Test
CV
Este test tiene tipos de pregunta que se abren en el reproductor de siempre.
Preguntas del test (90)
1Describe the Heart wall
• [blank_start]Endocardium[blank_end]
• [blank_start]Myocardium[blank_end]
• [blank_start]Epicardium[blank_end] – merging with Pericardium- AEndocardium
- BMyocardium
- CEpicardium
2What does the Pericardium consist of
[blank_start]Visceral[blank_end]
[blank_start]Parietal[blank_end]
- Create [blank_start]potential[blank_end] space to allow heart move freely- AVisceral
- BParietal
- Cpotential
3LA – RA separated by inter-[blank_start]atrial[blank_end] septum
LV-RV separated by inter-[blank_start]ventricular[blank_end] septum- Aatrial
- Bventricular
4Describe the Pleura – serous mem – lines thorax
VISCERAL-INVESTS [blank_start]LUNGS[blank_end].
PARIETAL – MEDIASTINAL – [blank_start]DIAPHRAGMATIC[blank_end], [blank_start]COSTAL[blank_end]- ALUNGS
- BDIAPHRAGMATIC
- CCOSTAL
5Describe generation of the normal heart sounds
S1 (‘lup’) – [blank_start]AV[blank_end] valves [blank_start]close[blank_end] and blood [blank_start]rebounds[blank_end] within the [blank_start]ventricles[blank_end] and accelerates within the [blank_start]aorta[blank_end].
S2 (‘dup’) – [blank_start]Semilunar[blank_end] valves [blank_start]close[blank_end] and blood [blank_start]decelerates[blank_end] in the great vessels.- AAV
- Bclose
- Crebounds
- Dventricles
- Eaorta
- FSemilunar
- Gclose
- Hdecelerates
6Descibe abnormal heart sounds
S3 – rare. Sometimes heard in heart failure due to [blank_start]turbulence[blank_end] in the [blank_start]left[blank_end] ventricle. Normal in horses.
S4 – uncommon. Occurs when ‘[blank_start]stiff[blank_end]’ ventricular wall, causing [blank_start]increased[blank_end] force of atrial contraction. Normal in horses.- Aturbulence
- Bleft
- Cstiff
- Dincreased
7What are heart murmurs
Generated by [blank_start]turbulence[blank_end] in the blood caused by anything which disturbs [blank_start]laminar[blank_end] flow.- Aturbulence
- Blaminar
8Descibe the auscultation of the heart
LEFT SIDE – Ribspace 3 = [blank_start]Pulmonic[blank_end] valve
4 = [blank_start]Aortic[blank_end] valve
5 = [blank_start]Mitral[blank_end] valve
RIGHT SIDE – Ribspace 5 = [blank_start]Tricuspid[blank_end] valve- APulmonic
- BAortic
- CMitral
- DTricuspid
9Where does the Diaphragm insert
[blank_start]central[blank_end] [blank_start]aponeuroic[blank_end] tendon- Aaponeuroic
- Bcentral
10CRANIALLY: [blank_start]Thoracic[blank_end] inlet
CAUDALLY: Banded by [blank_start]diaphragm[blank_end]
DORSALLY: Thoracic [blank_start]vertebrae[blank_end] (13)
1-9 [blank_start]sternum[blank_end] vert
Next 3 [blank_start]costal[blank_end] arch
1 floating
dorsal 2/3 [blank_start]Bone[blank_end]
ventral 1/3 [blank_start]cartilage[blank_end]
- AThoracic
- Bdiaphragm
- Cvertebrae
- Dsternum
- Ecostal
- FBone
- Gcartilage
11Describe and explain the route blood takes through the heart
LA- [blank_start]ox[blank_end] from lungs – LV –L. AV valve
RA – [blank_start]Deox[blank_end] from body – RV – R AV valve
Deox from body - via [blank_start]cranial[blank_end]/ [blank_start]caudal[blank_end] [blank_start]vena[blank_end] [blank_start]cavae[blank_end]- Aox
- BDeox
- Ccranial
- Dcaudal
- Evena
- Fcavae
12Describe and explain the route blood takes through the heart
LV- thick and muscular - pump around body via [blank_start]aorta[blank_end] through [blank_start]aortic[blank_end] valve
RV – to [blank_start]lungs[blank_end] via [blank_start]pulmonary[blank_end] artery through [blank_start]pulmonic[blank_end] valve- Aaorta
- Baortic
- Clungs
- Dpulmonary
- Epulmonic
13Outline the basic electrical pathway through the heart.
