Cardioresp Flashcards
1
Q
Haematocrit (PVC)
A
ratio of volume of red blood cells ( erythrocytes) to total volume ( 45%)
2
Q
Haemopoiesis
A
Formation of new blood cells and platelets
3
Q
Anaemia
A
Reduced haemoglobin or numbers of RBCs, often due to iron deficiency
4
Q
Haemostasis
A
The arrest of bleeding, involving the physiological processes of blood coagulation and the contraction of damaged blood vessels
5
Q
Haemophilia
A
Inability to make blood clots due to factor VIII deficiency ( haemophilia A) or factor IX deficiency ( haemophilia B - Christmas disease) A is more common.
6
Q
Erythrocytes
A
120 day lifespan
Simple cells, no nucleus, and no mitochondria
Biconcave disc, 7.5um diameter
Contain haemoglobin and glycolysis enzymes
RBCs are removed in the spleen, liver, bone marrow (reticuloendothelial cells ) and through blood loss
7
Q
Haemoglobin
A
Carries oxygen from lungs to tissues
Tetrameric protein with 4 globin chains, each with a haem group ( porphyrin with a central ferrous iron ion - Fe2+) capable of reversible binding oxygen
Several phenotypes exist :
Haemoglobin A - 2 a chains and 2 b chains ( 97% of adult population)
Foetal haemoglobin (HbF) 2 a, 2 y
HbA2 - 2 a, 2 d
Mutati9ns or absconded of a or b chains in adults referred to as thalassemia, potentially cashing anaemia
8
Q
Precursors of mature cells is adults and children
A
In adults are derived from the bone marrow of the axial skeleton ( not limbs) but all bones in children.
In embryos, it is in the yolk sac, liver, spleen, and bone marrow.
Stem cells are pluripotent and can differentiate into any RBCs, white blood cells ( leukocytes) or platelets
9
Q
Erythropoiesis
A
Production of RBCs
Hormonal stimulating factor - erythropoietin ( EPO) made in the kidneys. Low level constant release but also in response to hypoxia
10
Q
Myelopoiesis
A
Production of WBCs
Hormonal factor : granulocyte - macrophages colony stimulating factor (GM-CSF)
will only stimulate production of myeloblastic WBCs and not lymphoid cells
11
Q
Two types of leukocytes
A
Granulocytes - eosinophil, neutrophil, basophil
Agranulocytes - monocytes, lymphocytes
12
Q
Eosinophils
A
Stains orange
Bi-lobed nucleus
IgE receptors
Antagonistic to basophils : lowers mast cell histamine secretion
13
Q
Neutrophils
A
Don’t stain
( phagocyte - engulfs pathogens )
Granules -
1. Lysosomes - myeloperoxidase and acid hydrolyses
2. Inflammatory mediators
3. Gelatinises and adhesion molecules
14
Q
Basophils
A
Satin blue
Mature into mast cells
Express surface ige and secrete histamine
15
Q
Monocytes
A
Reinforce nucleus
Agranulocyte but have granules
Mature into macrophage
16
Q
Lymphycytes
A
Only blood cells that divide
Large nucleus
T cell - 80%
B cell - 20%
Indistinguishable, could be T cell b cell or nk cell
17
Q
T cell origin and maturation site
A
Originate in the bone marrow and mature in the thymus gland
18
Q
B cell origin and maturation site
A
Bone marrow
19
Q
Anaemia
A
Deficiency of Hb, male <130g/l and female <110g/l
20
Q
Anaemia signs and symptoms
A
include pallor, tachycardia, hyperventilation on exertion, malaise and angina in older people.
21
Q
Causes of anaemia
A
Acute blood loss ( haemorrhage )
Production mismatches - hypoplastic ( not enough)
Dyshaemotpoeitic ( ineffective production)
Increased removal of RBCs - haemolytic anaemia
Deficiencies in iron, folate ( macrocytic anaemia) or vitamin B12 ( pernicious)
22
Q
Haemostasis
A
Blood should remain fluid inside vessels and when outside, should clot.
