Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Phys 1412 > Topic 11: Cardiovascular Physiology > Flashcards

Topic 11: Cardiovascular Physiology Flashcards

1
Q

Cardiac Physiology Parts

A
  • Heart

- Conduction System

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Heart

A
  • dual pump with valves

- muscle cells connected by gap junctions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Conduction System

A
  • non-contractile cardiac muscle cells – modified to initiate & distribute impulses throughout the heart
  • produce APs spontaneously (no stimulus) BUT at different rates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Conduction System Parts

A
  • Sinoatrial (SA) node – in right atrium
  • Atrioventricular (AV) node – in right atrium
  • Bundle of His (AV bundle)
  • Purkinje fibers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Sinoatrial (SA) node

A
  • rate = 100 APs/min (modified by PSNS to be 75 APs/min at rest)
  • produces APs faster than other areas ∴ is the pacemaker
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Atrioventricular (AV) node

A

-rate = 50 APs/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Bundle of His (AV bundle)

A
  • originates at AV node
  • ONLY route for electrical activity to go from atria to ventricles + Bundle Branches (right and left)
  • 30 APs/min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Purkinje fibers

A
  • terminal fibers - stimulate contraction of the ventricular myocardium
  • 30 APs/min
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pathway of APs in heart

A
  • Interatrial
  • Intermodal
  • If conduction system damaged, next fastest part becomes pacemaker
    i. e. if SA node damaged, AV node takes over (atria may not contract + ventricles contract at AV speed = 50 beats/min)
  • Artificial pacemakers – stim. if SA or AV nodes damaged
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Interatrial

A

SA node through atrial contractile myocardium (rt and left) contract as a unit (gap junctions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Intermodal

A
  • SA node to AV node (delay of 0.1 sec to get through node due to small fibre size-allows vent. to fill with blood from atrial contraction)
  • To bundle of his
  • bundle branches
  • purkinjie fibers
  • Ventricular contractile myocardium (starts at apex, contracts as a unit-gap junctions)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

APs of SA & AV nodes

A
  • cells = non-contractile autorhythmic cardiac muscle cells (self-excitable)
  • threshold = -40mV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Phases of Pacemaker Activity

A
  • Pacemaker Potential
  • AP Depolarization
  • AP Repolarization
  • Na+ channels open at -50 mV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Pacemaker Potential

A
  • low K+ permeability (K+ voltage gates closed)
  • slow inward leak of Na+ (Na+ voltage gates open)
  • causes slow depolarization toward threshold (-40mV)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

AP Depolarization

A
  • at threshold ⇒ AP
  • Ca2+ voltage gates open - Ca2+ moves in ⇒ depol. (Na+ voltage-gates close at threshold ∴ not involved in AP)
  • Ca2+ voltage gates close at peak
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

AP Repolarization

A
  • K+ voltage gates open at peak, K+ out ⇒ repol.

- K+ gates close below threshold

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

 APs in Ventricular Myocardium

A

o cells = contractile
o Purkinje fiber AP ⇒ ventricular (contractile) myocardial AP (spread cell to cell by gap junctions)
o resting MP = -90mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

o Phases of Ventricular Myocardial APs

A

1) Depolarization
2) Plateau
3) Repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

1) Depolarization

A

 Na+ voltage gates open (fast) = same gates as neuron, skel. muscle
 MP to +30 mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

2) Plateau

A

 Na+ channels close + inactivate (slight drop in MP)

 Ca2+ slow voltage gates are open (Ca2+ influx maintains depolarization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

3) Repolarization

A

 Ca2+ channels close

 K+ voltage-gated channels open ⇒ ⇑ K+ outflux ⇒ ∴ MP ⇓ to resting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

o Absolute Refractory Period

A

 Long - Na+ channels inactivated until MP is close to - 70 mV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

o Excitation-Contraction Coupling in Myocardial Cells

A

1) AP on sarcolemma of contractile cell triggers…
2) voltage-gated Ca2+ channels open (plateau of AP) = small ⇑ cytosolic Ca2+ (from ECF) ⇒ not enough to trigger contraction BUT…
3) opens chemically-gated Ca2+ channels on SR
4) ⇑⇑ cytosolic Ca2+
5) binds to troponin, etc, etc ⇒ leads to contraction
6) Contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

