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PATHOLOGY OF THE CARDIOVASCULAR SYSTEM
Normal Structure and Function
Response to Injury
Shannon Martinson, 2017
VPM 222 – Systemic Pathology II
http://people.upei.ca/smartinson/
PATHOLOGY OF THE CARDIOVASCULAR SYSTEM
• There are excellent tutorials and quizzes available at :
• http://people.upei.ca/lopez
Miller, LM and Gal, A. Cardiovascular System and
Lymphatic Vessels: In, Pathological Basis of
Veterinary Disease, 6th Edition. Zachary Ed.
Elsevier. 2017
INTRODUCTION: STRUCTURE AND FUNCTION
RA
LA
• The heart is the first organ to
form in the embryo
• Mammalians and birds have 4
chambers:
• Left atrium
• Right atrium
• Right ventricle
• Left ventricle
RV
LV
Reptiles – 1 ventricle
INTRODUCTION: STRUCTURE AND FUNCTION
Function - maintain adequate
blood flow (cardiac output) to
deliver oxygen and nutrients
and remove waste
INTRODUCTION: STRUCTURE AND FUNCTION
The heart is composed of three layers:
1. Pericardium (Epicardium)
2. Myocardium (Heart muscle)
3. Endocardium (includes valves)
Myocardium
Endocardium
Epicardium
INTRODUCTION: STRUCTURE AND FUNCTION
Epicardium and Pericardium
Visceral Pericardium
= Epicardium
Parietal Pericardium
INTRODUCTION: STRUCTURE AND FUNCTION
Epicardium and Pericardium
Epicardial surface – pericardial space
Epicardium
PBVD Zachary, 2017
Myocardium
INTRODUCTION: STRUCTURE AND FUNCTION
Myocardium
Myocardium
INTRODUCTION: STRUCTURE AND FUNCTION
Myocardium
• Myocardiocytes
• Involuntary striated muscle
• Arranged in sarcomeres
• Branched fibers connect via
intercalated discs
• Contain↑ # mitochondria
• Left ventricular myocardial thickness is ~ 2
– 4 times thicker than the right
• Due to higher pressure on the left side
• Purkinje cells
• Modified myocardiocytes function in
conduction
INTRODUCTION: STRUCTURE AND FUNCTION
Endocardium
• Inner lining and the valves
• Equivalent to the tunica intima of BV
• Close contact with blood
• Important in hemostasis
Endocardium
INTRODUCTION: STRUCTURE AND FUNCTION
Endocardium
• 3 layers
1. Endothelium
2. Basal lamina
3. Subendothelial
connective tissue
Endocardium
Purkinje Fiber
• Also contains part of
the conductive system
and Purkinje fibers
Myocardium
INTRODUCTION: STRUCTURE AND FUNCTION
Endocardium
• There are four cardiac valves:
1. Right atrio-ventricular (Tricuspid)
2. Pulmonic
3. Left atrio-ventricular (Mitral)
4. Aortic
Right A-V valve
Prevent backflow in the heart
Right heart
Pulmonic valve
INTRODUCTION: STRUCTURE AND FUNCTION
Endocardium
Left A-V valve
• There are four cardiac valves:
1. Right atrio-ventricular (Tricuspid)
2. Pulmonic
3. Left atrio-ventricular (Mitral)
4. Aortic
Left heart
Aortic valve
INTRODUCTION: STRUCTURE AND FUNCTION
Endocardium
• Thin,
translucent and
shiny
INTRODUCTION: STRUCTURE AND FUNCTION
Endocardium
• AV valves
attach to the
papillary
muscles via the
chordae
tendineae
Valve
Chordae tendineae
Papillary muscle
POSTMORTEM EXAMINATION OF THE HEART
Silhouette in situ
Shape
Size
Weight
Color
Pericardial fluid
Fat deposits
Coronary vessels
Wall thickness
Valves
Endocardium
Great vessels
POSTMORTEM EXAMINATION OF THE HEART
Differentials for an
enlarged cardiac
silhouette:
• Cardiomegaly
• Tumor
• Cardiac effusions
• Hydropericardium
• Hemopericardium
• Pericarditis
Pay attention to the relative size of the cardiac silhouette!
