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Phase 1 > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is the structure of erythrocytes? What is their lifespan? Where are they removed?

A
  • Simple cell, anucleate, discoid, biconcave disc
  • Live for 100-120 days
  • O2/CO2 carrier
  • Contain haemoglobin and glycolytic enzymes
  • Formed: adults = bone marrow of axial skeleton, children = all bones, foetus = liver, spleen and yolk sac
  • Removed in spleen, liver, bone marrow + through blood tests
  • Reticulocyte = immature RBC, not usually found in blood
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2
Q

What is the structure of haemoglobin? What is its role?

A
  • Tetrameric protein with 4 globin chains, each with haem group (porphyrin with Fe2+) = capable of reversibly binding oxygen
  • Several haemoglobin types:
  • Haemoglobin: 2 alpha and 2 beta chains
  • Foetal haemoglobin: 2 alpha and 2 gamma chains, means it has a higher affinity for oxygen
  • HbA2: 2 alpha and 2 sigma chains
  • Carries oxygen from lungs to tissues
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3
Q

What is haemopoeisis? How are RBCs, WBCs and platelets produced?

A
  • Haemopoeisis = formation of new blood cells and platelets. Adults = precursors of mature cells derived from bone marrow of axial skeleton, but all bones in children. Embryos = in yolk sac, liver, spleen + bone marrow. Stem cells = pluripotent so can differentiate into RBCS, WBCs or platelets.
  • RBC production = erythropoeisis
  • WBC production = myelopoeisis
  • Platelet production = thrombopoeisis
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4
Q

What are the hormonal factors in erythropoeisis, myelopoeisis + thrombopoeisis?

A
  • Erythropoeisis = hormonal stimulating factor = erythropoeitin, made in kidneys
  • Myleopoeisis = hormonal factor = granulocyte-macrophage colony stimulating factor, will only stimulate production of myeloblastic WBCs + not lymphoid cells
  • Thromobopoeisis = hormonal factor = thrombopoeitin, leads to prodcution of megakaryocytes, which platelets bud from
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5
Q

What are leukocytes? What is their role? What are the different types?

A
  • Leukocytes = white blood cells
  • Two main groups, granulocytes + lymphocytes
  • Both involved in immune response, innate = granulocytes, adaptive = lymphocytes
  • Granulocytes:
  • Neutrophil = most abundant WBC, phagocytic and release chemo- + cytokines to induce inflammation. Multi-lobed nucleus, lasts ~10 hours. Granulocyte colony stimulating factor is the regulating hormone for most leukocytes (all the phils)
  • Monocytes = reniform (kidney bean-shaped) nucleus, mature into macrophages which then become tissue resident (common macrophages you should know: Kupffer cells, alveolar macrophages, osteoclasts), lasts 8-12 hours
  • Basophils = bi-lobed nucleus, very prominent dark blue granules of histamine, lasts 8-12 hours. Mature into mast cells, express IgE + release histamine. Mast cells are almost identical to basophils except are tissue-resident and come from a different cell lineage
  • Eosinophils = bi-lobed nucleus that is ‘lozenge-shaped’, distinct granules, lasts 8-12 hours. Role in fighting parasitic infections but also wide range of regulatory functions
  • Lymphocytes - ‘fried egg appearance’, comprise B and T cells (B cells mature in bone marrow, T cells mature in thymus gland). B lymphocytes = plasma cells/memory cells + produce antibodies, T lymphocytes = T helper, T cytotoxic, T suppressor. Lasts 8-12 hours
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6
Q

What do the terms haematocrit, anaemia and haemophilia mean?

A
  • Haematocrit = percentage of RBCs in cellular component of blood
  • Anaemia = reduced Hb, often due to iron deficiency. Two types: impaired production + increased haemolysis
  • Haemophilia = inability to make blood clots due to factor VIII deficiency (Haemophilia A) or Factor IX (Haemophilia B), A more common
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7
Q

What are the causes and symptoms of anaemia?

