Pathology of the Cardiovascular System 1

Question 1

NORMAL HEART

Answer 1

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.

Question 2

HEART MUSCLE

Answer 2

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.

Question 3

INTERNAL FEATURES OF THE HEART

Answer 3

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.

Question 4

CARDIAC CONDUCTION SYSTEM

Answer 4

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.

Question 5

MICROSCOPIC ANATOMY OF CARDIAC MUSCLE

Answer 5

Striated. 
Cells communicate via gap junctions. 
Cells are joined by intercalated disks.
Nucleated cells. 
Sarcoplasmic reticulum stores calcium. 
Fasciae adherens.

Question 6

CARDIAC OUTPUT

Answer 6

CO = SV x HR (stroke volume x heart rate)

Question 7

STROKE VOLUME

Answer 7

SV= EDV - ESV (end diastolic volume minus end systolic volume)

Question 8

STARLING’S LAW

Answer 8

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.

Question 9

STARLING’S LAW- HEART MUSCLE

Answer 9

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.

Question 10

PRELOAD

Answer 10

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)

Question 11

AFTERLOAD

Answer 11

Resistance.
Aortic pressure must be overcome in order to allow blood to be ejected from LV during systole.
Depends on aortic pressure.

Question 12

HEART FAILURE

Answer 12

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.

Question 13

ACUTE HEART FAILURE

Answer 13

New onset/transient.

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.

Question 14

(CHRONIC) CONGESTIVE HEART FAILURE

Answer 14

RIGHT SIDED CHF

LEFT SIDED CHF

Question 15

RIGHT SIDED CHRONIC HEART FAILURE

Answer 15

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.

Question 16

LEFT SIDED CHRONIC HEART FAILURE

Answer 16

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.

Question 17

SEVERE PULMONARY OEDEMA

Answer 17

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.

Question 18

INTRINSIC CARDIAC RESPONSES

Answer 18

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.

Question 19

NEUROENDOCRINE RESPONSE TO CARDIAC FAILURE

Answer 19

Sympathetic activation 
Renin Angiotensin Aldosterone System (RAAS)
Thromboxane
Endothelin
Natriuretic peptides (Atrial and Brain)

Question 20

SYMPATHETIC ACTIVATION

Answer 20

Increases heart rate and contractility, leading to increased CO, increased preload and increased blood pressure (short term benefits)

Question 21

RAAS

Answer 21

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)

Question 22

THROMBOXANE AND ENDOTHELIN

Answer 22

Vasoconstriction- Increases CO, preload and blood pressure (short term benefits)

Question 23

NATRIURETIC PEPTIDES (ANP, BNP)

Answer 23

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.

Question 24

HARMFUL EFFECTS OF RAAS ACTIVATION

Answer 24

• 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.

Question 25

PROGRESSION OF NEUROENDOCRINE RESPONSE TO CARDIAC FAILURE

Answer 25

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.

Question 26

FIVE MECHANISMS OF HEART FAILURE

Answer 26

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

Question 27

COR PULMONALE

Answer 27

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.

Question 28

BOVINE LUNG DISEASES ASSOCIATED WITH COR PULMONALE

Answer 28

- 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) - Pulmonary thromboembolism - Dirofilariasis

Question 29

BRISKET DISEASE aka. HIGH ALTITUDE DISEASE

Answer 29

Chronic hypoxia leads to pulmonary vasoconstriction and hypertension, resulting in OEDEMS. Cattle seem to be particularly susceptible. Subcutaneous and brisket oedema.

Question 30

UNDERLYING CAUSES OF DISEASE

Answer 30

``` DOUBLE MINT. Malformation, Metabolic Infection, Immune-mediated Neoplastic, Nutritional, Traumatic, Toxic. ``` Causes can be genetic and/or environmental- often multifactorial.

Question 31

HEART WALL

Answer 31

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. - Myocardium - INNER- Endocardium

Question 32

DISEASES OF THE PERICARDIUM

Answer 32

HYDROPERICARDIUM | HAEMOPERICARDIUM

Question 33

HYDROPERICARDIUM

Answer 33

-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.

Question 34

HAEMOPERICARDIUM

Answer 34

-Ruptured atria- dogs -Ruptured aorta- horses Can be caused due to trauma, neoplasia etc. Pericarditis eg. Hardware disease.

Question 35

PERICARDIAL RUPTURE

Answer 35

Can also occur. eg. Coronary arteries constrict, causing infarction.

Question 36

CARDIAC COMPRESSION

Answer 36

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.

Question 37

SIMPLE PERICARDITIS

Answer 37

Pericardium transforms in to granulation tissue- fibrovascular proliferation (connective tissue and blood vessels)

Question 38

CHRONIC CONSTRUCTIVE PERICARDITIS

Answer 38

A thick, dense fibrous layer replaces the epicardium (visceral pericardium) Heart cannot dilate due to this constrictive layer, leading to filling failure.

Question 39

PERICARDIAL HERNIA

Answer 39

Massive right atrial dilation can follow herniation.