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Cardiovascular Flashcards

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1
Q

How is oxygen supplied to the embryo?

A

Via the placenta

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2
Q

Describe the route of oxygen transport within the foetus.

A

Oxygen supplied via placenta into (L) umbilical vein -> liver (bypasses hepatic sinusoids via ductus venosus) -> caudal vena cava -> (R) atrium -> foramen ovale -> (L) atrium -> aorta
(R) atrium also goes to (R) ventricle (mixes with deoxygenated blood from head) -> pulmonary trunk -> lungs or ductus arteriosus -> caudal aorta (supplies thoracic and abdominal organs) -> returns to placenta via umbilical arteries.

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3
Q

What changes occur to the cardiovascular system at birth?

A

Placenta is replaced by the lungs as organ or respiratory exchange.
Thorax is compressed during birth - amniotic fluid is expelled from bronchial tree.

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4
Q

What occurs immediately prior to birth?

A

Umbilical artery contracts, decreases blood returning to placenta and results in the cord rupturing.
Umbilical vein contracts forcing placental blood into neonatal circulation. Blood flow through ductus venosus halted by wall contraction.

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5
Q

What occurs immediately after birth?

A

Ductus arteriosus contracts closing the foetal shunt. All blood in pulmonary arteries delivered to foetal lung.
Foramen oval is covered by septum primium, decreases pressure in (R) atrium due to loss of placental blood flow. Increased pressure in (L) atrium due to increased pulmonary flow.

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6
Q

What allows the blood to bypass pulmonary circulation in the foetal body?

A

Foramen ovale

Ductus arteriosus

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7
Q

What is the foramen ovale?

A

Opening between the atria

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8
Q

What is the ductus arteriosus?

A

Connecting vessel between aorta and pulmonary artery.

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9
Q

What is the ductus venosus?

A

Joins umbilical vein and caudal vena cava. Bypasses liver (mostly) as it is not yet required to function. THIS IS NOT PORTAL.

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10
Q

Why is pulmonary vascular resistance so high in the foetus?

A

Because the lungs are collapsed.

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11
Q

Describe the changes that occur with the onset of ventilation.

A

First breath must overcome strong surface tension (-60mmHg).
Loss of placental blood flow doubles the systemic vascular resistance.
Expansion of lungs reduces pulmonary vascular resistance; increased pulmonary blood flow, decreased pulmonary arterial pressure, pulmonary oxygenation releases hypoxic pulmonary vasoconstriction, pulmonary venous return is at higher PO2 and hydrostatic pressure.
Reversal of pressure gradients in aorta/pulmonary artery and (L) atrium/(R) atrium; direction of flow in ductus arteriosus reverses (PO2 increases to 100mmHg causes contraction of ductus smooth muscle - occurs d1-8), foramen oval flap on (L) atrium side closes.
Contraction of ductus venosus (1-3hrs); decreases blood flow due to rupture of umbilical vessels, increases portal tension (6-10mmHg) and forces hepatic perfusion by portal blood, liver function increases.

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12
Q

Compare the post-natal respiratory system to an adult.

A

Increased thoracic compliance (FRC, Vt decreased)
Increased closing volume when Vt decreased.
Increased RR
VE doubled.
Respiratory fatigue more likely during respiratory distress.

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13
Q

Compare the post natal cardiovascular system to an adult.

A 
Decreased cardiac contractile tissue
Decreased ventricular compliance
Decreased cardiac reserve
CO increased only by rate
Decreased SNS output (decreased baroreceptor reflex for BP changes and decreased beta-adrenoreceptors).
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14
Q

Compare the post-natal cardiorespiratory system to an adult.

A

Decreased hepatic function (decreased plasma, colloid osmotic pressure and drug binding albumin = increased [free drug]).
Increased total body water (80% compared to 60% in adults).
Fixed circulation volume (decreased central space compliance, increased risk of preload failure or pulmonary oedema if body water varies).
Increased metabolic rate (2x that of adult).
Decreased thermoregulatory capacity.
Decreased PCV and therefore O2 carrying capacity.
Decreased renal function.