POSTMORTEM EXAMINATION OF THE HEART
Differentials for an
enlarged cardiac
silhouette:
• Cardiomegaly
• Tumor
• Cardiac effusions
• Hydropericardium
• Hemopericardium
• Pericarditis
Pay attention to the relative size of the cardiac silhouette!
POSTMORTEM EXAMINATION OF THE HEART
When opening the
pericardium – pay
attention to the content.
POSTMORTEM EXAMINATION OF THE HEART
When opening the
pericardium – pay
attention to the content.
POSTMORTEM EXAMINATION OF THE HEART
• Examine the heart in situ before removing it
• Pay careful attention in young animals to
look for congenital defects
• Check the epicardium, epicardial fat
stores and great vessels
Lymphatic vessels may be visible
POSTMORTEM EXAMINATION OF THE HEART
• Evaluate the myocardium and endocardium
• Samples for histopathology
• Routine: LV, RV and IVS
• Full thickness
• +/- Atria , +/- Valves/ +/- Conduction system
RESPONSE TO INJURY
• Healing is limited
• Compensatory mechanisms:
• Activation of neurohumoral mechanisms
• Cardiac dilation
• Cardiac hypertrophy
Depression in
Cardiac
Output
Release of
norepinephrine
Redistribution
/↓ renal
blood flow
↑ADH
↑ HR and
contractility +
vasoconstriction
↑Renin /
Angiotensin
/Aldosterone
↑Retention of
water
↑Na water
reabsorption +
Vasoconstriction
↑blood
volume
Expansion of the blood volume
induces secretion of atrial natriuretic
peptide: Induces Na and water
excretion and vasodilation
RESPONSE TO INJURY
Normal
Increased Heart Rate (beats/min)
Cardiac output = heart rate x stroke (blood) volume
Cardiac Dilation
-Increased stroke volume
Myocardial hypertrophy
- Greater contractility and ejection force
Cardiac hypertrophy and dilation are beneficial to a point
RESPONSE TO INJURY - CARDIAC DILATION
• Myocardial fibers stretch:
• ↑ Contractile force
• ↑ Stroke volume
• ↑ Cardiac output
• ↑ Contractile force has a limit
• ↑ stretch causes ↓ tension
• Chronically - addition of sarcomeres
and lengthening of myocytes.
• Acute volume overload leads to
dilation
• Chronic volume overload causes
hypertrophy
Response to ↑ workload in both physiologic or pathologic states
RESPONSE TO INJURY - CARDIAC HYPERTROPHY
Increase in heart mass due to increased cell size
• Primary cardiac hypertrophy (=cardiomyopathy)
• Primary (idiopathic) disease of the myocardium
• Secondary cardiac hypertrophy
• Due to sustained ↑ in cardiac workload
• Volume overload
• Pressure overload
• Due to trophic signals (hyperthyroidism)
• Limited benefit – eventually develop:
• Impaired intrinsic contractility
• Impaired ventricular relaxation
• Decreased compliance
• Can be right or left sided or biventricular
• Can also be classified as:
• Eccentric
• Concentric
RESPONSE TO INJURY - CARDIAC HYPERTROPHY
Eccentric
Concentric
Images: Maxie, Pathology of Domestic Animals, 2015
RESPONSE TO INJURY - CARDIAC HYPERTROPHY
Eccentric
Note thin ventricular wall (line) and
distended ventricle (arrow)
Concentric
Note thick ventricular wall (line) and
reduced ventricular space (arrow)
RESPONSE TO INJURY - CARDIAC HYPERTROPHY
Eccentric
Note thin ventricular wall (line) and
distended ventricle (arrow)
Concentric
Note thick ventricular wall (line) and
reduced ventricular space (arrow)
RESPONSE TO INJURY - CARDIAC HYPERTROPHY
Gross changes
Heart Side
Right
Left
Bi-ventricular
Normal
Gross Changes
Broad base
Increased length
Globose (rounded)
Right
Underlying cause (egs)
Pulmonic stenosis, pulmonary hypertension
Aortic stenosis, feline hyperthyroidism
HCM, tetralogy of Fallot
Left
Biventricular
RESPONSE TO INJURY - CARDIAC HYPERTROPHY
Cellular stages in cardiac hypertrophy:
1. Initiation: Increase cell size (sarcomeres / mitochondria)
2. Compensation: Stable hyperfunction with no clinical signs