6) Contraction

A

 sliding filament mechanism
 begins a few msec after AP begins
 duration of AP = ~250 msec and duration of twitch = ~ 300 msec
 ∴ contraction almost over when AP ends
 Result = NO summation ∴ NO tetanus - get alternation of contraction/relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Cardiac Cycle

A

 3 components

1) Electrical Activity (ECG)
2) Mechanical Activity
3) Blood flow through heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

1) Electrical Activity (ECG)

A

 small currents due to depol/repol. of heart move through salty body fluids
 potential difference measured on body surface using electrode pairs: one pair = a lead
 recording seen as waves
o = sum of electrical activity of ALL myocardial cells (NOT an AP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

 ECG Waves

A

a) P wave = atrial depol ⇒ followed by contraction
b) QRS wave = ventricular depolarization ⇒ contraction
 also atrial repolarization (⇒ relaxation) - masked by larger vent. electrical event (larger muscle mass)
c) T wave = ventricular repolarization ⇒ followed by relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

 ECG Intervals

A

a) P-Q = atria contracted, signals passing through AV node
b) S-T = ventricles contracted, atria relaxed
c) T-P = heart at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

 Abnormalities of Heart Beat

A

a) Tachycardia = resting HR more than 100 bpm
b) Bradycardia = resting HR less than 60 bpm
c) Heart block = when conduction through the AV node slowed, get an increased P⇒Q interval ⇒ ventricles may not contract after each atrial contraction
 e.g. 3rd degree heart block - no conduction through AV node - atria fire at SA node rate (∼ 75 APs/min), ventricles at Bundle/Purkinje rate (∼ 30 APs/min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

2) Mechanical Activity

A

 2 main events:
a) Systole = contraction, emptying
b) Diastole = relaxation, filling
 both events initiated by electrical activity
 1 complete heartbeat = diastole + systole of atria AND diastole + systole of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

 Timing of mechanical events

A

o average resting Heart Rate (HR) = 75 beats/min
o ∴ 0.8 sec/beat = 1 cardiac cycle (60 sec/min÷75 beats/min)
o In 0.8 sec (start with atrial contraction at time 0):
 atria in systole for 0.1 sec, then diastole for 0.7 sec
 ventricles enter systole after atria (0.1 sec delay at AV node) ∴ ventricles begin systole as atria begin diastole ⇒ in systole for 0.3 sec, then diastole for 0.5 sec

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

3) Blood flow through heart

A

 Due to:

a) emptying pressure changes (high P ⇒ low P)
b) valves
c) myocardial contraction (raises P)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

 Path of Blood Flow

A
  • large veins (venous return)
  • atria relaxed (80% of blood into centrical passively)-diastole
  • ventricles relaxed-diastole
  • atria contract (increase in atrial pressure, remaining 20% of blood delivered to ventricle)-systole
  • ventricles contract-systole-and atria relax-diastole
  • ventricles relas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

 During Ventricular Systole

A

a) higher P in ventricles than atria forces AV valves shut ⇒ turbulence of blood gives first heart sound (= LUB) - shortly after QRS wave starts
b) P rises - higher P in ventricle than aorta/pulm trunk pushes semilunar valves open ⇒ blood enters vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

 During Ventricular Diastole

A

a) P drops - higher P in aorta/pulmonary trunk than ventricles forces semilunar valves to shut ⇒ turbulence ⇒ 2nd heart sound (= DUB) – mid-T wave
b) AV valves open when P in ventricles drops below P in atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

 Heart Sounds

A

o Turbulent flow – noisy due to blood turbulence when valves shut
o Laminar flow - no sound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

