Cardiovascular-Heart defects Flashcards
Function of heart
-perfusion of oxygen and nutrients and removal of waste products
Heart development
-first organ to form in embryo
Four cardiac valves
- Right AV (Tricuspid)
- Left AV (Bicuspid/Mitral)
- Aortic (semilunar)
- Pulmonic
three layers of the heart
- Pericardium (epicardium)
- Myocardium (muscle)
- Endocardium (atria, ventricles, valves)
Parts of the pericaridum
- Parietal- external, thicker layer
- Visceral- internal, thinner layer covering muscle (epicaridum)
pericardium serosa composition
-thin layer of mesothelium and connective tissue
**important for support of blood vessels, lymphatic vessels, nerves, adipose tissue
Pericardial space
-space between the epicardium and pericardium
-contains small amounts of clear lubricant fluid which is important for preventing friction between the layers
Myocardium
-muscle of heart
-contraction (systole), relaxation (diastole)
Myocardium histology
-involuntary striated muscle
-branched fibres connected through intercalated disks
-lots of mitochondria
Endocardium
-thin layer lining the internal surface of heart (equivalent to tunica intima of vessels)
-contains the purkinje fibres
Endocardium microscope layers
1.Endothelium
2.Basal lamina
3. Sub-endothelial connective tissue (elastin and collagen)
Purkinje fibres
-specialized myocardial cells
-responsible for electrical impulse conduction
Chordae tendinae
attach the papillary muscles of the ventricular myocardium to the AV valves
Postmortem exam of heart
- silhouette
-colour - wall thickness
-shape - pericardial fluid
- valves
- size
- fat deposits
- endocardium
- weight
-post mortem changes
-blood vessels
-check for effusion or exudate
When do enlarged hearts occur?
-cardiac dilation or hypertrophy
- pericarditis
-tumour or pericardial effusion
Compensatory mechanisms when cardiac function is impaired
- Neurohumoral systems
- Cardiac dilation and hypertrophy
Neurohumoral system
**NE/ RAA
When activated, leads to vascular redistribution of blood, increase heart rate, increase in blood volume.
Leads to atrial natriuretic peptide secretion (counter mechanism)
Myocardial hypertrophy
-greater contractility and ejection force
Cardiac Dilation
- increased stroke (blood) volume… AND contractile force and cardiac output
-occurs because the myofibrils become longer through addition of sarcomeres and myocyte lengthening (while diameter stays the same) which thins the wall and increased volume of chamber
Acute overload vs. chronic overload on the heart
Acute: leads to dilation
Chronic: causes hypertrophy
Cardiac hypertrophy cause
-can be primary (idiopathic) or secondary (occurs due to sustained increase in cardiac workload)
What are ways that the heart workload can be increased?
1.pump more blood (volume overload)
2. pump at higher pressure (pressure overload)
Is hypertrophy reversible?
yes, if workload demand is corrected
Cons to cardiac hypertrophy
- impaired intrinsic contractility
-impaired ventricular relaxation - decreased compliance (not able to fill)
Eccentric cardiac hypertrophy
-due to volume overload and leads to dilation
-thin ventricular wall and distended ventricle
Concentric cardiac hypertrophy
- due to reduced volume of the ventricular chamber
-thick ventricular wall and reduced ventricular space
Cellular stages in cardiac hypertrophy
- Initiation- increase cell size (sarcomeres/mitochondria)
- Compensation- stable hyperfunction with no clinical signs
- Deterioration - degeneration of hypertrophied cardiomyocytes and loss of contractility followed by heart failure
Heart shape- right sided cardiac hypertrophy/dilation?
-broad base of heart
Examples: pulmonic stenosis, brisket disease
What results from left sided cardiac hypertrophy/dilation?
increased length of the heart
Examples: aortic stenosis, feline hyperthyroidism
What results from bi ventricular cardiac hypertrophy/dilation?
-a rounded, globose heart
Examples: hypertrophic cardiomyopathy
Cardiac failure
-heart is unable to pump blood at rate sufficient to meet the metabolic demands of the tissues
When does cardiac failure occur?
when the cardiac dysfunction is not properly compensated
What does decreased cardiac output result in?
Decreased cardiac output via the aorta and/or pulmonic arteries (anterograde) leads to hypotension, depression, lethargy, and syncope
What does an inability to adequately empty the venous reservoirs result in?
Inability to empty venous reservoirs (retrograde) leads to swollen abdomen, tachypnea, and dyspenia (from pleural effusion and pulmonary edema)
Basic mechanisms in heart failure
- pump failure- weak contractility and emptying from fibrosis, inflammation, myocardial degeneration
- Outflow obstruction- stenosis or hypertension
- Blood flow regurgitation- valve insufficiency, endocardiosis, endocarditis, volume overload
- shunting of blood- congential heart defects or persistence of fetal circulation
- Restriction of filling- cardiac tamponade, pericarditis, tumour
- Conduction disorders- arrhythmias
Retrograde vs anterograde components
Retrograde- systemic/pulmonary venous stasis
Anterograde- decreased cardiac output
Diseases associated with right sided heart failure
-pulmonic stenosis
-pulmonary hypertension
- brisket disease
-hardware disease
- pulmonary fibrosis
Diseases associated with left sided heart failure
-aortic stenosis
-systemic hypertension
-mitral endocardiosis
-mitral dysplasia
-feline hyperthyroidism
Diseases associated with bilateral heart failure
-tetralogy of fallot
-hypertrophic cardiomyopathy
Extracardiac lesions in right side heart failure
-systemic venous congestion, portal congestion and hypertension
-generalized edema, ascited, hydrothorax, passive liver congestion (nutmeg liver)
Extracardiac lesions in left side heart failure
-pulmonary venous congestion
-pulmonary edema and intra-alveolar hemorrhage
-red cells phagocytized by alveolar macrophages leading to iron pigment within them= heart failure cells
Brisket disease
-pulmonary hypertension, leads to hypertrophy RV, leads to right side heart failure and then ascites and SQ edema (brisket swelling) and nutmeg liver
Mitral endocardiosis
-mitral insufficiency leads to passive congestion of the lung, pulmonary edema, intra-alveolar hemorrhages= heart failure cells
Myocardial Hypertrophy
-greater contractility and ejection force
Cardiac Dilation
-increased stroke volume
Eccentric Hypertrophy
-thin vascular wall and distended ventricle
Concentric Hypertrophy
-thick ventricular wall and reduced ventricular space
Right sided heart
-broad base
-examples: pulmonic stenosis, brisket disease
Left sided heart
-increased length
-Examples: aortic stenosis, feline hyperthyroidism
Bi-ventricular heart
-globose (rounded)
-Examples: hypertrophic cardiomyopathy
Brisket Disease= Right sided heart failure
-edema
-nutmeg liver/ congestion/necrosis
Mitral insufficiency= left sided heart failure
-pulmonary edema
-congestion of lung
-intra-alveolar hemorrhage
-heart failure cells (iron laden macrophages)
