Practice questions for Cardio physiology Flashcards

1
Q

Briefly describe the components of the circulatory system

A
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2
Q

Briefly describe the cardiovascular system as it relates to its function

A
  • transports nutrients to tissues
  • transports waste products from tissues
  • transport hormones
  • dissipation of heat
  • immune response
  • maintain homeostasis
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3
Q

Briefly describe the coronary circulation

A
  • left + right coronary arteries drain into coronary sinus into right atrium
  • thebesian veins drain ventricular wall which drains into left ventricle
  • have venous admixture which is bypassing pulmonary circulation
  • blood flow through coronary arteries being late systole with 80% occurring during late diastole
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4
Q

Name the 4 phases of the cardiac cycle

A
  1. inflow phase
  2. isovolumetric contraction
  3. outflow phase
  4. isovolumetric relaxation
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5
Q

Indicate what is happening during each phase of the cardiac cycle including which valves are open and closed

A
  1. Av open + SL close, rapid ventricular filling, atrial contraction makes the p wave top up the ventricle, diastole
  2. ventricular contraction causes AV closed = both valves closed, no blood flow, ventricular pressure increasing, when pressure exceeds = aortic valve opens, systole
  3. aortic valve open + blood flow from left ventricle to aorta, ventricular pressure decrease, aortic pressure increase, SL open + AV closed, systole
  4. both valves closed, no blood flow, pressure falls rapidly in left ventricle, diastole
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6
Q

Briefly describe cardiac output, and the 4 main factors that affect it

A

cardiac output = quantity of blood pumped by heart each minute
- factors:
- preload = amount ventricular wall stretch immediately prior to contraction
- afterload = amount of tension that contracting ventricle must produce to open semilunar valves
- heart rate = sinus node controls rate + many conditions affect it
- contractility = myocardial performance independent of pre + afterload
= factors that affect it = ANS, hormones, drugs, ion conc, myocardial disease

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7
Q

What is the frank starling mechanism, and how does it relate to function of the heart

A
  • enables heart to pump automatically amount of blood that returns to right atrium = thus cardiac output rapidly adjusted
  • more cardiac monocytes stretched = greater force of contraction = frank law = enables beat to beat modification of stroke volume
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8
Q

What are the clinical parameters that are used to assess cardiovascular function. Briefly describe their assessment

A
  • heart rate = SA node sets intrinsic HR which changes in response to ANS + extrinsic factors affected by baroreceptors, chemoreceptors, low pressure receptors
  • mucous membranes = oral mucous membrane, conjunctive + vulva/prepuce = pale (vasoconstriction or anaemia) = hyperaemic (vasodilation)
  • capillary refill time = assess time = normal <2 sec, >2 sec decreased perfusion,<1 sec rapid refill + pooling of blood
  • pulse quality = small animals (femoral or dorsal pedal), large animals (submandibular or facial)
  • peripheral temp = temp of extremities vs core temp = assess limp temp = cool (decreased blood flow), warm (increased blood flow)
  • heart rate
  • blood pressure
  • ECG
  • radiograph
  • echo
  • fluid accumulation
  • mentation = consider age + personality
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9
Q

What are primary and secondary cardiac disturbances and give an example of each.

A
  • cardiac disturbances = prevention of cardiac disease
  • primary = congenital disease such as abnormal communication, acquired cardiac disease such as cardiomyopathy
  • secondary = direct effect on heart vasculatureq
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10
Q

Define circulatory shock

A

without oxygen = not energy production in tissues = undergo anaerobic metabolism = less efficient + lactic acidosis develops = damage
- caused by cardiogenic = failure of cardiac pump, hypovolaemia = loss of intravascular volume, obstructive = obstruction of venous return, distributive = maldistribution of blood

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11
Q

Briefly describe the compensation of circulatory shock

A

= body attempts to restore core tissue perfusion + oxygnation
- activation of sympathetic nervous system + release catecholamines
= peripheral vasoconstriction
= tachycardia
= increased contractility
-activate RASS

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12
Q

Describe the anatomy and function of cardiac muscle

A
  • has actin + myosin filaments and gap junctions which allow for rapid diffusion of ions
  • pacemaker triggers AP which propagates throughout cardiac myocytes + when its threshold is reached = fast sodium channels open triggering AP
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13
Q

Compare and contrast cardiac muscle to skeletal muscle

A
  • cardiac muscle have actin and myosin filaments
    • they are connected by intercalated discs which forms 2 syncytial ( atria + ventricle)
    • have gap junctions for rapid diffusion of ions
  • action potentials are longer for skeletal muscle due to activation of slow sodium channels + inactivition of potassium channels preventing rapid depolarisation
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14
Q

