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VET377 > Lectures 10, 11, 12 - Cardio 1-3 > Flashcards

Lectures 10, 11, 12 - Cardio 1-3 Flashcards

1
Q

What is the formula for cardiac output?

A

Cardiac output = heart rate x stroke volume

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2
Q

What is the formula for stroke volume?

A

Stroke volume = End diastolic volume (EDV) - End systolic volume (ESV)

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3
Q

What is the normal percentage of systolic ejection on diastolic ejection? Why is this?

A

In reality is is 60 to 70% this is seen because of the wringing action of the heart allowing to to achieve a much greater value than the 60-70% that would be expected.

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4
Q

For optimal performance the ventricles need to cycle efficiently between the two states of systole and diastole. Briefly explain why:

A

Stiff chamber during systole efficiently ejects blood into arteries at high pressure (systolic ejection). A compliant chamber during diastole that permits rapid filling from a low atrial pressure (diastolic filling)

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5
Q

Briefly describe the relationship between increasing preload and cardiac output and name the mechanism that is responsible for this relationship:

A

Increased preload leads to left ventricular distention which then leads to increased stroke volume (Frank-Starling mechanism). However in systolic dysfunction (heart failure) - the curve shifts downward - reflecting reduced cardiac performance at a give preload

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6
Q

What is the definition of afterload?

A

is the systemic load that the heart needs to overcome

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7
Q

What is the difference between heart disease and hear failure?

A

Heart disease = the presence of an abnormality in cardiac function and structure Heart failure = the clinical manifestation of heart disease

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8
Q

What is cardiac dysfunction?

A

Heart failure occurs when the hear is unable to maintain sufficient cardiac output to satisfy the needs of the body

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9
Q

Briefly describe the three different manifestations of heart disease:

A

No clinical disease but pathological changes at necropsy or ultrasonography

Clinical cardiac abnormalities detectable (murmur, arrhythmia but no heart failure)

Clinical and systemic abnormalities (heart failure)

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10
Q

What is an arrhythmia?

A

a disturbance in the normal cardiac rhythm due to an abnormality in impulse initiation and/or impulse propagation

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11
Q

What is a murmur?

A

an auditory vibration of longer duration than the normal heart sounds - created due to disruption of laminar flow

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12
Q

What two clinical signs are often attributable to heart failure?

A

Accumulation of fluid (congestion)- dry to wet Tissue/organ ischemia (decreased cardiac output) - warm to cold - forward failure

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13
Q

What are the clinical signs of poor cardiac output?

A

weak pulses, pale mucous membrane, prolonged capillary refill time, tachycardia, cold extremeties

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14
Q

What are the signs of left-sided heart failure?

A

pulmonary oedema, adventitial sounds, cyanosis, tachypnoea (sleeping rate)

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15
Q

What are the signs of right-sided heart failure?

A

ascites, pleural effusion, peripheral oedema, jugular distension and pulses hepatojugular reflex - small animals

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16
Q

What are the physiological mechanisms for improving cardiac output?

A
  1. The Frank-Sarling mechanism - increased venous return increases. ventricular (EDV) and hence preload 2. Activation of sympathetic nervous system - results in increased inotropic (contractility) and chronotropic (heart rate) 3. Activation of RAAS system
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17
Q

What are the adverse affects of the activation of the sympathetic nervous system to maintain cardiac output?

A

Increased afterload Reduced peripheral tissue. perfusion Increased heart muscle oxygen requirements Enhance potential for. arrythmias Down regulation of beta receptors

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18
Q

What is the net result of the RAAS system?

A

renal sodium retention and water retention (volume expansion)

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19
Q

What is the effect of atrial natriuretic peptide and what is it released in response to?

A

Atrial natriuretic peptide is released in response to atrial stretch. It has natriuretic and diuretic properties. This causes decreased blood volume which then decreases preload and decreases cardiac output

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20
Q

What are the mechanisms of cardiac failure?

A
  1. Sustained pressure overload (afterload)
  2. Sustained volume overload (preload)
  3. Altered cardiac muscle contractility (systolic dysfunction)
  4. Altered cardiac muscle compliance (diastolic function)
  5. Altered normal cardiac rhyhthm
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21
Q

What is the effect on the structure of the heart of increased ventricular preload (volume overload)?

