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Equine Emergency and Critical Care Certificate > Equine Critical Care and Analgesia - physiology > Flashcards

Equine Critical Care and Analgesia - physiology Flashcards

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1
Q

Functions of the cardiovascular system?

A

Deliver oxygenated blood to body tissues = perfusion
Deliver deoxygenated/hypercapnic blood to lungs
Deliver waste products/toxins to sites of detoxification and excretion
Deliver hormones

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2
Q

When is the heart perfused? How much of the cardiac output does it receive?

A

During diastole from the coronary circulation
5-10% of the cardiac output at rest

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3
Q

Which symathetic receptors in the heart are responsible for increasing the contractility? How is an increased heart rate ahieved?

A

B1 receptors increase contractility
Heart rate increases by reducing vagal/parasympathetic tone

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4
Q

How does the parasympathetic system affect the heart?

A

Reduce heart rate, stroke volume and contractility

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5
Q

What causes the heart sounds?

A

S1 - Closure of AV valves
S2 - Closure of aortic valve
S3 - End of rapid ventricular filling
S4 - Atrial contraction

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6
Q

What makes up the conducting network of the heart?

A

SAN -> Conduction through atria -> AVN -> Bundle of His -> Purkinje fibres -> Ventricular myocytes (contracts apex first)

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7
Q

What predisposes horse to atrial fibrillation?

A

Large atria
High vagal tone

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8
Q

Cardiac output and blood pressure equations?

A

Cardiac output = Blood pressure/Systemic vascular resistance

Blood pressure = Cardiac output x Vascular resistance

Blood pressure = Heart rate x Stroke volume x Vascular resistance

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9
Q

What factors affect heart rate?

A

Autonomic influences
Exercise, stress, pain
Dysrhthmias
Electrolyte disturbance
Drugs

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10
Q

What factors affect stroke volume?

A

Preload - Effective circulating blood volume (ECBV), filling
Contractility - autonomic influences, Ca2+, structural heart disease
Afterload - vessel tone

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11
Q

What factors affect vascular resistance (afterload)?

A

Vasodilation - sepsis/endotoxins, drugs

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12
Q

Does good blood pressure always mean sufficient blood flow?

A

No
E.g. if arteries supplying a muscle belly are constricted, vascular resistance will be high, sop BP will appear high, but might not have sufficient blood able to reach tissue

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13
Q

How to calculate MAP?

A

Diastolic + 1/3(Systolic - Diastolic)

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14
Q

Does a bounding pulse mean good health?

A

No
A pulse will feel stronger if the diastolic pressure is very low and systolic is very high - the heart is trying to make up for the low diastolic pressure by putting systolic as high as possible - horse may not be doing well!

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15
Q

What counts as upper and lower respiratory systems?

A

Upper - nares to cervical trachea
Lower - thoracic trachea to lungs

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16
Q

Functions of respiratory system?

A

Delivery of O2
Removal of CO2
Non respiratory functions of the lungs:
- Trap airborne particles
- Reservoir of blood (stores about 10% of circulating volume)
- Metabolism - e.g. degrade angiotensin I
- Acid-base modulation - eliminating CO2
- Clotting modulation
- Filtration of blood - large particles e.g. tumour cells (so lungs common site for metastasis), emboli, clots are trapped and filtered
- Immune functions - macrophages in alveoli etc, IgA in mucus
- Modulation of body temperature - changes to ventilation
- Phonation
- Olfaction

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17
Q

What is ventilation?

A

= The exchange of air between the lungs and the atmosphere (prior to gas exchange happening)

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18
Q

What controls ventilation?

A

Sensory organs - peripheral chemoreceptors (carotid and aortic bodies), central chemoreceptors (ventral medullary sensing body), stretch and proprioception receptors
Respiratory control centres - brainstem and cortex
Feedback includes responses to changes in pH, PaCO2 and PO2

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19
Q

What stimuli can carotid bodies and aortic bodies detect?