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15
Q

Why are neonates so sensitive to changes to normal state (eg. dehydration, blood loss, over hydration)?

A

Due to inability to modify physiology in response to conditions.
Eg. 5% dehydration = decreased preload and CO resulting in shock.
Anaesthesia destroys most compensatory mechanisms.
Medical treatments for shock rely on beta-1-adrenoreceptors which are slow to develop in neonates.

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16
Q

In the foetus, does the (L) or (R) side of the heart have higher pressure?

A

(R)

(L) receives blood from lungs - little of this.

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17
Q

In the foetus, does the pulmonary trunk or aorta have higher pressure?

A

Pulmonary trunk.

Blood is forced from pulmonary trunk into aorta via ducts arteriosus.

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18
Q

What does the ductus arteriosus become post natally?

A

Ligamentum arteriosum - fibrous band between pulmonary trunk and aorta.

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19
Q

What local mechanisms control the cardio-respiratory system at rest?

A

Myogenic auto regulation
Arteriolar flow regulation (Nitric Oxide system)
Tissue auto regulation

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20
Q

What is myogenic auto regulation?

A

Contraction of arteriolar smooth muscle in response to stretch accompanying increased pressure within a vessel.

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21
Q

What is arteriolar flow regulation/NO system?

A

Nitric oxide causes local arteriolar vasodilation by relaxing arteriolar smooth muscle cells within its vicinity.

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22
Q

What is local tissue auto regulation?

A

Pre-capillary sphincters have sensors of H ions, purines (ADP, AMP) and potassium.
The sensor is in afferent blood supply so requires counter-current feedback.

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23
Q

What systemic mechanisms control the cardio-respiratory system at rest?

A 
Baroreceptor reflex
Bainbridge reflex
Acidaemia reflex pathway
CO2 reflex pathway
Renin-angiotensin pathway
ANP/BNP reflex pathway
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24
Q

What is the baroreceptor reflex?

A

Autonomically mediates HR and blood vessels to adjust CO and TPR in attempt to maintain BP close to normal values. Sensors in carotid and aortic arch.