- ASAN
- BAVN
- CAVN bundle
- DL limb
- ER limb
- FSeptomarginal band
14Explain the structure and function of the valves of the heart
Atrioventricular valves
• [blank_start]Mitral[blank_end] ([blank_start]Bicuspid[blank_end]) - L
• [blank_start]Tricuspid[blank_end] – R
Supported by [blank_start]annulus[blank_end] [blank_start]fibrosis[blank_end]
[blank_start]Cordae[blank_end] [blank_start]Tendineae[blank_end] (preventing everting into atrium )
[blank_start]Papillary[blank_end] muscles (extend from [blank_start]myocardium[blank_end])
[blank_start]Traberculae[blank_end] [blank_start]carnae[blank_end] – muscle irregularities of the [blank_start]interior[blank_end] ventricular walls
Function
• Prevent backflow of blood – pressure differences open + close- AMitral
- BBicuspid
- CTricuspid
- Dannulus
- Efibrosis
- FCordae
- GTendineae
- HPapillary
- Imyocardium
- JTraberculae
- Kcarnae
- Linterior
15Describe Coronary circulation - Supplies heart tissues
Coronary arteries arise from [blank_start]aortic[blank_end] bulb
Caudosinistral sinus = [blank_start]left[blank_end] coronary artery
Cranial sinus = [blank_start]right[blank_end] coronary artery
Major branches = [blank_start]circumflex[blank_end] and [blank_start]interventricular[blank_end]
Venous drainage via [blank_start]great[blank_end] [blank_start]cardiac[blank_end] vein to [blank_start]coronary[blank_end] sinus in right atrium- Aaortic
- Bleft
- Cright
- Dcircumflex
- Einterventricular
- Fcardiac
- Ggreat
- Hcoronary
16Veins
Systemic venous drainage to right atrium
[blank_start]Deoxygenated[blank_end] blood
[blank_start]Cranial[blank_end] and [blank_start]caudal[blank_end] vena cava
[blank_start]Great[blank_end] [blank_start]cardiac[blank_end] vein
Pulmonary venous drainage to left atrium
[blank_start]Oxygenated[blank_end] blood- ADeoxygenated
- BGreat
- Ccardiac
- DCranial
- Ecaudal
- FOxygenated
17List the major branches of the aorta
- APulmonary trunk
- BDesending aorta
- Cinstercostal arteries
- DL subclavian artery
- ER subclavian artery
- FBrachiocephalic trunk
- GVertebral artery
- Hcostochondral junction
- IL + R common carotids
- JSuperficial cervical artery
- KAxillary artery
- Linternal thoracic artery
18Describe the major venous drainage into the venae cavae
Venae cavae
• Cranial VC
Internal/external [blank_start]jugulars[blank_end]
C[blank_start]ephalic[blank_end]
A[blank_start]xillary[blank_end]
S[blank_start]ubclavian[blank_end]
• Caudal VC
Iliac
Testicular/ovarian
[blank_start]Renal[blank_end]
[blank_start]Hepatic[blank_end]- Ajugulars
- Bephalic
- Cxillary
- Dubclavian
- ERenal
- FHepatic
19Capillaries
• flow through bed controlled by pre cap [blank_start]sphincter[blank_end] zone, through [blank_start]fare[blank_end] channels + [blank_start]arteriovenous[blank_end] anastomes
• Large SA – [blank_start]high[blank_end] ratio Cap: Arterioles
• [blank_start]Fenestrated[blank_end] in renal glomerulus
• [blank_start]Intercellular[blank_end] cleft – gap junctions – H2O sol
• [blank_start]Tight[blank_end] junctions – Na+ and H2O- Asphincter
- Bfare
- Carteriovenous
- Dhigh
- EFenestrated
- FIntercellular
- GTight
20Define different vessel types based on their gross and basic histological features
i. tunica intima which is the [blank_start]internal[blank_end] layer with an endothelial lining,
ii. middle tunica media which contains varying amounts of [blank_start]smooth[blank_end] muscle and [blank_start]elastic[blank_end] [blank_start]tissue[blank_end] depending on the vessel
iii. external tunic adventitia, which is a layer of [blank_start]connective[blank_end] tissue.- Ainternal
- Bsmooth
- Ctissue
- Delastic
- Econnective
21Define bulk flow
Bulk flow
• Derived from [blank_start]HSP[blank_end]
• Movement of fluid by means of [blank_start]pressure[blank_end] difference
• Along [blank_start]vessels[blank_end]
Bulk flow out of capillary = [blank_start]Filtration[blank_end]
Define Diffusion
• [blank_start]High[blank_end]-[blank_start]Low[blank_end] conc of solute- AHSP
- Bvessels
- Cpressure
- DHigh
- ELow
- FFiltration
22Explain how perfusion pressure is generated and how it can be affected
Perfusion pressure –[blank_start]difference[blank_end] at two points
P(inlet) - P(oulet)
[blank_start]Transmural[blank_end] pressure – pressure difference In+Out
TransM pressure exceeds outside +filtration out into [blank_start]ISF[blank_end]- ATransmural
- BISF
- Cdifference
23Describe how variation of hydrostatic and oncotic pressures affect the movement of fluid across a vessel wall
Oncotic pressure – osmotic pressure exerted by [blank_start]plasma[blank_end] [blank_start]proteins[blank_end]
Hydrostatic pressure – pressure exerted on blood vessels ([blank_start]High[blank_end]-[blank_start]Low[blank_end])
Starlings Law of Cap - [blank_start]Hydrostatic[blank_end] and [blank_start]oncotic[blank_end] pressure differences across the vessel wall balance to determine movement of fluid
Net pressure = (Pcapillary – Pinterstitium) – (Ocapillary – Ointerstitium)
(where P = hydrostatic pressure and O = oncotic pressure)- Aplasma
- Bproteins
- CHigh
- DLow
- EHydrostatic
- Foncotic
24* A positive answer to the Starling equation = water is filtered [blank_start]out[blank_end] of capillary.
* A negative answer = water is absorbed [blank_start]into[blank_end] capillary- Aout
- Binto
25
* Along the vessels by [blank_start]BULK[blank_end] [blank_start]FLOW[blank_end].
* Across the capillary walls by [blank_start]BULK[blank_end] [blank_start]FLOW[blank_end] and [blank_start]DIFFUSION[blank_end].
