Heart Failure & Oedema Flashcards

1
Q

List different causes of heart failure

A

Degenerative valvular disease
Aortic/mitral

Heart muscle disease - cardiomyopathy

Valve/Endocardial infection

Pericardial disease

Rate/rhythm abnormalities

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2
Q

Explain how degenerative valvular disease leads to heart failure

A

Develops later in life

Cause unknown

May/may not develop heart failure

Regurgitation into atrium during systole meaning less forward flow into aorta
Compare atrial and aortic/pulmonic pressures

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3
Q

Explain how heart muscle disease leads to heart failure

A

Cardiomyopathy
-Disease of the heart muscle making it harder for blood to be pumped. Three types Dilated, restrictive and hypertrophic

Develops later in life

Cause unknown
Some primary causes?

Usually develop heart failure

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4
Q

Outline Dilated cardiomyopathy

A

Common in dogs

Dilated
Some inherited forms in cattle

Disease of the heart muscle

Muscle function is poor

Reduced contractility leads to reduction in forward flow

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5
Q

Outline Dilated cardiomyopathy

A

Common in cats

Rarely dilated

Usually restrictive - heart is stiff

Or hypertrophic (heart is thick walled)

Reduction in space decreases forward flow as the heart cannot fill

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6
Q

Compare concentric and eccentric cardiac hypertrophy and their causes and effects

A

Remodelling of ventricular chamber due to a chronic increase in cardiac work

-Eccentric:
Occurs with volume overloading (increased preload)
E.g. valve incompetence/dilated CMO

Compensatory mechanism: leads to replication of sarcomeres in series resulting in elongation of myocytes, increasing the diameter of the ventricle with a normal wall thickness and external diameter also grows as a result
Eventually the O2 demand of the myocardium outstrips ability of coronary circulation leading to myocardial ischemia

-Concentric
Occurs with Pressure load (increased afterload)
e.g. hypertension or aortic/pulmonic stenosis

In HCM – concentric hypertrophy is a consequence of the disease

Compensatory mechanism: leads to replication of sarcomeres in parallel resulting in increased wall thickness (& decrease in internal diameter)

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7
Q

List the pathophysiological responses which occur in cases of cardiac failure

A

Sympathetic NS
RAAS
Cardiac enlargement

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8
Q

Explain the pathophysiological responses of the sympathetic NS which occur in cases of cardiac failure

A

When arterial pressure falls there is a decreased firing of baroreceptors, consequently the medullary cardiovascular centre responds to this by increasing sympathetic activity, and decreasing parasympathetic activity.

Sympathetic increase and parasympathetic decrease increase the heart rate. The sympathetic system individually increased the contraction of arteries and veins, leading to an increase in stroke volume. The contraction of the vessels leads to increased peripheral resistance in effort to normalise arteriole pressure.

The combination of increased stroke volume and heart rate results in larger cardiac output, this again is in effort to normalise arterial pressure

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9
Q

Explain the pathophysiological responses of the renin-angiotensin system which occur in cases of cardiac failure

A

A multi-organ response to defend BP

A decrease in blood pressure, leads to a drop in renal perfusion pressure

Due to this the kidneys release renin, which is interacts with angiotensinogen (produced in liver) creating angiotensin I which is converted to Angiotensin II by the angiotensin converting enzyme (ACE). These bind to AT1 receptors, having affects on system vasoconstriction, increased blood volume and renal sodium and fluid retention

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10
Q

Describe the compensatory mechanisms and their faults

A

-Increased Heart Rate
Aim to increase oxygen perfusion to tissues

-Vasoconstriction
When CO falls after load increases
Increased afterload leads to leaking valves

-Contractility increases
Aims to increase oxygen perfusion to tissues by increasing bp

-Salt and Water Retained
This is to compensate for blood volume lost. Increase in fluid volume increases the amount of blood returned to the heart. However, it increases the pressure in capillaries and can lead to oedema

-Cardiac Enlargement
Develops in response to increased preload. The hypertrophy of the myocardial mass has a higher demand for O2 than the coronary arteries are a

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11
Q

Outline the viscous circle of heart failure

A

Heart failure occurs

Decrease in cardiac output

Compensatory mechanisms induced
-SNS activity
-RAAS system activated
-Antidiuretic hormone release

Excessive vasoconstriction
-sodium and water retention

Increase in preload and afterload

Leading to heart failure

Ideal in short term
E.g. Volume loss

Inappropriate in the long term
Worsens heart function

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12
Q

Explain the processes leading to lymph formation

A

Blood is bought from the arterioles into the met-arterioles. It enters the capillaries where it is regulated by precapillary sphincters.

Between the endothelial cells there are openings where the fluid is able to escape and enter the capillary, transporting nutrients and oxygen to the tissues, and removing carbon dioxide and waste products out of the tissues.

Plasma from the capillaries becomes tissue fluid and surrounds the tissues collecting waste products, excess water and toxins from the cells.

The majority is reabsorbed by the capillaries, but the remainder is known as lymph, which then drains into the lymphatic capillaries

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13
Q

Explain Starling’s forces and outline the equation

A

Applied to work out Net Filtration Pressure

Starling force = (Pc + Pi) - (Pi + Pp)

Pc = CHP:
Hydrostatic pressure in the capillary.

Pi = IOP:
Colloid osmotic pressure of the interstitial fluid.

Pi = IHP:
Hydrostatic pressure in the interstitial fluid.

Pp = COP:
Colloid osmotic pressure of the blood plasma.

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14
Q

Outline the use of hydrostatic pressure in the capillaries

A

HPc
Push plasma out of capillary bed (Net filtration pressure). Promoting formation of tissue fluid
32mmHg
Directly dependant upon systolic BP
PA (32mmHg) > PV (15mmHg)

HPIF
Pushes interstitial fluid back into the capillaries
1mmHg

Net outward pressure (filtration) = HPc - HPIF

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15
Q

Outline the use of oncotic pressure in the capillaries

A

Pressure that is exerted by plasma proteins (colloid) which promotes fluid absorption
Example of protein is alabamium which is made in the liver

OPc (/COP)
Pulls fluid back into the capillaries
25mmHg

OPIF
Pulls substances into extracellular space from the capillaries
6mmHg

Net inward pressure (absorption) = OPc - OPIF

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16
Q

Briefly outline the function of the lymphatic system

A

Assists in circulation of body fluids between cells and bloodstream

Returns tissue fluid to circulation

protects body against foreign material

Carries material/organisms to lymph nodes

Transports dietary fats

17
Q

Describe the mechanisms by which oedema may develop

A

-Vasogenic – leaky vessels
Local (inflammation) or generalised (vasculitis)
Histamine released by mast cells increases the gaps between the capillaries leading to increased fluid entering the tissue beds

-Lymphatic disease - lymphangiectasia

-Hyperaemic/hydrostatic
Obstruction – localised
High venous pressures – heart failure

-Osmotic
Low plasma COP – generalised?
Reduced protein synthesis
Increased protein loss

18
Q

Outline some clinical finding in the development of oedema

A

-Localised or generalised

-Fluid in skin – “pitting” swelling
Often “dependent”
Hypoproteinaemia
Cattle, horses – heart failure
“brisket” oedema

-Fluid within i/s tissue in a body system
e.g. lungs (L heart failure), brain

-Free fluid in body cavities
Pleural fluid - cat – Heart failure
Ascites - dog – R heart failure