Blood is a fluid inside vessels because :
Platelets and proteins of the coagulation cascade circulate in an inactive state
Endothelial cells , anticoagulant pathway and fibrinolytic pathways ensure fluidity
Bleeding - when blood fails to clot outside the vessel
Thrombosis - clotting inside the vessel
23
Q
Platelets
A
Circulate in an inactive form
Anucleate
Originate from magakaryocytes which enter endomitosis where the chromosomes duplicate but the cells do not divide so more. Chromosomes than normal - polyploidy
Platelets break off from the megakaryocytes
24
Q
Plasma
A
Fluid component of blood ( 55%)
Transportation media that contains water, salt glucose and proteins
Serum is blood plasma without any clotting factors
25
Proteins in blood plasma
Albumin - produced in the liver
-determines oncotic pressure of blood
- keeps intravascular fluid within that space
- lack of albumin leads to oedema
- seen in liver disease and nephrotic syndrome ( loss of protein into urine )
Carrier proteins
Coagulation proteins
Immunoglobulins - produced by activated b lymphocytes
26
Coagulation cascade
Process of blood clotting, ( not platelet plug formation which allows the bleeding to stop by closing the area )
Coagulation helps stabilise the plug
Ultimately converts soluble fibrinogen into fibrin which then forms a stable fibrin clot
27
Two initiating separate pathways the the coagulation cascade
Extrinsic and intrinsic
28
Coagulation cascade extrinsic pathway
Damage to endothelial lining of vessels releases tissue factor which activates factor VII.
TF VIIa then has a direct effect on factor X to initiate common part of the cascade
29
Coagulation cascade intrinsic pathway
Blood contacting endothelial collagen outside the lumen activates factor XII ( serum protease) > XI > IX
Factor X then activated by IXa along with cofactors VIII, phospholipids and ca2+
30
Coagulation cascade common pathway
Xa converts prothrombin ( factor II) into thrombin ( factor IIa)
Thrombin converts fibrinogen (I) into fibrin (Ia) and activates factor XIII
Fibrin and factor XIIIa leads to the cross linking of fibrin and a clot
Thrombin also gives positive feedback on factors V, VII, VIII and XI but also prevents over-coagulation by activating pas in which is fibrinolytic
31
Components of platelets
Plasma membrane
Cytoskeleton
Dense tubular system
Secretory granules
- alpha
- dense
- lysosome
-peroxisome
32
Heart shunts in embryonic development
Bypassing pulmonary circulation - not required in utero
Foremen ovals ( between atria)
Ductus arteriorsus ( pulmonary artery to aorta)
33
Arteries vs vein shunts in embryonic development
Umbilical vein carries oxygenated blood
Umbilical artery carries deoxygenated blood
34
The heart during birth
First breaths of life > lungs expand > the alveoli I. The lungs are cleared of fluid
An increase in the baby’s BP and a significant reduction in the pulmonary pressures reduces the need for the ductus arteriosus to shunt blood > closure of the shunt
These changes increase the pressure in the left atrium of the heart > decrease the pressure in the right atrium > foremen ovale closes > newborn circulation
35
Descriptive embryology
Repeated observation of last mortem specimens to determine stages of development
36
Mechanistic embryology
Experimentation (accidental or deliberate) to determine role of genes / proteins / environmental factors in cardiac development
37
Gastrulation
Mass movement and invagination of the blastula to form three layers - ectoderm, mesoderm ( middle layer) and endoderm
38
What comes from the ectoderm following gastrulation
( outside layer) - skin, nervous system, neural crest ( which contributes to cardiac outflow, coronary arteries )
39
What comes from the mesoderm following gastrulation
Middle layer - all types of muscle, most system, kidneys, blood, bone
40
What comes from the endoderm following gastrulation
Gastrointestinal tract ( including liver, pancreas, but not smooth muscle,) endocrine organs
41
Where is the cardiovascular system derived from
Most is derived from cells situated in the mesoderm ( blood, heart, smooth muscle, endothelium)
Ther is some contribution from the cardia neural crest cells from the ectoderm
42
The heart fields
First heart field - future left ventricle
Second heart field - outflow tract, future right ventricle, atria
The first heart field generates a scaffold which is added to by the second heart field and cardia neural crest
43
Evolution / gene duplication
As organisations evolve, gene duplication occurs sporadically ( from single gene to entire genome ) each copy of each gene can then evolve separately into different ( but related) gene
This accounts for increasing complexity of development
44
Stages of cardiac formation
Formation of the primitive heart tube
Cardiac looping
Cardiac separation
45
Which way is left
All vertebrate hearts have a leftward ventricle
Any mutations are associated with improper left-right positioning ( e.g. kartagener’s syndrome )
During development, the node secretes nodal, which circulates to the left due to ciliary movement
A cascade of transcription factors ( e.g. lefty, pitx2, fog-1) transducer looping
46
Why do we need circulation to
Every cell in our body needs to be bathed in fluid and within 2mm of a source of oxygenation
This reproduces the extra cellular environment of primitive unix and multicellular organisms in the primeval ocean.