* Excess fluid in the ISF is removed by the [blank_start]lymphatic[blank_end] system and returns to the [blank_start]circulation[blank_end]
* Failure of this = [blank_start]Oedema[blank_end]- ABULK
- BFLOW
- CBULK
- DFLOW
- EDIFFUSION
- Flymphatic
- Gcirculation
- HOedema
26Explain how cardiac output is generated and varied in the normal animal
([blank_start]CO[blank_end]) = [blank_start]heart rate[blank_end] ([blank_start]HR[blank_end]) x [blank_start]stroke volume[blank_end] ([blank_start]SV[blank_end]).
CO can only be altered by changing the [blank_start]stroke volume[blank_end] or [blank_start]heart rate[blank_end]- ACO
- Bheart rate
- Cstroke volume
- DHR
- ESV
- Fstroke volume
- Gheart rate
27SV = [blank_start]EDVV[blank_end]-[blank_start]ESVV[blank_end]
• [blank_start]Vol[blank_end] of blood ejected into the circulation by one stoke or cont of ventricle
[blank_start]EDVV[blank_end]- vol in vent at end of diastole
[blank_start]ESVV[blank_end]- vol left in vent at end of systole
R SV= L SV
SV/EDVV = [blank_start]Ejection[blank_end] Fraction – measure of [blank_start]systolic[blank_end] function of heart- AEDVV
- BESVV
- CVol
- DEDVV
- EESVV
- FEjection
- Gsystolic
28Increasing EDVV
• Increase [blank_start]preload[blank_end] = filling pressure of ventricle
* Increase [blank_start]diastolic[blank_end] filling time
* Increasing ventricular [blank_start]compliance[blank_end] (stretchiness)- Apreload
- Bdiastolic
- Ccompliance
29Describe the concepts of preload as they pertain to the heart
Preload –
* Filling pressure of the [blank_start]ventricle[blank_end]
* = atrial pressure
* = venous pressure
* = end [blank_start]diastolic[blank_end] ventricular pressure
- Increased by increasing [blank_start]volume[blank_end]
* Reducing [blank_start]perfusion[blank_end] to non-essential tissues
End [blank_start]diastolic[blank_end] vol that stretches R/L vent to [blank_start]greatest[blank_end] dimension- Aventricle
- Bdiastolic
- Cperfusion
- Dvolume
- Egreatest
- Fdiastolic
30Describe the concepts of afterload as they pertain to the heart
Afterload
* Afterload = [blank_start]vascular[blank_end] resistance
* ↑Afterload = ↑ESVV = ↓[blank_start]SV[blank_end] = ↓[blank_start]CO[blank_end] (higher pressure is needed in the ventricle- Avascular
- BSV
- CCO
31Describe Heterometric autoregulation
- inc [blank_start]preload[blank_end] +incr [blank_start]EDVV[blank_end] – Incr [blank_start]SV[blank_end]
- inc SV on one side + inc other side- Apreload
- BSV
- CEDVV
32What is Compliance
= change in [blank_start]volume[blank_end] ÷ change in [blank_start]pressure[blank_end]- Avolume
- Bpressure
33Poiseuilles law - resistance varies inversely with 4th power of radius
- increase radius of vessel= resistance [blank_start]drops[blank_end]
- reduce radius of vessel= resistance [blank_start]incr[blank_end]
- most of vascular resistance caused by [blank_start]arterioles[blank_end]- Adrops
- Bincr
- Carterioles
34Total peripheral resistance – net [blank_start]resistance[blank_end] of whole circulation
TPR – mean aortic pressure – mean [blank_start]vena[blank_end] [blank_start]caval[blank_end] pressure / [blank_start]CO[blank_end]- Aresistance
- Bvena
- Ccaval
- DCO
35Explain the circulatory adaptations of the mammalian foetus in utero
- Foramen ovale open – [blank_start]oxy[blank_end] blood pass from [blank_start]RA[blank_end]-[blank_start]LA[blank_end]
- Oxy blood to foetus via [blank_start]umbilical[blank_end] [blank_start]vein[blank_end] – drains into [blank_start]caudal[blank_end] [blank_start]vena[blank_end] [blank_start]cavae[blank_end] then RA
- Lungs collapsed – little blood flow through [blank_start]pulmonary[blank_end] [blank_start]circ[blank_end] – flow from [blank_start]pulmonary[blank_end] [blank_start]trunk[blank_end] to aorta via [blank_start]ductus[blank_end] [blank_start]arteriosis[blank_end]
- Liver largely bypassed die to [blank_start]ductus[blank_end] [blank_start]venosus[blank_end]- Aoxy
- BRA
- CLA
- Dumbilical
- Evein
- Fcaudal
- Gvena
- Hcavae
- Ipulmonary
- Jcirc
- Kpulmonary
- Ltrunk
- Mductus
- Narteriosis
- Oductus
- Pvenosus
36Describe the changes in circulation that occur at birth in mammals and explain the stimuli for these changes
Umbilicus
- Umbilical arteries [blank_start]contract[blank_end] = flow stops from neonate to [blank_start]placenta[blank_end]
- Umbilical artery becomes [blank_start]round[blank_end] [blank_start]ligament[blank_end] of the [blank_start]bladder[blank_end]
- Umbilical veins [blank_start]contract[blank_end] – venous blood delivered to the [blank_start]neonate[blank_end]
- Umbilical vein becomes [blank_start]round[blank_end] [blank_start]ligament[blank_end] of the [blank_start]liver[blank_end].
