Increased cardiac work leads to myocardial hypertrophy

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25
Q

How can tachyarrhythmias be reduced?

A

Reduce firing rate or slow conduction of impulses.

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26
Q

Briefly describe the Vaugh-Williams classification of antidisrhythmics.

A

Ia,b,c - sodium channel blockersII - Beta blockersIII - K channel blockers that act to prolong the APIV - calcium channel blockersV - Miscellaneous

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27
Q

What overall effects do class I antidisrhythmics have on the body?

A

Na channel blockade . Preferably effect open or refractory channels . The more active the channels, the better they work Therefore they reduce the heart rate in tachyarrhythmias but have little effect on other heart rates.

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28
Q

Briefly summarise each of the V-W antidisrrhythmic class I and subgroups.Give an example for each.

A

IC > IA > IB

  • 1A - Moderate reduction in phase 0 slope; increase APD; increase ERP.
  • IB - Small reduction in phase 0 slope; reduce APD; decrease ERP.
  • IC - Pronounced reduction in phase 0 slope; no effect on APD or ERP.

ADP - action potential duration, ERP - effective refractory period

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29
Q

Name a class II A/D.

A

Atenolol - β1 selective .

A - Oral/Parenteral.

D - Hydrophillic

E - Excreted in urine.

ADVERSE: limited to CVS

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30
Q

Class III A/Ds block K+ channels, what effect does it have and how does it prolong the AP?

A

Slows repolarisation Increases refractory period

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31
Q

Name and summarise a Class III A/D

A

Sotalol.

  • Racemic mixture of two isomers.
    • L- isomer is non selective beta-blocker.
    • D- isomer inhibits K channels

Oral admin, Excreted unchanged by kidneys

ADVERSE: Hypotension, Bradycardia, AV blockade GI signs

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32
Q

Summarise Digoxin as an A/D

A
  • Oral
  • Fair plamsa protein binding
  • Minimal hepatic metabolism
  • Renal excretion
  • VERY specific theraputic range
  • ADVERSE: calcium overload, Automaticity, GI toxicity
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33
Q

What sort of arrhythmias can you use Digoxin to treat?

A

Supraventricular - it is contraindicated in ventricular arrhythmias

34
Q

How does Digoxin act as an A/D Vagomimetic, increases vagal outflow

A

Slows conduction through the AV node, increases the refractory period

35
Q

Digoxin is a positve inotrope, what is it also?

A

Negative chronotrope - Class V A/D (it increases the refractory period)

36
Q

Name and summarise a Class IV A/D

A
  • Diltiazam
  • Also a coronary and systemic dilator.
  • Oral/parenteral.
  • Extensive first pass metabolism - Liver metabolised
  • ADVERSE: Uncommon - bradycardia, Liver enzyme elevation, Personality changes
37
Q

When are Class IV A/Ds useful?

A

Supraventricular tachycardias and Atrial fibrillation

38
Q

What is significant about Class IV A/Ds

A

Block Ca channels in cardiac muscle only. Also Negative inotropes and positive lusiotropesThey shorten the plateau phase of contraction (slow SA to AV conduction)

39
Q

Outline the process of cardiac muscle contraction.

A

Voltage change caused by an influx of positive ions (Na+/Ca2+) through the gap junctions initiates depolarisation by opening Na+ channels. Rapid entry of Na+ causes opening of slow Ca channels. This triggers CICR from SR; When K+ channels open Ca2+ briefly = K+ (plateu - allows ventricular filling) VGCC are inactivated leading to repolarisation alongside K+ efflux. Ca2+ is actively transported out of the cell and into ECF and SR. K+/Na+ pump restores membrane potential.

40
Q

Outline the MOA of Nitrate vasodilators.Name examples.

A

They are direct vasodilators (act on vessel smooth muscle) They act via cGMP to cause hyperpolarisation.Nitroglycerine and nitroprusside.

41
Q

Name a direct vasodilator which acts as a Ca2+ channel blocker.

A

Amlodipine (istin)

42
Q

Name a direct arteriodilator which has a particular at coronary, renal and cerebral arteries.

A

Hydralazine

43
Q

Which phosphodiesterase enzyme is a receptor targeted to cause vasodilation of arteries?Name an inhibitor of this enzyme.

A

FiveSildenafil (viagra)

44
Q

How do indirect vasodilators work?

A

Influence a system which causes vasodilation, for example, RAAS or SNS (via a1 adrenoceptors)

45
Q

Outline three targets of the RAAS which cause vasodilation.Name examples from each.

A

ACE inhibitors - Enalapril, Ramipril and Benzapril (Fortekor)Angiotensin 2 receptor agonist - TelmisartanAldosterone antagonist - Spironolactone

46
Q

Name a class IV A/D.

A

Diltiazem (aka hypercard)

47
Q

What drug classes are considered negative inotropes?

A

Sympathetic antagonists (beta blockers), Ca2+ channel blockers, Cholinergics

48
Q

Name a positive inotrope which acts by agonising Beta1 adrenoceptors

A

Dobutamine

49
Q

How do methyxanthines work in the CV system?