 Korotkoff Sounds

A

o turbulence heard in brachial artery during blood pressure measurements:
 begin = systolic pressure
 stop = diastolic pressure
 due to cardiac cycle events

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Cardiac Output (CO):

A

volume of blood ejected by each ventricle in 1 min (ml/min)

-heart rate multiplied by stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

 Stroke Volume (SV)

A

-volume ejected by each ventricle per beat
o is equal to the difference between EDV and ESV (i.e. EDV – ESV)
 End Diastolic Volume (EDV) = volume of blood in each ventricle at end of ventricular diastole (= preload)
o i.e. max ventricular volume ~ 120 ml
 End Systolic Volume (ESV) = volume of blood in each ventricle at the end of ventricular systole (i.e. what’s left after ejection) ~ 50 ml
o therefore SV = 120ml – 50ml = 70ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

 Control of CO

A

1) Control of Heart Rate

2) Stroke Volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

1) Control of Heart Rate

A

 basic rate set by SA node = intrinsic control (built in)
 modifiers of HR = extrinsic control
o change pacemaker potential (AP does not change)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

 types of extrinsic control

A

a) Neural
b) Hormonal
c) Other Factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

a) Neural

A

i. SNS (thoracic nerves)

ii. PSNS (Vagus nerve)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

i. SNS (thoracic nerves)

A

 Na+ channels open wider ∴ ⇑ Na+ permeability at SA node ∴ ⇑ slope of pacemaker potential ∴ reach threshold faster ∴ ⇑ HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

ii. PSNS (Vagus nerve)

A

 keeps resting HR lower than pace set by SA node alone (sends continuous impulses)
 ⇑ K+ permeability at SA node ∴ more –ve on repol. ∴ further to go to get to threshold ∴ takes longer ∴ ⇓ HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

b) Hormonal

A

 epinephrine, NE - ⇑ HR - same mechanism as SNS
 thyroid hormone - directly ⇑ HR (but slow, so takes days)
o also ⇑ # of epi receptors ∴ more sensitive to epi

47
Q

c) Other Factors

A

i. ions
ii. fever
 ⇑ temp - ⇑ HR
iii. age
 newborn = high
iv. fitness
 ⇑ fitness = ⇓ HR

48
Q

i. ions

A

 e.g.1: High K+ in ISF
o MP more +ve than normal ⇒ pacemaker Na+ channels may not open
o also slows repol.
o ∴ ⇓ HR ⇒ may lead to cardiac arrest
 e.g.2: Low K+ in ISF
o evidence that K+ channels in some cells change specificity: allow Na+ through instead of K+ ∴ depolarizes membrane ⇒ ⇑ HR - feeble beat, abnormal rhythms

49
Q

 Control of Stroke Volume

A

a) Intrinsic Control: (heart’s built-in ability to vary SV - adjust to demands)
b) Extrinsic Controls:

50
Q

a) Intrinsic Control: (heart’s built-in ability to vary SV - adjust to demands)

A

 ⇑ venous return ⇒ ⇑ EDV ⇒ ⇑ heart muscle stretch ⇒ ⇑ force of contraction (at rest, cardiac fibers are at less than optimal length ∴ stretch ⇒ approach optimal length = more cross bridges attach = more force) ⇒ ⇑ SV (within physiological limits)
o i.e. more blood in ⇒ more blood out

51
Q

 relationship between EDV and SV

A

o Frank-Starling’s Law of the Heart: ⇒ force of ejection is directly proportional to length of ventricular contractile fibers (within physiological limits).