A

Carotid bodies - pH, PaCO2, PaO2, temperature, hypoglycaemia
Aortic bodies - pH, PaO2, PaCO2, and also blood carrying content e.g. anaemia, carboxyHb

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20
Q

What do the central chemoreceptors in the ventral medulla respond to for ventilation?

A

pH - concentration of H+ ions

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21
Q

What are the 3 main things measured in the blood by the ventilatory system?

A

PaO2
PaCO2
pH

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22
Q

What is hypoxaemia? What are possible causes?

A

Low oxygen levels in the blood (<60mmHg in arterial blood)
Causes:
- Low FiO2 (breathing in low O2 e.g. barn fires)
- Diffusion impairment
- Hypoventilation (common cause)
- V/Q mismatch
- Hypotension (as then have poor perfusion to pulmonary tissues)

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23
Q

What is hypoventilation?

A

= Inadequate minute ventilation
Minute ventilation (amount of air we move in and out of our lungs per minute) = Tidal volume x RR

Would not be blowing off enough CO2, so this then reduces space for O2

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24
Q

Calculation for minute ventilation?

A

Minute ventilation = tidal volume x RR

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25
Q

What is diffusion capacity? What influences this?

A

How much of a gas can diffuse across a surface - O2 and CO2 diffusing from alevoli into/out the blood stream

Influenced by:
- gas properties (CO2 is more soluble than O2 so will find it easier to diffuse than O2)
- surface area (age of horse, lung size etc)
- membrane thickness (e.g. thickened with equine asthma)
- uptake of RBCs - affinity of Hb for O2, Hb concentration, CO

26
Q

What are the two things alveolar gas exhnage depends on?

A

Ventilation and perfusion

Ie need the gases present in alveoli and need the blood supply there too

27
Q

What are ventilation: perfusion shunts and phyisologic dead space mismatches (V/Q)?

A

V = ventilation
Q = perfusion (flow)

Ideally want V = 1 and Q = 1

Shunt = good perfusion to alveoli, but poor ventilation (e.g. alveoli blocked with mucus, atelectasis)

Physiological dead space = good ventilation to alveoli, but poor perfusion (e.g. due to emboli, low CO, horse lying in lateral recumbency)

28
Q

What is oxygenation?

A

Adding oxygen to the body by movement of O2 into the blood stream

29
Q

How to divide up the causes for a horse presenting with respiratory distress?

A

Non respiratory? E.g. pain, shock
Respiratory? URT vs LRT?
If LRT - parencymal vs pleural?

30
Q

How much of the cardiac output do the kidneys receive? From which artery?

A

20%
Renal artery (direct branch of aorta)

31
Q

Functions of the kidneys?

A

Regulation:
- Plasma volume
- Electrolyte concentration
- Plasma osmolarity
- Removal of waste products
- Maintaining acid-base balance
- Gluconeogenesis

Hormonal:
- Synthesises EPO
- Activates Vitamin D
- Secretes renin

31
Q

Structure of the kidney and nephrons?

A

Cortex and medulla
Functional unit is a nephron
Nephron starts at the glomerulus, where a small artery (afferent arteriole) coils up into glomerus where plasma contents are filtered out
The filtrate is collected by the Bowman’s capsule and enters a series of tubes which make up the nephron
Along the nephron, useful chemicals are reabsorbed, whilst waste products remain
Urine is discharged into the collecting duct
Collecting ducts coalesce to form the ureters

32
Q

How is the blood supply split between the renal cortex and medulla?

A

Cortex - 90% of blood flow
Medulla - 10%
But medulla is nearly 50% of renal volume and many resorptive active processes occur here, so it is essential this blood flow is maintained

33
Q

What are the two types of renal nephrons?

A

Most are short cortical nephrons - after leaving glomerulus, blood runs through peritublar capillaries next to collecting duct for perfusion and resorption
Juxtamedullary nephrons (25% of nephrons) - after leaving glomerulus, blood runs down around the loop of Henle, vital for fluid exchange and fluid balance, these vessels are the only vessels responsible for the perfusion of the medulla

If renal blood flow is poor, the medulla can quickly become under perfused and injured

34
Q

What does the filtrate in the kidney’s bowman’s capsules contain?

