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Module 10 > Cardiovascular Pathology 1 > Flashcards

Cardiovascular Pathology 1 Flashcards

1
Q

what is the preload and what does it approximate

A

initial stretch of cardiac fibres prior to contraction

related to sarcomere length and dependent on venous return

approximates to end diastolic volume (EDV)

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2
Q

what is the afterload

A

resistance

pressure (squeeze) that chambers must develop to eject blood during systole

dependent on aortic pressure

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3
Q

what is frank starling’s law

A

force of muscle contraction is proportional to initial length of muscle fibre

as heart rate increases, cardiac output increases linearlly until plateau reached then further heart rate increase results in cardiac output decrease due to decreased diastolic filling

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4
Q

what is stroke volume

A

SV = EDV - ESV

end diastolic volume - end systolic volume

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5
Q

what is the significance of frank starling’s law and heart disease

A

as the volume of blood entering the heart increases, the amount leaving the heart must also increase

the heart adjusts for this by increasing the contractile force and stroke volume to move more blood out (this allows the heart to compensate for increased work-load)

if it can’t keep up –> heart failure

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6
Q

what is heart failure

A

progressive clinical syndrome –> impaired pumping, decreased ventricular ejection, impedes venous return

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7
Q

how does heart failure occur

A
  1. decreased blood pumping into pulmonary artery or aorta
  2. failure to maintain arterial pressure
  3. low output heart failure (depression, lethargy, syncope, hypotension)

or inability to adeqautely empty the venous reservoirs –> congestive heart failure (ascites, pleural effusion, pulmonary edema)

end result of a wide range of causes NOT a specific disease

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8
Q

what is acute heart failure

A

usually decompensation of chronic disease

de novo disease uncommon

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9
Q

what is chronic heart failure

A

congestive heart failure

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10
Q

what are the pathophysiologic mechanisms of heart failure

A
  1. pump failure
  2. obstruction to forward flow
  3. regurgitant blood flow
  4. shunted blood flow from congenital defects
  5. heart/major vessel rupture
  6. cardiac conduction disorders (arrythmias)
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11
Q

what is pump failure

A

weak contractility and emptying of chambers

impaired filling of chambers

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12
Q

what causes obstruction to forward flow

A

valvular stenosis, valvular narrowing

systemic or pulmonary hypertension

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13
Q

what causes regurgitant blood flow

A

volume overload of chamber behind failing valve

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14
Q

what causes shunted flow from congenital defects

A

septal defects, shunts between vessels

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15
Q

what causes heart/major vessel rupture

A

cardiac temponade, massive internal hemorrhage

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16
Q

what causes cardiac conduction disorders (arrhthymias)

A

failure of synchronized cardiac contraction

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17
Q

what are the mechanisms that lead to systolic failure

A
  1. failure of myocardium
  2. volume overload
  3. pressure overload
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18
Q

what is failure of myocardium leading to systolic failure

A

dilated cardiomyopathy, myocarditis, doxorubicin toxicity, myocardial infarcts

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19
Q

what is volume overload leading to systolic failure

A

valvular diseases, PDA(patent dutuctus arteriosus)/VSD(ventricular septal defect)/ASD (atria septal defect), chronic anemia

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20
Q

what is pressure overload leading to systolic failure

A

subaortic stenosis, pulmonic stenosis, systemic hypertension, pulmonary hypertension

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21
Q

what are mechanisms of diastolic failure

A
  1. impaired E-dependent ventricular relaxation or abnormal ventricular chamber or muscle properties
  2. obstruction to ventricular filling at veins, atria and AV valves
  3. pericardial abnormalities
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22
Q

what are examples of impaired E-dependent ventricular relaxation or abnormal ventricular chamber or muscle properties

A

hypertrophic cardiomyopathy (HCM)

pulmonic/subaortic stenosis

heartworms

systemic hypertension

DCM, RCM (restrictive cardiomyopathy)