47
Arterial system
Conduits of blood ; physical properties ( elastic arteries) increase efficiency whilst regulatory control (muscular arteries) control distribution
48
Parts of the arterial system
Elastic arteries - major distribution vessels ( aorta, brachiocephalic, carotids, subclavian, pulmonary)
Muscular arteries - main distributing branches
Arterioles - terminal branches ( < 300mm diameter)
49
Capillaries
Functional part of the circulation
Blood flow regulated by precapillary sphincters
Between 3-40 microns in diameter
Three types of capillary; continuous ( most common) fenestrated ( kidney, small intestine, endocrine glands), discontinuous ( liver sinusoids)
Slow flow rate ( more nutrient exchange)
50
Venous system
Return blood to the heart
System of valves allows “muscular pumping”
Some peristaltic movement
51
General structure of an artery / vein
Tunica intima ( endothelium basement membrane )
Tunica media ( vascular smooth muscle cells )
Internal elastic laminate
Vasa vasoorum
Tunica adventitious ( fibroblasts)
External elastic lamina
52
Embryology of the circulation
Aberrant embryology accounts for many congenital abnormalities and fetal death
Many of the processes which pattern blood vessels in embryo are also used in post- natal physiological and pathological processes
53
Formation of the primitive heart tube
During the third week of development, the heart is formed from cells that form a horseshoe shaped region called the cardiogenic region
By day 19 ( third week). Two endocardia’s tubes form. These two tubes will fuse to form a single, primitive heart tube.
Day 21 : as the embryo undergoes lateral folding, the two endocardia’s tubes have fused to form a single heart tube
54
Bulbis cordis
Part of the primitive heart tube
Forms most of the right ventricle and parts of the outflow tracts for the aorta and pulmonary trunk
55
Primitive ventricle
Forms most of the ventricle
56
Primitive atrium
Forms the anterior parts of the right and left atria
57
Sinus venosus
Forms the superior vena cava and part of the right atrium
From left and right horns of the primitive heart tube
58
Cardiac looping
By day 22, the heart begins to beat , the bulbis cordis moves inferiority, anteriorly and to the embryos right , the primitive ventricle moves to the embryos left side, the primitive atrium and sinus venosus move superiorly and posteriorly, the sinus venosus is now posterior to the primitive atrium
59
Cardiac septation
At this stage in heart development, there is one common atrium and one common ventricle they are connected by an internal opening called the atrioventricular canal
Blood first enters the atrium
Passes through the atrioventricular canal and into the ventricle then exits through the turn us arteriosus
Masses of tissue called endocardia’s cushions grow from the sides of the atrioventricular canal to partition it into two separate openings.
As the endocardia’s cushions grow together, the atrioventricular canal also is being repositioned to the right of the heart.
The superior and inferior endocardia’s cushions fuse, forming two separate openings that are now called the right and left atrioventricular canals and become the right and left atrioventricular openings of the heart ( now as blood flows through the heart, it will pass from the atrium, through both atrioventricular openings, into the ventricle and up through the truncus arteriosus
60
Days 17-21
Formation of blood islands
Vascularisation of the yolk sac, chorionic villus and stalk,
Vasculogenesis commences
This is added to by angiogenesis
( driven by angiogenic growth factors and takes place via proliferation and sprouting )
61
1st and 2nd aortic arches
Become minor head vessels
1st - small part of maxillary
2nd - artery to stapedius
62
3rd aortic arches
Portion between 3rd and Ruth arch disappears
Become common carotid arteries, and proximal internal carotid arteries
Distal internal carotids come from extension of dorsal aortae
63
Right dorsal aorta and right 4th aortic arch
R dorsal aorta looses connections with midline aorta and 6th arch, remaining connected to r 4th arch
Acquires branch 7th cervical intersegmental artery which grows into r upper limb
Right subclavian artery is derived from right 4th arch, right dorsal aorta and right 7th intersegmental artery
64
Left dorsal aorta and left 4th aortic arch
Left dorsal aorta continues into trunk
Left 7th cervical intersegmental artery, which grows into left subclavian artery
Right subclavian artery is derived from right 4th arch, right dorsal aorta, and right 7th intersegmental artery
65
6th aortic arches
Right arch may form part of pulmonary trunk
Left arch forms ductus arteriosus - communication between pulmonary artery and aorta
66
4 major types of blood
A B AB O
67
ABO antigens inheritance
Mendelian pattern
Gene on chr 9 codes for an enzyme rather than the sugar itself
Another gene codes for the sugar base of the ABO antigen
68
ABO antibodies
Infants <3 months produce a few ( first true abo antibodies >3 months )
Mix of igM and IgG
IgM mainly fro group Aand B.