A

Used to combat bradyarrhythmias, they reduce hyperpolarisation and speed up pacemaker potentials. (they are also bronchodilators)

50
Q

What does an eCG measure?

A

Electrical activity of the heart from one location to another

51
Q

Explain what is seen on a normal eCG waveform.

A

P - Atrial depolarisation

Q - Early ventricular depolarisation (within the intraventricular septum)

R - Ventricular depolarisation

S - Late ventricular depolarisation

T - Ventricular depolarisation

52
Q

What is the relevance of the three AV leads?

A

AVR - RF with average of LF and LHAVL - LF with average of RF and LHAVF - LH with average of RF and LFThese are the unipolar lead sets

53
Q

What can we use an eCG for?

A

Measuring: heart rate, rhythm, mean elecrical axis, interval timings/ voltage, heart chamber size

54
Q

What can be interpreted from the intervals seen on an eCG?

A

PR/PQ interval - Time to transmit from AV node and bundle.ST segment - Indicates the voltage between depolarisation and repolarisation (should be at baseline)

55
Q

Outline how changes in chamber size can be indicated on an eCG.

A

Right atrial enlargement (P pulmonale) - tall P wave Left atrial enlargement (P mitrale) - wide P wave Ventricular enlargement - Tall R waveLeft ventricular enlargement and hypertrophy - Wide R wave

56
Q

How can you calculate mean electrical axis from an eCG?

A
  1. Find the isoelectric lead - the one where the sum of the positive and negative deviations of the qrs complex is zero. 2. The MEA is the angle perpendicular to this using Baileys hex axial diagram.
57
Q

What is meant by forward heart failure? What effects does it have?

A

Systolic failure - reduced cardiac contractility causes reduced cardiac output and mean arterial pressure, this leads to reduced perfusion pressure and capillary refil time.

58
Q

Sinus arrhythmia

A

Regular abnormal rhythm

59
Q

Supra ventricular premature complex

A

Out of place QRS complex, electrical initiation arises from above the ventricle.

60
Q

Ventricular premature complex

A

QRS and T complexes oppose each other, the action potential is not following the his purkinje route normally taken

61
Q

Benazepril is an example of what class of drugs used to treat heart failure?

A

ACE inhibitor

62
Q

Outline the coronary circulation of the heart.

Which vessels drain the heart and where do they drain into?

A

Supplies cardiac mesenchyme.

L - caudosinistral sinus passes between left auricle & pulm trunk to coronaryG > left intervent artery in the interventG > apex + circumflex artery in the coronaryG to caudal side of the heart, terminates close to (H/P)/ in (C/R) right AVG.

Right - cranial sinus passes between right auricle and pulmonary trunk to coronaryG runs round to right side of the heart and peters out (C/R)/ ends in right AVG.

Drained via great cardiac vein into right atrium or viathespian veins into all chambers

63
Q

Which vessels arise from the brachiocephalic trunk?

What is special about one of the vessels in the dog and pig?

A

Paired carotid and paired subclavian vessels.

In the dog and pig the left subclavian remains distinctly separate from the trunk, arising distal to the heart.

64
Q

Visceral pleura.

Branches and what they cover.

Outline the significance of a cranial pneumothorax in the dog.

A

Reflected back at the root of the lung on to the mediastinum forming the mediastinal pleura, the ribcage forming the costal pleura and the diaphragm forming the diaphragmatic pleura. These last three together form the parietal pleura.

This forms the pleural cavity - a potential space filled with a few mls of fluid.

The cupula pleura protrudes beyond the first rib, a deep wound to this area can result in pneumothorax since it is not protected by the ribcage.

65
Q

Outline the circulatory changes which occur at birth in the neonate.

A

First breath = drop in pulmonary pressure, increased pulmonary flow. This decreases afterload on the right side of the heart. Venous return to the left side of the heart increases therefore closeing the foramen ovale.

The ductus arteriosus shuts due to smooth muscle contraction which is stimulated by reduced flow since aortic pressure is now greater than pulmonary pressure.

Ductus venosus also closes due to sm contraction.

66
Q

Describe these four neonatal heart pathologies.

  1. Stenosis of greater vessels
  2. Vascular ring abnormalities
  3. Septal defect
  4. Patent ductus arteriosus

A teralogy of fallot is a combination of which four pathologies?

A
  1. Narrowed vessels - increased afterload and ESVV - thickened left side if aortic and thickened pulm vessels if pulmonary
  2. 4th aortic arch persists - traps trachea and oesophagus - megaoesophagus
  3. Atrial - mixing of oxygenated and deoxygenated blood. Ventricular - moves from L to R = right overload
  4. Aorta to pulmonary flow - Pulmonary hypertension (^afterload, thickened right heart)

TOF - VSD, aorta moved, PS and RVHypertrophy

67
Q

The umbilical artery and vein form which structures in the mature animal?

A

Artery = round ligament of the bladder

Vein = round ligament of the liver (found within the falciform ligament)

68
Q

What do the heart sounds correspond to?

