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RES anatomy part 2 > SAR PHYSIO > Flashcards

SAR PHYSIO Flashcards

1
Q

.Briefly describe the components of the circulatory system

A 
Heart
Arteries
Arterioles
smooth muscle
Most resistance
Capillaries
Venues and veins
act as a reservoir for blood
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2
Q

Briefly describe the cardiovascular system as it relates to its function

A

transports nutrients, waste products, hormones
Heat dissipation
Immune response
Maintain homeostasis

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3
Q

Briefly describe the coronary circulation

A

receives 5% of rest of resting cardiac output
Left and right coronary arteries = drain into coronary sinus —> right atrium
Thebesian veins drain the ventricular wall
Drain into the left ventricle
Venous admixture - bypass the pulmonary circulation
Paradoxical flow = vessel compression during ventricular contraction

Issues with tachycardia = decrease of time in diastole -> can affect coronary vascular supply
Right atrial pressure increase in CPR = crucial

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4
Q

Name the 4 phases of the cardiac cycle and indicate what is happening during each phase including which valves are open and closed

A
  1. Inflow
    AV open, SL closed
    Ventricular filling
    P wave filles ventricle
  2. Isovolumetric contraction
    both valves closed, no blood flow
    Ventricular contractions causes AV valves to close
    Ventricular pressure builds
    No blood flow
    When pressure exceeds aortic pressure, aortic valve opens
  3. Outflow phase
    SL open, AV closed
    Aortic valve opens
    Ventricular pressure decreases, while aortic rises
    When aortic pressure is greater than left ventricular pressure the aortic valve closes
  4. Isovolumetric relaxation
    both valves closed, no blood flow
    Start of ventricular diastole
    Aortic valve has snapped shut, mitral valve still closed
Diastole = 1 and 4
Systole = 2 and 3
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5
Q

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

A

Cardiac output = stroke volume x Heart rate
Preload
Amount of ventricular wall stretch right before contraction
Normally the primary controller of cardiac output
Measured by central venous pressure + wedge pressure

Afterload
= amount of tension that the contracting ventricle must produce to open the semilunar valves
Aka the force the heart must overcome to eject blood during systole

Contractility
myocardial performance independent of preload and afterload
Factors which affect this = ANS, Circulating hormones, drugs, ion concentration, myocardial disease

Heart rate
Sinus node controls rate (ANS)
Influenced many conditions can induce a change in heart rate (fever, thyrotoxicosis, exercise, excitement)
Influenced by anything that increases oxygen demand
Increase in heart rate is usually good, but excess of 200bpm is detrimental = reduced diastolic filling time

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6
Q

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

A

The more cardiac myocytes are stretched the greater the force of contraction

How this is achieved
better alignment of actin and myosin
Releasing more Ca2+ from sarcoplasmic reticulum
Increased tropinin-C to Ca2+

How it relates to heart fx
beat to beat rapid modifications

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7
Q

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

A

Clinical Parameters
• Perfusion parameters
- hyperaemic (injected) = vasodilation
Auscultation

Blood Pressure
Pulse quality
large animals (submandibular, facial)
Invasive and non-invasive methods

Electrocardiography

Diagnostic Imaging
• Ejection fraction (the fraction of ejected blood)
• Ventricular volumes
• Radiographic enlargement

• Cardiac Output
• Requires a pulmonary artery catheter (PAC)
Peripheral temperature
Temperature of extremities -v- core temperature
Decreased (cool extremities), Increased (warm)

Fluid accumulation
venous distension + Jugular distension
Body cavity fluid (Ascites, pleural effects, pericardial effusion)
Subcutananeous oedema

Auscultation

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8
Q

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

A

listen for normal heart sounds
heart rate and rhythm
assess in conjunction with pulse
diagnose abnormal heart

blood pressure
ECG

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9
Q

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

A 
Primary heart disease
(Congenital, acquired valve/cardiomyopathy
Mechanical
myocardial disease
Valvular disease
Shunt
= Congestive heart failure

