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Cardiology.CV.hemolymph > Marr& Bowen. CardiologyoftheHorse > Flashcards

Marr& Bowen. CardiologyoftheHorse Flashcards

1
Q

Right atrium is made up of what two parts?

A

Sinus venarum cavarum: veins empty
Auricle: conical out pouching

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2
Q

What are the structures that drain into the right atrium?

A

Cranial vena cava: draining structures of head and neck
Coronary sinus: draining coronary circulation

Caudal vena cava: drianing abdominal structures into the azygous vein

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3
Q

What is the ova fossa?

A

Diverticulum at the point of entrance of the caudal vena cava
** remnant of the foramen ovale— the communicaiton between the 2 stria of the

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4
Q

Leaflets of the tricuspid valve

A
  1. Septal
  2. Parietal: lies on the right margin
  3. Angular: between the AV opening & right outflow tract
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5
Q

What the the pulmonary valve leaflets?

A

Right
Left
Intermediate

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6
Q

What are the mitral valve leaflets?

A
  1. Septal
  2. Parietal
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7
Q

The interventricular septum is made up of what tissues?

A

Muscular tissue (primarily)
Fibrous tissue: at its most dorsal extennt (membranous/nonmuscular)

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8
Q

Where is the location of the sinus of Valsalva?

A

At the base of the Aorta
**boulbous in shape—- is hte sinus of valsalva

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9
Q

Where do the 2 coronary arteries originate?

A

The sinus of valsalva

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10
Q

The ductus arteriosus connects what?

A

Joints the pulmonary artery to the descending aorta in the fetus

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11
Q

The degree of AV conduction delay is influenced by autonomic tone. With what causing increase/decrease in rate of conduction

A

Vagal tone: reducing
Sympathetic tone: increasing

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12
Q

Systole is made up of:

A

Isovolumetric contraction phase & ventricular ejection

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13
Q

Diastole is made of:

A

Isovolumic relaxation phase
Rapid filling phase
Diastasis
Atrial contraction

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14
Q

What marks the beginning and ending of systole?

A

Beginning: onset of the QRS complex
Ending: closure of the aortic valve

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15
Q

What makes up the phase of isovolumetric diastole?

A

Start when AV closes
Ventricular pressure continues to rapidly decline
**all cardiac valves are closed

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16
Q

The rate of intraventricular pressure decline during the isovolumic relaxation of diastole?

A

Determined by the rate of active relaxation of the myofibers

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17
Q

When do mitral valve leaflets open?

A

When when left ventricular pressure drops below left atrial pressure
** onset of rapid filling phase of diastole

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18
Q

Describe/define diastesis (of diastole)

A

The atriovetnricular pressure difference approaches zero
Ventricular volume reaches a plateua

**minimal changes in intraventricular pressure and volume

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19
Q

The duration of diastesis is determined by?

A

Inversely related to heart rate

**resting heart rate— diastesis is longest phase of diastole

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20
Q

S1 heart sounds

A

Closure of the AV valves

mechanical onset of systole

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21
Q

S2 heart sound

A

Closure of the semilunar valves

**end of systole

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22
Q

S3 heart sound

A

Early ventricular filling

**rapid filling phase of diastole

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23
Q

S4 heart sound

A

Atrial contraction

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24
Q

Systolic function refers to

A

Ability of the ventricles to contract and eject blood

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25
Q

Diastolic function refers to

A

The ability of the ventricles to adequately relax and fill

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26
Q

What are the major factors that affect ventricular systolic function

A

Preload (ventricular end-diastolic volume)
Inotropic/contractiel state of myocardium
Afterload: impedence to ventricular outflow
Heart Rate

27
Q

Events that cause an increase in pre-load?

A

Exercise
Anaemia
Fever
Pregnancy

28
Q

Factors that affect myocardial contractility

A

Autonomic output
Circulating substances (hormones, pharmacologic agents, endogenous & exogenous toxins, etc)
Locally produced metabolites
Pathologic processes (ischemia, acidosis, infarction, etc.)

29
Q

Ventircular filling is affected primarily by:

A

Venous return
Atrioventricular valve function
Atrial function
Pericardial compliance
Heart rate
Myocardial relaxation
Compliance

30
Q

Inadequate end-diastolic volume will result in:

A

Inadequate stroke volume
**reduced coronary perfusion

31
Q

What are the two major factors that affect ventricular diastolic performance

A

Chamber compliance
Mycoardial relaxation

32
Q

If ventricular compliance is reduced what is required to achieve a given diastolic volume?

A

A greater filling pressure

33
Q

Examples of conditions that cause a decrease in ventricular compliance

A

**chronic conditions

Reduction in LV lumen size
Pathological hypertrophy
Fibrosis
Infiltrative diseases
Pericardial tamponade or constriction
Dz or dilatation fo the opposite ventricle

34
Q

Myocardial relaxation may change acutely in response to

A

Hypoxia
Ischaemia
Altered afterload
Tachycardia
Catecholamines
Various pharmacological agents

35
Q

What are disease processes that produce diastolic dysfunction

A

Pressure overload states— myocardial hypertrophy or fibrosis (aortic and pulmonic stenosis,, systemic or pulmonary hypertension)

36
Q

What are examples of dysrhythmias that produce a loss of effective atrial systole resulting in poor exercise tolerance, wekaness or syncope

A

Atrial fibrillation
Ventricular tachycardia
High degree AV conduction block

37
Q

What are factors that affect systolic & diastolic function of the atria?