- Rupture - arteries undergo [blank_start]elastic[blank_end] recoil to prevent haemorrhage- Acontract
- Bround
- Cligament
- Dbladder
- Econtract
- Fround
- Gligament
- Hliver
- Iplacenta
- Jneonate
- Kelastic
37Foramen ovale
- 1st breath – large drop in [blank_start]resistance[blank_end] to flow in [blank_start]pulm[blank_end] [blank_start]circ[blank_end]
= decreased [blank_start]R[blank_end] [blank_start]Vent[blank_end] [blank_start]afterload[blank_end]
= incr [blank_start]pulm[blank_end] blood flow
- Incr venous return to L atrium = incr [blank_start]L[blank_end] [blank_start]atrial[blank_end] pressure
= closure of [blank_start]foramen[blank_end] [blank_start]ovale[blank_end] as [blank_start]septum[blank_end] [blank_start]primum[blank_end] is pushed against [blank_start]septum[blank_end] [blank_start]secundum[blank_end]
- Remnant of foramen ovale = [blank_start]fossa[blank_end] [blank_start]ovalis[blank_end]- Aresistance
- Bpulm
- Ccirc
- DR
- EVent
- Fafterload
- Gpulm
- Hatrial
- IL
- Jforamen
- Kovale
- Lseptum
- Mprimum
- Nsecundum
- Oseptum
- Pfossa
- Qovalis
38Ductus arteriosus
- Pressure in aorta [blank_start]increases[blank_end]
- Pressure in pulmonary trunk [blank_start]decreases[blank_end]
- Smooth muscle of ductus [blank_start]constricts[blank_end], stopping flow through [blank_start]ductus[blank_end]
- Connective tissue proliferates causing permanent closure of [blank_start]ductus[blank_end] within 2-3 months – becomes [blank_start]ligamentum[blank_end] [blank_start]arteriosum[blank_end]- Aincreases
- Bdecreases
- Cconstricts
- Dductus
- Eductus
- Fligamentum
- Garteriosum
39Ductus venosus
- Smooth muscle of [blank_start]ductus[blank_end] [blank_start]venosus[blank_end] contracts stopping flow and diverting blood into [blank_start]hepatic[blank_end] [blank_start]circulation[blank_end].
- Permanent closure within [blank_start]2[blank_end]-[blank_start]3[blank_end] weeks of birth.- Aductus
- Bvenosus
- Chepatic
- Dcirculation
- E3
- F2
40Explain how this (changes in circulation) affects blood pressure in different parts of the circulation
- [blank_start]Increased[blank_end] pulmonary blood flow
o Due to drop in [blank_start]PVR[blank_end]
- [blank_start]Oxygenated[blank_end] blood returned to left atrium
o Increased [blank_start]left[blank_end] atrial pressure > R atrial pressure
- Increased [blank_start]aortic[blank_end] pressure- APVR
- BIncreased
- COxygenated
- Dleft
- Eaortic
41Aortic stenosis
- Narrowing of [blank_start]aortic[blank_end] valve/below valve
- Harder to eject L.V ([blank_start]turbulence[blank_end])
- Incr L.V [blank_start]afterload[blank_end]
- Decr [blank_start]CO[blank_end]- Aaortic
- Bturbulence
- Cafterload
- DCO
42Pulmonic stenosis
- Thickening of [blank_start]valve[blank_end]/[blank_start]artery[blank_end]
- Incr RV [blank_start]afterload[blank_end]- Avalve
- Bartery
- Cafterload
43Patent ductus arteriosus
- More blood in [blank_start]aorta[blank_end]/ [blank_start]pulmonary[blank_end] trunk – incr
[blank_start]pulmonary[blank_end] overcirculation
- Incr preload [blank_start]L.A[blank_end] – incr pressure [blank_start]LA[blank_end] – incr [blank_start]HSP[blank_end]
in cap and lungs – incr movement of fluid out of
vessels - [blank_start]edema[blank_end]- Aaorta
- Bpulmonary
- Cpulmonary
- DL.A
- EHSP
- FLA
- Gedema
44Ventricular septal defect
- Failure of [blank_start]ventricular[blank_end] [blank_start]septum[blank_end]
- Overloading of [blank_start]RV[blank_end]
- Loudest on [blank_start]R[blank_end] side- Aseptum
- Bventricular
- CRV
- DR
45Atrial septal defect
- Faulty development of [blank_start]septa[blank_end]/[blank_start]foramen[blank_end] ovale to close
- Mix [blank_start]deox[blank_end]/[blank_start]oxy[blank_end] blood- Asepta
- Bforamen
- Cdeox
- Doxy
46Vascular ring abnormalities
- Entrapment of [blank_start]oestophagus[blank_end]
- Defect in development of [blank_start]aortic[blank_end] [blank_start]arch[blank_end] arteries
- [blank_start]Megaoesophagus[blank_end] + regurgitation- Aoestophagus
- Baortic
- Carch
- DMegaoesophagus
47Tetralogy of fallot
- [blank_start]Ventricular[blank_end]-[blank_start]septal[blank_end] effect
- [blank_start]Dextraposed[blank_end] aorta
- [blank_start]Pulmonic[blank_end] stenosis – hypertrophy of [blank_start]RV[blank_end]- Aseptal
- BVentricular
- CDextraposed
- DPulmonic
- ERV
48Portosystemic shunt
- Portal vein – blood to [blank_start]gut[blank_end]
- Toxin in blood [blank_start]remain[blank_end] – not decontaminated by [blank_start]liver[blank_end]- Agut
- Bremain
- Cliver
49Describe how an action potential is generated and propagated in cardiac muscle.