Electrical disease
= low output failure

Secondary heart disease
- systemic disease can affect cardiovascular fx

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10
Q

Define circulatory shock

A

Shock is the clinical expression of circulatory failure that results in inadequate cellular oxygen utilization

with less O2 its less efficient and lactic acidosis develops
Many causes (cardiac disease, loss of blood volume, vascular dysfunction/obstruction)
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11
Q

Briefly describe the compensation of circulatory shock

A

Attempts to restore corse tissue perfusion and oxygenation
sympathetic release (Catecholamines)
peripheral vasoconstriction
Tachycardia
Increased constraciltiy
Activation of RAAS (renin- angiotensin-aldosterone system

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12
Q
  1. Describe the anatomy and function of cardiac muscle and compare and contrast to skeletal muscle.
A

the usually things

Intercalated discs = direct communication
Action potential is significant longer than skeletal muscle

Cardiac muscle = contraction is impacted by both sarcoplasmic and extracellular Ca2+ concentration, whereas skeletal muscle is based on sarcoplasmic only

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13
Q
  1. Briefly describe what is occurring during the phases of the cardiac muscle action potential
A
  • pacemaker triggers the action potential which propagates throughout the cardiac myocytes

When the threshold potential of the cardia myocyte is reached, fast sodium channels open triggering an action potential
Involving sarcoplasmic reticulum and from the T-tubules
Calcium concentration in ECF is very important
The influx of calcium channels makes the depolarisation 15x longer

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14
Q
  1. What is the refractory period.
A

Absolute refectory period —> cardiac muscle is refracted, cannot be stimulated
Relative refractory period —> Additional period

Purpose of refractory period = make sure the signal only goes one way

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15
Q
  1. Briefly describe cardiac conduction.
A

Sinoatrial node (pacemaker)
Atrioventricular AV node
R and L branches of AV bundle (bundle of His)
Purkinje fibers either side

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16
Q
  1. Why is the sinus node the pacemaker and describe its activation and automaticity.
A

atria contract 1/6 of a second ahead of ventricles

Activation is spontaneous caused by the ‘funny current’ = constant slow leak of sodium, this results in the pacemaker cell never really at resting membrane potential.
as it is far not at resting potential it takes less to depolarise, thus only slow sodium channels
Then why depolarised slow calcium channels activate
Then potassium channels open to depolarise the cell
Constantly going

Overdrive suppression
SA node fires the fastest and is therefore the offical pacemaker —> exerts overdrive suppression on the remainder of the conductive tissue
IMPORTANTs - if SA fails another component of the conductive pathway takes over, the heart rate becomes slower if its triggered further down the conductive pathway

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17
Q
  1. Briefly describe the sympathetic and parasympathetic activation of the heart.
A

Sympathetic chain
Beta adrenergic receptors in the heart = 1. increase Ca2+ and Na2+ permeability —> increase contractility and increase Sinus node discharge = fast HR
2. More potassium channels open = reduced refractory period
Alpha adrenergic receptors in blood vessels = vasoconstriction

Parasympathetic (vagus nerve)
- Mainly affect the two nodes
 cholinergic receptors (acetylcholine)
Increased potassium ion permeability = hyperpolarization (less excitable membrane)
Decrease sinus node = slow HR
Decrease AV nodal conduction
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18
Q
  1. Identify the different components of the normal ECG.
A
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19
Q
  1. What are the standard and augmented limb leads of the ECG?
A

Negative and positive electrodes are placed on the skin

Lead = voltage of the difference between two electrodes

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20
Q
  1. What is the mean electrical axis and why?
A

Mean electrical axis is 59 degrees because that is the direction that SA= AV to bundle of his go based on anatomy
So lead II is 60 degrees so is the standard bipolar lead with the greatest amplitude of QRS complex