A

Metabolic waste products
Water
Electrolytes
Glucose
Amino acids

Should not contain blood cells or plasma proteins

35
Q

Where does most resorption in the nephrons take place? What is resorbed here?

A

Proximal convoluted tubules
The fluid is resorbed into peritubular capillaries, formed from the efferent arteriole which has left the glomerulus
2/3 of NA, K and Cl and 85% of bicarb is resorbed
All of the glucose and amino acids are resorbed

36
Q

What is resorbed and excreted by the loop of Henle?

A

Thin descending loop - Water is resorbed
Thick ascending loop - electrolytes are resorbed, H+ ions are excreted

37
Q

What is resorbed and excreted by the distal convoluted tubule and collecting duct?

A

Na, Cl, bicarb, some K and water are resorbed
H+ and K can be excreted

38
Q

Where is urea resorbed?

A

Medullary collecting duct

39
Q

What is the juxtaglomerular apparatus and what happens here?

A

Where the distal convoluting tubule passes very close to the glomerulus/afferent arteriole
Juxtaglomerular cells within the walls of the afferent arteriole - store renin and can release this into the blood stream

40
Q

What are the 3 stimuli which cause the juxtaglomerular cells in the afferent arteriole to release renin?

A
  • Mechanical - if BP drops, the walls of the afferent arteriole are less stretched -> renin released
  • B1 adrenergic stimulation from adrenaline/noradrenaline -> renin release
  • Prostaglandin release from macula densa which lines distal convoluted tubule and monitors Na ion concentrations - if BP drops, less blood reaches afferent arteriole, less Na is filtered, so less Na in DCT –> release of prostaglandin –> release of renin (this is one reason why need to be careful giving NSAIDs to hypotensive/hypovolaemic patients)
41
Q

What does renin do?

A

Renin released from juxtaglomerular apparatus in kidneys
-> renin cleaves angiotensinogen (made by liver) to ANG I
-> ANG I converted to ANG II by ACE, mostly in the lungs
-> ANG II in circulation
-> vasoconstriction, increase Na+ resorption from kidneys (PCT), stimulates ADH release from pituitary (-> vasoconstriction, increases water retention in kidney DCT/CD), acts on adrenal cortex to stimulate release of aldosterone (-> increases Na+ retention by kidneys DCT)
-> increases BP and blood volume

42
Q

How much of the cardiac output does the brain receive?

A

15%

43
Q

What are the 3 protective meningeal membranes of the brain?

A

Dura mater (outer)
Arachnoid mater
Pia mater (inner)

44
Q

What makes up the blood brain barrier? What is excluded from the brain

A

ECF within the brain is separated from the brain capillaries by the blood brain barrier, comprising of:
- Endothelial cells with tight junctions
- Thick basement membrane
- Astrocyte foot processes (reduce capillary permeability)

Excludes catecholamines, ammonia, amino acids, some drugs

45
Q

What are the 5 functional regions of the brain?

A

Cerebellum - motor coordination, balance, posture
Diencephalon - thalamus (relays sensory info to cerebral cortex, pain perception, sleep), hypothalamus (autonomic function, neuroendocrine, pituitary, hunger, thirst, thermoregulation)
Telencephalon - cerebral hemispheres (4 lobes), basal ganglia (fine motor control), limbic system (memory, emotion, behaviour)
Rhombencephalon - medulla (autonomic control of respiration, CV system, consciousness), pons (stimulation of breathing, sleep cycle control)
Mesencephalon - midbrain (vision, arousal, temperature regulation, motor control, hearing)

Rhombencephalon + mesencephalon = brainstem (all cranial nerves, except olfactory, emerge from here)

46
Q

What is the equation for cerebral blood flow?

A

Cerebral blood flow = cerebral perfusion pressure/cerebral vascular resistance

Perfusion pressure = MAP - ICP

So, cerebral blood flow = (MAP - ICP)/CVR

Vascular resistance depends on the diameter of the cerebral arteries

47
Q

What supplies the blood flow to the brain?