Cardiac AP
- RMP [blank_start]–ve[blank_end] inside rel to outside
- [blank_start]+[blank_end] charge into into cell = depolarises = less [blank_start]–ve[blank_end] = cell reaches threshold = AP generated = [blank_start]contraction[blank_end]
Skeletal AP
- [blank_start]Na[blank_end]+ , [blank_start]K[blank_end]+ Dependent
- Resting – K+ conc [blank_start]>[blank_end] Na+ conc
- K+ [blank_start]open[blank_end]
- Na+ [blank_start]closed[blank_end]
- Depolarisation = [blank_start]Na[blank_end]+ into cell
- [blank_start]Ca2[blank_end]+ released from SR = contraction- A–ve
- B+
- C–ve
- Dcontraction
- ENa
- FK
- G>
- Hopen
- Iclosed
- JNa
- KCa2
50Describe the movement of cations during a cardiac action potential and extrapolate how electrolyte abnormalities could affect this.
Electolyte disturbance
- [blank_start]incr[blank_end] K+ = less K+ out of cell = decr [blank_start]HR[blank_end]
- [blank_start]decr[blank_end] Na+ = conc gradient reduced = less outside cell = decr HR
- [blank_start]decr[blank_end] Ca2+ = excitation coupling – decr [blank_start]Ca2[blank_end]+ release- AHR
- Bincr
- Cdecr
- Ddecr
- ECa2
51Explain how the pacemaker potential is generated
- No [blank_start]fast[blank_end] Na+ channels (slow AP)
- Funny Na+ channels [blank_start]closed[blank_end] during AP – [blank_start]Open[blank_end] after AP
- K+ [blank_start]open[blank_end] at end of AP – less [blank_start]K[blank_end]+ out
- Ca2+ [blank_start]open[blank_end] as Na+ [blank_start]close[blank_end]
- Rises slowly towards [blank_start]threshold[blank_end] after an AP is complete- Afast
- Bclosed
- COpen
- Dopen
- EK
- Fopen
- Gclose
- Hthreshold
52Excitation - contraction coupling
Extracellular Ca++ enters through the [blank_start]voltage[blank_end] [blank_start]gated[blank_end] [blank_start]calcium[blank_end] channels of the T-tubule.
Stimulates [blank_start]calcium[blank_end]-induced [blank_start]calcium[blank_end] release from [blank_start]sarcoplasmic[blank_end] reticulum
Ca2+ binds to [blank_start]troponin[blank_end] – reveal binding site for [blank_start]myosin[blank_end] – power stroke- Avoltage
- Bgated
- Ccalcium
- Dcalcium
- Ecalcium
- Fsarcoplasmic
- Gtroponin
- Hmyosin
53ANS – affects freq + speed of [blank_start]AP[blank_end]
- [blank_start]Sympathetic[blank_end] – speed up HR + force of contraction
- [blank_start]Parasympathetic[blank_end] – decr via vagus nerve- AAP
- BSympathetic
- CParasympathetic
54Explain how an ECG is generated
- Records [blank_start]electrical[blank_end] activity of the heart - [blank_start]comparing[blank_end] voltage at a +ve / –ve electrode.
- Voltage against time – measure [blank_start]amplitude[blank_end] of each wave and HR/Rhythm duration- Acomparing
- Belectrical
- Camplitude
55State the electrode position in the 3 bipolar limb leads and the 3 augmented unipolar limb leads.
I – compare volt [blank_start]LFL[blank_end]/[blank_start]RFL[blank_end] - [blank_start]+[blank_end]ve el.LFL
II – [blank_start]LHL[blank_end]/[blank_start]RHL[blank_end] - [blank_start]+[blank_end]ve el.LHL
III – [blank_start]LHL[blank_end]/[blank_start]RFL[blank_end] - [blank_start]-[blank_end]ve el LHL
• AVR compares the right forelimb (+ve) with the average of the [blank_start]left[blank_end] forelimb and [blank_start]left[blank_end] hindlimb.
• AVL compares the left forelimb (+ve) with the average of the [blank_start]right[blank_end] forelimb and [blank_start]left[blank_end] hindlimb.
• AVF compares the left hindlimb (‘F’ for foot!) (+ve) with the [blank_start]average[blank_end] of the [blank_start]two[blank_end] forelimbs.- ALFL
- BRFL
- C+
- DLHL
- ERHL
- F+
- GLHL
- HRFL
- I-
- Jleft
- Kleft
- Lright
- Mleft
- Naverage
- Otwo
56Explain what the waves of a normal ECG trace represent.
P – [blank_start]ATRIAL[blank_end] [blank_start]DEPOLARIATION[blank_end]
([blank_start]+[blank_end]ve deflection )
(more [blank_start]+[blank_end]ve outside L)
QRS – [blank_start]VENTRICULAR[blank_end] [blank_start]DEPOLARISATION[blank_end]
P-R interval – Delay in conduction due to [blank_start]AP[blank_end] traveling through [blank_start]AV[blank_end] node
T – [blank_start]VENTRICULAR[blank_end] [blank_start]REPOLARISATION[blank_end] (can be +/-)
* Height of deflection = size of electrical [blank_start]potential[blank_end] difference
* Width of deflection = [blank_start]time[blank_end] [blank_start]taken[blank_end] for potential difference to return to 0.- AATRIAL
- BDEPOLARIATION
- C+
- D+
- EVENTRICULAR
- FDEPOLARISATION
- GAP
- HAV
- IVENTRICULAR
- JREPOLARISATION
- Kpotential
- Ltime
- Mtaken
57Identify basic abnormalities in wave form and rhythm and relate these to physiology.
