Flashcards in Pathology of the Cardiovascular System 1 Deck (39):
Apex comprises left ventricle.
LV contains oxygenated blood- pushed out in to the aorta on systole -> systemic circulation.
After blood has passed round the body, it is deoxygenated -> re-enters heart in cranial and caudal vena cavas/azygos vein -> RA -> RV -> pulmonary artery.
PA carries deoxygenated blood to the lungs to be oxygenated. Once this has occurred, blood is brought back to the LA by the pulmonary vein. It can then pass to LV and aorta etc.
The heart muscle is arranged in circular and spiral bundles, which make it fit for purpose- it ENSURES THE PROPER DIRECTION OF SQUEEZING BLOOD.
Muscle structure is fit for purpose until heart failure occurs.
INTERNAL FEATURES OF THE HEART
Tricuspid valve- between RA and RV.
Bicuspid/Mitral valve- between LA and LV.
Pulmonary Semilunar valve- between RV and pulmonary artery.
Aortic Semilunar valve- between LV and aorta.
CARDIAC CONDUCTION SYSTEM
TIME ordered stimulation allows SYNCHRONOUS myocardial contractility.
-Sinoatrial and Atrioventricular nodes are impulse generating.
-Sinoatrial nodes initiates conduction.
-His-Purkinje System is impulse propagating- passes electrical impulse from atria to ventricles.
-The heart muscle acts as a FUNCTIONAL SYNCYTIUM.
MICROSCOPIC ANATOMY OF CARDIAC MUSCLE
Cells communicate via gap junctions.
Cells are joined by intercalated disks.
Sarcoplasmic reticulum stores calcium.
CO = SV x HR (stroke volume x heart rate)
SV= EDV - ESV (end diastolic volume minus end systolic volume)
The force of muscle contraction is proportional to the length of the muscle fibre.
The relationship is not linear, and it has limits- SV eventually plateaus, then over stretching decreases SV.
STARLING'S LAW- HEART MUSCLE
As the volume of blood entering the heart increases, the volume leaving must also increase.
The heart adjusts for this- it increases contractile force and stroke volume- more blood is pushed out on systole.
Force of contraction increases in response to increased filling.
The heart compensates for the increased workload.
However, if the heart cannot keep up, heart failure will occur.
Initial stretch of cardiac fibres before contraction.
Related to sarcomere length and depends on venour return (pulmonary vein)
Approximates to END DIASTOLIC VOLUME- volume of blood at end of diastole (relaxation and filling)
Aortic pressure must be overcome in order to allow blood to be ejected from LV during systole.
Depends on aortic pressure.
INABILITY OF THE HEART TO MAINTAIN ADEQUATE PERFUSION.
Heart failure is a clinical syndrome.
It can present acutely or chronically.
Heart disease does not mean heart failure will also be seen.
Heart failure can be secondary to non-cardiac disease.
ACUTE HEART FAILURE
1. SUDDEN DEATH- often due to cardiomyopathy.
2. DECREASED CARDIAC OUTPUT- cardiogenic shock (heart fails to pump efficiently) -> sudden collapse
Cardiogenic shock is uncommon.
3. VOLUME OVERLOAD- too much fluid leads to mass vasoconstriction and movement of blood.
ACUTE PULMONARY CONGESTION- lungs fill with fluid due to pulmonary artery/vein.
SYSTEMIC CONGESTION- most obvious in periphery- subcutaneous oedema/congested mucous membranes. Due to cranial and caudal vena cavae.
(CHRONIC) CONGESTIVE HEART FAILURE
RIGHT SIDED CHF
LEFT SIDED CHF
RIGHT SIDED CHRONIC HEART FAILURE
Venous congestion (back pressure of vena cavae) leads to hypoperfusion of lungs.
Back pressure in liver/kidneys -> increased vena cava pressure, excessive right atrial pressure -> systemic venous congestion
-> jugular distension, hepatic/splenic enlargement, ascites, peripheral oedema.
Mucous membranes are dark and congested in right sided CHF.
Chronic venous congestion leads to nutmeg appearance of liver.
LEFT SIDED CHRONIC HEART FAILURE
Back pressure from pulmonary veins leads to atrial dilation -> pulmonary congestion and oedema
Clinical signs- Dyspnoea, cough.
Systemic circulation is hypoperfused.
Mucous membranes are pale in left sided CHF due to systemic hypoperfusion.
Most cases of left CHF present as congestive diseases.
SEVERE PULMONARY OEDEMA
Seen with chronic left sided heart failure.
Wet, frothy fluid in lungs and trachea.
HISTO- Chronic thickening of alveolar walls
- MACROPHAGES movie in to flooded air spaces.
Macrophages remove protein and extravasated blood cells.
Haemosiderin-laden macrophages are seenwithin alveoli in the lungs in left sided CHF- haemosiderophages, aka. HEART FAILURE CELLS.
INTRINSIC CARDIAC RESPONSES
1. CARDIAC DILATION
2. CARDIAC HYPERTROPHY
3. INCREASED CARDIAC RATE.
Intrinsic cardiac responses can occur in physiological or pathological situations.
They are INITIALLY BENEFICIAL, but ultimately contribute to stresses on the myocardial wall.
The heart cannot compensate indefinitely.
Adaptive and maladaptive signalling molecules and pathways have been identified.