Briefly describe what is occurring during the phases of the cardiac muscle action potential

A
  • phase 0 = depolarisation. = fast sodium channels open
  • phase 1 = initial repolarisation = fast sodium channels close + fast potassium channels open
  • phase 2 = plateau = calcium channels open + fast potassium channels close
  • phase 3 = rapid repolarisation = calcium channels close + slow potassium channels open
  • phase 4 = restoration of resting membrane potential
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15
Q

What is the refractory period

A
  • absolute refractory period
    • period of time where cardiac muscle is refractory to restimulation
  • relative refractory period
    • additional period of time after AP whistle cardiac muscle is more difficult to excite
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16
Q

Briefly describe cardiac conduction

A
  • atria contract abut 1/6 of a second ahead of ventricles = allow for ventricular filling
  • ventricular conduction must be coordinated
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17
Q

Why is the sinus node the pacemaker and describe its activation and automaticity

A
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18
Q

Briefly describe the sympathetic and parasympathetic activation of the heart

A

Sympathetic:

  • adrenaline/noradrenaline
  • beta adrenergic receptors in heart:
    • increase calcium and sodium permeability = increase contraction + sinus node discharge = fast HR
    • more potassium channels open = reduce refractory period
  • alpha adrenergic receptors in blood vessels = vasoconstriction

Parasympathetic

  • acetylocholine
  • cholinergic receptors
    • increase potassium ion permeability = hyper polarisation = less excitable membrane
    • decrease sinus node = slow HR
    • decrease AV nodal conduction
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19
Q

Identify the different components of the normal ECG

A
  • measures electrical conductivity from skin surface
  • P wave = atrial depolarisation
  • QRS wave = ventricular depolarisation
  • T wave = ventricular repolarisation
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20
Q

What are the standard and augmented limb leads of the ECG

A
  • neg + pos electrodes placed on skin
  • standard leads mostly used in animals attached to limbs
  • appearance of ECG trace dependent for each lead
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21
Q

What is the mean electrical axis and why?

A
  • lead 2 = closest to mean electrical axis
    = mean electrical axis = 59 degrees C and lead 2 = 60 degrees C
    = highest magnitude of electrical activity from base to apex
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22
Q

Briefly describe the base apex lead system used in large animals

A
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23
Q

Briefly describe the steps of rhythm analysis and apply these to interpret an ECG trace

A
  1. calculate heart rate = count no. of QRS complexes in 6 secs + multiple by 10 to give no of QRS complexes in 60 sec
  2. is rhythm regular? = r-r intervals equidistant = regular
  3. P wave for every QRS? = do P waves occur at regular rate + for every QRS
  4. are waves of normal shape + consistence? = p waves - are they all similar in appearances, is appearance normal, QRS - are all same shape + polarity, is shape, duration + polarity appropriate for this lead + species, T waves - is wave appropriate size
  5. are segments + intervals normal = is PR of appropriate duration, is ST depressed or elevated, is T wave appropriate size
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24
Q

What are common causes of sinus bradycardia and sinus tachycardia?

A

brachycardia = slow HT
tachycardia = fast HR
- normal response to decreased output
- stress, anxiety, fever

