W6: CVS1; Overview; ECG; Cardiac Cycle; Regulation Flashcards

1
Q

Define the function of the cardiovascular system.

A

bulk flow
O2, nutrients, metabolites hormones, HEAT

varying outputs
store and redirect blood

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2
Q

Justify the significance of pressure, resistance and capacitance with respect to the cardiovascular system.

A
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3
Q

Indicate the significance of vascular beds being arranged in parallel or in series.

A

series: one after another, where output is equal both sides
parallel: ensures all tissues recieve get oxygenated blood + regional redirection and varying output

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4
Q

Explain the functions of elastic arteries, muscular arteries, resistance vessels and capacitance vessels

A
  1. elastic art.: wide lumen ↓resistance, THICK ELASTIC = absorb energy and dampen pressure variations (major vessels)
  2. muscular art.: wide lumen + non-elastic. LOW RESISTANCE CONDUIT.
  3. arterioles: narrow lumen, contractile smc wall = control of resistance = flow
  4. RESISTANCE VESSELS = control regional flow; CAPACITANCE VESSELS: slow movement and reserve volume
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5
Q

What are the features of cardiac synctium

A

Collection of myocytes acting as one unit
*GAP JUNCTION: cytoplasm and passage of current and messenger molecules

*DESMOSOMES: physical linking + unify contractions

=> intercalated discs

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6
Q

Myocyte Vs Skeletal

A

Skeletal: Short APs, TETANIC contraction, saturation occuring @ twitch contraction

Cardiac: Long APs, no saturation, Ca2+ modulatory, no tetanic activity

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7
Q

List the sequence events occurring during excitation-contraction coupling in cardiac muscle.

A

AP propagation along sarcolemma > T-Tubules > SR release Ca2+

Ca bind calmodulin > complex bind to myosin light chain kinase > x-bridges w/ M Head

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8
Q

AP in Non-Pacemaker

A
  1. -90MV d/t K+ leaving
  2. DEPOL: ↑PNa+ . SHORT AP
  3. ↑Ca2+: slower + longer => PLATEAU
    ↑Ca2+L-Type ↓PK+
  4. repol: ↓Ca2+ ↑PK+
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9
Q

AP in Pacemaker

A
  1. Pacemaker Potential: gradual ↓PK+, ↑EarlyNa (PF), late ↑Ca(T) => DEPOL
  2. AP: ↑Ca2+ (L) = slower AP
  3. repol: ↓Ca2+ then ↑PK+ = channels open
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10
Q

Describe the initiation and spread of electrical activity throughout the heart.

A
  1. SA
  2. Annulus Fibrosis: non-conducting ring of tissue
  3. AV Node (DELAY BOX): slows depol to give atria time to expel before ventricular expulsion
  4. BoH: widespread dispersion
  5. Purkinje Fibres: rapid 5m/s, uniform depol. spread
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11
Q

Correlate the various components of the electrocardiogram with the electrical events in the heart.

A

P: Atrial Depol

QRS: Ventricular

T: Ventricular Repol.

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12
Q

ECG Intervals

A

PR: Time between atrial and ventricular depol
(0.12-0.25) ~3/4 small squares

QRS: Whole ventr depol. (0.08s) ~1square or less

QT: duration of ventricular systole
(0.42s @ 60bpm) ~1.5 L.Squares

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13
Q

Conduction via limb leads

A

SLL2: L Leg wrt R Arm

  1. Ventr. depol to L Leg = +ve inflection wrt R arm
    (repol to R Arm)
  2. L Leg to R Arm = -ve inflection wrt R arm
    (repol. to L LEg)
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14
Q

What are the stages of the cardiac cycle?

A
  1. ATRIAL SYSTOLE
    - contraction and ejection into ventr.
  2. ISOVOLUME VENTR. CONTR.
    - AV delay; ↑pressure AV shut; semilunar valves remain close
  3. VENTR. EJECTION
    - ↑↑pressure exceeds arterial pressure
    - semis open = EJECT into atrial and pulmonary
    (Ca2+ uptake)
  4. ISOVOLUME VENTRE. RELAXATION
    - ↓pressure, blood falls back, SEMIS CLOSE
    - muscle relaxation
  5. LATE DIASTOLE
    - passive filling
    - pacemaker reaches depol.
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15
Q

Systolic and diastolic pressures

A

Systolic Pressure is based off the peak pressure of the AORTA ) aortic arterial

Diastolic Pressure is based off the lowest pressure of the AORTA aortic arterial

MAP: 1/3 of the way between diastolic and systolic

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16
Q

What is pulse pressure

A

Difference between systolic and diastolic

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17
Q

What is the dicrotic notch

A

Ao pressure, post-ao valve closure. Elastic recoil exerts pressure onto column of blood. Then mitral valves open.

