Heart failure Flashcards
Hydrostatic pressure
- Outward filtration pressure
- Exerted against the inner capillary wall
- Promotes the formation of tissue fluid
Colloid osmotic pressure
- Inward absoprtion pressure
- Exerted by plasma proteins which are too big to leave the capillary
- Promotes fluid reabsorption into the circulatory system
How does capillary hydrostatic pressure change over the course of the capillary?
- It is higher at the arterial around (~32mmHg) than the venous end (~15mmHg)
*Do not need to memorise numbers*
Describe the two main categories for heart failure causes
- Congenital (rare)
- Acquired
What are some causes of heart failure?
- Degenerative valve disease
- Cardiomyopathy
- Valve/endocardial infection
- Pericardial disease
- Rate/rhythm abnormalities
Cardiomyopathy
Disease of the heart muscle. The muscle function is poor and the heart does not pump effectively.
It develops later in life.
True/false: there are inherited forms of cardiomyopathy in cattle.
True.
What is the most common form of cardiomyopathy in dogs?
Dilated
What is the most common form of cardiomyopathy in cats?
Restrictive. This is due to hypertrophy of the walls of the heart.
How does hypertrophy, as seen with restrictive cardiomyopathy in cats, affect heart function?
- The heart becomes thick-walled
- There is hardly any lumen for the blood to be in during diastole (thus filling of the heart between beats is compromised)
What type of hypertrophy is shown here?
Concentric hypertrophy
The external diameter of the heart in unchanged, but the internal diameter has narrowed due to deposition of additional muscle within the ventricle lumen.
Differentiate between eccentric and concentric hypertrophy
- Eccentric hypertrophy: both internal and external diameter increase (heart = like balloon). This occurs with volume loading e.g. dilated cardiomyopathy, valve incompetence.
- Concentric hypertrophy: external diameter of heart unchanged, internal diameter (lumen) narrows. Occurs with pressure loading e.g. hypertension and aortic/pulmonic stenosis.
What is valve stenosis?
Type of valvular heart disease where the valve narrows and doesn’t open fully.
Aortic stenosis → reduces blood flow from left ventricle to aorta
Pulmonic stenosis → reduces blood flow from right ventricle to pulmonary artery
What is the cardiovascular system’s main aim (the one that tends to take priority over all others)?
Maintenance of blood pressure
This is very important as some tissue have very particular perfusion pressure requirements e.g kidneys
Why might preload fall in an animal with a very high heart rate?
The heart rate may be so high that the heart does not have time to fill.
This diagram shows how different causes of heart failure can all have the downstream impact of less forward flow.
Fill in the blanks.
1 and 2
3
4
Describe the incidence and causes of acute heart failure
- Acute heart failure is common in people but rare in animals
- In people, acute heart failure is caused by vascular disease/acute myocardial infarct
What mechanisms are activated to restore blood pressure when it falls?
What is the eventual consequence of these mechanisms being continually employed?
- Sympathetic nervous system activation
- Renin Angiotensin Aldosterone System (RAAS)
Eventually, this will result in cardiac enlargement.
What are the clinical signs of heart failure?
Case/species dependent. Broadly:
- Coughing
- Panting
- Dyspnoea/elevated respiratory rate even at rest
- Exercise reluctance
- Tiring faster with previously-tolerated exercise
- Fatigue
- Blue-tinged gums (cyanosis)
Describe how sympathetic nervous system activation increases blood pressure.
Include: neurotransmitter involved, receptors involved, location, effect.
Which works faster: SNS activation or RAAS?
SNS activation
RAAS is still reasonably quick though.
Describe how the Renin Angiotensin Aldosterone System (RAAS) responds to low blood pressure.
What does ACE represent in this diagram?
Angiotensin-converting enzyme.
It converts Angiotensin I to Angiotensin II.
Aldosterone causes renal sodium retention. How does this affect blood pressure?
Renal sodium retention → fluid retention
Fluid retention → increase in BP
Where is aldosterone released from? What stimulates its release?
Angiotensin II stimulates the release of aldosterone from the Zone glomerulosa in the adrenal cortex (adrenal glands).
What are the effects of Angiotensin-II?
- Systemic vasoconstriction
- Increased blood volume
- Renal sodium and fluid retention
Describe the vicious cycle by which the body’s compensatory mechanisms can worsen heart failure.
- Compensatory mechanisms result in increased preload and afterload at a cost of even greater oxygen needs
- This means the sick heart must cope with increased preload and afterload.
How does oedema develop in heart failure?
- Sodium and fluid retention occurs due to RAAS
- Volume of fluid in the blood vessels, esp. veins, increases
- Pressure in capillaries increases
- Excess interstitial fluid (=oedema) develops
Why is a patient’s respiratory rate elevated in heart failure?
- To restore blood pressure, heart rate increases, meaning the sick heart must work harder, and thus it demands more oxygen.
- SNS activation leads to increased contractility, meaning the sick heart must work harder, and thus demands more oxygen.
- Cardiac enlargement results in increased leakiness of AV valves. Therefore, more oxygen is required to provide the body with the same amount as before.
- Increased oxygen needs → increased respiratory rate.
Why does AV valve regurgitation increase in the vicious cycle of heart failure? What effect does this have on cardiac output?
- SNS activation causes peripheral vasoconstriction
- Peripheral vasoconstriction increases afterload
- Increased afterload increases AV valve regurgitation
Increased afterload and valve leakiness results in a fall in cardiac output
Outline how heart failure leads to feelings of weakness and fatigue.
- SNS activation causes peripheral vasoconstriction.
True/false: the lower the patient’s SNS activation and plasma noradrenaline levels, the less chance they have of surviving heart failure.
False.
Lower SNS activation and plasma noradrenaline levels = better chance of survival.
High NA plasma levels = bad news :(
1
Increased venous return
2
Peripheral vasoconstriction
3
Increased peripheral resistance
4
Increased rate and force of myocardial contraction