3. Deterioration: Degeneration of hypertrophied cardiomyocytes and loss of
contractility followed by heart failure
Histology
• ↑ Size of cardiomyocytes
• +/- Dissarray
With chronicity:
• Cardiomyocytes loss
• Fibrosis
CARDIAC DYSFUNCTION AND FAILURE
No clinical disease
Heart
Disease
Lesion at necropsy
Clinically detectable but no heart
failure
Uncompensated
Congestive heart failure
(fluid accumulation, edema)
Heart failure
Acute heart failure
(collapse, weakness)
CONGESTIVE HEART FAILURE
Decreased contractibility of myocardial fibres (myocardial failure)
is the pathophysiological hallmark of clinical heart failure
Retrograde component:
Systemic/pulmonary
venous stasis
Anterograde component:
Decreased cardiac output
Often both occur together
• Inability to empty the venous reservoirs ( =
congestive heart failure)
• Ascites
• Pleural effusion
• Pulmonary edema
• Insufficient blood pumping into the
aorta/pulmonary artery ( = low output heart
failure)
• Depression
• Lethargy
• Syncope
• Hypotension
CARDIAC DYSFUNCTION
BASIC PATHOPHYSIOLOGICAL MECHANISMS OF CARDIAC DYSFUNCTION AND FAILURE
Change
Example
Pump failure
Weak contractility: ↓emptying of the chambers due to myocardial
damage
Outflow obstruction Vascular or valvular stenosis, systemic or pulmonic hypertension
Blood flow
regurgitation
Valvular insufficiency, endocardiosis, endocarditis, volume overload
Shunted blood
Congenital heart defects
Restricted atrial /
ventricular filling
Cardiac tamponade, pericarditis, tumour
Conduction
disorders
Arrhythmias – die to functional or structural abnormalities in the
conduction system
CONGESTIVE HEART FAILURE
• CHF occurs when the heart
is unable to pump blood at
a rate sufficient to meet
the metabolic demands of
tissues
• Can occur at the end stage
of many forms of chronic
heart disease
• Acute hemodynamic
stresses can cause CHF to
appear suddenly
CONGESTIVE HEART FAILURE
Heart failure can be right sided, left sided or bilateral:
Pulmonic stenosis
Pulmonary
hypertension
Brisket disease
Hardware disease
Pulmonary
fibrosis
Aortic stenosis
Systemic
hypertension
Mitral
endocardiosis
Mitral dysplasia
Feline
hyperthyroidism
Tetralogy of Fallot
Hypertrophic
Cardiomyopathy
CONGESTIVE HEART FAILURE – EXTRACARDIAC LESIONS
Right sided
failure
Left sided
failure
Systemic venous
congestion
Pulmonary
venous
congestion
Edema and ascites
Pulmonary
edema and
intra-alveolar
macrophages
Chronic passive
hepatic
congestion
RBCs
phagocytosed
by alveolar
macrophages
Iron in alveolar
macrophages
Nutmeg
liver
Heart
failure cells
CONGESTIVE HEART FAILURE – RIGHT HEART FAILURE
Right sided
failure
3-yr-old dog
• Presented for distended abdomen (ascites) and dyspnea
• 2.5 L of fluid in the abdomen and 400 ml in the thorax
• Liver dark with rounded margins (hepatic congestion)
• Notably enlarged heart wide on the base
• RV concentric hypertrophy
• Final Diagnosis: Pulmonic valve stenosis
CONGESTIVE HEART FAILURE – RIGHT HEART FAILURE
Image: Noah’s arkive
Right sided
failure
Chronic passive hepatic congestion
“Nutmeg Liver”
CONGESTIVE HEART FAILURE – LEFT HEART FAILURE
Left sided
failure
Aged cat
• Lethargy and anorexia
• Difficulty breathing
• Pulmonary edema and congestion, hydrothorax
• LV eccentric hypertrophy
• Final Diagnosis: LAV dysplasia
CONGESTIVE HEART FAILURE – LEFT HEART FAILURE
Left sided
failure
Aged cat
• Lethargy and anorexia
• Difficulty breathing
• Pulmonary edema and congestion, hydrothorax
• LV eccentric hypertrophy
• Final Diagnosis: LAV dysplasia +/- excess
moderator bands
Heart failure cells
I would like to thank Dr A Lopez and Dr E Aburto, Atlantic
Veterinary College, for their contributions to this material.