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
Explain the effects of preload and afterload on stroke volume.
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
CO in Exercise
* ↑HR * ↑Venous return d/t VENOCONSTR. + SKELETAL PUMPS * ↓TPR d/t arteriole dilation = ↓Afterload = ↑SV
27
Changes in the aortic pressure wave as it passes through the vascular tree.
1. Elastic arteries act as pressure resevoirs, with arterioles acting as resistance vessels 2. BP varies greatly, with ↓pressure going down the tree
28
Changes in blood velocity and total cross-sectional area of the vessels throughout the vasculature.
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
Systemic filling pressure
Difference in pressure entering vein and pressure entering heart
30
Indicate the factors affecting pressure & flow in veins.
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
What is the main driving force of venous pressure?
Systemic Filling Pressure suppl. by other factors
32
Describe the mechanisms that prevent blood clotting in vessels.
1. PT PLUC + FIBRIN CLOT | 2. ENDOTHELIAL BARRIER: collagen, NO + prostaglandin inhibit PT aggr.; TFPI; thrombomodulin
33
Capillary Types
1. Continuous 2. Fenestrated (intestine, kidney) fluid exch. 3. Discontinuous: clefts and massive pores (liver)
34
Identify the processes involved in transport between capillaries and tissues.
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
Oedema causes
lymphatic obs, HYPOPROTEINEMIA, ↑CVP, ↑cap permeability
36
Justify the importance of Poiseuille’s Law in relation to the control of resistance and blood flow.
Poiseuille’s Law = Radius of vessel controls and redirects flow * flow INVERSE resistance, viscocity = resistance * TPR = MAP => controlled by smc surr. arterioles
37
LOCAL INTRINSIC CONTROLS of FLOW
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
Identify the various neural, hormonal and local factors affecting arteriolar tone.
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
Describe the dominant factors controlling blood flow in cardiac, cerebral, pulmonary and renal vascular beds.
1. CORONARY CIRC. * metab. sensitivity 2. CEREBRAL CIRC. * pressure autoreg. 3. PULM. 4. RENAL ↓map = ↓filtr. = ↓urine MAP = blood vol.
40
Describe the components and function of the arterial baroreceptor reflex.
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
Identify other inputs to the medullary cardiovascular centres.
1. HIGHER CENTRES: hypothalamus, cerebral cortex 2. JOINT RECEPTORS 3. muscle and central chemoreceptors 4. cardiopulm. baroreceptors
42
Explain the relationship between cardiac output, total peripheral resistance, and mean arterial pressure.
MAP = CO X TPR
43
VALSALVA MANOEUVRE
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
What does valsalva detect?
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
role of the kidneys in regulating plasma volume and therefore blood pressure
*[Na] extracel fluid determined water permeability at collection duct via osmostic gradient => diuresis => reabs
46
Triggers of RAAS
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
RAAS
*** 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
ADH: triggers & effects
Trigger: ↓blood vol (cardiopulm.) . ↑osmolarity of ISF (hypothal. osmoreceptors); Ang II = ↓diuresis ↑plasma vol. * increased permeability of collecitng duct * vasoconstr. = ↑MAP
49
ANP + BNP: what? triggers? effects?
(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