A

Circle of Willis, from internal carotid arteries

48
Q

What makes up intracranial pressure?

A

CSF, arterial blood and venous blood
If get a bleed in the brain or tumour etc, ICF can quickly increase as skull cannot expand and limited ability of CSF to reduce to compensate

49
Q

What does raised ICP look like in horses?

A

Unknown
Humans - vomiting, headaches, optic disc swelling
Dogs - altered consciousness, abolition of brainstem reflexes, abnormal postures

50
Q

What happens physiologically if ICP increases?

A

Cushings response
= Bradycardia, hypertension and abnormal respiration

Cerebral blood flow will fall
CNS ischaemia stimulates sympathetic response –> widespread vasoconstriction –> to increase BP and then cerebral blood flow
If large increase in BP, baroreceptor reflex will cause decrease in HR

If ICP increases further, possibly leading to herniation of brainstem –> abnormal breathing pattern

51
Q

How to reduce ICP medically?

A

Difficult to do practically
Attempt to shrink brain tissue by giving hypertonic saline, or by reducing blood volume by giving osmotic diuretic like mannitol
May be possible to do in foals with head injuries

52
Q

Where do the sympathetic and parasympathetic systems outflow from?

A

Sympathetic - thoracolumbar
Parasympathetic - craniosacral

53
Q

Which neurotransmitters do sympathetic and parasympathetic use at the effector?

A

Para - Acetylcholine
Symp - Noradrenaline/adrenaline

54
Q

Clinical signs of heart failure in horses?

A

Due to reduced CO:
- Tachycardia
- Weight loss
- Weakness
- Exercise ontolerance
- Pale mucous membranes
- Weak arterial pulses
- Weakness
- Ataxia
- Syncope
- Reduced renal output (but difficult to document clinically in horses)
- Increased serum creatinine

Due to increased ventricular filling pressure:
- If left heart failure e.g. severe mitral insufficiency and large VSDs –> congestion of pulmonary circulation –> pulmonary oedema (-> inc RR esp after exercise and crackles if slowly progressive, if acute rapid lesions then may be dyspnoea, coughing, profuse nasal frothy discharge)
– Pulmonary hypertension can lead to dilation and eventually rupture of pulmonary artery - not necessarily immediately fatal, may be several episodes of syncope and distress before death
- right sided heart failure less common in horses as an isolated state, but clinical signs of left heart failure often go unnoticed if slowly progressive disease, until the right heart fails in response to pulmonary hypertension, clinical signs include jugular distension, pulsations of the jugular veins extending beyond normal distal one third of neck, distension of other peripheral veins such as lateral thoracic veins, ventral/muzzle/prenuptial/limb oedema, ascites on US, pleural effusions with absence of resp sounds over ventral lung field and ventral thoracic dullness on percussion (and visualised by radiography and US)

55
Q

Why is atrial fibrillation a common finding in CHF in horses?

A

Many lesions associated with heart failure lead to enlargement of the left or right atrium -> predisposes to development of AF

Important to differentiate primary AF from AF secondary to CHF, because quinidine sulfate is indicated for primary, but contraindicated for CHF

56
Q

Differential diagnosis for horses presenting with acute severe clinical signs of congestive heart failure?

A

Diseases with recent onset
Disruption of valvular apparatus
Bacterial endocarditis
Myocardial disease (bacterial, viral, toxic, nutritional, idiopathic, neoplastic)
Pericarditis (bacterial, viral, idiopathic, immune mediated, toxic)
Aortocardiac fistula
Rapid ventricular tachycardia
Chronic diseases that can decompensate acutely
Degenerative valvular disease
Large ventricular septal defect
Complex congenital cardiac anomaly

56
Q

What signs accompanying a horse with AF may make you suspect CHF is present?

A

HR >60
Loud cardiac murmurs
Echo evidence of valvular or other cardiac lesions

57
Q

What is the most common form of acute mitral valve disease in the horse?

A

Rupture of chordae tendinae
Either spontaneously, or secondary to degenerative or inflammatory valve disease

58
Q
A

Equine Emergency and Critical Care Certificate (7 decks)

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