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25
What is the bainbridge reflex?
Increased HR due to increased central venous pressure. Increased blood volume detected by stretch receptors located in atria and venoatrial junctions. Increased preload.
26
What is the academia reflex pathway?
Acidosis leads to academia - may be respiratory or metabolic. Buffered by bicarb, intracellular, respiratory or renal.
27
What is the CO2 reflex pathway?
Ventilation is adjusted depending on PaCO2 reaching ventral medulla.
28
What is the ratio of Adrenaline and noradrenaline secretion?
3:2
29
When is SNS stimulation the lowest?
Horizontal sleep
30
What are the characteristics of the SNS adrenoreceptors?
``` All g-protein coupled (Gs, Gi/o, Gq/11). All metabotropic - indirectly linked with ion channels on plasma membrane. Respond to Ad, NAd. Transduction times vary. Receptor synapse regulation is slow. NAd re-uptake is slow. ```
31
What are Gs receptors?
Beta 1 and 2. Upregulate cAMP. 1 is inotrope, chronotrope, dromotrope, lusitrope, bathmotrope. 2 relaxes smooth muscle in vascular beds of skeletal muscle.
32
What are Gi/o receptors?
Alpha 2 - decrease intracellular [cAMP], protein kinase A and increase smooth muscle function.
33
What are Gq/11 receptors?
Alpha 1 - releases Ca from intracellular stores into cytoplasm.
34
What are the characteristics of PNS muscarinic receptors?
Metabotropic - Gi/o in M2 and M4, Gq/11. Responds to acetylcholine (vasodilation). N-ACh receptors are ionotropic (open ion channels when activated). Destruction of ACh in synapse is almost immediate (pseudocholinesterase). Fine control function achieved using Each transmitters.
35
Why is NAd less clearly targeted than ACh?
NAd has local and humoral leakage due to high output - results in overflow. It has slow receptor transduction (30sec) and so requires longevity of agonist. ACh is always targeted and leakages destroyed.
36
What are the important functions of the PNS?
1. Slows HR at SA node (M2). 2. Slows AV node takeover rate and bundle conduction (M2). 3. Decreased atrial dromotrophy via increased K conductance. 4. Constriction of bronchi (M3). 5. At rest, HR predominantly under vagal (PNS) control. 6. Untrained subjects increase HR to mediate CO during exercise (vagal mediation).
37
What are the important functions of the SNS?
1. NAd | 2. Ad
38
What does NAd do?
Alpha 1 and beta 1 agonist. Minimal alpha 2 agonist effect. No beta2 agonist activity. Chronotrope, Inotrope, Dromotrope, Lusitrope, Bathmotrope. Causes splenic contraction - increased PCV. Contraction of great veins and central venous space (increased preload and SV). Contraction of pulmonary veins (decreased compliance, increased preload). Constriction of resistance arterioles and increased arterial BP. Afferent arterioles constrict (renal cortex=decreased GFR). Decreased integument blood flow (thermoregulation). Dilation of pupil Increased ADH secretion. Uterine contraction. Decreased urination Ejaculation Decreased insulin production Increased blood coagulability
39
What effect do beta1 receptors have?
Cardiac mediator. | Causes short term phosphorylation of ion channels in cardiac cells = earlier gating and increased channel recruitment.
40
What is a Chronotrope?
Increases HR by increasing Na leak rate in atria
41
What is a Inotrope?
Increases contraction
42
What is a dromotrope?
faster AP propogation
43
What is a Lusitrope?
Increased relaxation
44
What is a bathmotrope?
Increased excitability
45
What are the effects of Ad?
Alpha 2, beta 1 and 2 agonist. Weak alpha 1 agonist. ONLY beta 2 agonist in body. Co-secreted with NAd (NEVER ALONE). Secreted by adrenal gland. Bronchodilation Vasodilation in skeletal and cardiac muscle. Increased glycogenolysis in skeletal muscle. Increased gluconeogenesis in liver. Uterine, gall bladder, urinary bladder relaxation. Increased sweat production in horses. Increased insulin production. Blocks histamine release. Increased renin secretion. Decreased ADH secretion - increased urine.
46
What other hormones play a role in stress?
Cortisol - release glucose, glycogen, fat and protein catabolism. Insulin - increased glucose transport and uptake. ADH - increased osmolarity and water retention. RAAS - decreased blood volume, vasoconstriction, increased pressure and Na via aldosterone. ANP - Increased blood volume, vasodilation, decreased aldosterone and Na reabsorption.
47
What does homeothermic mean?
Maintains temperature within close range. | Not homothermic - same temp.
48
Why is thermoregulation important?
Provides specific conditions for enzymes to work. Increased temperature increases chemical reaction speeds. pH of neutral H2O changes with temperature.
