Marr& Bowen. CardiologyoftheHorse Flashcards
Right atrium is made up of what two parts?
Sinus venarum cavarum: veins empty
Auricle: conical out pouching
What are the structures that drain into the right atrium?
Cranial vena cava: draining structures of head and neck
Coronary sinus: draining coronary circulation
Caudal vena cava: drianing abdominal structures into the azygous vein
What is the ova fossa?
Diverticulum at the point of entrance of the caudal vena cava
** remnant of the foramen ovale— the communicaiton between the 2 stria of the
Leaflets of the tricuspid valve
- Septal
- Parietal: lies on the right margin
- Angular: between the AV opening & right outflow tract
What the the pulmonary valve leaflets?
Right
Left
Intermediate
What are the mitral valve leaflets?
- Septal
- Parietal
The interventricular septum is made up of what tissues?
Muscular tissue (primarily)
Fibrous tissue: at its most dorsal extennt (membranous/nonmuscular)
Where is the location of the sinus of Valsalva?
At the base of the Aorta
**boulbous in shape—- is hte sinus of valsalva
Where do the 2 coronary arteries originate?
The sinus of valsalva
The ductus arteriosus connects what?
Joints the pulmonary artery to the descending aorta in the fetus
The degree of AV conduction delay is influenced by autonomic tone. With what causing increase/decrease in rate of conduction
Vagal tone: reducing
Sympathetic tone: increasing
Systole is made up of:
Isovolumetric contraction phase & ventricular ejection
Diastole is made of:
Isovolumic relaxation phase
Rapid filling phase
Diastasis
Atrial contraction
What marks the beginning and ending of systole?
Beginning: onset of the QRS complex
Ending: closure of the aortic valve
What makes up the phase of isovolumetric diastole?
Start when AV closes
Ventricular pressure continues to rapidly decline
**all cardiac valves are closed
The rate of intraventricular pressure decline during the isovolumic relaxation of diastole?
Determined by the rate of active relaxation of the myofibers
When do mitral valve leaflets open?
When when left ventricular pressure drops below left atrial pressure
** onset of rapid filling phase of diastole
Describe/define diastesis (of diastole)
The atriovetnricular pressure difference approaches zero
Ventricular volume reaches a plateua
**minimal changes in intraventricular pressure and volume
The duration of diastesis is determined by?
Inversely related to heart rate
**resting heart rate— diastesis is longest phase of diastole
S1 heart sounds
Closure of the AV valves
mechanical onset of systole
S2 heart sound
Closure of the semilunar valves
**end of systole
S3 heart sound
Early ventricular filling
**rapid filling phase of diastole
S4 heart sound
Atrial contraction
Systolic function refers to
Ability of the ventricles to contract and eject blood
Diastolic function refers to
The ability of the ventricles to adequately relax and fill
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
Events that cause an increase in pre-load?
Exercise
Anaemia
Fever
Pregnancy
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.)
Ventircular filling is affected primarily by:
Venous return
Atrioventricular valve function
Atrial function
Pericardial compliance
Heart rate
Myocardial relaxation
Compliance
Inadequate end-diastolic volume will result in:
Inadequate stroke volume
**reduced coronary perfusion
What are the two major factors that affect ventricular diastolic performance
Chamber compliance
Mycoardial relaxation
If ventricular compliance is reduced what is required to achieve a given diastolic volume?
A greater filling pressure
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
Myocardial relaxation may change acutely in response to
Hypoxia
Ischaemia
Altered afterload
Tachycardia
Catecholamines
Various pharmacological agents
What are disease processes that produce diastolic dysfunction
Pressure overload states— myocardial hypertrophy or fibrosis (aortic and pulmonic stenosis,, systemic or pulmonary hypertension)
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
What are factors that affect systolic & diastolic function of the atria?
Atrial preload
Impedance to atrial emptying
Inotropic state of atrial myocytes
Atrial compliance
What are the 3 methods commonly used to determine cardiac output
- Fick method
- Thermodilutioon method (overestimates cardiacoutput)
- Lithium dilution method
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
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
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
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
Parasympathetic nervous system controls what (in regards to the heart)
Heart rate (chronotropic effects)
Sympathetic nervous system controls what (in regards to the heart)?
Heart rate
Contractility (inotropic effects)
The sympathetic and parasympathetic control of the heart is controlled by what part of the brain?
Integrated by the brain stem
Baroreceptors sense
Stretch
— detect high pressure within the vascular system
Where are baroreceptors located? that detect high pressure
Within the aortic arch and carotid sinus
Baroreceptors that detect low pressure are located (central volume receptors) where?
Atrial tissue (primarily at junction with the great veins)
Pulmonary arteries & ventricles
Affarent input to the CNS from the heart are transmitted via the
Glossopharyngeal and vagal nerves
Glossopharyngeal and vagal nerves terminate where
Nucleus tractus solitarius (NTS)
Alpha 2 adrenoreceptor agonists effect o nheart
Increase vagal tone to heart
Reduce sympathetic tone to blood vessels
**bradycardia, hypotension
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
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
Vasomotor nerves are controlled by which system and hormone?
Sympathetic nerves—
Noradrenaline on alpha 1 adrenoreceptors
Acetylcholine is the neurotransmitter that acts on what receptors of the SA and AV nodes
M2 muscarinic receptors
Renin is produced by what cells?
Modified smooth mm cells o the afferent arterioles in the juxtaglomerular apparatus
Renin then acts on angiotensin 1 which is then converted via (BLANK ) to (BLANK)
Angiotensin converting enzyme (ACE)
Angiotensin II
Where is angiotenson converting enzyme located?
Endothelial cells— especiallly in the lung
What is synthesized in response to angiotensin II?
Aldosterone
Aldosterone MOA
Mineralocorticoid receptors — to preserve Na reabsorption from teh distal nephrome
**results= INC in circulating volume
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)
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)
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
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