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23
Q

what is obstruction to ventricular filling at veins, atria, and AV valves

A

mitral/tricuspid stenosis

intracardiac neoplasia

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24
Q

what is pericardial abnormalities

A

constrictive disease

cardiac tamponade

25
Q

what are clinical signs of acute heart failure syndrome

A

may see intermittent weakness and syncope due to significant drop in cardiac output

26
Q

what typically occurs in acute heart failure syndrome

A

sudden death due to either:

  1. decreased cardiac output: cardiogenic shock, failure to pump blood effectively (decreased SV and CO, dilated or hypertrophic cardiomyopathies, arrhythmias, obstruction to blood flow, acute myocardial infarction in humans)
  2. volume overload (acute pulmonary congestion and/or systemic congestion)
27
Q

what is congestive heart failure

A

failure to empty venous reservoirs leads to congestion and edema

gradual loss of myocardial pumping ability due to volume or P overload or myocardial damage

28
Q

what does right sided congestive heart failure lead to

A

increased right atrial pressure

systemic venous congestion

29
Q

what are the clinical signs of right sided heart failure

A

jugular distention, hepatic and splenic enlargement, ascites, peripheral edema

30
Q

what does left sided congestive heart failure lead to

A

dilated left atrium

pulmonary congestion and edema

31
Q

what are the clinical signs of left sided congestive heart failure

A

dyspnea and cough

32
Q

what does failure of one side of the heart lead to

A

almost always leads to failure to the other side

global/biventricular failure

33
Q

what are the intrinsic cardiac responses

A
  1. cardiac dilation
  2. cardiac hypertrophy
  3. increased cardiac rate

can occur in physiological or pathological conditions –> initially beneficial but ultimately contribute to stresses on myocardial wall

adaptive and maladaptive signalling molecules and pathways have been indentified

34
Q

what are neuroendocrine responses to cardiac failure and what are their mechanisms and benefits

A

1. sympathetic activation (RAAS, thromboxane, endothelin) –> increase heart rate & contractility, Na & water retention, vasoconstriction –> increases cardiac output, increases preload and CO, increases BP

2. natriuretic peptides (ANP; atrial natriuretic peptide and BNP; brain natiuretic peptide) –> inhibition of RAAS –> diuresis, natriuresis, vasodilation –> increased tissue perfusion, inhibit maladaptive cardiac hypertrophy

35
Q

what is the renin-angiotensin-aldosterone system

A
  1. kidney releases renin in response to decrease in renal perfusion (juxtaglomerular apparatus) which causes the liver to convert angiotensinogen to angiotensin II
  2. lungs release angiotensin converting enzyme (ACE) which converts angiotensin I to angiotensin II
  3. angiotensin II has positive effect on:
    - pituitary gland: which causes ADH release –> ADH secretion –> collecting duct in kidney causes H2O absorption
    - arteriole: vasoconstriction, increase in blood pressure
    - adrenal cortex: aldosterone secretion –> tubular Na, Cl and K excretion, H2O retention
    - increase in sympathetic activity
  4. water and salt retention –> effective circulating volume increases –> perfusion of juxtaglomerular apparatus increases which negatively inhibitsthe kidney from releasing renin
36
Q

what are the harmful effects of RAAS activation (5)

A

angiotensin II causes:

  1. degenerative cardiac changes: cardiac remodelling, myocyte fibrosis and necrosis
  2. degenerative renal changes: glomerular hypertension
  3. stimulation of sympathetic nervous system: increased heart rate
  4. vasoconstriction: increased cardiac workload
  5. aldosterone –> sodium and water retention: volume overload
37
Q

how is the progression of neuroendocrine repsonse to cardiac failure harmful

A

1. sympathetic activation: increases rate & contractility –> increases CO –> decreases tissue perfusion

2. RAAS: Na & water retention –> increases preload –> increase CO –> cardiac remodelling and myofibre dysfunction

3. thromboxane, endothelin: vasoconstriction –> increases BP –> cardiac remodelling and myofibre dysfunction

