Cardiovascular Pathology 1

Question 1

what is the preload and what does it approximate

Answer 1

initial stretch of cardiac fibres prior to contraction

related to sarcomere length and dependent on venous return

approximates to end diastolic volume (EDV)

Question 2

what is the afterload

Answer 2

resistance

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

dependent on aortic pressure

Question 3

what is frank starling’s law

Answer 3

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

Question 4

what is stroke volume

Answer 4

SV = EDV - ESV

end diastolic volume - end systolic volume

Question 5

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

Answer 5

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

Question 6

what is heart failure

Answer 6

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

Question 7

how does heart failure occur

Answer 7

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

Question 8

what is acute heart failure

Answer 8

usually decompensation of chronic disease

de novo disease uncommon

Question 9

what is chronic heart failure

Answer 9

congestive heart failure

Question 10

what are the pathophysiologic mechanisms of heart failure

Answer 10

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)

Question 11

what is pump failure

Answer 11

weak contractility and emptying of chambers

impaired filling of chambers

Question 12

what causes obstruction to forward flow

Answer 12

valvular stenosis, valvular narrowing

systemic or pulmonary hypertension

Question 13

what causes regurgitant blood flow

Answer 13

volume overload of chamber behind failing valve

Question 14

what causes shunted flow from congenital defects

Answer 14

septal defects, shunts between vessels

Question 15

what causes heart/major vessel rupture

Answer 15

cardiac temponade, massive internal hemorrhage

Question 16

what causes cardiac conduction disorders (arrhthymias)

Answer 16

failure of synchronized cardiac contraction

Question 17

what are the mechanisms that lead to systolic failure

Answer 17

1. failure of myocardium
2. volume overload
3. pressure overload

Question 18

what is failure of myocardium leading to systolic failure

Answer 18

dilated cardiomyopathy, myocarditis, doxorubicin toxicity, myocardial infarcts

Question 19

what is volume overload leading to systolic failure

Answer 19

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

Question 20

what is pressure overload leading to systolic failure

Answer 20

subaortic stenosis, pulmonic stenosis, systemic hypertension, pulmonary hypertension

Question 21

what are mechanisms of diastolic failure

Answer 21

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

Question 22

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

Answer 22

hypertrophic cardiomyopathy (HCM)

pulmonic/subaortic stenosis

heartworms

systemic hypertension

DCM, RCM (restrictive cardiomyopathy)

Question 23

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

Answer 23

mitral/tricuspid stenosis

intracardiac neoplasia

Question 24

what is pericardial abnormalities

Answer 24

constrictive disease

cardiac tamponade

Question 25

what are clinical signs of acute heart failure syndrome

Answer 25

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

Question 26

what typically occurs in acute heart failure syndrome

Answer 26

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)

Question 27

what is congestive heart failure

Answer 27

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

Question 28

what does right sided congestive heart failure lead to

Answer 28

increased right atrial pressure systemic venous congestion

Question 29

what are the clinical signs of right sided heart failure

Answer 29

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

Question 30

what does left sided congestive heart failure lead to

Answer 30

dilated left atrium pulmonary congestion and edema

Question 31

what are the clinical signs of left sided congestive heart failure

Answer 31

dyspnea and cough

Question 32

what does failure of one side of the heart lead to

Answer 32

almost always leads to failure to the other side global/biventricular failure

Question 33

what are the intrinsic cardiac responses

Answer 33

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

Question 34

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

Answer 34

**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

Question 35

what is the renin-angiotensin-aldosterone system

Answer 35

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

Question 36

what are the harmful effects of RAAS activation (5)

Answer 36

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

Question 37

how is the progression of neuroendocrine repsonse to cardiac failure harmful

Answer 37

**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

Question 38

what is cor pulmonale

Answer 38

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)

Question 39

what is brisket disease

Answer 39

high altitude disease chronic hypoxia --\> pulmonary vasoconstriction and pulmonary hypertension --\> cor pulmonale

Question 40

what are diseases of the pericardium

Answer 40

1. hypopericardium 2. hemopericardium

Question 41

what is cardiac compression (acute and chronic)

Answer 41

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

Question 42

what are the two causes of hydropericardium

Answer 42

1. transudate (edema) --\> congestive heart failure, hypoproteinemia, neoplasia 2. modified transudate --\> mulberry heart disease (pigs)

Question 43

what are the causes of hemopericardium

Answer 43

1. ruptured atria: dogs 2. ruptured aorta: horses

Question 44

what does hydropericardium cause (6)

Answer 44

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)

Question 45

what are inherited conduction disorders and arrhythmias

Answer 45

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

Question 46

what are conduction disorders

Answer 46

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)

Question 48

what occurs during right sided heart failure

Answer 48

increase right atrial pressure and systemic venous congestion hypoperfusion of the lungs --\> blood has to go somewhere so it pools in the systemic circulation

Question 49

what are clinical signs of right sided heart failure

Answer 49

Question 50

what are clinical signs of right sided heart failure

Answer 50

Question 51

what causes left sided failure clinical signs

Answer 51

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

Question 52

what are the PM changes in right sided heart failure

Answer 52

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

Question 53

what are the PM changes seen with left sided heart failure

Answer 53

mucosal pallor pulmonary edema --\> froth is surfactant (clara cells in alveoli) lungs huge, rib implants, heavy, wet

Question 54

what is shown here

Answer 54

severe pulmonary edema thickened alveolar walls and macrophages (round cells) --\> mopping up blood in flooded air spaces ("heart failure cells")

Question 55

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

Answer 55

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

Question 57

what are the PM findings of cor pulmonale

Answer 57

dilated right side of the heart

Question 58

what is an example of cor pulmonale in the bovine

Answer 58

brisket disease/high altitude disease

Question 59

what is an example of cor pulmonale in the canine

Answer 59

Dirofilaria (heartworm)