49
What is a poikilotherm?
Animal whose temperature is allowed to vary with environmental temperature.
50
How does homeothermic regulation occur?
Temperature regulation - 2 principle theories; 1) adjustable set point control (increased temp makes it more difficult for virus to function), 2) reciprocal inhibition. Heat regulation Temperature regulation theories don't account for decreased hear shedding at completion of exercise before patient has cooled.
51
How is temperature sensing achieved?
Rostral hypothalamic-preoptic area - hot and cold Skin surface - hot and cold Deep body (viscera, spinal cord, great veins) - cold only Caudal hypothalamus integrates signals for response.
52
How is temperature managed?
Production of heat and transfer must balance. Transfer governed by radiation (cool/heat), conduction (cool/heat), evaporation (cool), convection (increases conduction and evap.)
53
What is the most important heat transfer mechanism?
Evaporation. | Without it you will die.
54
How is heat in the body produced?
BMR Muscle activity incl. shivering. Thermogenic hormones (thyroxine, GH, testosterone). Ad, NAd. Increased temperature means increased chemical activity in cells and increased metabolism and heat. Thermogenic effect of food.
55
How does passive heat transfer occur?
Wavelengths absorbed by skin are converted to heat except for light waves that cause chemical changes (UVb, VitD). Conduction Convection - increased heat conductance in any fluid medium.
56
How does evaporative heat transfer occur?
Loss governed by perspiration and ventilation. H2O only vaporises to saturation point. Heat dissipation is proportional to surface area.
57
How does blood flow effect temperature?
Increased temperature increases blood flow to skin for heat loss. Decreased temperature causes vasoconstriction - heat maintained centrally.
58
What is piloerection?
Hairs raise, makes coat layer thicker and traps more air. Reduces convective loss.
59
What effect can anaesthesia have on thermoregulation?
Can cause vasodilation - increased blood flow to surfaces - can result in hypothermia.
60
What adaptations have been made in animals adapted to cold environments?
Decreased skin blood flow - less moist skin. Thermogenesis - shivering and non-shivering Hibernation
61
What is shivering and how does it occur?
Primary motor centre is dorsomedial portion of caudal hypothalamus. Stimulated by signals from skin and spinal cord. Increased muscle tone, once critical level is reached shivering starts. Generates 4 x heat than BMR.
62
What is non-shivering thermogenesis?
Chronic cold exposure - increased metabolic heat production independent of muscle contraction. Maintained by hormones Ad and TH. Can be rapid (brown fat) or slow control (TRH). Incidental control is via testosterone and GH which both increase BMR.
63
How is thermoregulation maintained in hot environments?
Main transfer is via evaporation (vasodilation). Increased animal temperature increases H2O loss. Sweating Panting Excess heat causes hyperventilation and alkalosis (increases CO2 loss). Strong inhibition of chemical thermogenesis.
64
How is sweating in horses controlled?
Ad and beta2 receptors only. No control from NAd or cholinergic fibres. No control by aldosterone (iso-osmotic sweat).
65
What effect does training have on heat tolerance?
Increased speed of response to heat stress. | Doesnt improve temperature to which subjects can exercise.
66
What are the forms of clinical heat overload?
Heat stress - approaching limit of ability to adequately cool, increased sweating, HR and temp. Heat exhaustion - decreased fluids and electrolytes, rapid shallow breathing. Heat stroke (emergency) - prolonged exhaustion, high HR and temp, sweating failure, exhaustion, agitation, seizure, coma, death.
67
True or false, most energy is dissipated as heat?
True
68
Describe the ways in which energy can be stored.
Storage with low total energy can produce high output - anaerobic (ATP produced on demand, phosphorus-creatine). Large stores have lower output rates - aerobic (glycogen, fat, protein).
69
What is the phosphagen energy system?
ATP and phosphocreatine as rapid suppliers for high energy output. Creatine can be phosphorylated and used to regenerate ATP very rapidly. Longer duration exercise uses up these reserves very rapidly (8-10sec).
70
What is the glucose anaerobic pathway/Glycogen-Lactic acid system?
Break down of glycogen to produce ATP. Causes lactate to build up - requires O2 for transport to liver where it is converted back to glucose. Lasts 1.3-1.6 minutes
71