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25
Briefly describe the effect of high potassium on the membrane potential, threshold potential and the resulting clinical findings with each of these electrolyte disturbances.
= hyperkalaemia - decrease resting membrane potential = partially depolarise membrane with less sodium channels open - causes bradycardia, atrial arrest and even death
26
Briefly describe the effect of low calcium on the membrane potential, threshold potential and the resulting clinical findings with each of these electrolyte disturbances
= low calcium - decrease membrane potential - most common = tremors, seizures, behaviour changes + cardiovascular changes ( less common) = hypotension + decreased cardiac contractility
27
What is the difference between a physiologic and pathologic arrhythmia?
``` physiological = disturbances in normals minus rhythm caused by canes in sympathetic tone pathologic = defect in cardiac system ```
28
common arrhythmias
-
29
supraventricular -vs- ventricular
This is a pathological arrhythmia which has caused a third degree AV block - supra ventricular is atrial in origin - atrial premature depolarisation - atrial filling - ventricular in origin - ventricular premature depolarisation - ventricular tachycardia - ventricular fibrillation
30
sinus arrhythmia
= changes in vagal tone during respiration - inspiration = blood sucked into lungs, decreased vagal tone, increased heat rate - expiration = blood squeezed from lungs, increased vagal tone, decreased heart rate
31
AV block
AV block = variable conduction from atria to ventricle - classified as 1st, 2nd or 3rd degree - 1st = characterised by prolonged P-R interval - 2nd = p wave not followed by QRS + high parasympathetic tone - 3rd = no conduction through AV node + supra or ventricular in origin
32
atrial fibrillation
= multiple re=entrant pathways causing rapid + disorganised depolarisation without atrial contraction - depolarises continuously bombard AV junction - results from atrial enlargement - irregular irregular rhythm - no p waves
33
APDs and VPDs
``` APD = atrial premature depolarisation = P wave early + different on appearance from sinus P wave + P wave may be buried in T wave of previous beat VPD = ventricular premature depolarisation = QRS occurs early + wide and bizarre in appearance, QRS not associated with P wave, T wave opposite polarity ```
34
ventricular tachycardia
= lots of VPC joined together + rapid regular rhythm - QRS wide + bizarre + not associated with P - high heart rate = reduced cardiac output
35
Ventricular fibrillation
impulse propagates into area of non-refractory muscle; - slow conduction velocity - long circuit - short refractory period - terminal arrhythmias = form of cardiac arrest
36
Briefly describe the abnormalities that may be identified during auscultation?
diagnose abnormal heart sounds/arrhythmia - murmurs - arrhythmias - bradycardia - tachycardia - muffled heart sounds - pericardial/pleural space disease
37
What are the normal heart sounds that are heard during auscultation in small animals, and when do they occur?
- S1 = Av valve closure - S2 = semi-lunar valve closure - S3 = rapid diastolic filling of ventricle - S4 = atrial contraction - S1 + S2 = high frequency normal heart sounds = caused by vibrations within ventricles - S3 + S4 = gallop rhythms = abnormal in dogs + rarely heard in normal cats + can be heard in larger animals
38
What are the abnormal heart sounds that may be heard during auscultation and when do they occur?
39
What is a gallop rhythm?
s3 +s4
40
What is a heart murmur?
= sounds created by turbulent blood flow - high velocity - obstruction to flow - low viscosity
41
What is the different between a physiologic and a pathologic heart murmur and give an example of each?
Physiological - low intensity, high frequency, early systolic murmurs - turbulent flow in aorta or pulmonary artery - e.g anaemia Pathological - most due to high velocity flow through narrow orifice - insufficiency (regurgitation) - leaky valve - stenosis - narrowing of valve
42
Identify when murmurs are heard with regurgitant -vs- stenotic heart valves
- murmurs of valvular regurgitation occur when valve is suppose to be closed - blood flows at high speed through defect in valve because pressure different between ventricle + atrium during systole - murmurs of stenosis occur when valve is suppose to be open - some blood goes into ventricle down normal pressure gradient - blood pushed by atria through stenotic valve
43
Discuss how blood flow changes from the large arteries down to the capillaries
44
What are the main determinants of blood flow through a vessel?
dependent on pressure gradient along vessel
45
What are the main differences between veins and arteries?
``` arterties = thick walled + move blood to tissues veins = carry blood to heart + thinner walls ```
46
What vessels provide the largest contribution to total peripheral resistance?
47
What effect does vasoconstriction and vasodilation have on total peripheral resistance?
vasoconstriction - increases blood pressure + therefore increases TPR - vasodilation - decreased blood pressure + therefore TPR
48
What factor has the most significant factor on laminar blood flow?
describes flow of fluid through laminar tube is dependent on: - change in pressure along tube - radius of tube - viscosity of fluid - length of tube - BUT diameter of vessel plays greatest role in determining
49
What are the main factors that determine blood pressure?
determined by: - cardiac output (SVxHR) - resistance from vessels
50
Define mean arterial pressure?
average pressure within arteries
51
What determines the pulse pressure?
pulse pressure = SBP - DB
52
Briefly describe the vasomotor centre and its regulation of arterial blood pressure
