Cardiovascular Pathology 1 Flashcards
what is the preload and what does it approximate
initial stretch of cardiac fibres prior to contraction
related to sarcomere length and dependent on venous return
approximates to end diastolic volume (EDV)
what is the afterload
resistance
pressure (squeeze) that chambers must develop to eject blood during systole
dependent on aortic pressure
what is frank starling’s law
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
what is stroke volume
SV = EDV - ESV
end diastolic volume - end systolic volume
what is the significance of frank starling’s law and heart disease
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
what is heart failure
progressive clinical syndrome –> impaired pumping, decreased ventricular ejection, impedes venous return
how does heart failure occur
- decreased blood pumping into pulmonary artery or aorta
- failure to maintain arterial pressure
- 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
what is acute heart failure
usually decompensation of chronic disease
de novo disease uncommon
what is chronic heart failure
congestive heart failure
what are the pathophysiologic mechanisms of heart failure
- pump failure
- obstruction to forward flow
- regurgitant blood flow
- shunted blood flow from congenital defects
- heart/major vessel rupture
- cardiac conduction disorders (arrythmias)
what is pump failure
weak contractility and emptying of chambers
impaired filling of chambers
what causes obstruction to forward flow
valvular stenosis, valvular narrowing
systemic or pulmonary hypertension
what causes regurgitant blood flow
volume overload of chamber behind failing valve
what causes shunted flow from congenital defects
septal defects, shunts between vessels
what causes heart/major vessel rupture
cardiac temponade, massive internal hemorrhage
what causes cardiac conduction disorders (arrhthymias)
failure of synchronized cardiac contraction
what are the mechanisms that lead to systolic failure
- failure of myocardium
- volume overload
- pressure overload
what is failure of myocardium leading to systolic failure
dilated cardiomyopathy, myocarditis, doxorubicin toxicity, myocardial infarcts
what is volume overload leading to systolic failure
valvular diseases, PDA(patent dutuctus arteriosus)/VSD(ventricular septal defect)/ASD (atria septal defect), chronic anemia
what is pressure overload leading to systolic failure
subaortic stenosis, pulmonic stenosis, systemic hypertension, pulmonary hypertension
what are mechanisms of diastolic failure
- impaired E-dependent ventricular relaxation or abnormal ventricular chamber or muscle properties
- obstruction to ventricular filling at veins, atria and AV valves
- pericardial abnormalities
what are examples of impaired E-dependent ventricular relaxation or abnormal ventricular chamber or muscle properties
hypertrophic cardiomyopathy (HCM)
pulmonic/subaortic stenosis
heartworms
systemic hypertension
DCM, RCM (restrictive cardiomyopathy)
what is obstruction to ventricular filling at veins, atria, and AV valves
mitral/tricuspid stenosis
intracardiac neoplasia
what is pericardial abnormalities
constrictive disease
cardiac tamponade
what are clinical signs of acute heart failure syndrome
may see intermittent weakness and syncope due to significant drop in cardiac output
what typically occurs in acute heart failure syndrome
sudden death due to either:
- 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)
- volume overload (acute pulmonary congestion and/or systemic congestion)
what is congestive heart failure
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
what does right sided congestive heart failure lead to
increased right atrial pressure
systemic venous congestion
what are the clinical signs of right sided heart failure
jugular distention, hepatic and splenic enlargement, ascites, peripheral edema
what does left sided congestive heart failure lead to
dilated left atrium
pulmonary congestion and edema
what are the clinical signs of left sided congestive heart failure
dyspnea and cough
what does failure of one side of the heart lead to
almost always leads to failure to the other side
global/biventricular failure
what are the intrinsic cardiac responses
- cardiac dilation
- cardiac hypertrophy
- 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
what are neuroendocrine responses to cardiac failure and what are their mechanisms and benefits
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
what is the renin-angiotensin-aldosterone system
- kidney releases renin in response to decrease in renal perfusion (juxtaglomerular apparatus) which causes the liver to convert angiotensinogen to angiotensin II
- lungs release angiotensin converting enzyme (ACE) which converts angiotensin I to angiotensin II
- 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 - water and salt retention –> effective circulating volume increases –> perfusion of juxtaglomerular apparatus increases which negatively inhibitsthe kidney from releasing renin
what are the harmful effects of RAAS activation (5)
angiotensin II causes:
- degenerative cardiac changes: cardiac remodelling, myocyte fibrosis and necrosis
- degenerative renal changes: glomerular hypertension
- stimulation of sympathetic nervous system: increased heart rate
- vasoconstriction: increased cardiac workload
- aldosterone –> sodium and water retention: volume overload
how is the progression of neuroendocrine repsonse to cardiac failure harmful
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
what is cor pulmonale
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)
what is brisket disease
high altitude disease
chronic hypoxia –> pulmonary vasoconstriction and pulmonary hypertension –> cor pulmonale
what are diseases of the pericardium
- hypopericardium
- hemopericardium
what is cardiac compression (acute and chronic)
- acute: cardiac tamponade –> acute cardiac compression due to accumulated fluid
- chronic: gradual accumulation of fluid –> constriction pericarditis –> +/- herniated tissue
what are the two causes of hydropericardium
- transudate (edema) –> congestive heart failure, hypoproteinemia, neoplasia
- modified transudate –> mulberry heart disease (pigs)
what are the causes of hemopericardium
- ruptured atria: dogs
- ruptured aorta: horses
what does hydropericardium cause (6)
- transudate in pericardium
- generalized edema (CHF, also hydrothorax, ascites)
- pulmonary hypertension (high altitude disease)
- renal failure
- hypoproteinemia –> decreased colloid osmotic pressure
systemic diseases (african horse sickness)
what are inherited conduction disorders and arrhythmias
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
what are conduction disorders
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)
what occurs during right sided heart failure
increase right atrial pressure and systemic venous congestion
hypoperfusion of the lungs –> blood has to go somewhere so it pools in the systemic circulation
what are clinical signs of right sided heart failure
what are clinical signs of right sided heart failure
what causes left sided failure clinical signs
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
what are the PM changes in right sided heart failure
- chronic venous congestion of liver: expanded congested liver, full of blood
- 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
what are the PM changes seen with left sided heart failure
mucosal pallor
pulmonary edema –> froth is surfactant (clara cells in alveoli)
lungs huge, rib implants, heavy, wet
what is shown here
severe pulmonary edema
thickened alveolar walls and macrophages (round cells) –> mopping up blood in flooded air spaces (“heart failure cells”)
how does pulmonary edema lead to increased left ventricular pressure and remodelling
- decreased oxygenated blood (hypoperfusion)
- renal hypoperfusion –> release renin –> RAAS
- fluid retention
- increased systemic venous pressure
- increased end diastolic L ventricular volume
- increased L ventricular pressure and remodelling
what are the PM findings of cor pulmonale
dilated right side of the heart
what is an example of cor pulmonale in the bovine
brisket disease/high altitude disease
what is an example of cor pulmonale in the canine
Dirofilaria (heartworm)