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21
Q
  1. Briefly describe the base apex lead system used in large animals.
A
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22
Q
  1. Briefly describe the steps of rhythm analysis and apply these to interpret an ECG trace.
A

Steps

  1. calculate HR
  2. is the rhythm regular
  3. is there a P wave for every QRS? Is there a QRS for every P?
  4. Are the wave forms consistent and normal shape?
  5. Are the intervals and segments normal
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23
Q
  1. What are common causes of sinus bradycardia and sinus tachycardia?
A

Different species
All complexes housed be normal
Increased vagal tone = Bradycardia

Tachycardia normal reasons
Stress/anxiety
Pain
Fever/hyperthermia

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24
Q
  1. Briefly describe the effect of high potassium and low calcium on the membrane potential, threshold potential and the resulting clinical findings with each of these electrolyte disturbances.
A 
High potassium effect (hyperkalaemia
- normal = small range kept usually 
- resting membrane potential decreases
threshold potential is increased
Resulting clinical findings = slows myocardial electrical conductance = brachycardia
Severe = serial arrest —> death
No Ps high Ts 
Case = cats with urethral obstruction affecting kidneys which regulate K (Bradycardia in a stressed cat)
FLUTD as treatments
Hypo K rare
Low calcium membrane potential
- membrane potential
threshold potential
Resulting clinical findings
Common
muscle fasciculations/tremors
Seizures
Behaviour change - agitation, hypersensitivity

Cardiovascular effects, less common
Hypotension
Decreaed cardiac contractility

Hypercalcaemia = rare
- usually diarrhoea

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25
Q
  1. What is the difference between a physiologic and pathologic arrhythmia?
A 
Physiologic arrhythmia
Caused by sympathetic tone
normal ecg trace
Irregular rhythm
Eg sinus arhythmia - common rhythm in resting dogs, especially large, fit individuals
Increase in HR occurs during inspiration
Decrease HR during and after exhalation
Due to fit animals have more vagal tone

!st -2nd AV blocks

Pathologic arrhythmia
Third degree AV block

26
Q

Be familiar with common arrhythmias, supraventricular -vs- ventricular, sinus arrhythmia, AV block, atrial fibrillation, APDs, VPDs, ventricular tachycardia, and ventricular fibrillation.

A 
Supra ventricular vs ventricular
Above and below the AV
AV blocks
1st = increased P-R interval (dw)
2nd = some P without QRS
3rd = no communication, subsidiary pacemaker = escape rhythm

Atrial fibrillation
fine uncoordinated contractions which results in ineffective work being done. Caused by multiple re-entrant pathways causing a rapid and disorganised depolarisation without atrial contraction
Loose 20% of volume, an issue when exercise
Enlargement of stria

F waves

APDs (Atrial premature depolarisation)
an early P wave and different in appearance from sinus P waves
P wave may be buried in T wave of previous beat
QRS complexes are normal in appearance
Extra P from the SA node
Unlikely to negatively impact cardiac output
Not always pathological has many causes

VPDs (ventricular premature depolarisations)
QRS occurs early
QRS is wide and bizarre in appearance 
QRS is not associated with p wave
T wave often opposite
  • could be from surgery, trauma, GDV, splenectomy
Ventricular tachycardia 
lots of VPCs joined together
Rapid regular rhythm
QRS complexes are wide and bizarre
QRS complexes not associated with p waves although p waves are present and often buried in QRS complexes

Ventricular fibrillation = death

27
Q

Auscultation: Heart Sounds

A

• S1: AV valve closure
• S2: Semi-lunar valve closure
• S3: Rapid diastolic filling of ventricle • S4: Atrial contraction
S1 and S2 are high frequency normal heart sounds, caused by vibrations within the ventricles.
S3 and S4 (gallop rhythms) – abnormal in dogs and rarely heard in normal cats. Can be heard in larger animals