IgM antibodies don’t cross placenta but rhesus antibody (IgG) can cross the placenta
69
Rhesus antigens
>45 different Rh antigens
2 genes, hromosome 1 ( RHD - codes for Rh D and RHCE - codes for Rh C and Rh E )
Highly immunogenic
Can cause haemolytic transfusion reactions and haemolytic disease of the foetus and newborn ( HDFN)
70
Haemolytic disease of the foetus/newborn (HDFN)
RhD sensitisation most common cause
Develop anti-Rh antibodies
Severe fetal anaemia
Hydrous fetalis
Prevention - detect mothers at risk, maternal fetal free DNA, anti D prophylaxis
( mothers antibodies attacks baby’s erythrocytes
Mother (dd) has kids with DD/Dd
1st child - no immune response- treated like foreign material by the mother because it has no anti-d antibodies
( mother will make rhesus D auntibodies )
2nd child - rapid immune response - Rhd antibodies from birth and attack foetus can ¡dad to anaemia and death.
71
Indirect anti globulin test
( indirect Coombs test)
Blood grouping for ABO and rhesus d
Detects antibodies in patients serum
72
Blood donation exclusion criteria
Temporary- travel, tattoos/body piercings, lifestyle
Permeant - certain diseases, received blood products or organ/tissue transplant since 1980, notified risk of vCJD
73
Indications for transfusions
Hypovolaemia due to blood loss
Severe anaemia with inadequate oxygenation of tissues
Anaemia - check b12 deficiency before considering blood transfusion, not included for iron deficiency of b12 deficiency
74
Early hazards of transfusions
ABO incompatibility reaction - can be fatal
Fluid overload - pulmonary oedema
Febrile reaction - antigens target donor antigens. Can cause life- threatened respiratory failure
Bacterial and malarial infection.
75
Late hazards of transfusions
Rhesus d and other antibody sensitisation
Delayed transfusion reaction
Viral infection, hepatitis b, c and hiv
Prior infection
Iron overload resulting in cardiac, hepatic and endocrine damage
76
Operative erythropoietin alternative to transfusion
Stimulates RBC production
77
Plasma alternative to transfusion
Can be used as it is of fractioned to produce concentrates of specific components such as factor 8 or 9.
78
Fresh frozen plasma alternative to transfusion
Contains coagulation proteins and clotting factors. Used in massive transfusion , dilutions and coagulopathy ( impaired coagulation), liver disease, and disseminated intravascular coagulation ( DIC).
79
Cryoprecipitate alternative to transfusion
Frozen blood rich in fibrinogen. Used in DIC and massive transfusion is there is a lack of fibrinogen in coagulation cascade
80
Platelet use in alternative to transfusion
Used in thrombocytopenia ( low platelet count ) however not useful if deficiency is due to immune anti-platelet antibody
81
Albumin alternative to transfusion
Can be used in cases of oedema to correct the oncotic pressure of blood and keep fluid in. Used in liver disease or nephrotic syndrome
82
Anti-D globulin alternative to transfusion
Collected from people sensitised to D and used to prevent Rh D disease
83
Intravenous immunoglobulin alternative to transfusion
Pooled immunoglobulin, use din immunodeficiency, congenital or acquired and some auto-immune diseases.
84
Cardiac output
Volume of blood ejected by each ventricle per minute
Co = hr x sv
85
Extra-embryonic blood vessel formation day 17-21
Lateral plate mesoderm - blood islands - vasculogenesis
86
Extra-embryonic blood vessel formation day 28
Angiogenesis - proliferation and sprouting - mesodermal cell recruited for tunica media and adventitia
87
Arteries
Low resistance, high pressure - maintain perfusion during diastole
Elastic - largest and closest to the heat x elastin in tunica media / external - expand / recoil to absorb pressure
Muscular - includes coronary arteries, thick muscular walls
88
Arteriole
High resistance
Myogenic auto regulation - increase stretch - vasoconstriction : smooth muscle contraction ( thermogenesis) - more pressure and more perfusion.