52
Q

 Get ⇑ venous return due to:

A

o exercise – venous return speeded up

o lower HR - has longer to fill ⇒ less of an effect than exercise

53
Q

b) Extrinsic Controls:

A

i. ANS – SNS
ii. Hormones
iii. Other Factors

54
Q

i. ANS – SNS

A

 ⇑ force of contraction (for a given EDV) ∴ ⇑ SV (SNS stimulation ⇑ opening of Ca++ channels ⇒ ⇑ Ca++ into cytosol ∴ more cross bridges ∴ ⇑ force)
 BUT SNS also ⇑ HR = less time to fill ∴ have ⇓ EDV at higher HR. However, ⇑ force ⇒ ⇓ ESV - compensates for ⇓ in EDV
 By ⇑ both force + HR, allows at least maintenance of SV even at high HR (usually an increase)
 PSNS – no significant effect
 Overall: SNS ⇑ CO; PSNS ⇓ CO

55
Q

ii. Hormones

A

 Epi, NE - same mechanism as SNS - ⇑ force

 thyroid hormone - ⇑ force (+ ⇑ epi receptor #)

56
Q

iii. Other Factors:

A

 force ⇑ by:
o ⇑ external Ca++ (more Ca++ moves in on AP)
o digitalis (drug) - ⇑ Ca++ inside
 force ⇓ by:
o acidosis
o ⇑ external K+
o Ca++ channel blockers (drugs) e.g. verapamil

57
Q

Blood Circulation

A

 Blood flow = volume of blood flowing through any tissue/min (i.e. ml/min)
 Blood flow in a vessel is determined by pressure and resistance

58
Q

Blood flow calculated as

A

f=change in P/R
o Where:
1) F = Flow
2) ΔP = blood pressure gradient (difference) between 2 points
 ⇓ blood pressure from: aorta ⇒ arterioles (resistance vessels) ⇒ large veins (capacitance vessels).
3) R = Resistance

59
Q

3) R = Resistance

A

 opposes flow - friction of blood rubbing against vessel walls
 depends on:
a) vessel length
b) blood viscosity
c) radius of arterioles (major resistance vessels) controlled by smooth muscle innervated by SNS
 vasodilation = ⇑ radius ∴ ⇓ R, ⇑ F
 vasoconstriction = ⇓ radius ∴ ⇑ R, ⇓ F

60
Q

 Blood Flow to Organs Controlled by

A

1) Vasoconstriction
2) Vasodilation
a) = opposite of constriction

61
Q

1) Vasoconstriction

A

a) ⇓ radius ∴ ⇑ R, ⇓ F
b) P in artery ⇑ (backs up)
c) P in organ ⇓ (less blood flows into organ capillaries)

62
Q

 Blood Flow to Organs

A

o If vasoconstriction/dilation is local (i.e. to 1 organ) - no observable change in systemic (arterial) BP
o If vasoconstriction/dilation is systemic, then systemic BP will change

63
Q

 Control of vasoconstriction/dilation (arteriolar radius)

A

1) Intrinsic Regulation-allows organ to control its own blood flow
a) myogenic regulation
b) metabolic regulation
 both a) and b) - maintain blood gases + pH levels - very important in heart, skeletal muscle, brain
2) Extrinsic Regulation-external control by Nervous System and Endocrine System
a) neural regulation (SNS)
b) hormonal regulation

64
Q

a) myogenic regulation

A

 when smooth muscle is stretched, it contracts ∴ if ⇑ systemic bp ⇒ arterioles constrict
 e.g. on standing ⇒ high arterial bp in feet (gravity) ∴ arterioles constrict ⇒ ⇓ flow into capillaries
 e.g. on standing ⇒ low arterial bp in brain (gravity) ∴ arterioles dilate ⇒ ⇑ flow into capillaries

65
Q

b) metabolic regulation

A

 blood levels of ⇓ O2, ⇑ CO2, ⇓ pH (⇑ metabolism in organ) - endothelial cells + hemoglobin release nitric oxide ⇒ vasodilation ⇒ ⇑ blood flow to organ
 if ⇑ O2, pH ⇑, CO2 ⇓ (= low metabolism) - endothelial cells release endothelins ⇒ vasoconstriction ⇒ ⇓ blood flow to organ

66
Q

a) neural regulation (SNS)

A

 arteriolar vasocon. (except in brain - intrinsic regulation only)
 vasodilation due to ⇓ SNS signals (only important PSNS effect = dilation of arterioles of penis/clitoris)
 also venoconstriction (vein constriction)

67
Q

b) hormonal regulation

A

i. epinephrine
 vasoconstriction - skin, viscera - reinforces SNS
 vasodilation - heart, skeletal muscle, liver - opposes SNS
ii. other hormones
 angiotensin II, ADH – vasoconstriction
 histamine – vasodilation

68
Q

Blood Pressure

A

 = hydrostatic P exerted by blood on wall of vessel (clinically on the walls of the arteries) – results when F is opposed by R
 What we measure in an artery: 120/80 = syst./diast.