Increase in height
Increase in the [blank_start]voltage[blank_end] difference perceived – [blank_start]thickening[blank_end] of tissue?- Avoltage
- Bthickening
58Increase in width
Increase in [blank_start]time[blank_end] taken for [blank_start]AP[blank_end] to move through [blank_start]tissue[blank_end] (i.e. the chamber might be [blank_start]larger[blank_end])- Atime
- BAP
- Ctissue
- Dlarger
59Change in direction
The AP is not following the [blank_start]normal[blank_end] pathway (e.g. there may be an [blank_start]ectopic[blank_end] [blank_start]pacemaker[blank_end])- Aectopic
- Bpacemaker
- Cnormal
60Change in baseline
There is a [blank_start]potential[blank_end] [blank_start]difference[blank_end] present when there shouldn’t be – i.e. polarised tissue remains between [blank_start]phases[blank_end] of the cycle (e.g. [blank_start]myocardial[blank_end] hypoxia)- Apotential
- Bdifference
- Cphases
- Dmyocardial
61Tall P wave (P.[blank_start]pulmonale[blank_end] wave) – [blank_start]R.A[blank_end] enlargement
Wide P wave ( P [blank_start]mitrale[blank_end] wave ) –[blank_start]L.A[blank_end] enlargement
Tall R wave – [blank_start]V[blank_end]. enlargement
Wide R/QRS wave – V .[blank_start]enlargement[blank_end] + [blank_start]hypertrophy[blank_end]- Apulmonale
- BR.A
- CL.A
- Dmitrale
- EV
- Fenlargement
- Ghypertrophy
62Measure R-R interval / 60sec
PQRST complex 3-6 sec
Normal – [blank_start]sinus[blank_end] [blank_start]rhythm[blank_end]
Fast – [blank_start]tachycardia[blank_end]
Slow – [blank_start]Brachycardia[blank_end]
Abnormal – [blank_start]arrhythmia[blank_end]
NORMAL
DOG – [blank_start]70[blank_end]-[blank_start]160[blank_end]bpm
CAT – [blank_start]120[blank_end]-[blank_start]220[blank_end]bpm- Asinus
- Brhythm
- Ctachycardia
- DBrachycardia
- Earrhythmia
- F70
- G120
- H160
- I220
63Describe the development of the lymphatic system in the foetus.
[blank_start]6[blank_end] lymph sacs
thymus arises from [blank_start]3rd[blank_end] [blank_start]pharangeal[blank_end] pouch, endo/ecto/mesoderm
spleen develops from [blank_start]mesoderm[blank_end] in dorsal [blank_start]mesogastrium[blank_end]- A6
- B3rd
- Cpharangeal
- Dmesoderm
- Emesogastrium
64Describe the lymphatic drainage pathway
[blank_start]Tracheal[blank_end] ducts – head, neck + proximal FL
[blank_start]R[blank_end] [blank_start]Lymphatic[blank_end] duct – R thorax
[blank_start]Cisterna[blank_end] [blank_start]chyli[blank_end] – abonormal lymphocenters, HL + Pelvis via lumbar ducts
[blank_start]Lumbar[blank_end] ducts – form plexus on roof of abdomen
[blank_start]Thoracic[blank_end] ducts – into central vena cava- ATracheal
- BR
- CLymphatic
- DCisterna
- Echyli
- FLumbar
- GThoracic
65Explain how the lymphatic system acts to maintain fluid balance in the body
* Net filtration of fluid from blood capillaries = fluid moves into [blank_start]ISF[blank_end]
* [blank_start]Bulk[blank_end] [blank_start]flow[blank_end] into lymphatic capillaries
* [blank_start]Protein[blank_end] uptake also – lowers [blank_start]ISF[blank_end] oncotic pressure & [blank_start]increases[blank_end] diffusion from ISF into lymphatics- AISF
- BBulk
- Cflow
- DProtein
- EISF
- Fincreases
66Flow within lymphatic system due to bulk flow
* Overall [blank_start]HSP[blank_end] gradient leading into venous system (P lowest in veins)
* External pressure from [blank_start]skeletal[blank_end] muscle
* Smooth muscle in walls of [blank_start]larger[blank_end] lymphatics
* Valves prevent [blank_start]backflow[blank_end]- AHSP
- Bskeletal
- Clarger
- Dbackflow
67Failure of lymphatic drainage leads to formation of [blank_start]oedema[blank_end] (fluid in the interstitial space) or effusions (free fluid within a cavity– e.g. pleural effusion).
• Disease of the lymphatic system (e.g. lymphangitis)
• Capacity is overwhelmed (e.g. [blank_start]congestive[blank_end] [blank_start]heart[blank_end] failure (CHF) leads to excessive [blank_start]ISF[blank_end] volume)
• Derangement of [blank_start]hydrostatic[blank_end] [blank_start]pressure[blank_end] [blank_start]gradient[blank_end] preventing drainage (e.g. a tight bandage)- Aoedema
- Bcongestive
- Cheart
- DISF
- Ehydrostatic
- Fpressure
- Ggradient
68List functions of the lymphatic system
* Removal of excess water from the [blank_start]interstitial[blank_end] [blank_start]fluid[blank_end].