89
Capillary
Slow flow - enables time for nutrient/ waste exchange
Continuous, discontinuous or fenestrated
Pericytes regulate flow
Flow determined by : arteriolar resistance, pre capillary sphincters and plasma/ifs flow
90
Vein
Low resistance capacitance vessels : contain 70% of blood volume
Venous return is aided by :
Valves - unidirectional blood flow
Skeletal muscle contraction
Sns mediated vasoconstrictions
Respiratory pump - diaphragm contraction creates pressure difference
91
Sphygmomanometer
Compress brachial artery with cuff above sbp- deflate
Systolic : pressure in arteries when heart beats - 100-150 mmHg x korotohoff sounds start -turbulent blood flow
Diastolic : pressure in arteries when heart is at rest beats 60-90 mmHg - korotohoff sounds stop : laminar blood flow
92
Baroreceptors
Present in the carotid sinus ( carotid artery birfurcation) and aortic arch primarily. Secondary found in vein, myocardium and pulmonary vessels
Afferent - glossopharyngeal nerve to medulla
Efferent - sympathetic and vagus x.
Firing rate proportional to medulla
93
How Baroreceptrs work
Increased bp sensed by baroreceptors which is then sent via the glossopharyngeal nerve ( is) to the medulla where there is increased firing which results in stimulation of parasympathetic ( x) nerves and decrease in sympathetic stimulation
. Results in decreased co and tar. By = co x tpr
94
Arterial baroreceptors
Short term regulation of bp. New baseline formed if arterial pressure has deviated from the normal baseline for more than a few days. Can lead to hypertension if new baseline is higher.
95
Cardiopulmonary baroreceptors
Atria, ventricles and pulmonary artery. When these baroreceptors are stimulated, you have a decreased vasoconstrictor and decreased bo. Decreased release of angiotensin, aldosterone and vasopressin leads to fluid loss - key in blood volume regulation.
96
Blood vessel auto regulation
Is both intrinsic (responds to blood flow ; should be constant)
And extrinsic ( myogenic vasocontriction / dilation)
Myogenic tone of blood vessels - smooth muscle never relaxes
97
Hyperaemia
Increased blood flow
Active - metabolic response ( increases intensity e.g. excersize )
Reactive - occluded tissue - once removed more blood flow to it
98
Peripheral chemoreceptors
Aortic arch and carotid sinus
Sensitive to
High co2
Hypoxia ( low oxygen)
And low ph
Will always act ina sympathetic way to increase blood pressure
Does this by sending impulses to the pressor region of the medulla
99
Arterial baroreceptors
Aortic arch and carotid sinus
Responds to high bp
More distortion of baroreceptors means higher firing rate
Sends impulses to depressor centre of medulla
Lowers bp in a parasympathetic way
100
Cardiopulmonary baroreceptors
In atria ventricle and pulmonary artery
Responds to high blood volume
Increased by - increased bp = more distorted baroreceptors
Impulses to depressor region of medulla
Lowers bp in a parasympathetic way
101
Central control of circulation
Medulla
Two centres
Pressor - sympathetic
Depressor - parasympathetic
102
Cardiac output equation
Stroke volume x heart rate
103
Blood pressure equation
Cardiac output x total peripheral resistance
104
Pulse pressure equation
Systolic - diastolic
105
Mean arterial pressure equation
Diastolic pressure + 1/3 of pulse pressure
106
Pouisseile’s law
Blood flow = (pi) r ‘4/ 8 x length x viscosity
107
Frank starling law
Higher end diastolic volume ( more vent filling) = harder contraction
( higher edv means more myocytes stretching - contraction strength - higher stroke volume so higher cardiac output