28
Q

Auscultation: Murmurs

A

High velocity
• Obstruction to flow • Low viscosity

Physiologic
• Ejection(flow )murmur
• Anemia, fever, young animals

Pathologic
• Valvularregurgitation • Stenosis
• Congenitaldefects

29
Q

physiologic Murmurs

A

Low intensity, high frequency early systolic murmurs • Turbulent flow in the aorta or pulmonary artery
• Innocent murmur in young animals
• Usually due to large stroke volume relative to patient size
• Anaemia
• Decreased viscosity due to reduction in haematocrit
• Dynamic Right Ventricular Outflow Tract Obstruction–cats
• No cardiac disease, related to normal ventricular contraction

30
Q

pathologic murmurs

A
31
Q

murmurs and timing

A
32
Q

murmurs sounds, av or semilunar

A
33
Q

Murmur location

A

• Heart base
Aortic and pulmonic stenosis
Physiologic murmurs

• Left apex
Mitral regurgitation

• Cranial left axillary region
Patent ductus arteriosus

34
Q

murmur gradin system

A

1 low intensity only heard in a quiet room
2 low intensity but easily heard
3 moderate intensity
4 high intensity, no thrill
5 high intensity with a precordial thrill
6 precordial thrill and can be heard with the stethoscope off the chest wall

35
Q

Mitral and Tricuspid Regurgitation:

A

this murmur is systolic
• Murmurs of valvular regurgitation occur when the valve is supposed to be closed
• Blood flows at high speed through the defect in the valve because of the pressure different between the ventricle and atrium during systole

36
Q

Pulmonic Stenosis

A
  • Weight loss & low milk yield
  • Pulmonic stenosis caused by endocarditis • What type of murmur?
  • WHY?
37
Q

Aortic Regurgitation

A
38
Q

Mitral / Tricuspid Stenosis

A
  • Murmurs of stenosis occur when the valve is supposed to be open
  • Some blood goes into ventricle down normal pressure gradient
  • Blood is pushed by the atria through the stenotic valve
39
Q

`Congenital heart disease

A

Variety of cardiac malformations:
• Aortic/Pulmonic stenosis • Mitral/tricuspid dysplasia • Tetralogy of Fallot
• Ventricular Septal Defect Persistent fetal circulation: • Patent foramen ovale
• Patent ductus arteriosus

40
Q
  1. Discuss how blood flow changes from the large arteries down to the capillaries.
A

Higher pressure in arteries, then goes down at veins

41
Q
  1. What are the main determinants of blood flow through a vessel?
A 
Flow = change in pressure/resistance
Clinically it is based on diameter “diameter of vessel plays the greatest role”
Poiseuilles law = flow dependent on 
change in pressure
Radius of the tube
Viscosity of the fluid
Length of the tube
42
Q
  1. What are the main differences between veins and arteries?
A

A - more elastic with higher flow going through

V- less elastic with low pressure flow

43
Q
  1. What vessels provide the largest contribution to total peripheral resistance?
A

Arterioles

44
Q
  1. What effect does vasoconstriction and vasodilation have on total peripheral resistance?
A

Vasoconstriction = increase TPR

Vasodilation = Decrease TPR

45
Q
  1. What factor has the most significant factor on laminar blood flow?
A

Diameter of the blood vessel

46
Q
  1. What are the main factors that determine blood pressure?
A 
Poiseuilles law = flow dependent on 
change in pressure
Radius of the tube
Viscosity of the fluid
Length of the tube
47
Q
  1. Define mean arterial pressure?
A

True MAP an only be determined by invasive monitoring,

Not arithmetic mean as more time is sent in diastole than systole

MAP (SBP + 2 (DBP))/3

48
Q
  1. What determines the pulse pressure?
A

Pulse pressure = SBP-DBP

Map (BP) = CO x TPR

Thus pulse pressure magnitude is based on the difference between SBP - DBP. But this magnitude is not directly related to the blood pressure.