A
  1. AV valve has closed, blood turbulence within the ventricle, blood is being squeezed towards the great vessels.
  2. Pulmonary and aortic valves are opened, blood turbulence within the great vessels and deceleration
  3. Turbulence in the left ventricle as blood flows from the atria under pressure
  4. Increased force of contraction due to slowed relaxation of the ventricles (stiff walls)

Remember S3 and 4 are pathological in small animals.

69
Q

Explain the circulation in the neonate BEFORE birth.

(x5 aspects + brief description)

A
  1. Foramen Ovale - oxygenated blood moves from right atrium to left atrium to the body
  2. Pulmonary circulation - hypoxic pulmonary vasoconstriction
  3. Ductus Arteriosum - blood moves from pulmonary artery to the aorta due to high pulmonary tension
  4. Ductus Venosus - supplies caudal vena cava with oxygenated placental blood
  5. Umbilical vessels - vein brings oxygenated blood from placenta to the right atrium - bypassing the liver
70
Q

What are the names of the embryological lymphatics which give rise to mature lymphnodes?

(there are 6)

Which one doesn’t develop in the mature animal?

A
  1. 2x jugular sacs - head neck and forelimb
  2. Cisterna chyli - viscera
  3. Retroperitoneal - viscera
  4. 2x illiac sacs - hindlimb and pelvic region
71
Q

Frank-Starling law

How does this relate to the contraction of smooth muscle?

A

Stroke volume increases with increase EDVV but only up to a certain point.

Beyond a certain point sarcomere length is stretched beyond the optimal, therefore SM contraction does not occur.

72
Q

Preload vs Afterload

When considering SV = EDVV - ESVV which do preload and afterload effect?

A

Preload - Pressure in ventricles before contraction - cardiomyocyte stretch - Affects EDVV (lower preload, lower EDVV) > Stroke volume

Afterload - Pressure the heart works against to eject blood during systole - Affects ESVV (higher afterload, higher ESVV) < Stroke volume

73
Q

Pulse pressure.

Which four factors affect PP and how?

A

P = systolic pressure - diastolic pressure

  1. Stroke volume >
  2. Aortic compliance < (increases afterload therefore increasing systolic pressure but decreasing diastolic pressure)
  3. Total peripheral resistance >
  4. Heart rate <
74
Q

How can we measure systolic function of the heart?

How can we measure diastolic function of the heart?

A

Systolic

  • Ejection fraction = SV/EDVV

Diastolic

  • Compliance = Change in volume/change in pressure
75
Q

Outline the electrical pathway of the heart.

How are the atria and ventricles electrically separates?

A

Separated by the annulus fibrosus

76
Q

How do pacemaker potentials of the heart work?

A
  1. L-type Calcium channels open = hyperpolarised
  2. Ca2+ channels close, K+ channels open = repolarised and depolarised
  3. K+ close and FUNNY Na+ channels open = back to threshold (+T-type Ca2+ channels)

Remember SAN > AVN so that atria contract before ventricles.

77
Q

Draw the action potential of a cardiomyocyte.

Why do cardiomyocytes have prolonged action potentials?

A

Prolonged due to to L-type calcium channels, this prevents tetany of the cells.

78
Q

Outine the intrinsic controls of blood pressure.

(x3-x7)

A
  • Metabolic
    • ​>rate - >O2 used, >waste, >K+ outflow = increased blood flow = active hyperaemia
    • reactive hyperaemia - increased waste & oxygen debt
  • Paracrine
    • ​NO - vasodilator released with increased flow velocity
    • Endothelial damage - endothelin 1 and TX = vasoconstrictors
    • Inflammation - PGI2, histamine, bradykinin = vasodilator
  • Mechanical
    • ​skeletal muscle pump
    • ischemia = pain
79
Q

What are the extrinsic controls of blood pressure?

Which part of the brain do they relay to?

A
  • Baroreflex - aortic arch
  • RAAS - kidney
  • Further angiotensin 2 - ^ thirst and ADH release

The cardiac centre recieves this info and can activate the SNS or PSNS

80
Q

What are the three treatment goals for forward heart failure?

What classes of drugs could you give and why?

A

Forward heart failure = systolic dysfunction

  • Improve systolic function
    • B1 agonists
  • Reduce afterload
    • Arteriodilator
  • Improve contractility
    • PDE-inhibitor
    • Calcium sensitisers
81
Q

What are the effects of backwards heart failure and how do they cause clinical signs?

What are treatment goals in these cases?

A

> atrial press > venous pressure > hydrostatic pressure > leakage of fluid

  • Left handed - Pulmonary veins leak = pulmonary oedema
  • Right handed - Vena Cava leaks = **ascites. **Increased venous pressure = jugular vein distends, hepato/splenomegaly

Treatment goals - increase water loss, improve CO, reduce compensations

  • Diuretics - potassium sparing (spironolactone) + loop
  • ACE inhibitors - reduce RAAS
  • PDE 3 inhibitors - vasodilator/ ^ CO
  • Reduce cardiac remodelling

NSF (14 decks)

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