* Removal of [blank_start]infectious[blank_end] agents and dead cells
* [blank_start]Antigen[blank_end] presentation
* Movement of [blank_start]lymphatic[blank_end] cells
* Transport of some [blank_start]proteins[blank_end]
* Transport of dietary lipids from [blank_start]gut[blank_end]- Ainterstitial
- Bfluid
- CAntigen
- Dlymphatic
- Eproteins
- Fgut
- Ginfectious
69Chylomicrons
Chyle – once drainage in GIT has been added, proportion of chylomicrons [blank_start]incr[blank_end]= fluid in thoracid duct = [blank_start]white[blank_end]= chyle- Aincr
- Bwhite
70Intrinsic controls of blood flow
• Metabolic autoregulation – matches blood flow to [blank_start]metabolic[blank_end] rate
• Paracrine control – locally acting chemicals which alter flow rate in response to local [blank_start]environment[blank_end]
[blank_start]Nitric oxide[blank_end] - ↑ BF velocity – [blank_start]VD[blank_end]
Prostacyclin/[blank_start]Histamine[blank_end]/ Bradykinin – Local irritation –[blank_start]VD[blank_end]
[blank_start]Endothelin[blank_end] ↑ / Thromboxane A2 – [blank_start]Endothelial[blank_end] damage - [blank_start]VC[blank_end]- Ametabolic
- Benvironment
- CNitric oxide
- DVD
- EVD
- FVC
- GEndothelin
- HEndothelial
- IHistamine
71Extrinsic controls
• CNS coordinates response via [blank_start]ANS[blank_end]
• [blank_start]Baroreflex[blank_end]
• RAAS
• Hypothalamus
• Pituitary- AANS
- BBaroreflex
72Explain metabolic autoregulation of blood flow to tissues and describe how this maintains brain blood flow.
An increase in BP leads to [blank_start]increase[blank_end] in [blank_start]perfusion[blank_end] of tissue = delivers more [blank_start]oxygen[blank_end] and removes waste products more rapidly = [blank_start]VC[blank_end] = [blank_start]decr[blank_end] perfusion.
= [blank_start]BP[blank_end] and perfusion in ess organs maintained within small range.- Aincrease
- Bperfusion
- Coxygen
- DVC
- Edecr
- FBP
73Active hyperaemia
[blank_start]VC[blank_end] of arterioles
[blank_start]Reduced[blank_end] BF in capillaries
Reduced [blank_start]HSP[blank_end] inside capillaries
= less blood perfuse- AVC
- BReduced
- CHSP
74Explain the implications of short- and long-term compression of blood vessels in different tissues
Vessel compression
Short term – [blank_start]reactive[blank_end] hyperaemia
• depletion of [blank_start]oxygen[blank_end] and build-up of waste products continues - when flow is re-established the blood flow increases above [blank_start]normal[blank_end] for a short time until the waste products have been removed and the oxygen [blank_start]debt[blank_end] repaid.
Long term
• [blank_start]reduces[blank_end] BF to tissues ([blank_start]ischemia[blank_end]) = damage(infarction) + death (necrosis)- Areactive
- Boxygen
- Cnormal
- Ddebt
- Eischemia
- Freduces
75
Describe the baroreflex and explain how it acts in response to changes in blood pressure
Baroreceptors – stretch receptors situated in [blank_start]aortic[blank_end] arch / [blank_start]carotid[blank_end] sinus
Drop in [blank_start]BP[blank_end]- ↓ A.P from bareorecptors
↑ [blank_start]Symp[blank_end] output
↓ [blank_start]parasymp[blank_end] output- Aaortic
- Bcarotid
- CBP
- DSymp
- Eparasymp
76Describe the effects of the sympathetic nervous system on the cardiovascular system.
Sympathetic- “fight/flight”
* Causes [blank_start]increased[blank_end] heart rate & contractility, [blank_start]vasodilation[blank_end] of working skeletal muscle.
* Also causes reduced activity and [blank_start]vasoconstriction[blank_end] in non-essential organs
Thoracolumbar origin – supply to heart from sympathetic ganglia [blank_start]C5[blank_end] –[blank_start]T3[blank_end]- Aincreased
- Bvasodilation
- Cvasoconstriction
- DC5
- ET3
77Describe the effects of the parasympathetic nervous system on the cardiovascular system.
Parasympathetic – primary function is at rest
• Moderates [blank_start]HR[blank_end] and [blank_start]contractility[blank_end]
• Opposes action of [blank_start]sympathetic[blank_end] NS
• Local
Craniosacral origin – CN [blank_start]X[blank_end] supplies thoracic viscera- AHR
- Bcontractility
- Csympathetic
- DX
78Effector organ receptors
Parasympathetic
* Blood vessels = [blank_start]M3[blank_end] cholinergic
* Heart = [blank_start]M2[blank_end] cholinergic
Sympathetic
* Blood vessels = α1 α2 β2 [blank_start]adrenergic[blank_end]
* + M3 [blank_start]cholinergic[blank_end]
* Heart = β1 [blank_start]adrenergic[blank_end]- AM3
- BM2
- Cadrenergic
- Dcholinergic
- Eadrenergic
79Explain cardiovascular responses to exercise
Metabolic autoregulation ↑ skeletal muscle activity = [blank_start]VD[blank_end]
As ↑ CO2, H+, K+ build up in [blank_start]ISF[blank_end]
= ↓ [blank_start]Arterial[blank_end] pressure
Psychogenic response
↑ [blank_start]symp[blank_end] activity , ↓ [blank_start]parasymp[blank_end] activity
= ↑ CO ↑ [blank_start]Preload[blank_end] = ↑ SV
= VC non essential organs
= ↑ [blank_start]TPR[blank_end]
Exercise reflex
- joint + muscle receptors
- modifies degree of [blank_start]AN[blank_end] activity
- feedback system- AVD
- BISF
- CArterial
- Dsymp
- Eparasymp
- FPreload
- GTPR
- HAN
80Fight or flight response
Response to sudden stress = large increase in [blank_start]CO[blank_end] and Skeletal muscle activity.