A

Ventricle undergoes compensatory hypertrophy (eccentric)

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22
Q

What is the effect on the structure of the heart as a result of increased ventricular afterload (pressure overload)?

A

The ventricle undergoes compensatory hypertrophy (concentric)

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23
Q

Under what conditions would there be sustained pressure overload?

A

due to impedance to chamber outflow (e.g. stenosis or hypertension)

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24
Q

Under what conditions would a sustained volume overload occur?

A

due to increased preload. An example could be abnormal patterns could be valvular insufficiency and congenital defects (e.g. septal defect, shunt)

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25
Q

What pathological changes result from a sustained pressure overload?

A

concentric ventricular hypertrophy post-stenotic vascular dilation

26
Q

What pathological changes result from sustained volume overload?

A

Eccentric chamber dilation and hypertrophy Endocardial fibrosis (jet lesions) - typically seen on the distal side of an orrifice between a high pressure and a low pressure chamber

27
Q

What are the clinical signs see in pulmonary hypertension?

A
  1. Rapid breathing 2. Split S2 valve (premature closing of pulmonic valve relative to the aortic valve) 3. Pulmonary thromboembolism 4. If prolonged there would be hypertrophy of the right ventricle with secondary tricuspid regurgitation and right atrial enlargement 5. Cor pulmonale - hypertrophy of the right heart resulting from diseases affecting structure or function of the lung
28
Q

What are the main causes of systemic hypertension?

A

Primary = no identifiable cause (extremely uncommon in dogs and may occur in cats) Secondary = more common. (seen with renal disease, adrenal causes, diabetes mellitus, acromegaly and polycythemia

29
Q

What are the three mechanisms of diastolic abnormalities?

A
  1. Slowed or incomplete relaxation (due to myocyte calcium, decreased ATP, activation of angiotensin II) 2. Reduced left ventricular filling 3. Altered passive elastic properties (wall stiffness due to endomyocardial fibrosis and altered collagen structure)
30
Q

What are the mechanisms of systolic disfunction and what is an example of each?

A
  1. Altered normal contractility (unable to generate sufficient force to maintain CO) 2. Insufficient myocytes - toxic damage 3. Dysfunctional myocytes - unknown or hereditary causes or iatrogenic
31
Q

What are the effects of DCM?

A

Eventually manifests as left-sided heart failure - lethargy and weakness is seen, pulmonary oedema, progression to biventricular heart failure Cardiac arrythmias Sudden death in some cases

32
Q

What is restrictive cardiomyopathy?

A

Is where the heart chambers are unable to fill to their normal size due to the stiffness of the heart. Can have congenital or acquired causes

33
Q

What species is hypertrophic cardiomyopathy commonly seen in and what are the problems associated with it?

A

Most commonly seen in cats. Caused by. left ventricular outflow obstruction and the reduced compliance means it cannot relax and fill. The left atrial dilation increases the potential for clot formation.

34
Q

Is pleural effusion more common in dogs or cats?

A

Pleural effusion is more common in cats. It does not occur in dogs except for cases of biventricular failure

35
Q

Rank the SA node, AV node and purkinje fibres in order of rate of spontaneous depolarisation (in the dog):

A

SA node - 60-180/min AV node - 40-60/min Purkinje fibres - 20-40/min

36
Q

What are the three main mechanisms of impulse conduction bradyarrythmias?

A
  1. Conduction delays and blocks 2. Sinoatrial blocks 3. Atrioventricular blocks
37
Q

What is the main mechanism of tachyarrythmia impulse disorders?

A

Re-entry - the re-stimulation of a cell by nearby tissue after it has been depolarised

38
Q

Name the arrythmia that is seen below:

A

Sinus arrythmia - regularly irregular rythym

This is commonly seen in horses - the respiratory form the P-P interval shortens during inspiration (due to reflex inhibition of vagal tone and lengthens during expiration)

39
Q

What is sinus bradycardia and what is a potential cause of it?