69
Q

 Systolic pressure

A

produced by ventricular contraction against vascular resistance

70
Q

 Diastolic pressure

A

produced by elastic arteries against vascular resistance (when ventricles are relaxed)

71
Q

 Pulse Pressure

A

systolic - diastolic

72
Q

 Mean Arterial Pressure (MAP)

A

=regulated by the body i.e. what the body measures
o = average blood P through cardiac cycle BUT diastole is longer than systole, so:
o MAP = diast P + 1/3 pulse P

73
Q

 MAP Regulation

A

MAP= Cardiac Output multiplied by Total Peripheral Resistance
o MAP is regulated by controlling:
1) Cardiac Output
2) TPR (arteriolar radius)
3) Blood Volume (affects venous return ∴ SV; also MAP directly)

74
Q

o Extrinsic Regulation of MAP

A

1) Neural Control

2) Hormonal Control

75
Q

1) Neural Control

A

a) Baroreceptor Reflexes - short term changes e.g. standing

b) Chemoreceptor Reflexes

76
Q

a) Baroreceptor Reflexes - short term changes e.g. standing

A

 stretch receptors - monitor MAP in:

i. carotid sinus (brain bp)
ii. aortic arch (systemic bp)

-increase in MAP, increase baroreceptor impulses, medulla, increases PSNS (decreases CO), decreases SNS impluses (decrease epidemic secretion, vasoconstriction, venoconstriction-blood pools in veins decreasing venous return and CO), decreases MAP

77
Q

b) Chemoreceptor Reflexes

A

 peripheral chemoreceptors – respond to pH, CO2 (and O2)
 found in aortic arch and carotid sinus (called “bodies”)
 involved in regulation of respiration, but affect bp

-increase CO2 and decrease pH or O2, increase chemoreceptor impulses, medullary cardiovascular centre, increase SNS and epinephrine, increase vasoconstriction and heart rate and force of contraction, increase MAP

78
Q

2) Hormonal Control

A

a) Epinephrine
 ⇑ HR, force of contraction ∴ ⇑ CO ⇒ ⇑ MAP
b) Renin-Angiotensin System
c) Atrial Natriuretic Peptide (ANP) causes

79
Q

b) Renin-Angiotensin System

A

-plasma angiotensinogen (renin), angiotensin I (angiotensin-converting-enzyme (ACE)), angiotensin II
 Angiotensin II causes:
o ⇑ vasocon, ⇑ venocon ∴ ⇑ MAP
o ⇑ aldosterone, ADH ∴ ⇑ renal Na+, H2O abs; ⇑ thirst ∴ ⇑ blood vol ⇒ ⇑ MAP

80
Q

c) Atrial Natriuretic Peptide (ANP) causes

A

o ⇓ renin (∴ ⇓ angio II) ⇓ aldosterone, ⇓ ADH = ⇑ urine production ∴ ⇓ blood vol
o ⇓ vasoconstriction
o so overall = ⇓ MAP

81
Q

Capillary Exchange

A

 between blood and ISF

82
Q

 solutes enter and leave capillaries by

A

1) Diffusion = major route (except brain)
 CO2, O2, ions, aa, glucose, hormones etc
 usually between endothelial cells
2) Vesicular transport – large proteins (e.g. antibodies)
 occurs via transcytosis
o = endocytosis from blood into endothelial cell, then exocytosis from endothelial cell into ISF
3) Mediated Transport – requires a membrane carrier protein
 Important mainly in the brain