α adrenergic activation = VC of non ess organs + abdominal organs = ↑ [blank_start]preload[blank_end].
β1 activation = increased [blank_start]heart[blank_end] [blank_start]rate[blank_end] and contractility, shorter refractory period.
β2 activation = [blank_start]vasodilation[blank_end] in cardiac and skeletal muscle, along with sympathetic cholinergic [blank_start]M3[blank_end] activation
Pa = [blank_start]CO[blank_end] x [blank_start]TPR[blank_end]- ACO
- Bpreload
- Cheart
- Drate
- Evasodilation
- FM3
- GCO
- HTPR
81Return to normality
* Parasympathetic activation of [blank_start]M2[blank_end] cholinergic receptor at sympathetic nerve endings in heart and on cardiac [blank_start]myocytes[blank_end] = reduced heart rate and contractility
* Coronary blood flow is maintained via [blank_start]parasympathetic[blank_end] activation of [blank_start]M3[blank_end] receptor- AM2
- Bmyocytes
- Cparasympathetic
- DM3
82Explain the cardiovascular responses to hypovolaemia
Hypovolemia - perceived by [blank_start]atrial[blank_end] vol receptors + atrial [blank_start]baroreceptors[blank_end]
- ↑ in [blank_start]symp[blank_end] stimulation = ↑ [blank_start]contractility[blank_end]. HR + speed
Vc in non essential organs- Aatrial
- Bbaroreceptors
- Csymp
- Dcontractility
83Hypovolemic shock
↓ vol of [blank_start]circulating[blank_end] blood = acute drop in [blank_start]MAP[blank_end]
- Haemorrhage
- Severe dehydration
- [blank_start]Sequestration[blank_end] of blood- Acirculating
- BMAP
- CSequestration
84Splenic contraction
- Expels blood contained in spleen into [blank_start]circulation[blank_end]
- Blood in spleen = [blank_start]haematocrit[blank_end]- Acirculation
- Bhaematocrit
85Starlings law of Capillaries
- ↓ [blank_start]vent[blank_end] + art pressure
= ↓ [blank_start]HSP[blank_end] = H2O absorbed from [blank_start]ISF[blank_end]- Avent
- BHSP
- CISF
86Cells + Proteins
- If whole blood has been lost = PCV + TP [blank_start]unchanged[blank_end]
- BM replaces cells within few [blank_start]weeks[blank_end]
- protein synthesis in liver in a few [blank_start]days[blank_end]
Reduce as replacement of fluid (through [blank_start]RAAS[blank_end]) dilute blood- Aunchanged
- Bweeks
- Cdays
- DRAAS
87Features of forward heart failure
Forwards ([blank_start]systolic[blank_end])
- ↓[blank_start]CO[blank_end] ↓ [blank_start]MAP[blank_end]
Signs
- ↓[blank_start]perfusion[blank_end] + [blank_start]slow[blank_end] cap R T + [blank_start]pale[blank_end] mm
Unable to exercise + [blank_start]vasovagal[blank_end] syncope when under physiology stress (sudden loss of consciousness)- Asystolic
- BCO
- CMAP
- Dperfusion
- Eslow
- Fpale
- Gvasovagal
88Features of backwards heart failure
Backwards (congestive)
- inability of hear to cope with [blank_start]preload[blank_end]
↑ [blank_start]Venous[blank_end] pressure
↑ [blank_start]Capillary[blank_end] pressure
= leakage of fluid into [blank_start]ISF[blank_end] due to ↑ [blank_start]HSP[blank_end] in capillaries
e.g Mitral valve dx (L CHF)
Pulmonary oedema
Tachypnoea
Dyspnoea- Apreload
- BVenous
- CCapillary
- DISF
- EHSP
89Decompensation
Persistent vasoconstriction of “non-essential” organs
* [blank_start]Azotaemia[blank_end] -uraemia & renal failure
* GI [blank_start]ischaemia[blank_end] - ulceration & sepsis
Fluid retention
* Oedema - [blank_start]myocardial[blank_end] hypoxia
Increased [blank_start]afterload[blank_end] and exposure to aldosterone
* Myocardial remodelling –fibrosis- AAzotaemia
- Bischaemia
- Cmyocardial
- Dafterload
90Vicious cycle
Compensatory mechanisms fail to correct cardiac output
- Further stimulation of [blank_start]RAAS[blank_end] etc
- More retention of water and [blank_start]vasoconstriction[blank_end]
- Increased [blank_start]workload[blank_end] on failing heart
- Heart failure worsens
- More stimulus for compensatory mechanisms!- ARAAS
- Bvasoconstriction
- Cworkload
Información
- Descripción
- CV Test sobre CV , creado por hanna sayedi el 04/02/2019.
- Autor
- hanna sayedi
- Idioma
- English
- Visitas
- 3
- Etiquetas
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