NEUROENDOCRINE RESPONSE TO CARDIAC FAILURE
Renin Angiotensin Aldosterone System (RAAS)
Natriuretic peptides (Atrial and Brain)
Increases heart rate and contractility, leading to increased CO, increased preload and increased blood pressure (short term benefits)
Hypoperfusion of kidney stimulates increased renin production.
Renin stimulates conversion of angiotensinogen to angiotensin I.
Angiotensin I is converted to angiotensin II by ACE in the lungs.
Angiotensin II increases sympathetic activity, renal tubular Na and Cl resorption, K excretion and water retention. Also increases aldosterone secretion, causes arterial vasoconstriction (increase blood pressure), and stimulates ADH production from the posterior pituitary.
ALL OF THESE ACT TO INCREASE SALT AND WATER RETENTION, INCREASE EFFECTIVE CIRCULATING VOLUME, AND INCREASE PERFUSION OF THE JUXTAGLOMERULAR APPARATUS (this then exerts negative feedback on the kidney to decrease renin production)
-> increased CO, preload, blood pressure (short term benefits)
THROMBOXANE AND ENDOTHELIN
Vasoconstriction- Increases CO, preload and blood pressure (short term benefits)
NATRIURETIC PEPTIDES (ANP, BNP)
Counteract RAAS, causing diuresis, naturesis, vasodilatin.
This occurs via re-expression of the CARDIAC HYPERTROPHY GENE.
-> reduced water retention, increased tissue perfusion, inhibition of maladaptive cardiac hypertrophy.
HARMFUL EFFECTS OF RAAS ACTIVATION
-DEGENERATIVE CARDIAC CHANGES- Cardiac remodelling, cardiomyocyte fibrosis and necrosis.
-DEGENERATIVE RENAL CHANGES- Glomerular hypertension.
-SODIUM AND WATER RETENTION- via aldosterone, can lead to volume overload.
-STIMULATION OF SYMPATHETIC NERVOUS SYSTEM- increased heart rate.
-VASOCONSTRICTION- increased cardiac workload.
PROGRESSION OF NEUROENDOCRINE RESPONSE TO CARDIAC FAILURE
As CHF progresses, the neuroendocrine responses that were at first beneficial become HARMFUL.
Tissue perfusion decreases (due to vasoconstriction), and cardiac remodelling and myofibre dysfunction occur.
These are also due to increased stress on the ventricular wall.
As the heart is harmed, congestive heart failure progresses.
FIVE MECHANISMS OF HEART FAILURE
1. FAILURE OF HEART TO EXPAND (filling failure)
2. DAMAGE TO MYOCARDIUM (pump failure)
3. INCREASED RESISTANCE TO OUTFLOW (output failure)
4. VALVULAR DEFECTS
5. IRREGULAR RHYTHMS
RIGHT SIDED HEART FAILURE SECONDARY TO PULMONARY DISEASE.
Cardiac dilatation and hypertrophy.
Heart tries but fails to push blood to lungs.
Secondary to pulmonary hypertension (eg. pulmonary disease- diffuse lung pathology, hypoxia- altitude disease, or vascular disease- pulmonary thromboembolism, dirofilariasis)
Rare in horses with COPD, as COPD is intermittent.
BOVINE LUNG DISEASES ASSOCIATED WITH COR PULMONALE
-Diffuse Fibrosing Alveolitis (DFA, Allergic Alveolitis, Hypersensitivity Pneumonitis)
-Bovine Respiratory Virus infection
-Chronic Suppurative Pneumonia- widespread pus makes it hard for blood to enter the lungs
-Chronic Obstructive Pulmonary Disease (COPD)
BRISKET DISEASE aka. HIGH ALTITUDE DISEASE
Chronic hypoxia leads to pulmonary vasoconstriction and hypertension, resulting in OEDEMS.
Cattle seem to be particularly susceptible.
Subcutaneous and brisket oedema.
UNDERLYING CAUSES OF DISEASE
Causes can be genetic and/or environmental- often multifactorial.
OUTER- Fibrous pericardium
-Serous pericardium (parietal layer)
-Pericardial space (between parietal and visceral pericardium, normally contains a small volume of fluid to reduce friction)
-Serous pericardium (visceral layer, epicardium)
-Fatty connective tissue, coronary artery and vein- supply heart.
DISEASES OF THE PERICARDIUM
-Serous transudate (due to altered hydrostatic pressure) eg. due to heart failure, neoplasia.
-Modified transudate (toxaemia, bacterial infection) eg. Mulberry Heart Disease (pigs- selenium/vit E deficiency), bowel oedema (pigs- E. coli toxaemia)
Often bloody at post mortem examination.
-Ruptured atria- dogs
-Ruptured aorta- horses
Can be caused due to trauma, neoplasia etc.
Pericarditis eg. Hardware disease.
Can also occur. eg. Coronary arteries constrict, causing infarction.
ACUTE= cardiac tamponade- pericardium becomes 'massive bag of fluid'; the heart is put under pressure due to accumulation of fluid.
eg. in horse, following cardiac rupture.
CHRONIC= gradual accumulation of fluid allows the heart to adapt to an extent, but it will eventually fail, due to constrictive pericarditis and herniated tissue.
Pericardium transforms in to granulation tissue- fibrovascular proliferation (connective tissue and blood vessels)
CHRONIC CONSTRUCTIVE PERICARDITIS
A thick, dense fibrous layer replaces the epicardium (visceral pericardium)
Heart cannot dilate due to this constrictive layer, leading to filling failure.