1 – Introduction and Heart Failure Flashcards
3 layers of the heart:
-pericardium
-myocardium
-endocardium
Pericardium: epidcardium
o Parietal and visceral pericardium
Thin layer of mesothelium and connective tissue
Pericardial space contains small amounts of clear lubricant fluid
Myocardium: heart muscle
o Striated, connected by intercalated disks
o Lots of mitochondria
Endocardium: atria, ventricles, valves
- Endothelium (superficial)
- Basal lamina
- Sub-endothelial connective tissue
*Purkinje fibres
AV valves
- Attached to papillary muscles by chordae tendinea
Postmortem examination of the heart
- Check in situ (relative size)
Most important compensatory mechanisms of the heart:
- Activation of neurohumoral systems (NE/RAA
- Cardiac dilation and hypertrophy
- Activation of neurohumoral systems (NE/RAA)
o Vascular redistribution of blood
o Increase HR
o Increase in blood volume
o *all leads to atrial natriuretic peptide secretion (counter mechanism)
o Cardiac dilation
Increased stroke (blood) volume
Myocardial fibers stretch=increase contractile force
* Limit to stretch (too far=decrease tension)
Chronic dilation through addition of sarcomeres (lengthening of myocytes)
*acute overload=dilation, chronic overload=hypertrophy
o Myocardial hypertrophy
Greater contractility and ejection force
* Pump more blood (volume overload)
* Pump at a higher pressure (pressure overload)
Due to sustained increase in cardiac workload OR due to trophic signals (ex. hyperthyroidism)
*reversible if workload demand is corrected
Eccentric hypertrophy:
- Accompanied by dilation
- *thin wall and distended ventricle
Concentric hypertrophy:
- Reduced volume of ventricular chamber
- *thick wall and reduced ventricular space
Cellular stages in cardiac hypertrophy:
- Initiation
- Compensation
- Deterioration
- Initiation
a. Increase cell size (sarcomeres/mitochondria)
- Compensation
a. Stable hyperfunction with no clinical signs
- Deterioration
a. Degeneration of hypertrophied cardiomyocytes
b. Loss of contractility followed by heart failure
Gross changes in cardiac hypertrophy/dilation: Right side
o Broad base
o Ex. pulmonic stenosis, brisket disease
Gross changes in cardiac hypertrophy/dilation: left side
o Increased length
o Ex. aortic stenosis, feline hyperthyroidism
Gross changes in cardiac hypertrophy/dilation: bi-ventricular
o Globose (rounded)
o Ex. hypertrophic cardiomyopathy
Cardiac failure
- Heart unable to pump blood at a sufficient rate to meet metabolic demands of tissues
- Cardiac dysfunction is NOT properly compensated
- Retrograde and anterograde component
Anterograde component of cardiac failure
- Decreased CO via the aorta and/or pulmonic arteries
- Leads to:
o Hypotension
o Depression
o Lethargy
o Syncope: temporary loss of consciousness
Pathophysiological mechanisms in heart failure: pump failure
- Weak contractility and emptying of chambers caused by myocardial degeneration, fibrosis, inflammation and/or neoplasia
Retrograde component of cardiac failure
- Inability to adequately empty the venous reservoirs
- Leads to
o Swollen abdomen (ascites)
o Tachypnea
o Dyspnea
o *due to pleural effusion and pulmonary edema
Pathophysiological mechanisms in heart failure: outflow obstruction
- Vascular or valvular stenosis
- Systemic or pulmonic hypertension
Pathophysiological mechanisms in heart failure: blood flow regurgitation
- Valvular insufficiency
- Endocardiosis
- Endocarditis
- Volume overload
Pathophysiological mechanisms in heart failure: shunting of blood
- Congenital hear defects
- Persistence of fetal circulation
Pathophysiological mechanisms in heart failure: restriction of atrial/ventricular filling
- Cardiac tamponade
- Pericarditis
- Tumor
Pathophysiological mechanisms in heart failure: conduction disorders
- Arrhythmias caused by functional or structural abnormalities in the conduction system
Congestive heart failure
- Unilateral (left or right) or bilateral
- Acute or chronic
Right sided heart failure due to
- Pulmonic stenosis
- Pulmonary hypertension
- Brisket disease
- Hardware disease
- Pulmonary fibrosis
Left sided heart failure due to
- Aortic stenosis
- Systemic hypertension
- Mitral endocardiosis
- Mitral dysplasia
- Feline hyperthyroidism
Bilateral heart failure due to
- Tetralogy of Fallot
- Hypertrophic
- Cardiomyopathy
Extra cardiac lesions in right-sided heart failure
- Systemic venous and portal congestion and hypertension
- LUNGS are the target
- Generalized edema
- Hydrothorax
- Passive liver congestion
Cor pulmonale
- Pulmonary hypertension and R. heart failure secondary to PULMONARY disease
Extra cardiac lesions in left-sided heart failure
- Pulmonary venous congestion
- Pulmonary edema and intra-alveolar hemorrhage
- Red cells phagocytized by alveolar macrophages
- Iron pigment in alveolar macrophages=’heart failure cells’
Specific animal diseases causing R and L heart failure
- High altitude
- Brisket disease in cattle
- Mitral endocardiosis in dog
High altitude
- Pulmonary hypertension
- Hypertrophy RV
- R. heart failure
- Ascites and subcutaneous edema
Brisket disease in cattle
- Extensive subcutaneous edema caused by R. sided heart failure
- Nutmeg liver
o Chronic passive congestion
o Zonal pattern caused by congestion/necrosis/fibrosis of centrilobular regions
Mitral endocardiosis in dog
- Mitral insufficiency
1. Passive congestion of lung
2. Pulmonary edema
3. Intra-alveolar hemorrhages
4. ‘heart failure cells’