A
  • Causes:
  • acute blood loss (haemorrhage)
  • production mismatches - hypoplastic (not enough), dyshaematopoeitic (ineffective production)
  • increased removal of RBCs - haemolytic anaemia
  • deficiencies of iron, folate (macrocytic anaemia) or vitamin B12 (pernicious)
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8
Q

What is haemostasis? Why is blood fluid inside vessels?

A
  • Haemostasis = the process to prevent + stop bleeding, is mediated by coagulation (where blood changes from liquid to gel/solid, also known as clotting, 3 main mechanisms = vascular constriction, platelet plug formation and clot formation)
  • Blood should remain fluid inside vessels, should clot when outside
  • Blood = fluid inside vessels as platelets + proteins of coagulation cascade circulate in inactive state, endothelial cells, anticoagulant pathway + fibrinolytic pathways ensure fluidity
  • Bleeding = blood fails to clot outside vessel
  • Thrombosis = clotting inside vessel
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9
Q

What are platelets? Where do they originate from? What is the regulatory hormone? What are the two types of granules?

A
  • Platelets = 2-5um, last 7-10 days, circulate in inactive form + anucleate and discoid but become spiculated with pseudopia once activated, form blood clots (coagulation cascade)
  • Originate from megakaryocytes, 1 megakaryocyte = 4000 platelets = membrane blebbing process
  • Regulatory hormone = thrombopoeitin - produced by liver + kidneys
  • Plasma have 2 types of granules: alpha (coagulation factors, fibrinogen and other clotting mediators) and dense (ADP + platelet-activation mediators)
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10
Q

What is plasma? Which proteins does it contain? What is serum?

A
  • Plasma = fluid component of blood (55%)
  • Transport medium containing water, salt, glucose + proteins
  • Proteins:
  • Albumin = produced in liver, determines oncotic pressure of blood, keeps intravascular fluid within that space, lack of albumin leads of oedema
  • Carrier proteins
  • Coagulation proteins. These are all prodcued by the liver
  • Immunoglobins = produced by plasma cells, key role in immunity + vaccination
  • Serum = plasma without clotting factors
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11
Q

What are the two main systems of erythrocyte antigens?

A

ABO and Rhesus

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12
Q

What are the 4 blood groups of the ABO blood group system?

A
  • A: A antigen, dominant, 40%, has anti-B antibodies, means you don’t attack own cells
  • B: B antigen, dominant, 12%, has anti-A antibodies
  • AB: A + B antigens, universal acceptor, 3%, no antibodies. AB+ is universal plasma donor as no antibodies in plasma
  • O: universal blood donor, 45%, no antigens but anti-A + anti-B antibodies. O- = universal blood donor
  • ABO antigens made from carbohydrates
  • A, B, AB + O are either Rhesus + or Rhesus -. Rh + contains D-antigen + no antibodies. Rh - contains no antigens, has anti-D antibodies
  • When looking at recipient, focus on antibody
  • When looking at donor, look at antigens
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13
Q

What are ABO antibodies generally a mixture of?

A
  • Mixture of IgM + IgG antibodies. IgM antibodies don’t cross placenta but IgG (Rhesus) antibodies do
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14
Q

What are the Resus antigens?

A
  • Series of C, D + E antigens, D = most important
  • High proportion of D negative people will form Anti-D if exposed to D positive blood, can cause Rhesus disease
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15
Q

What is Rhesus disease? How can this be treated?

A
  • D negative woman with D positive father, if baby’s Rhesus D positive antigens cross placenta then mother makes anti-D antibodies that can destroy baby’s erythrocytes by attacking D antigens, baby can become anaemic. As this is first time mother has been exposed to Rh+, baby will be okay. Subsequent baby with Rh+ blood will be affected (Rhesus disease)
  • Treatment = anti-D immunoglobulin injections, prevents mother from making her own anti-D antibodies
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16
Q

How do we perform ABO and Rh D grouping?