A

Atrial preload
Impedance to atrial emptying
Inotropic state of atrial myocytes
Atrial compliance

38
Q

What are the 3 methods commonly used to determine cardiac output

A
  1. Fick method
  2. Thermodilutioon method (overestimates cardiacoutput)
  3. Lithium dilution method
39
Q

What are the parameters measured on echocardiogram to determine LV systolic function?

A

Fractional shortening: percent decrease of LV minor axis
Ejection fraction: percent decrease in end-diastolic volume
Mean VCF: veloicty of circumferential fiber shortening

40
Q

Used pulsed doppler on echocardiogram, what measurements can estimate LV systolic function/indexes

A

Peak and mean velocity
Acceleration
Ejection time
**aortic root or pulmonary artery

41
Q

Indexes of diastolic function on M-mode echocardiography?

A

-peak and mean velocites of early (passive) ventricular filling (peak and mean E-wave velociteies)
Peak and mean velocities of late (atrial systolic) ventricular filling (peak and Mean A wave velocites)

-E/a ratio

42
Q

What is starlings law of the heart?

A

The more blood which returns to the heart (venous return) and stretches the heart in diastole, the large the stroke volume ejected per beat

43
Q

Parasympathetic nervous system controls what (in regards to the heart)

A

Heart rate (chronotropic effects)

44
Q

Sympathetic nervous system controls what (in regards to the heart)?

A

Heart rate
Contractility (inotropic effects)

45
Q

The sympathetic and parasympathetic control of the heart is controlled by what part of the brain?

A

Integrated by the brain stem

46
Q

Baroreceptors sense

A

Stretch
— detect high pressure within the vascular system

47
Q

Where are baroreceptors located? that detect high pressure

A

Within the aortic arch and carotid sinus

48
Q

Baroreceptors that detect low pressure are located (central volume receptors) where?

A

Atrial tissue (primarily at junction with the great veins)
Pulmonary arteries & ventricles

49
Q

Affarent input to the CNS from the heart are transmitted via the

A

Glossopharyngeal and vagal nerves

50
Q

Glossopharyngeal and vagal nerves terminate where

A

Nucleus tractus solitarius (NTS)

51
Q

Alpha 2 adrenoreceptor agonists effect o nheart

A

Increase vagal tone to heart
Reduce sympathetic tone to blood vessels

**bradycardia, hypotension

52
Q

Cardiac glycosides (digoxin) cause

A

Increase in parasympathetic tone to heart
Increased baroreceptor stimulation

** reflec reduction in sympathetic vasoconstrictor nerve activity

**variable depending on physiological state of animal

53
Q

Why is the effect of cardiac glycosides (digoxin) dependent on

A

Degree of activation of the natural hormone: endogenous digitalis-like substance— which binds to these receptors

54
Q

Vasomotor nerves are controlled by which system and hormone?

A

Sympathetic nerves—
Noradrenaline on alpha 1 adrenoreceptors

55
Q

Acetylcholine is the neurotransmitter that acts on what receptors of the SA and AV nodes

A

M2 muscarinic receptors

56
Q

Renin is produced by what cells?

A

Modified smooth mm cells o the afferent arterioles in the juxtaglomerular apparatus

57
Q

Renin then acts on angiotensin 1 which is then converted via (BLANK ) to (BLANK)

A

Angiotensin converting enzyme (ACE)

Angiotensin II

58
Q

Where is angiotenson converting enzyme located?

A

Endothelial cells— especiallly in the lung

59
Q

What is synthesized in response to angiotensin II?

A

Aldosterone

60
Q

Aldosterone MOA

A

Mineralocorticoid receptors — to preserve Na reabsorption from teh distal nephrome

**results= INC in circulating volume

61
Q

Hormone: Adrenaline

CV and Renal effects:

A

INC HR and force of contraction (beta 1)
Increase vascular resistance, decrease venous capacitance (alpha 1 on vascular smooth mm, beta 2 on sympathetic nerve terminals)
Increase in blood flow to skeletal & cardiac mm (Beta2)

62
Q

Hormone: Angiotensin II

Cardiovascular and renal effects

A

Inc vascular resistance, decrease venous capcitance (receptors on vascular smooth mm and on sympathetic nerve termianl which in rease noradrenaline release)

Increase in heart rate and force of contraction and sitmualte cardiac mm cell hyeprtrophy

Enhance sodium retention by the kidney 9direct effect in proximal tubule and mediated via aldosterone in distal tubule)

Increase thirst and possible salt appetite, enhance ADH secretion (effects on brain)

63
Q

Hormone: Antidiuretic hormone (vasopressin)

Cardiovascular and renal effects

A

Increase water retention at the kidney (V2 receptors)

Vasoconstriction (V1 receptors on vascular smooth mm) seen at higher ADH concentrations

64
Q

Hormone: Aldosterone Natriuertic peptides (ANP & BNP)

A

Increase sodium retention and potassium excretion by kidney

Increase salt and water excretion by kidney (direct effects and inhibition of aldosterone)

Inhibit renin and ADH secretion

Inhibit the peripheral and central actions of angiotensin II

Vasodilatation (modest) of resistance of blood vessels

Increase in capillary permeability— reduction in circulating volume

Cardiology.CV.hemolymph (6 decks)

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