What is the oxidative system?
Takes over before fatigue sets in. Takes pyruvate to CAC in mitochondria instead of turning it into lactate (anaerobic). 36ATP yielded from each glucose molecule.
72
What is the order of energy system activation?
``` ATP Phosphocreatine Glycogen-lactic acid Aerobic In heavy chronic output fat and protein will then begin to be used as well. ```
73
Why must the body discharge metabolic acids?
Produce shifts in pH (buffering and excretion).
74
What is the most limiting factor in exercise for metabolic oxygen supply?
Heart | Not the lungs.
75
What are the three main stores of oxidisable substrate?
Muscle Liver Fat - adipose is not a ready source of fat for energy, instead the fats used for energy are stored in muscle or liver cells or still in blood. Conversion from major adipose is very slow.
76
How is oxygen acquired for energy production?
Stored in myoglobin, haemoglobin, ECF. | Ventilation
77
How are oxidisable substrates and oxygen supplied to tissues for energy production?
Blood and heart. | Regulation of blood flow via pre-capillary sphincters (acids, purine receptors).
78
What are the metabolic by-products of energy production?
Excess heat. Aerobic - CO2. Anaerobic - lactic acid Protein oxidation - CO2, NH3, strong ion acids (require renal secretion).
79
What effects do higher temperatures have on the body and energy production?
Increases the strength of attraction required to hold proteins in correct shape. Decreases dissolved gas carried in plasma. Decreases O2 in Hb. Less effective blood buffering of respiratory acid. Increased channel opening. Increased AP in heart (dromotropy). Mental incapacitation
80
What effects does pH have on energy production?
High [H+] reduces maximal energy production by mitochondria and decrease gradient between cells and ECF. Protein conformation very dependent on pH (ionisation of side chains, shape, charge). Low pH effects Ca+ flux in/out of SR. Acidosis increases ventilation. Severe pH changes close Cx45 in heart muscle - decrease dromotropy (decreased AP conduction).
81
Discuss lactate in horses.
Horses tolerate higher lactate than humans. Blood lactate peaks 5-10minutes after exercise. Production increases with increased work. Above 75% VO2 max, lactate clearance doesn't increase and so limits exercise.
82
How are acids excreted?
Respiratory acids - ventilation | Metabolic acids - metabolised in liver or muscle to respiratory acid, renal compensation.
83
How is ammonia excreted?
Converted to urea in liver and excreted renally.
84
How can strong ions be excreted?
Renally.
85
What is the acute response to heavy exercise?
Neurohumeral and SNS control is dominant. | MMR
86
What respiratory changes occur in response to high energy output?
Increased pulmonary artery blood flow and pressure - decreased perfusion differences, decreased PVR, recruitment of alveolar vessels. Broncho-dilation mediated by adrenaline (Beta2). Increased ventilation - same effects as increased pulmonary artery blood flow and pressure. Increased rates and depth increase VO2 and heat loss.
87
What is different in horses in terms of respiration during high intensity exercise?
Higher VO2 max. May not reach VO2 max depending on type of work, environmental conditions. Active exhalation. Airway resistance means higher vacuum on inspiration (probably promotes pulmonary bleeding).
88
What cardiac changes occur in response to high energy output?
MMR and cerebral premonition; Rapid, positive chronotropic response SV increases - positive inotropy. Increased rate of conduction - positive dromotropy. Increased rate of ventricular relaxation - positive lusitropy. Increased excitability - positive bathmotropy. All mediated by SNS.
89
What vascular and rheological changes occur in response to high energy output?
MMR increases SNS vasoconstriction - increases preload, and PCV from splenic contraction. Decreased pre-capillary sphincter open time. Cerebral and renal artery constriction protects against upstream pressure (alpha2 mediated).
90
What hepatic changes occur in response to high energy output?
Increased production of glucose from gluconeogenesis and beta-oxidation of FA. Governed by glucocorticoids.
91
What other neuro-humoral changes occur in response to high energy output?
Increased SNS - splenic contraction and direction of blood flow away from viscera. Angiotensin II production - causes vasoconstriction, increases aldosterone (Na and H2O sparing), increases BP. ANP and BNP secretion - secreted in response to increased preload, causes vasodilation, inhibits ADH and aldosterone. Cortisol secretion - decreases glucose uptake, increases insulin, increases fat metabolism and protein catabolism. NAd and Ad don't work without cortisol. Increases sensitivity to catecholamines.