A
  • Forward typing = patient’s RBCs mixed with anti-A, anti-B and anti-D (separately). If antibody binds to antigen in blood, colour change
  • Reverse typing = patient’s plasma, add known red blood cells (A or B). Adding know antigen, looking for antibody
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17
Q

What are the the three rules to help remember what blood groups can donate to and receive?

A
  • Group O = no antigens = universal donor
  • Group AB = both antigens = universal recipient
  • Negative can donate to positive but positive can’t donate to negative
  • O- can donate to all, can receive O- only
  • O+ can donate to AB+, A+, B+ and O+, can receive O- and O+
  • A- can donate to AB-, AB+, A+ and A-, can receive O- and A-
  • A+ can donate to AB+ and A+, can receive O-, O+, A- and A+
  • B- can donate to B-, B+, AB- and AB+, can receive O- and B-
  • B+ can donate B+ and AB+, can receive O-, O+, B- and B+
  • AB- can donate to AB- and AB+, can receive O-, A-, B- and AB-
  • AB+ can donate to AB+, can receive from all
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18
Q

What is a Direct Antiglobulin Test (DAT)?

A
  • Some RBCs may already be coated in antibodies, this method detects them
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19
Q

Which non-RBC components are used in transfusions?

A
  • Plasma = can be used as fractionated to produce specific components
  • White blood cell = rare due to antibiotics that work
  • Fresh frozen plasma = contains coagulation proteins + clotting factors, from male donors only
  • Platelets = used in thrombocytopaenia (low platelet count), ABO type still important even though platelets don’t have red cell antigens as there will be some plasma within unit that contains RBC antibodies)
  • Cryoprecipitate = made by thawing out FFP. Rich in fibrinogen, used in DIC and massive transfusion if there is a lack of fibrinogen required for aggregation + precursor to fibrin in coagulation cascade
  • Intravenous immunoglobulin (IVIg) = made from large pools of donor plasma, contains antibodies to common circulating viruses (normal IVIg), can also be specific (from pateint who’s had disease)
  • Albumin = used in cases of oedema to correct oncotic pressure of blood
  • Anti-D globulin = collected from people sensitised to D + used to prevent Rh D disease
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20
Q

How can we try and avoid transfusion?

A
  • Optimise patients with planned surgical procedures pre-op
  • Use of erythropoeitin stimulating drugs
  • Cell salvage (re-infusing own blood lost in surgery)
  • IV iron for severe iron deficiency
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21
Q

What does gastrulation mean (embryologically)?

A
  • Mass movement + invagination of the blastula to form 3 layers - ectoderm (skin, nervous system, neural crest which contributes to cardiac outflow), mesoderm (all types of muscle) + endoderm (gastrointestinal tract)
  • Most of cardiovascular system derived from cells that were situated in mesoderm. Some contribution from cardiac neural crest cells from ectoderm
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22
Q

What are the two heart fields on day 15?

A

Have no cardiac function. First heart field (red) = future left ventricle. Second heart field (yellow) = outflow tract, future right ventricle, atria

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23
Q

What happens to the heart fields between day 15 and day 50?

A

First heart field generates a scaffold which is added to by second heart field and cardiac neural crest. 4 chambers by day 50

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24
Q

What do the terms gene and transcription factor mean?

A
  • Gene = DNA which when expressed is transcribed into RNA which is translated into protein with a function
  • Transcription factor = type of protein which when expressed ‘turns on/off’ many other gene(s) expression. In heart formation, examples = GATA, Tbx, Fog-1 (expressed in different parts of heart depending on whether they come from FHF or SHF)
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25
Q

What are the 3 stages of cardiac formation?

A
  1. Formation of primitive heart tube
  2. Cardiac looping
  3. Cardiac septation
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26
Q

What happens in the formation of the primitive heart tube?