A

Regular sinus rhythym with a sinus that is firing that is too slow (less than 60 bpm in the awake dog, less than 60 bpm in the awake horse)

40
Q

How does a sinoatrial block and sinoatrial arrest appear on an ECG?

A

Absence of electric PQRST activity. It can be asymptomatic but can cause syncope. Long periods are interupted by junctional or ventricular escape complexes.

41
Q

What is seen on an ECG trace with atrial standstill?

A

QRST complexes without P waves (assuming atrial fibrillation not present)

Pathology is due to atrial muscle loss and fibrosis

42
Q

What is the name of the condition that is shown below?

A

Sick sinus syndrome - degenerative disease of the sinus node

Persistant bradycardia - rapid regular or irregular atrial and tachycardia and SA block or arrest

fixed with a pacemaker implant

43
Q

What is seen on an ECG trace with a first degree AV block?

A

prolonged PR interval

44
Q

What is seen on a ECG trace with a second degree AV block?

A

some sinus depolarisations conduct through the AV node to depolarise the ventricles while others do not. Some P-waves without a following QRST wave are seen.

45
Q

What type of block is seen below?

A

Second degree AV block

46
Q

What type of block is seen below and how is this distinguished from other types of blocks?

A

Third degree atrioventricular block - no relationship between. P waves and QRS complexes (AV dissociation)

47
Q

How can supraventricular tachdysrrythmias be differentiated from ventricular tachydysrythmias?

A

In a supraventricular tachycardia the QRS complex appear normal whereas in the ventricular tachycardia it will appear wide and bizarre.

48
Q

What is a sinus tachycardia and under what conditions would a sinus tachycardia be observed?

A

Higher than normal heart rate but with a regular rhythym. This would be observed with pain, anxiety, hypoxia etc.

49
Q

How would supraventricular premature depolarisation be seen on an ECG?

A

Premature beat arising from an ectopic focus from within the atria or the AV junction. It is seen as a single premature beat arising from an ectopic focus in the atria/AV junction. Seen on ECG as an abnormal P wave but a normal looking QRS complex

50
Q

How would a supraventricular (atrial or junctional) tachycardia be seen on an ECG?

A

Would be seen as 3 or more severe ventricular premature depolarisations - result of atrial flutter (re-entry circuit in right atrium)

51
Q

What type of tachycardia is shown in the image below?

A

Supraventricular (atrial or junctional) tachycardia

52
Q

What factors can predispose to atrial fibrillation?

A
  1. Large atrial mass - horses can develop AF in absence of heart disease since their atrial mass is very large
  2. Elevated vagal tone (shortens the refractory period - predisposes to AF, horses have naturally high vagal tone)
  3. Low heart rate

Re-entry –> multiple wavelets

53
Q

How is atrial flutter normally seen on an ECG?

A

irregularly irregular rythym (irregularl RR intervals) - no P waves normally normal QRS complexes

54
Q

How do premature ventricular contractions appear on an ECG trace?

A

Appear as premature ventricular contractions. Premature often wide and bizzarre QRS complexes - originates below the bundle of his

55
Q

How are ventricular tachycardias - ideoventricular rythyms seen on ECG traces?

A

Appear as three or more succesive PVC’s with wide QRS complexes

56
Q

Describe the pattern that is seen below:

A

ventricular tachycardia - ideoventricular rythym

57
Q

Describe the pattern seen below and the clinical consequences that are likely to arise from it:

A

Ventricular fibrillation - preterminal event that is fatal if not treated

58
Q

What are the cause of mulberry heart disease and what are the likely clinical consequences as a result of it?

A

Vitamin E/Se deficiency in pigs and likely to result in arryhtmias of a ventricular origin causing death

59
Q

How do ergot alkaloids result in vasocontriction?

A

Ergot alkaloids result in potent contriction of arterial smooth muscle and ischameic necrosis of distal limbs

60
Q

What are the four mechanims of oedema?

A

Decreased colloid osmotic pressure

Increased hydrostatic pressure

Increased vascular permeability

Decreased lymphatic drainage

VET377 (60 decks)

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