located in medulla + pons - vasoconstrictor area - vasodilator area
53
Briefly describe the short-term neural mechanisms present for the rapid control of blood pressure, including the baroreceptor reflex
SNS can cause rapid changes in arterial pressure by: - 1. Vasoconstriction = control of TPR + distribution of blood flow - 2. Constriction of veins = increase preload + therefore CO - 3. Increased contractility + HR = increased by SV + therefore CO negative feedback loop - increased mean arterial pressure - stretch of barorecpetors -> vagus+ glossopharyngeal nerves -> nucleus tractus solitaries of medulla -> inhibition of vasoconstrictor centre -> decreased sympathetic nervous system activation -> vasodilation -> bradycardia -> decreased contractility = thus decreased TPR + CO = thus decreased BP
54
Briefly describe the humoral (longer term) mechanisms of blood pressure control
- pressure diuresis = increased urine production - activation of RAAS - vasoconstriction - retention of Na + water - thirst - ADH secretion by hypothalamus - ANP released from atrial myocytes = natiuresis
55
Briefly describe the Bainbridge reflex
- stretch of atrium causes increase in heart rate - ANS control of sinus node - thus effect of increased intravascular volume is net effect of baroreceptor reflex which reduces HR + Bainbridge reflex which increases HR - when blood volume increase above normal Bainbridge reflex usually prevails whereas low blood volume barorecpetors reflex prevails
56
Briefly describe the production and mechanism of action of atrial natriuretic peptide
57
Briefly describe how the arterioles work to regulate the local control of blood flow to individual tissues (including the vasodilator and oxygen demand theories).
- stop cocks of circulation - regulate flow through capillaries - constriction - dilation - offer greater résistance to flow - maintenance of vascular tone - vasodilator theory - vasodilator substances - released in response to decreased O2 conc - adenosine reasoned from heart msucle cells when coronary blood flow is reduced - oxygen demand theory - smooth muscle surrounding pre-capillary sphincters + met-arterioles constrict in presence of oxygen - high flow delivering high oxygen -> precapillary constricts reducing blood flow - decreased oxygen -> relaxation of smooth muscle -> vasodilation -> increased blood flow
58
What is autoregulation and why is it important?
- maintaining local blood flow during changes in arterial blood pressure - increase in blood pressure immediately increases blood flow, auto regulation returns blood flow to normal - particularly precise in brain + heart - maintains normal blood flow
59
Briefly describe the metabolic and myogenic mechanisms by which autoregulation is thought to occur
Metabolic theory - arterial pressure increases - increased delivery of oxygen + other nutrients - increased blood flow also washes out local vasodilators - vasoconstriction Myogenic mechanism 1. Increased BP -> increase blood flow 2. Blood flow increase -> stretch of vascular smooth muscle 3. Muscle starts responding to stimulus by contracting 4. Contraction narrows lumen -> increased resistance to flow 5. Greater stretch = greater contraction - low pressure = less stretch = vasodilation
60
Briefly describe the functional anatomy of the capillary bed, and how it differs in different tissues
- at their organ a smooth muscle fibre completely encircles capillary = pre-capillary sphincter - unicellular layer of endothelial cells surrounded by thin basement membrane - intercellular spaces (clefts) through which water-soluble substances diffuse - brain - tight junctions that only allow water + gases to permeate - liver - are wide open to allow passage of all molecules including proteins - kidney - glomerular capillaries are fenestrated + allow tremendous amount of small molecular + ionic substances
61
Describe the fluid compartments of the body
- extracellular compartment = 1/3 - interstitial space = 3/4 - intravascular space = 1/4 - intracellular compartment = 2/3
62
Briefly describe the movement of fluid and particles across the capillary wall, what factors can affect this movement
hydrostatic forces push fluid through capillary pores into interstitium - osmotic forces (colloid on optic pressure) within capillary lumen act to keep fluid within vessel - lymphatics return excess fluid + proteins to circulation (some proteins leak through) - diffusion - most important means of substance transfer between IVS + interstitium - H2O + particles move back + forth through capillary wall - lipid soluble = cell membrane = extremely fast/easy movement - H2O soluble = intercellular clefts = still very fast flow - net rate of disunion of substance through any membrane is proportional to conc different of substance between two sides of membrane - O2 flows from capillary into tissue - CO2 flow from tissues into capillaries
63
What are starlings forces?
components of startling forces - hydrostatic pressure - osmotic pressure - colloid osmotic pressure - endothelial (blood vessel wall) permeability
64
Briefly describe the lymphatics system and its function?
- small amount of net filtration that occurs within capillaries result in slight excess of fluid within interstitium - this fluid is returned to circulation via lymphatic system - network of channels/ducts that drain excess interstitial fluids - accessory route from interstitium to intravascular space - lymph vessels drain to thoracic duct + right lymph duct before draining into venous system - in addition to excess fluid = also carries proteins + large molecules that cant be removed by absorption into capillaries - lymphatic endothelial cells overlap so edge is free to fold inward forming a one way flap that opens to allow passage of large suspended particles - these flaps are present on all lymphatic vessels