83
Q

 Fluid (H2O) enters (absorption) or leaves (filtration) capillaries by

A

1) Osmosis

2) Bulk Flow – due to pressure differences

84
Q

 4 pressures involved

A

a) blood hydrostatic P (BHP) = blood pressure
b) blood osmotic P (BOP) – mainly due to plasma proteins
c) ISF hydrostatic pressure (IFHP) = 0 mmHg
d) ISF osmotic pressure (IFOP) – mainly due to ISF proteins

85
Q

 Net Filtration Pressure (NFP)

A

o sum of hydrostatic and osmotic pressures acting on the capillary
NFP=(BHP+IFOP)-(BOP+IFHP)

86
Q

o In the body:

A

 90% of filtered fluid reabsorbed to blood
 10% enters lymph
 ∴ ISF vol remains relatively constant

87
Q

o Clinical Application: Edema

A

 = accumulation of fluid in the tissue (ISF) causing swelling
 due to:
1) High blood pressure (⇑ BHP)
2) leakage of plasma proteins into ISF ⇒ inflammation (⇑ IFOP)
3) ⇓ plasma proteins (malnutrition, burns) (⇓ BOP)
4) obstruction of lymph vessels - elephantiasis, surgery

88
Q

Circulatory Shock

A

 = inadequate blood flow (⇓ O2, nutrients to cells)

89
Q

1) Hypovolemic Shock

A

 ⇓ blood volume

 due to: blood loss, severe burns, diarrhea, vomiting

90
Q

2) Vascular Shock

A

 blood volume normal, but vessels expanded
 due to: systemic vasodilation of blood vessels ⇒ ⇓ bp
 examples:
a) anaphylactic shock - allergic reactions
 due to: = lots of histamine released from mast cells
b) septic shock
 due to: bacterial toxins
c) cardiogenic shock
 pump failure ⇒ ⇓ CO
 heart cannot sustain blood flow

91
Q

 stages of shock

A

1) Compensatory
2) Progressive
3) Irreversible

92
Q

1) Compensatory

A 
	mechanisms can restore homeostasis by themselves
	involves:
a)	baroreceptors
b)	chemoreceptors
c)	ischemia (lack of O2) of medulla
	all trigger SNS
93
Q

 all trigger SNS:

A

o ⇑ HR, generalized vasoconstriction (except to heart, brain) = ⇑ bp
o ⇓ blood flow to kidneys triggers renin release - get angio II, aldosterone, ADH release ∴ vasocon, ⇑ Na+, H2O retention (maintain blood volume), ⇑ thirst

94
Q

2) Progressive

A

 mechanisms inadequate to restore homeostasis - requires intervention
 ⇓ CO ∴ ⇓ bp in cardiac circulation ∴ ⇓ cardiac activity
 ⇓ blood to brain ⇒ ⇓ cardiovascular control
 damage to viscera due to ⇓ blood flow, especially kidneys (can lead to renal failure)

95
Q

3) Irreversible

A

 ⇓ CO ⇒ too little blood to heart ⇒ ⇓ CO

 self-perpetuating cycle - leads to death

96
Q

Blood contains:

A

1) Plasma

2) Formed Elements

97
Q

1) Plasma

A 
a)	H2O (90.5%) 
	transport medium and carries heat
b)	Proteins (7%) 
c)	Electrolytes (ions)
	functions:
i.	membrane excitability
ii.	buffers (HCO3-)
d)	Other solutes
	nutrients, wastes, gases, hormones
98
Q

b) Proteins (7%)

A

 albumins (58% of proteins)
 globulins (38%)
 fibrinogen (4%)
 functions:
i. produce osmotic pressure (especially albumins)
ii. buffer pH (7.35-7.45) - keep it from changing
iii. α, β globulins - transport lipids, metal ions, hormones
iv. γ (gamma) globulins = antibodies
v. clot formation