D/t elasticity, there is a slower drop in aortic pressure

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18
Q

Atrial waves

A

a - atrial contraction (p-wave)
c - ventr contract and stops when ao valve opens
v - ejection, gradual increase until mitral valve opens d/t atrium relatively smaller

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19
Q

Cardiac volumes

A
  1. END DIASTOLIC VOLUME
    - peak volume at end of diastole
  2. END SYSTOLIC VOL.
    - minimum vol @ end of ejection phase
  3. STROKE VOL.
    - difference between “” “”, therefore vol of blood pumped out w/ each beat of heart
  4. EJECTION FRACTION.
    - how much end systolic volume pumped out
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20
Q

Rapid Ejection Phase

A

HR of 150++ = cuts into the rapid ejection phase

  • first 1/3 of ejection phase most significant and 2/3 slower diastolic filling

RHS: HR + timing + vol same d/t lower pressure going into pulm. circulation

21
Q

Heart Sounds

A

1 - AV Closure

2 - Ao + Pulm Closure

3 - Rapid Passive Filling

4 - Active Filling

22
Q

Pathological Murmurs

A
  1. Systolic Murmur: MR. ASS
  2. Diastolic Murmur: MS. ARD
  3. Continuous Murmur: Septal defect; hole in septum (L pressure higher)
23
Q

Explain the chronotropic and ionotropic effects of the sympathetic and parasympathetic systems

A
  1. SYMPATHETIC:
    * +ve chronotropic: NA (adr. medulla) -> B1 R on SA = TACHY
    * +ve ionotropic: NA -> B1 = ↑contractility d/t ↑Ca = ↑SV
  2. PARASYMP.
    * -ve chronotropic: hyperpol. d/t ACh (vagus) -> muscarinic R on SA = ↓pacemaker potential slope

*ionotropic: nil d/t lack of innervation of ventr. muscle

24
Q

** Cardiac output equation **

A

CO = HR x SV

25
Q

Explain the effects of preload and afterload on stroke volume.

A
  1. PRE-LOAD: length of muscle fibre before stimulated to contract.
    * starling law: contraction proportional to length of muscle fibre
    * ↑EDV = ↑Stretch = ↑Preload = ↑SV
    * capacitance influences input into heart
  2. AFTER-LOAD: load against which the muscle tries to contract
    * TPR = ↑Constriction = ↑Ao. P = ↑Work = ↓SV
    * ↑TPR = ↓SV
26
Q

CO in Exercise

A
  • ↑HR
  • ↑Venous return d/t VENOCONSTR. + SKELETAL PUMPS
  • ↓TPR d/t arteriole dilation = ↓Afterload = ↑SV
27
Q

Changes in the aortic pressure wave as it passes through the vascular tree.

A
  1. Elastic arteries act as pressure resevoirs, with arterioles acting as resistance vessels
  2. BP varies greatly, with ↓pressure going down the tree
28
Q

Changes in blood velocity and total cross-sectional area of the vessels throughout the vasculature.

A

FLOW: vol blood going through particular area

VELOCITY: speed of cells passing through area

tot cross-sect. area of specific part of circulation INVERSELY PROP. to velocity

29
Q

Systemic filling pressure

A

Difference in pressure entering vein and pressure entering heart

30
Q

Indicate the factors affecting pressure & flow in veins.

A
  1. RESP PUMP: ↑RR + ↑Depth = ↑EDV = ↑Venous Return
  2. SKELETAL MUSCLE PUMP = ↑
    * peripheral vein valves
  3. GRAVITY: pressure gradients do not drive blood back
    * ** DISTENSION in legs pools fluid and ↓↓EDV, SV, CO, MAP *** (orthostatic hypoT)
  4. VENOMOTOR TONE: smc contraction around veins mobilises capacitance d/t symp. activity
  5. ** SYSTEMIC FILLING PRESSURE ** pressure from ventricles exerted to veins main driving force
31
Q

What is the main driving force of venous pressure?

A

Systemic Filling Pressure suppl. by other factors

32
Q

Describe the mechanisms that prevent blood clotting in vessels.

A
  1. PT PLUC + FIBRIN CLOT

2. ENDOTHELIAL BARRIER: collagen, NO + prostaglandin inhibit PT aggr.; TFPI; thrombomodulin

33
Q

Capillary Types

A
  1. Continuous
  2. Fenestrated (intestine, kidney) fluid exch.
  3. Discontinuous: clefts and massive pores (liver)
34
Q

Identify the processes involved in transport between capillaries and tissues.

A
  1. CAP. HYDROSTATIC PRESSURE (OUT) - reduces along, fluid uses clefts and pores
    => ↑[int. solute]
  2. PLASMA ONCOTIC (IN) - increases along, osmosis of water d/t solute increase
35
Q

Oedema causes

A

lymphatic obs, HYPOPROTEINEMIA, ↑CVP, ↑cap permeability

36
Q

Justify the importance of Poiseuille’s Law in relation to the control of resistance and blood flow.