A
  • During 3rd week, heart formed from cells that form horseshoe shaped region called cardiogenic region
  • By day 19, two endocardial tubes form, fuse to form single primitive heart tube
  • Day 21, embryo undergoes lateral folding, the two endocardial tubes fused to form single heart tube
  • Learn these parts of primitive heart tube and what they become:
  • Truncus arteriosus = ascending aorta, pulmonary trunk
  • Bulbus cordus = smooth (outflow) parts of L + R ventricles
  • Primitive ventricle = forms majority of ventricles
  • Primitive atrium = both auricular appendages, entire L atrium, anterior part of R atrium
  • Sinus venous = smooth part of R atrium, vena cavae, coronary sinus
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27
Q

What happens in cardiac looping?

A
  • Bulbis cordis moves inferiorly, anteriorly + to embryo’s right
  • Primitive ventricle moves to embryo’s left side
  • Primitive atrium + sinus venosus (bottom part of heart) move superiorily + posteriorly
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28
Q

How does the body know which way is left?

A
  • All vertebrae hearts have a leftward ventricle
  • During development, the node secretes nodal, which circulates to the left due to ciliary movement. This switches on transcription factors that cause looping
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29
Q

What happens in cardiac septation?

A
  • At this stage, one common atrium + one common ventricle connected by internal opening called the atrioventricular canal
  • Masses of tissue called endocardial cushions grow from the sides of the atrioventricular canal to partition it into two separate openings
  • Superior + inferior endocardial cushions fuse, forming two separate openings (left and right atrioventricular canals)
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30
Q

Picture summary of the development of the heart.

A
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31
Q

Why do we need a circulation?

A

Every cell in our body needs to be bathed in fluid + within 2mm of a source of circulation

  • Heart - arterial system, capillaries, venous system - heart
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32
Q

What are the features of the arterial system? What type of arteries come away from the heart?

A

Elastic to increase efficiency, muscular to control distribution. Arteries coming away from heart = elastic arteries = aorta, subclavian, pulmonarc etc. Muscular arteries = main distributing branches. Arterioles = terminating branches

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33
Q

What are the 3 different types of capillaries?

A

Capillaries = functional part of circulation, blood flow regulated by precapillary sphincters. 3 types:

  • Continuous (common)
  • Fenestrated (kidney, small intestine, endocrine glands)
  • Discontinuous (liver sinusoids)
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34
Q

What is the function of the venous system?

A
  • Return blood to the heart
  • System of valves allows “muscular pumping” (got to get from toes to heart)
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35
Q

General structure of arteries/veins

A
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36
Q

Elastic artery with H&E stain

A
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37
Q

Muscular artery (Van Gieson stain)

A
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38
Q

Arterioles

A
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39
Q

Capillaries

A
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40
Q

Red blood cells in capillaries (H&E stain)

A
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41
Q

Arteries + veins often run side by side

A
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42
Q

Vein with valve shown

A
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43
Q

Do we have blood vessels on day 17?

A

No, we have blood islands

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44
Q

What happens between day 17 - 21 (embryology of circulation)?

A

Yolk sac, chorionic villus + stalk become vascularised

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45
Q

Where does vasculogenesis occur?

A

Lateral mesoderm. Very first axial vessels are formed.

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46
Q

What happens on day 18 (embryology of circulation)?

A

Vasculogenesis commences. Angioblasts from mesoderm coalesce to form angioblastic cords throughout embryonic disc. All other blood vessels arise from this core of central vessels

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47
Q

What happens from day 18 onwards (embryology of circulation)?

A

Vasculogenesis is added to by angiogenesis (driven by angiogenic growth factors + takes place by proliferation and sprouting). Endothelial cells proliferate, causing growth of blood vessels

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48
Q

How do the endothelial cells etc. know where to go?

A

Attractive signals make cells migrate towards them, repulsive signals push the cells away from going in the wrong place. Angiogenic growth factors cause endothelial cells to proliferate

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49
Q

At 29 days, how many pairs of aortic arches do we have?