49
Q
  1. Briefly describe the vasomotor centre and its regulation of arterial blood pressure.
A

Changes the resistance of the blood vessels
Coordinated this ANS fx by vasomotor centre
Lx -brain stem
Fx- increasing sympathetic output
Maintains normal sympathetic tone

50
Q
  1. Briefly describe the short-term neural mechanisms present for the rapid control of blood pressure
A

Baroreceptor reflex is the main one,

  1. Vasoconstrictions (TPR and distribution of blood flow)
  2. Constriction of veins - increasing preload and therefore Cardiac output
  3. Increasing contractility

neg feedback loop
A detector of blood pressure changes
Consists of special nerves (stretch receptors)
Carotid sinus and aortic arch
Very rapid change minute by minute
Fx more firing of baroreceptors when more stretch
= more firing = more inhibition of sympathetic

Other- chemoreceptors = also regarded as fast

51
Q
  1. Describe how the baroreceptor reflex would respond in a patient with acute haemorrhage.
A
  • decreased blood flow= decreased stretch of vessels = decreased baroreceptors firing = less inhibition of sympathetic system = increased sympathetic fx = increased contractility
52
Q
  1. Briefly describe the humoral (longer term) mechanisms of blood pressure control.
A

Pathway targets BVs and kidneys in the control of ECF volume
ADF, ANP, RAAS
Fx = hormones

53
Q
  1. Briefly describe the Bainbridge reflex.
A

The opposing of barinbridge reflex

where there is increased volume = increased rate to move along the

54
Q
  1. Briefly describe the production and mechanism of action of atrial natriuretic peptide.
A

IDK

55
Q
  1. Briefly describe how the arterioles work to regulate the local control of blood flow to individual tissues (including the vasodilator and oxygen demand theories).
A

thick smooth muscle layer
Thing adventitial layer
Endothelial lining

56
Q
  1. What is autoregulation and why is it important?
A

maintaining local blood flow during changes in arterial BP
Regulating BF based on flow not O2 demand
Important and especially precise in brain and heart

57
Q
  1. Briefly describe the metabolic and myogenic mechanisms by which autoregulation is thought to occur.
A

Metabolic Theory
arterial pressure is used on O2 required and other nutrients
Increased blood flow also washes out local vasodilators
Overall its vasoconstriction

Myogenic theory
low pressure = less stretch —> vast dilation
Greater the stretch = greater constriction
Thus self regulating

58
Q
  1. Briefly describe the functional anatomy of the capillary bed, and how it differs in different tissues.
A

Precapillary sphincter
unicellular layer of endothelial cells surrounded by thin BM
Allow diffusion of solute and water

Different tissues
Brain = tight junctions that only allow water and gases to permeate to go through
Liver = v leaky, proteins
Kidney = glomerular cap, fenestrated = lots of small molecules and ionic substances

59
Q
  1. Describe the fluid compartments of the body. (VERY IMPORTANT)
A

Extracellular compartments 1/3
interstitial space 3/4 (between vessels and cells)
Intravascular space 1/4 (vessels)

Intracellular compartment 2/3

60
Q
  1. Briefly describe the movement of fluid and particles across the capillary wall, what factors can affect this movement. (VERY IMPORTANT)
A

Molecular size
- intercellular cleft = 6-7 nm wide
Small amounts of plasma proteins will pass through
Concentration gradients

Overall
hydrostatic forces (blood pressure)
Osmotic forces (concentration gradient)
Lymphatic return excess fluid and proteins to the circulations (some proteins leak through)
61
Q
  1. What are starlings forces?
A
  • Hydrostatc pressure
    osmotic pressure
    Endothelial permeability
62
Q
  1. Briefly describe the lymphatics system and its function?
A

The small amount of net filtration that occurs within the capillaries results in slight excess of fluid within the interstitium 

Flaps present on all lymphatic tissue to make sure one direction flow

  • look at Dees lecture

RES anatomy part 2 (4 decks)

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