A

Poiseuille’s Law = Radius of vessel controls and redirects flow

  • flow INVERSE resistance, viscocity = resistance
  • TPR = MAP

=> controlled by smc surr. arterioles

37
Q

LOCAL INTRINSIC CONTROLS of FLOW

A
  1. ACTIVE HYPERAEMIA
    * ↑[metab. output] (skeletal) = ↑EDRG + local paracrine = RELAXATION = ↑Flow d/t ↓RES.
  2. PRESSURE AUTOREG.
    * ↓MAP = ↓Flow = same rate of metab !!!
    = ↑EDRG + local paracrine = RELAXATION = ↑Flow d/t ↓RES.
  3. REACTIVE HYPERAEMIA
    * OCCLUSSION of supply = ↑Flow
    = +++EDRG = +++DILATATION
  4. INJURY RESPONSE
    *c-fibres activate = AP to dorsal root gang.
    *peptipe p released
    = mast cell activation = histamine
    = dilatation + ↑capillary junct perm
    = ↑flow + ↑perm
38
Q

Identify the various neural, hormonal and local factors affecting arteriolar tone.

A
  1. NEURAL: symp. NA, A1 receptors = art. constr. = ↓flow = ↑MAP d/t ↑TRP
  2. HORMONAL: adrenaline (adr. medulla)
    * smc art. A1 = constr.

*skel = B2 = dilatation

39
Q

Describe the dominant factors controlling blood flow in cardiac, cerebral, pulmonary and renal vascular beds.

A
  1. CORONARY CIRC.
    * metab. sensitivity
  2. CEREBRAL CIRC.
    * pressure autoreg.
  3. PULM.
  4. RENAL
    ↓map = ↓filtr. = ↓urine
    MAP = blood vol.
40
Q

Describe the components and function of the arterial baroreceptor reflex.

A

stretch receptors, APs increase @ differing MAPS
1. AORTIC ARCH => AO. ARCH. BARORECEPTORS =>
(vagus nerve)
2. CAROTID SINUS => carotid sinus receptors =>
(glossopharyngeal nerve)

=> both to medullary cardiovasc centre in brainstem

=> medullary output (parasymp) => vagus => SA node
=> symp effects via NA release => SA node

=> ventircular muscle innervation => Ca influx
=> vasc. innervation => vaso and veno constr.

41
Q

Identify other inputs to the medullary cardiovascular centres.

A
  1. HIGHER CENTRES: hypothalamus, cerebral cortex
  2. JOINT RECEPTORS
  3. muscle and central chemoreceptors
  4. cardiopulm. baroreceptors
42
Q

Explain the relationship between cardiac output, total peripheral resistance, and mean arterial pressure.

A

MAP = CO X TPR

43
Q

VALSALVA MANOEUVRE

A
  1. ↑thoracic p. = ↑ao p. = ↑BP, venous return stopped ↓CO
  2. ↑+ve pressure in thorax = ↓EDV = CO
  3. ↓MAP detected => reactive tachy = ↑venoconstrictio
  4. STOP. ↓throacic p = ↓ao p
  5. Blood building floods into heart => ↑↑EDV, preload, SV (reversed pressure to thorax prevents blood going forwards - capacitance released). VR RESTORED AND ++
  6. ↓HR and CO balanced out via ↑vagal activity to SA node (reactive brady)
44
Q

What does valsalva detect?

A
  1. assess Baroreflex stretch. ↓stretch = continuous BP drop (no reactive tachy)
    * d/t autonomic nerve dmg
  2. ↑strain on heart d/t ↓preload therefore
45
Q

role of the kidneys in regulating plasma volume and therefore blood pressure

A

*[Na] extracel fluid determined water permeability at collection duct via osmostic gradient

=> diuresis
=> reabs

46
Q

Triggers of RAAS

A
  1. symp. activation = ↑activity = ↑renin release
    = ↓BP
  2. ↓distension of afferent arterioles (renal baroflex)
    = ↓MAP = ↓distension
  3. ↓Na/Cl delivery: macula densa
    ↓delivery d/t BP (direct)
47
Q

RAAS

A

** renin release (juxtaglomerular cells); **
renin converts ANGIOTENSNGN -> ANG. I
ACE converts ANG. I -> ANG. II.

ANG II (active hormone) => 
• aldosterone release (adrenal cortex):
↑Na transporter = ↑Reabs = ↓diuresis ↑plasma vol.
  • ↑ADH (pituitary) = ↑thirst, ↑water perm, = ↑Reabs = ↓diuresis ↑plasma vol.
  • DIRECT VASOCONSTRICTOR = ↑TPR
48
Q

ADH: triggers & effects

A

Trigger:
↓blood vol (cardiopulm.) .
↑osmolarity of ISF (hypothal. osmoreceptors);
Ang II

= ↓diuresis ↑plasma vol.

  • increased permeability of collecitng duct
  • vasoconstr. = ↑MAP
49
Q

ANP + BNP: what? triggers? effects?

A

(atrial/brain) natriuretic peptide (atrial and ventr. myocardial cells)

TRIGGER: ↑atrial and ventr. distension d/t ↑MAP and ↑↑Blood vol.

=> ↑↑Na Excretion
renin inhib.
plasma vol reduction
medullary cardio centre => ↓↓MAP