108
Starling forces acting of blood vessels
Force keeping blood in = oncotic pressure ( by albumin pressing on by walls )
Force squeezing fluid out = hydrostatic pressure ( by more pressures of fluid inside - pressure gradient high to low )
109
Controlling blood pressure long term
Fluid intake
RAAS
ADH
Failing hearts go have a lower cardiac output
We can treat by increasing sv ( increase volume of extra cellular fluid by giving blood ) or increase hr
110
regulating circulation
Vasodilators
Hypoxia
Low ph / high h+ / high co2
Bradykinin
NO
prostacyclin ( ( released by healthy endothelium)
High K+
Acetylcholine (Ach) - acting on muscularinic type 2 receptors
ANP ( released by dialated atria when bp high j
Vasoconstrictors
Endothelin 1 ( released by injured endothelium)
Angiotensin II
ADH
NAd ( noradrenaline)
111
Stroke volume
Ventricular ejection at systole
112
Co
Ventricular ejection / unit time
113
TPR
total peripheral systemic resistance ( highest in the arterioles)
114
Preload
Amount of myocyte stretch in ventricular filling ; ( a volume )
115
After load
Resistance myocytes contract against in ventricular systole ( a resistance)
116
Contractility
How hard heart beats
117
Compliance
How easily heart fills in diastole
118
Diastolic distensibility
Pressure to fill ventricles at diastole to edv
119
Parasympathetic and sympathetic effects of cv system
Parasympathetic
ach - muscularinic type 2 (M2) receptors
Decrease in hr (chrinotropic )
Decrease in force if contraction ( ionotrophic )
Sympathetic
Noradrenaline- beta 1 (B1) receptors in heart
( increase hr - positive chronotropic )
Increase in force of contraction- positive ionotropic )
120
Pulmonary vs systemic vessels
Pulmonary
Thin walled
Hypoxia - vasoconstrict
Sys/ dia pressure - 25/8 ( trying to oxygenate deoxygenated blood from right side of the heart - only passing through the lungs so can’t have too high pressure )
Too high pressure can cause oedema- as hydrostatic pressure in vessels would be too big to withstand keeping fluid inside )
Systemic
Thick walled
Hypoxia - vasodilate
120/80
121
Precursor to all blood cells
Haematocytoblast - pluripotent
Proerythroblast - rbc
Monoblast - monocyte
Lymphoblast - t + b lymphocyte
Myeloblast - progranulocyte - basophil, eosinohil, neutrophil
Megakaryoblast - megakaryocytes - platelet
122
Granulocyte
Have visible granules
Neutrophils, (inflam response, multilobed, faint granules
eosinophil, ( antihistamines, pink granules, IgE receptors
basophil ( histamines, dark blue granules, IgE receptors
123
Agranulocytes
Monocytes - ( immature, become macrophages and arcs, reinforce nucleus
Lymphocytes ( cell mediated innate response, very little cytoplasm, mostly nucleus
124
Platelets
Megakaryocyte undergoes endomitosis ( dna doubles but cell doesn’t divide
C.s.m “ blebs “ ( ejects fragments = platelets )
Inactive platelets - smooth and discoid
Activated - increase sa and pseudopoid
Release e- granules ( energy)
Adp, ca2+, atp, serotonin
And dense granules ( scaffold )
Fibrinogen, pdgf ( platelet dense growth factor ) , heparin antagonist
125
Too high or low platelets
High - thrombocytosis ( more clots )
Thrombocytopenia ( cutes can cause bleeding)
126
Vascular contraction
Step before platelet plug formation
Endothelin 1 from damaged endothelium = vasoconstriction
( healthy endothelium = prostacyclin and NO release vasodilates and keeps vessels open
127
Platelet plug formation
Con willebrand factor ( vwf) ( factor 8) binds to exposed collagen at injured endothelium ( using the platelet receptor factor GP1b).