92
What are slow twitch fibres?
``` Type 1 Aerobic - red muscle Narrower diameter Slower development of force Many mitochondria Large stores of myoglobin Shorter distance to capillaries. Common in larger muscles. ```
93
What are fast twitch fibres?
Type II, a and b. Anaerobic - white muscle Twice the diameter of slow. Extensive SR. Fewer mitochondria. Greater proportion for rapid power development. Type IIa more like type 1, type IIb are ultra-fast twitch.
94
What is fatigue?
Relates to muscle, fibres, nerves and whole body. Whole body associated with lactic acid build up, depletion of muscle glycogen, psychological responses complicate this. Muscle associated with strong contraction for long periods occluding blood and O2 supply and waste removal. Fibre associated with loss of glycogen. Nerves fatigue and reduce strength of signal for contraction.
95
Discuss fatigue in high performance subjects?
Reduced ATP levels - phosphagen system has been depleted. | Mid-range sprints associated with ATP reduction and build up of lactic acid.
96
Discuss fatigue in medium performance subjects?
Usually due to build up of lactic acid and loss of glycogen stores.
97
Discuss fatigue in marathon/all day event subjects.
Loss of muscle glycogen stores. Oxidisable substrates come into play - protein and fat. Not as rapid in energy delivery.
98
What is central fatigue?
Lethargy and loss of drive due to decreased motor fibre recruitment. Increased serotonin levels. Associated with hyperthermia, acidosis, hypoglycaemia, dehydration.
99
Why might warm-up be important?
Need is well documented by not well understood. Overexertion less likely with warm up. Full system recruitment obtained before high output.
100
Why might warm-down be important?
Cerebral systems switch off at end of exercise however ongoing needs are still present (MMR). Continuing low level exercise maintains state in which deficits induced by exercise are repaired faster than reflexes (lactic acid, temp, CO2, pH, glycogen).
101
What is the purpose of training?
Increases heat loss ability to reduce rate of temperature increase - prolongs approach to cut-off point. Increases muscles ability to do more work. Increases cardiac, vascular and respiratory ability to service increases in work. Sweat is produced sooner but with less Na content.
102
What effects does training have on skeletal muscle?
Increased muscle bulk - widening of muscle fibres due to increased filaments. Aerobic; Increased mitochondria, Increased ability for lipolysis. Anaerobic; Increased glycogen storage, Faster lactate clearance, Angiogenesis (neovascularisation).
103
What are the effects of training on the heart?
Volume load - increased cardiac output. Pressure load - need to pump against increased after load. Very oxidative sports are more cardiac output driven. Weight lifting is almost entirely pressure load. Combined training effects produce increase in pressure output and SV. Heart size can increase up to 33% due to increased CO.
104
What is volume load training in the heart?
Increased volume to pump per unit time. Internal signalling causes muscle hypertrophy. Eccentric hypertrophy - larger ventricular lumen for increased venous return and SV. Also requires an increase in muscle wall thickness in order for CO to increase.
105
What is pressure load training in the heart?
Increased pressure to pump against (after load). Internal signalling causes muscle hypertrophy. Concentric hypertrophy - larger ventricular wall for increased pressure of output with same SV. Thicker wall is more viscous and slower to fill - maximum effective HR will be reduced.
106
What effect does SV have on HR and fitness?
Increased SV results in decreased max HR. | Increased heart size = decreased max CO.
107
What are some abnormal conditions of HR?
Elevated rate at rest Cardiac drift - increased rate not proportional to exercise intensity. Poor HR recovery May be due to lack of fitness, heat stress.
108
What effect does training have on tissue vascular supply?
Heavy work output increases tissue oxygen consumption. Lower O2 in tissues, higher [H], greater NO and adrenergic signalling. Combined signalling produces angiogenesis - capillary distance in tissues decreases (increased blood supply).
109
What effects does training have on ventilation?
Limited - about 10% improvement in VO2 max. | Horses can have more improvement as VO2 is there limiting factor for exercise rather than CO.

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