38
Q

what is cor pulmonale

A

failure of the right side of the heart: cardiac dilation and hypertrophy, heart tries but fails to push blood into the lungs

secondary to pulmonary hypertension: pulmonary disease (diffuse lung pathology, hypoxia –> high altitude disease), vascular disease (pulmonary thromboembolism, dirofilariasis –> heartworm)

39
Q

what is brisket disease

A

high altitude disease

chronic hypoxia –> pulmonary vasoconstriction and pulmonary hypertension –> cor pulmonale

40
Q

what are diseases of the pericardium

A
  1. hypopericardium
  2. hemopericardium
41
Q

what is cardiac compression (acute and chronic)

A
  1. acute: cardiac tamponade –> acute cardiac compression due to accumulated fluid
  2. chronic: gradual accumulation of fluid –> constriction pericarditis –> +/- herniated tissue
42
Q

what are the two causes of hydropericardium

A
  1. transudate (edema) –> congestive heart failure, hypoproteinemia, neoplasia
  2. modified transudate –> mulberry heart disease (pigs)
43
Q

what are the causes of hemopericardium

A
  1. ruptured atria: dogs
  2. ruptured aorta: horses
44
Q

what does hydropericardium cause (6)

A
  1. transudate in pericardium
  2. generalized edema (CHF, also hydrothorax, ascites)
  3. pulmonary hypertension (high altitude disease)
  4. renal failure
  5. hypoproteinemia –> decreased colloid osmotic pressure

systemic diseases (african horse sickness)

45
Q

what are inherited conduction disorders and arrhythmias

A

can occur in very young patients

either congenital heart disease or structurally normal heart

mutations responsible for majority of inherited arrhythmias occur in genes encoding for cytoskeletal proteins, sarcomeric proteins, ion channels

46
Q

what are conduction disorders

A

abnormalities in the conduction pathway of the heart –> SAN, AVN, bundle of His, purkinje fibres

conduction disorders often result in arrhythmia –> variation from the normal rhythm (bradycardia, tachycardia)

47
Q
A
48
Q

what occurs during right sided heart failure

A

increase right atrial pressure and systemic venous congestion

hypoperfusion of the lungs –> blood has to go somewhere so it pools in the systemic circulation

49
Q

what are clinical signs of right sided heart failure

A
50
Q

what are clinical signs of right sided heart failure

A
51
Q

what causes left sided failure clinical signs

A

left side failure –> can’t pump blood out and left atria swells and dilates –> blood build up in lungs –> pulmonary congestion and edema

hypoperfusion in systemic circulation

52
Q

what are the PM changes in right sided heart failure

A
  1. chronic venous congestion of liver: expanded congested liver, full of blood
  2. nutmeg liver: repeating pattern of red and tan mottling. red = dilated central veins + sinusoidal dilation and congestion. tan = uncongested parenchyma with lipid accumulation. blood backs up in liver –> liver in fibrous capsule and can’t expand much
53
Q

what are the PM changes seen with left sided heart failure

A

mucosal pallor

pulmonary edema –> froth is surfactant (clara cells in alveoli)

lungs huge, rib implants, heavy, wet

54
Q

what is shown here

A

severe pulmonary edema

thickened alveolar walls and macrophages (round cells) –> mopping up blood in flooded air spaces (“heart failure cells”)

55
Q

how does pulmonary edema lead to increased left ventricular pressure and remodelling

A
  1. decreased oxygenated blood (hypoperfusion)
  2. renal hypoperfusion –> release renin –> RAAS
  3. fluid retention
  4. increased systemic venous pressure
  5. increased end diastolic L ventricular volume
  6. increased L ventricular pressure and remodelling
56
Q
A
57
Q

what are the PM findings of cor pulmonale

A

dilated right side of the heart

58
Q

what is an example of cor pulmonale in the bovine

A

brisket disease/high altitude disease

59
Q

what is an example of cor pulmonale in the canine

A

Dirofilaria (heartworm)

Module 10 (27 decks)

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