99
Q

2) Formed Elements

A

a) Red Blood Cells (RBCs)
b) White Blood Cells (WBCs)
c) Platelets

100
Q

a) Red Blood Cells (RBCs) functions

A

i. transport – O2 on iron (Fe) of heme; CO2 on globin
ii. buffer – globin binds to H+ reversibly
iii. carbonic anhydrase (CA) – important for CO2 transport in blood

101
Q

 Hemoglobin

A 
o	Hb = 4 hemes + 4 globins (protein)
o	1 iron (Fe)/heme ∴ 4 Fe/Hb
o	broken down by macrophages into
i.	heme
ii.	globin
	converted to amino acids – recycled
102
Q

i. heme

A

 Fe removed and stored (liver, muscle, spleen)
 from stores (or diet) ⇒ bone marrow cells make heme ⇒ RBCs
 non-iron portion ⇒ bilirubin ⇒ excreted in bile from liver
 jaundice = excess bilirubin in blood because:
o excess RBC breakdown; or
o liver dysfunction (neonates ⇒ liver immature); or
o blockage of bile excretion

103
Q

b) White Blood Cells (WBCs)

A

i. Granulocytes

ii. Agranulocytes

104
Q

i. Granulocytes

A

Neutrophils
 phagocytic
 1st to enter infected area
Eosinophils
 attack parasites
 break down chemicals released in allergic reactions
Basophils
 secrete histamine (increases inflammation)
 secrete heparin (inhibits local clotting)

105
Q

ii. Agranulocytes

A

Monocytes
 enter tissues, enlarge to become phagocytic macrophages
Lymphocytes

106
Q

 Lymphocytes

A

 T lymphocytes - Helper T (TH) + cytotoxic T (CTLs) lymphocytes
 B lymphocytes - when activated, give rise to plasma cells - secrete antibodies
 Natural Killer Cells - attack foreign cells, abnormal cells (non-specific)

107
Q

c) Platelets

A

 cell fragments from megakaryocytes
 functions:
o form platelet plug – prevents excess blood loss
o contain granules = coagulation factors (proteins/chemicals involved in clotting)

108
Q

Hemostasis

A 
	= process of stopping bleeding
	involves:
1)	Vascular Spasm 
2)	Platelet plug formation 
3)	Clot Formation 
4)	Clot Retraction + Repair
5)	Fibrinolysis  
	thrombus = a stationary clot in an undamaged vessel
	embolus = free floating clot
	Hemophilia – clotting abnormal/absent
o	about 83% = type A - lack clotting factor VIII
109
Q

1) Vascular Spasm

A

 = vasoconstriction of damaged arteries, arterioles - ⇓ blood flow (minutes to hours)

110
Q

2) Platelet plug formation

A

 platelets stick to damaged blood vessel, release chemicals (factors) which:
a) cause more platelets to stick (+ve feedback)
b) promote clotting
c) begin healing
 neighbouring healthy endothelial cells release a chemical preventing spread of plug
 plug formation requires a prostaglandin - inhibited by aspirin

111
Q

3) Clot Formation

A

 3 stages:
a) production of prothrombin activator
b) Prothrombin converted to thrombin
c) Fibrinogen converted to fibrin
 Thrombin - +ve feedback to ⇑ its own formation
 NOTE: ~ 2 doz. factors involved
o from diet, liver (plasma proteins), damaged tissue, platelets
o e.g. vitamin K required for synthesis of 4 factors

112
Q

a) production of prothrombin activator

A

i. extrinsic pathway – uses factors released by damaged tissues
ii. intrinsic pathway - uses factors contained in blood
 usually both occur together - require Ca2+, tissue, platelet and/or plasma factors

113
Q

4) Clot Retraction + Repair

A

 retraction – blood vessel edges pulled together

 repair - fibroblasts form new CT, new endothelial cells repair lining

114
Q

5) Fibrinolysis

A

 clot dissolution
 fibrin digesting enzyme = plasmin
 phagocytes then remove clot in clumps

Phys 1412 (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions