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BIOL 273 Physiology > Unit 4 - Cardiovascular System > Flashcards

Unit 4 - Cardiovascular System Flashcards

1
Q

solution for diffusion distance limitation (for big organisms)?

A

i. cardiovascular system for transport of substances through body
ii. transported by flow of blood through circulatory system
iii. bulk flow rather than diffusion

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2
Q

material transported in cardiovascular system

A
  • from external environment to tissues: nutrients, water, gases (esp O2)
  • between tissues of body: wastes, nutrients, hormones
  • from tissues to external environment: metabolic wastes, gases (esp CO2), heat
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3
Q

components of cardiovascular system (3)

A

heart - pump
blood vessels - vasculature
blood cells & plasma - fluid

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4
Q

blood contains: (7)

A

erythrocyte (RBC)
platelets
leukocytes: neutrophil, lymphocyte, monocyte, eosinophil, basophil
(Never Let Monkeys Eat Bananas)

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5
Q

external heart anatomy

A

pericardium - tough membranous sac surrounding heart
- made of two layers with a small amount of fluid between them (lubricant)

coronary arteries:
- nourish heart muscle
- heart has high oxygen demand -> depends on adequate blood flow
- lack of blood supply to heart leads to heart attack

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6
Q

heart attack AKA

A

myocardial infarction

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7
Q

base and apex refer to?

A

base is top
apex is bottom, pointy area

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8
Q

internal heart anatomy

A

left atrium
- receives blood from pulmonary veins (sends to left ventricle)

left ventricle
- receive blood from left atrium (sends to body via aorta)

right atrium
- receives blood from vena cavae (sends to right ventricle)

right ventricle
- receive blood from right atrium (sends to lungs)

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9
Q

heart valve - direction and placement

A
  • valves ensure flow is unidirectional
  • no valves at entrance to right & left atria, due to weak atrial contraction relative to ventricular contraction
  • atrial contraction compresses veins at entry to heart -> closes exit to heart & reduces backflow
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10
Q

heart valves (4)

A

AV valves - tricuspid (RIGHT) & bicuspid/mitral (LEFT)
- attached on ventricular side to collagenous cords -> chordae tendineae (prevent valves from being pushed back into atrium)

Semilunar valves - aortic & pulmonary
- just inside aorta and pulmonary arteries -> prevent backflow into ventricles
- semilunar valves do not needs cords to brace them due to shape

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11
Q

path of blood flow (2 divisions)

A
  1. pulmonary circuit
    - right atrium -> right ventricle -> pulmonary arteries -> lungs
    - lungs have capillaries for O2 transfer -> increase resistance -> decrease pressure of blood
    - oxygenated blood has low pressure -> return to heart via pulmonary veins -> left atrium
  2. systemic circuit
    - left atrium -> left ventricle -> aorta -> arterioles -> body
    - O2 diffuses through capillary beds -> small venules -> larger veins
    - oxygen-poor blood has low pressure -> return to heart via superior vena cava & inferior vena cava -> right atrium

Note: heart increases pressure of blood at critical points in the double circuit

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12
Q

main definition difference of artery vs vein

A

arteries carry blood AWAY from heart
veins carry blood TOWARDS heart

NOT correlated to level of oxygenation

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13
Q

does heart need input form nervous system for contraction?

A

no! they have autorhythmic/pacemaker cells

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14
Q

what does SA node stand for?

A

sinoatrial node!

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15
Q

where are pacemaker cells located?

A

SA node
right atrium, near superior vena cava

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16
Q

pacemaker potential

A
  • pacemaker cells have an unstable membrane potential that slowly drifts upwards from -60 mV (pacemaker potential) until threshold (AP!)
    – unstable membrane potentials because they have different membrane channel than other excitable cells
    – special I(f) channels (I = current; f = funny channel)
    – permeable to K+ and Na+
  • when membrane potential -ve, Na+ influx > K+ efflux -> net influx of +ve charge -> slow depolarization
  • when membrane potential becomes more +ve, I(f) channels close; Ca2+ channels open -> continued depolarization -> threshold reached -> many Ca2+ channels open & rapid Ca2+ influx -> steep depolarization
  • at end of depolarization, Ca2+ channels close and K+ channels open slowly; efflux of K+ repolarizes
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17
Q

major difference between APs and pacemaker potentials in pacemaker cells?

A

Na+ & Ca2+ influx for pacemaker potential

only Ca2+ influx for AP

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18
Q

modulation of heart rate

A
  • autonomic division modulates RATE of pacemaker potentials

a. norepinephrine released from sympathetic neurons & epinephrine released from adrenal medulla -> bind to beta1 adrenergic receptor
- release of cAMP through signalling pathway which binds to open I(f) channels -> channels stay open longer -> increased permeability to Na+ and Ca2+
- increased depolarization rate which increases rate of APs -> heart rate increases

b. acetylcholine released from parasympathetic neurons -> binds to muscarinic receptors
- increases K+ permeability which hyperpolarizes cell -> pacemaker potential starts at more -ve value -> heart rate decreases

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19
Q

electrical communication in heart

A
  • pacemaker/autorhythmic cells initiate electrical excitation of heart
  • depolarization spreads to neighbouring cardiac cells via gap junctions in intercalated discs
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20
Q

events of conduction steps (5)

A
  1. APs fired from SA node
  2. rapid spread through internodal pathway
    (spread is slower though contractile cells of atrium)
  3. signal passed through AV node ONLY at AV junction (fibrous connective tissue - insulator)
    (signal slightly delayed by AV node, make sure atria complete contraction)
  4. signal carried to bottom of heart through bundle of His (AV bundle)
  5. bundle of His divides into left and right branches -> Purkinje fibres transmit VERY rapidly (all contractile cells at apex contract together)
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21
Q

why is it necessary to conduct signals only though AV node and bundle of His?

A
  1. want contraction signal to start at apex
  2. ensures contraction drives up blood since blood exits heart at top
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22
Q

events of conduction summary (locations in order) (6)

A

SA node ->
internodal pathway ->
AV node ->
AV bundle (bundle of His) ->
bundle branches ->
Purkinje fibresw

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23
Q

electrocardiogram AKA?

A

ECG/EKG

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24
Q

electrocardiogram 3 leads =

A

Einthoven’s triangle

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25
Q

each lead in EKG has?

A

+ve end and -ve end

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26
Q

nowadays clinically we use ___ leads

A

12

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27
Q

components of ECG: waves/segments = mechanical/electrical?

A

waves = electrical
segments = mechanical

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28
Q

components of an ECG (2):

A

waves (electrical)
- deflections above or below baseline
- 3 major waves:
i. P wave -> depolarization of atria
ii. QRS complex -> depolarization of ventricles
iii. T wave -> repolarization of ventricles

segments (mechanical)
- sections of baseline between two waves
- lag slightly behind electrical events
- 2 segments:
i. P-R segment -> atrial contraction
ii. S-T segment -> ventricular contraction, just after Q wave

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29
Q

heart rate recorded by ECGs are measured from ___ ___ to ___ ___

A

p wave to p wave

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30
Q

cardiac cycle: period from one ___ to ____

A

heartbeat to next (heartbeat)

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31
Q

cardiac cycle 2 phases

A
  1. systole - contraction
  2. diastole - relaxation
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32
Q

cardiac cycle steps (6)

A
  1. late diastole: both atria and ventricles are relaxed -> semilunar valves closed; AV valves open -> blood enters ventricles passively
  2. atrial systole: atria contract, ventricles relaxed -> semilunar valves closed; AV valves open -> small amount of blood enters ventricles
  3. isovolumic ventricular contraction: ventricles contract -> AV and semilunar valves closed
  4. ventricular ejection -> semilunar valves open, AV valves shut -> blood ejected
  5. isovolumic ventricular relaxation -> semilunar valves closed; AV valves closed
  6. repeat from step 1
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33
Q

lub-dub sounds are due to?

A

lub - closing of AV valves
dub - closing of semilunar valves

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34
Q

max volume in ventricle
min volume in ventricle

A

max volume in ventricle
- End Diastolic Volume (EDV)
- end of ventricular filling

min volume in ventricle
- End Systolic Volume (ESV)
- end of ventricular contraction

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35
Q

stroke volume = ?

A

EDV - ESV

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36
Q

how to calculate cardiac output?

A

cardiac output = heart rate x stroke volume
(amount of blood pumped in 1 min)

37
Q

factors influencing heart rate (3)

A
  1. parasympathetic stimulation - decreases heart rate, via vagus nerve (ACh)
  2. sympathetic stimulation - increases heart rate, via great cardiac nerve (NE)
  3. plasma epinephrine (from adrenal medulla) - increases heart rate
38
Q

factors influencing stroke volume (4)

A
  1. parasympathetic stimulation -> decreases contractility
  2. sympathetic stimulation -> increases contractility
  3. plasma epinephrine -> increases contractility
  4. increased end-diastolic volume -> increase stroke volume
39
Q

factors affecting venous return (4)

A
  1. total blood volume - more blood = more can be loaded into ventricles
  2. sympathetic vasoconstrictor nerves - constrict blood vessels pushes blood towards heart
  3. skeletal muscle pump - muscle contractions push blood toward heart
  4. respiratory pump - creates lower pressure in thorax and higher pressure in abdomen
40
Q

blood vessel structure parts

A
  1. lumen - central cavity
  2. wall - layers (inside->outside):
    a. inner lining - endothelial cells make up endothelium
    b. elastic connective tissue
    c. vascular smooth muscle
    - vasoconstriction -> narrowing of vessel
    - vasodilation -> widening of vessel
    d. fibrous connective tissue
41
Q

types of blood vessels (5) and their components

A

artery - thick-walled to withstand high pressure (all 4 layers)

arteriole - smallest arteries (inner lining, vascular smooth muscle)

capillary - smallest blood vessel -> exchange of material (inner lining)

venule - smallest veins (inner lining, fibrous connective tissue)

vein - transport blood at low pressure (all 4 layers)

42
Q

blood flow pressure gradient

A

blood flows due to pressure gradient (delta P) between arteries and veins, not absolute pressure
- flow is directly proportional to delta P

43
Q

factors that influence blood flow (arterioles) (4)

A
  1. myogenic autoregulation - stretch receptors in walls of arterioles when activated cause vasoconstriction (vascular smooth muscle)
  2. paracrine hormones - released from vascular endothelium and tissues, cause vasodilation or vasoconstriction
  3. innervation by sympathetic division of autonomic nervous system:
    - NE -> alpha receptors, vasoconstriction
    - E -> alpha receptors, reinforce vasoconstriction (longer-lasting response)
  4. hormonal signals via circulating E -> beta 2 receptors
    - found only in vascular smooth muscle of heart, liver, skeletal muscle
    - vasodilation
44
Q

pressure is increased when volume ___
how does the heart accomplish this?

A

decreases
the heart contracts

45
Q

pressure is ___ by friction

A

decreased

46
Q

friction

A

the force that resists relative motion between two bodies in contact
- in circulatory system, friction occurs between blood and blood vessel walls

47
Q

force exerted by a tube =?

A

resistance

48
Q

formula for resistance, define variables

A

R = (8 L η)/(π r^4)

L = length of tube
η = viscosity of liquid
r = radius of tube

49
Q

resistance variable notes; which variables are constant? which change?

A

L (length of tube) and η (viscosity) generally stay constant
r changes (vasodilation/vasoconstriction)

50
Q

flow is ____ to resistance

A

inversely proportional
F ∝ 1/R

51
Q

relationship of flow with pressure difference and resistance

A

F ∝ (ΔP)/R

52
Q

pulse is?

A

pulse is increase in pressure caused when ventricles contract and push blood into aorta

53
Q

2 parts make up blood pressure

A
  1. systolic pressure: time when heart is contracting (highest arterial pressure)
  2. diastolic pressure: time when ventricle relaxes (lowest arterial pressure)
54
Q

estimation of blood pressure is done by ___. what is that?

A

sphygmomanometry
use of pressure pressure cuff & stethoscope

55
Q

sphygmomanometry steps (5)

A
  1. inflate cuff (cut off blood flow)
  2. cuff gradually deflated; when pressure in cuff = systolic pressure -> blood flows again
  3. turbulent flow results in sound -> Korotkoff sound (with each heartbeat)
  4. cuff pressure further reduced
  5. eventually all sound stops (flow no longer turbulent) -> diastolic pressure
56
Q

what is MAP?

A

Mean Arterial Pressure:
since arterial pressure is pulsatile, use 1 value to represent driving pressure

57
Q

mean arterial pressure formula

A

mean arterial pressure =
diastolic P + 1/3(systolic P - diastolic P)

58
Q

factors affecting mean arterial pressure (3)

A
  1. cardiac output
  2. changes in blood volume (normally constant)
  3. peripheral resistance
    - largely controlled by arterioles w lots of smooth muscle to modify diameter
    - small changes in radius -> large changes in resistance
    - influenced by both reflex & local control mechanisms
59
Q

regulation of blood pressure is coordinated by?

A

CNS -> homeostatic reflex

60
Q

how is blood pressure monitored?

A

blood pressure monitored by baroreceptors (stretch sensitive mechanoreceptors found in vessel walls of the:)
- carotid artery -> monitors blood pressure to brain
- aorta -> monitors blood pressure to body

61
Q

blood pressure regulation steps (7)

A

baroreceptor reflex based on higher blood pressure:
1. membrane of baroreceptor stretches
2. increase firing rate of receptor
3. APs travel to cardiovascular control centre in CNS (medulla)
4. control centre integrates sensory input
5. efferent output carried by autonomic neurons
6. decrease in sympathetic output & increase in parasympathetic output, causes:
- vasodilation
- decrease in force of cardiac contraction and heart rate
- decrease in peripheral resistance and cardiac output
7. decrease in blood pressure (negative feedback loop)

62
Q

what is blood

A

the circulating component of ECF responsible for carrying substances around body

63
Q

4 major components of blood

A

plasma
red blood cells (erythrocytes)
white blood cells (leukocytes)
platelets (thrombocytes)

64
Q

plasma

A

fluid portion of blood

65
Q

red blood cells (AKA, characteristics, major function)

A

AKA erythrocytes
- biconcave shape
- most abundant cells in blood
- contain protein haemoglobin
- major function: gas transport (CO2, O2)
- in humans (mammals), lack nucleus & mitochondria

66
Q

white blood cells (AKA, function, types (mnemonic))

A

AKA leukocytes
- immune responses
i. lymphocytes
ii. monocytes (macrophage)
iii. granulocytes (3 types)
- neutrophils
- eosinophils
- basophils (mast cells)

macrophages and neutrophils are professional phagocytes

67
Q

platelets (AKA, function, derived from)

A

AKA thrombocytes
- blood clotting
- derived from megakaryocytes -> pinch off and have no nucleus

68
Q

haemoglobin synthesis

A
  • synthesis of haemoglobin required for RBC to transport O2
  • large complex molecule made of 4 protein chains (globins)
  • each globin subunit is wrapped around an iron-containing haeme group
  • haeme group C-H-N porphyrin ring contains an Fe in centre
    – haemoglobin synthesis requires adequate dietary Fe -> low Fe can result in anemia
69
Q

haemoglobin/oxygen saturation curve

A
  • curve is S-shaped with a steep portion, followed by plateau
  • highest in alveoli, lower in resting cells
  • diff haemoglobins ave slightly diff dissociation curves
70
Q

haemoglobin binding

A
  • factors can affect haemoglobin-O2 binding, which alter haemoglobin configuration (thus altering its properties)
  • a form of allosteric modification
  • e.g. temp, pH
    – increase in temp, decrease haemoglobin-O2 affinity
    – increase in blood CO2 and H+, decrease haemoglobin-O2 affinity
    – all these factors are elevated in lung tissue (higher temp, PCO2, H+)
    — leading to O2 unloading at lungs (more active, greater increases in PCO2&H+&temp, so more O2 released
71
Q

Bohr effect meaning

A

a shift in haemoglobin saturation due to pH

72
Q

haematopoiesis meaning

A

formation of blood

73
Q

where are blood cells produced?

A

red bone marrow

74
Q

what single precursor do blood cells arise from?

A

pluripotent haematopoietic stem cell

75
Q

haematopoiesis process

A

pluripotent haematopoietic stem cell -> uncommitted stem cells

-> progenitor cells (committed to one or two cell types)

  • path taken is guided by cytokines -> small peptides/proteins secreted by one cell to send signals to another (often called factors with a modifying word, e.g. growth factor, modifying factor)
76
Q

leukopoiesis meaning

A

formation of leukocytes

77
Q

leukopoiesis process

A
  • regulated by colony-stimulating factors (CSFs)
    – CSFs released by endothelial cells, marrow fibroblasts, WBCs
    – induce cell division and cell maturation in stem cells
  • cytokines released by leukocytes -> formation of more leukocytes
    – e.g. active bacterial infection -> release cytokines -> produce more macrophages & neutrophils
78
Q

thrombopoiesis process

A
  • megakaryocytes are parent cells that produce platelets
  • growth and maturation regulated by cytokine thrombopoietin (TPO)
  • cells undergo mitosis up to 7x without nuclear/cytoplasmic division

– megakaryocyte is polyploid w/ a lobed nucleus
— the ends fragment into disk-like platelets (no nucleus), which have mitochondria, smooth ER, granules filled with clotting proteins and cytokines
—- platelets always in blood -> not active unless damage happens to circulatory system walls

79
Q

erythropoiesis meaning

A

formation of RBCs

80
Q

erythropoiesis process

A
  • regulated by erythropoietin (EPO) -> commonly called hormone but is CYTOKINE!
  • EPO is a glycoprotein made primarily in kidney
  • EPO synthesis and release is regulated by hypoxia (low O2)
81
Q

haemostasis meaning

A

“stopping blood” - blood clotting

82
Q

haemostasis details

A
  • prevents blood loss from damaged vessels -> need to maintain integrity of blood vessels
    – blood flow cannot be turned off
    – must be fixed under pressure
    – if patch is too weak, will be blown off
83
Q

haemostasis major steps list (3)

A
  1. vascular spasm
  2. platelet plug to temporarily block break
  3. blood clot to seal break
84
Q

vascular spasm

A
  • like putting pressure on bleeding wound
  • via vasoconstrictive paracrines released by damaged endothelium of blood vessel
  • decreases blood flow in increasing resistance -> promotes formation of platelet plug
85
Q

platelet plug to temporarily block break

A
  • collagen is normally in sub-endothelial layer -> platelets stick & become activated
  • releases cytokines -> activate more platelets
  • activated platelets stick together (aggregation) to form a loss platelet plug -> this slows blood flow in vessel & provides clotting framework
86
Q

blood clot to seal break

A
  • a result of coagulation cascade
  • inactive plasma proteins are activated by either exposure to factor XII to collagen (intrinsic pathway) or exposure to tissue factor III (extrinsic pathway) released from damaged cells
  • several steps in each pathway (intrinsic & extrinsic) which involve protein factors that are turned on to activate next protein factor in pathway
  • both pathways merge into common pathway and lead to activation of thrombin which cleaves fibrinogen into fibrin
  • thrombin also activates factor XIII which cross-links fibrin into long fibres that intertwine to form a fibrin network
  • intertwined fibres reinforce platelet plug, making it a clot
87
Q

excessive clotting produces ___

A

thrombus, a clot which can block blood vessels

88
Q

healing (clot) details

A
  • during clot formation, plasminogen is converted into plasmin by either thrombin or tissue plasminogen activator (tPA)
  • enzyme plasmin dissolves clot -> fibrinolysis
  • as repairs progress, clot slowly shrinks

BIOL 273 Physiology (6 decks)

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