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

Marr& Bowen. CardiologyoftheHorse Flashcards

(64 cards)

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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
Diastolic function refers to
The ability of the ventricles to adequately relax and fill
26
What are the major factors that affect ventricular systolic function
Preload (ventricular end-diastolic volume) Inotropic/contractiel state of myocardium Afterload: impedence to ventricular outflow Heart Rate
27
Events that cause an increase in pre-load?
Exercise Anaemia Fever Pregnancy
28
Factors that affect myocardial contractility
Autonomic output Circulating substances (hormones, pharmacologic agents, endogenous & exogenous toxins, etc) Locally produced metabolites Pathologic processes (ischemia, acidosis, infarction, etc.)
29
Ventircular filling is affected primarily by:
Venous return Atrioventricular valve function Atrial function Pericardial compliance Heart rate Myocardial relaxation Compliance
30
Inadequate end-diastolic volume will result in:
Inadequate stroke volume **reduced coronary perfusion
31
What are the two major factors that affect ventricular diastolic performance
Chamber compliance Mycoardial relaxation
32
If ventricular compliance is reduced what is required to achieve a given diastolic volume?
A greater filling pressure
33
Examples of conditions that cause a decrease in ventricular compliance
**chronic conditions Reduction in LV lumen size Pathological hypertrophy Fibrosis Infiltrative diseases Pericardial tamponade or constriction Dz or dilatation fo the opposite ventricle
34
Myocardial relaxation may change acutely in response to
Hypoxia Ischaemia Altered afterload Tachycardia Catecholamines Various pharmacological agents
35
What are disease processes that produce diastolic dysfunction
Pressure overload states— myocardial hypertrophy or fibrosis (aortic and pulmonic stenosis,, systemic or pulmonary hypertension)
36
What are examples of dysrhythmias that produce a loss of effective atrial systole resulting in poor exercise tolerance, wekaness or syncope
Atrial fibrillation Ventricular tachycardia High degree AV conduction block
37
What are factors that affect systolic & diastolic function of the atria?
Atrial preload Impedance to atrial emptying Inotropic state of atrial myocytes Atrial compliance
38
What are the 3 methods commonly used to determine cardiac output
1. Fick method 2. Thermodilutioon method (overestimates cardiacoutput) 3. Lithium dilution method
39
What are the parameters measured on echocardiogram to determine LV systolic function?
Fractional shortening: percent decrease of LV minor axis Ejection fraction: percent decrease in end-diastolic volume Mean VCF: veloicty of circumferential fiber shortening
40
Used pulsed doppler on echocardiogram, what measurements can estimate LV systolic function/indexes
Peak and mean velocity Acceleration Ejection time **aortic root or pulmonary artery
41
Indexes of diastolic function on M-mode echocardiography?
-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
What is starlings law of the heart?
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
Parasympathetic nervous system controls what (in regards to the heart)
Heart rate (chronotropic effects)
44
Sympathetic nervous system controls what (in regards to the heart)?
Heart rate Contractility (inotropic effects)
45
The sympathetic and parasympathetic control of the heart is controlled by what part of the brain?
Integrated by the brain stem
46
Baroreceptors sense
Stretch — detect high pressure within the vascular system
47
Where are baroreceptors located? that detect high pressure
Within the aortic arch and carotid sinus
48
Baroreceptors that detect low pressure are located (central volume receptors) where?
Atrial tissue (primarily at junction with the great veins) Pulmonary arteries & ventricles
49
Affarent input to the CNS from the heart are transmitted via the
Glossopharyngeal and vagal nerves
50
Glossopharyngeal and vagal nerves terminate where
Nucleus tractus solitarius (NTS)
51
Alpha 2 adrenoreceptor agonists effect o nheart
Increase vagal tone to heart Reduce sympathetic tone to blood vessels **bradycardia, hypotension
52
Cardiac glycosides (digoxin) cause
Increase in parasympathetic tone to heart Increased baroreceptor stimulation ** reflec reduction in sympathetic vasoconstrictor nerve activity **variable depending on physiological state of animal
53
Why is the effect of cardiac glycosides (digoxin) dependent on
Degree of activation of the natural hormone: endogenous digitalis-like substance— which binds to these receptors
54
Vasomotor nerves are controlled by which system and hormone?
Sympathetic nerves— Noradrenaline on alpha 1 adrenoreceptors
55
Acetylcholine is the neurotransmitter that acts on what receptors of the SA and AV nodes
M2 muscarinic receptors
56
Renin is produced by what cells?
Modified smooth mm cells o the afferent arterioles in the juxtaglomerular apparatus
57
Renin then acts on angiotensin 1 which is then converted via (BLANK ) to (BLANK)
Angiotensin converting enzyme (ACE) Angiotensin II
58
Where is angiotenson converting enzyme located?
Endothelial cells— especiallly in the lung
59
What is synthesized in response to angiotensin II?
Aldosterone
60
Aldosterone MOA
Mineralocorticoid receptors — to preserve Na reabsorption from teh distal nephrome **results= INC in circulating volume
61
Hormone: Adrenaline CV and Renal effects:
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
Hormone: Angiotensin II Cardiovascular and renal effects
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
Hormone: Antidiuretic hormone (vasopressin) Cardiovascular and renal effects
Increase water retention at the kidney (V2 receptors) Vasoconstriction (V1 receptors on vascular smooth mm) seen at higher ADH concentrations
64
Hormone: Aldosterone Natriuertic peptides (ANP & BNP)
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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