A

We have 5 pairs of aortic arches (1, 2, 3, 4 + 6). The aortic arches exist during weeks 4-6

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50
Q

What do the 1st and 2nd aortic arches become?

A
  • Become minor head vessels
  • 1st = small part of maxillary
  • 2nd = artery to stapedius

You won’t be able to see these by the 7th week

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51
Q

What do the 3rd aortic arches become?

A

Become common carotid arteries + proximal internal carotid arteries

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52
Q

What do the left dorsal aorta and left 4th aortic arch become? What about the right 4th aortic arch?

A
  • Left dorsal aorta continues into trunk
  • Left 4th aortic arch becomes the arch of the aorta
  • Right 4th aortic arch becomes right subclavian artery
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53
Q

What do the 6th aortic arches become?

A
  • Right 6th aortic arch = pulmonary arteries
  • Left 6th aortic arch forms ductus arteriosus - communication between pulmonary artery + aorta
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54
Q

What are main components of the myocardium?

A

Myocardium = muscles of heart that make up middle + thickest layer of heart wall. Main components:

  • Contractile tissue = composed of cardiac myocytes
  • Connective tissue (keeps contractile tissue together)
  • Fibrous frame (sits in between filling + pumping chambers and holds valve)
  • Specialised conduction system
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55
Q

What is the function of cardiac myocytes? How are they activated? What leads to the heart relaxing?

A
  • Pumping action of heart dependent on contractile proteins in its muscular wall
  • Interactions transform chemical energy from ATP into mechanical energy - this moves blood from s/i v. cava to p.a., p.v. to aorta
  • Contractile proteins activated by excitation-contraction coupling. Action potential arrives (begins) + leads to influx of Ca2+ into cytosol. Ca2+ binds to Ca2+ receptor of contractile apparatus. Movement of Ca2+ into cytosol = passive (high to low conc.)
  • Heart relaxes when Ca2+ is transported out of cytosol by ion exchangers + pumps (low to high conc.)
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56
Q

What are the features of myocardial cells?

A
  • Cross striated myofibrils
  • Plasma membrane regulates excitation-contraction coupling + relaxation
  • Plasma membrane forms part of T-tubule
  • Mitochondria = ATP, aerobic metabolism + oxidative phosphorylation
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57
Q

What is a myocytes composed of?

A

Bundles of myofibrils that contain myofilaments

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58
Q

What is the structure of a myofibril?

A
  • Sarcomere = defines region by Z line on either sides
  • Thick filament = myosin
  • Thin filament = actin along with tropomyosin + troponin
  • H zone = region of sarcomere that only has thick filament
  • I band = contain thin actin filaments and regulatory proteins tropomyosin and troponin + binds to Z line (light)
  • A band = large portion of sarcomere, overlap between thick + thin filaments (dark)
  • M line = proteins that connect central points of thick filament
  • C zone = crosslinks thick + thin filament
  • Z line = anchoring point of thin actin filaments, bisect I-bands
  • Titin = elastic filaments that maintain alignment of sarcomere
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59
Q

What is the sarcoplasmic reticulum, the sarcolemma and the transverse tubules?

A
  • Sarcolemma = plasma membrane of muscle
  • Transverse tubules = invaginations of sarcolemma at Z-line
  • Sarcoplasmic reticulum = myocardial cell organelle, membrane network that surrounds contractile proteins
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60
Q

What is the structure of myosin?

A
  • 2 large heavy chains, responsible for 2 globular heads on myosin end which would join with actin
  • 4 light chains
  • Globular heads present 40 degrees from each other to maximise chance of connecting with actin
  • ATPase in head of myosin molecule
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61
Q

What is the structure of actin?