Platelet adhesion - bind to VWF on collagen via GP IIa / IIIb
Platelet activation - exocytosis of dense and e- granul3s - result = amplified +ve feedback to activate more platelets
This forms initial platelet plug
128
Coagulation cascade following platelet plug formation
Forms a mesh of fibrin 1 over primary platelet plug to form a stable secondary platelets plug
Intrinsic pathway - uncommon, trauma inside the blood vessels ( internal endothelial damage)
Factor 12 - 11 - 9 - 8 -10
Extrinsic pathway - common, extra vascular trauma
Tissue factor 3 from damaged tissue activates 7 then 10
Common pathway - 10 in centre - activates 2 ( with the help of 5) ( prothrombin- thrombin)
2 activates 1
Fibrinogen - fibrin
129
Hydrolysis the secondary platelet plug
tPa ( tissue plasminogen activator ) converts plasminogen to plasminogen
Plasmin eats fibrin; fibrin - fibrinogen (. It’s inactive form )
All clotting factors bar VIII ( VWF) produced by the liver
Vitamin k dependant factors are 10 9 7 2
130
Conduction of a heartbeat
SAN ( in wall of the right atrium, in one of the grooves in the right oricle) ( 60-80 bpm autorythmic sinus pattern - Myogenic and doesn’t need any neural signals to beat it does it on its own )
Electrical impulses to atria via bacchman bundles
AVN - delayed about 0.1s for ventricles to;fill
Lower condiction speed As less gap junctions and smaller fibre diameter
Impulses conducted down bundle of his ( spread from right and left ventricles down to the apex of the heart )
Then transmitted to lateral regions of the ventricles by purkinje fibres ( fastest conduction)
131
Myocytic contraction
1. AP wave of depolarisation; Na + influx
2. Plateau phase (2) ; ca ++ in causes ca ++ release via Ryr -2 receptors from sarcoplasmic reticulum ( Ca++ induced Ca++ release)
3. Ca++ binds to troponin c ( protein that sits on top of tropomyosin and inhibits actin forming cross bridges with the myosin)
- changes shape ; removes tropomysin from myosin head. Actin myosin bridges form
After this - atp needed to break cross bridges ( so myosin can move along / muscle can relax) and to return ca++ to sarcoplasmic reticulum.
132
Excitation contraction coupling ; contractile cell
Phase 4 - resting membrane potential ( -90 mV )
Increase in mV value to the threshold ( -70)
once threshold is exceeded - massive influx in Na+ ( fast sodium ion channels open) - phase 0
This cause’s potential difference of cell to increase to + 20.
Shutting of fast na + channels and transient k + open ( these allow k+ to leave ) causes minor decrease in potential diff in cell.
L type ca ++ channels open ( proportional to rate of transient k + ions leaving ) so charge will not change
Ca ++ L type channels eventually close and more k+ channels open to k+ can leave ( potassium rectifying channels) until rmp is reestablished.
No hyperpolsrisztion as heart muscle is autorythmic and continuous so needs to be consistent.
Refractory periods
Absolute - phase 1 and 2 - no further ap generated at this point
Relative - phase 3 can generate ap but stimulus needed.
133
Nodal cell depolarisation
cells that transmit electrical impulses
Rmp of -60. Threshold -40
T type ca ++ channels open allow small ca ++ influx
L type will open at threshold value and allow a bigger calcium influx
K+ channels open allow k effluent
This sinus rhythm generation needs to be shorter than contractile mechanism
134
ECG reading
P wave - atrial systole ( depolarisation)
QRS - ventricular systole ( depolarisation) and atrial repolarisation
T wave - ventricular repolarisation
135
St elevation
St segment isn’t isoelectric
So ventricles repolarise ( relax ) less
Lowered edv and co
Widow maker - cardiac arrest
136
Pr interval
Start of p to start of qrs
137
12 lead ecg
10 sticky pads
12 leads
A. 3 unipolar - aVR, aVL , avF
B. 3 bipolar - I, II, III ( 4 sticky pads)
C. 6 chest - ( 6 sticky pads)
A & B - 4 pads on each limb ( right leg emitted ; value 0)
- aVL, aVR, aVF correspond in one direction to a sticky pad on e limbs from heart
The 3 pads correspond with each other too ( bipolar leads).
C. 6 chest leads
V1-V6
138
Heart views of the 12 lead ecg
Septal - v1v2
Anterior - v3v4
Lateral - v5v6 II aVF
inferior - II IIaVF
139
What part of heart does the RCA supply
SAN, AVN, post IV septum
140
What part of heart does the RMA supply
RV & apex
141
What part of heart does the PDA supply
RV, LV, post 1/3 IV septum
142
What part of heart does the LCA supply
LA, LV, septum, AV, bundle of his
143
What part of heart does the LAD supply
Ant 2/3 of IV septum, RV, LV
144
What part of heart does the LMA supply
LV
145
What part of heart does the circulflex artery supply
LA, LV
146
Heart failure
Systolic failure - heart doesn’t pump hard enough
Diastolic - heart doesn’t fill to full volume
Left failure x blood backs up in lungs - pulmonary oedema
Right failure - blood back up in rest of body - peripheral oedema ( most commonly legs )