A
  • Globular protein, double stranded by monomers folding around each other to form helical structure
  • Has myosin binding site which is partially covered by tropomyosin + held in place by troponin
  • Tropomyosin is a wire like structure that occupies the longitudinal grooves between 2 actin strands. Regulates interaction between troponin, actin + calcium
  • Troponin has 3 subunits:
  • TnI = inhibitory. Inihibits actin + myosin interaction
  • TnT = tropomyosin binding. Troponin binding to tropomyosin
  • TnC = calcium binding. High affinity calcium binding sites which signal contraction + drives TnI from myosin binding site, allowing interaction between actin + myosin. When Ca2+ binds to TnC, TnI moves away from groove. Re-alignment of tropomyosin in groove brings actin closer to myosin heads (Z-lines get closer together). TnC-Ca2+ bond required energy from ATP hydrolysis to break bond + allow groove to be partially blocked by TnI again
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62
Q

Describe the excitation-contraction coupling.

A
  • Action potential arrives along sarcolemma + passes down T-tubule + depolarises membrane, causes Ca2+ channels to open = increase of Ca2+ in sarcoplasmic reticulum
  • Leads to release of Ca2+ from sarcoplasmic reticulum into cytosol
  • Ca2+ binds to TnC which pulls TnI away from groove with tropomyosin
  • This allows globular head of myosin to interact with groove of actin filament. Crossbridge formation
  • ATP required for contraction and ATP hydrolysis (ATPase on myosin) breaks apart the Ca2+-TnC bond + groove of actin is partially blocked by tropomyosin + TnI subunits
  • Power stroke action by myosin leads to sliding action if actin along myosin, shortening sarcomere + causing contraction
  • Crossbridge formation + release of Ca2+ from TnC requires ATP hydrolysis
  • Contraction stops when cystolic (Ca2+) returns to initial
  • Force of contraction depends on levels of CYSTOLIC Ca2+
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63
Q

What happens to contractions during hypoxia?

A

Anaerobic respiration of muscle only maintains muscle for survival but not contraction

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64
Q

What are the 3 events of the cardiac cycle?

A
  • LV contraction
  • LV relaxation
  • LV filling
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65
Q

What composes LV contraction and LV relaxation?

A
  • LV contraction:
  • Isovolumic contraction = pressure rising in ventricle, volume not (b)
  • Maximal ejection = most blood goes out of ventricle as pressure > aortic pressure, aortic valve opens (c)
  • LV relaxation:
  • Start of relaxation + reduced ejection (d)
  • Isovolumic relaxation (e)
  • Rapid LV filling + LV suction (f)
  • Slow LV filling (diastasis) (g)
  • Atrial booster (a)
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66
Q

What happens in ventricular contraction?

A

1) Isovolumetric contraction
- Depolarisation, opening of L calcium tubules, Ca2+ arrives at contractile proteins
- LV pressure rises above LA pressure, mitral valve closing M1 gives us 1st heart sound
- LV pressure rises (isovolumic contraction) > aortic pressure
- Aortic valve opens + ejection begins
- QRS complex
2) Ejection
- Ventricular pressure > arterial pressure
- SL valves open, blood ejected out of ventricle
- Aortic pressure increases as blood ejected out
- Ventricular pressure + velocity of ejection falls as blood is ejected
- Atria begin to fill with blood

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67
Q

What happens in ventricular relaxation?

A

1) Isovolumetric relaxation
- Ventricular pressure < aortic pressure, SL valves close
- Ventricular pressure decreases
2) Passive blood flow
- Atrial pressure > ventricular pressure, AV valves open
- 70-80% of blood passively fills ventricles
3) Atrial booster
- Extra kick to move the remaining blood of out of atria
- PR interval

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68
Q

What happens in ventricular filling?

A
  • LV pressure < atrial pressure and MV opens, rapid filling starts
  • Ventricular suction (active diastolic relaxation) can also contribute to filling
  • Diastasis (separation) is when LV pressure = LA pressure, filling temporarily stops
  • Filling renewed when atrial contraction (booster) raises LA pressure
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69
Q

What is the difference between physiological and cardiological systole and diastole?

A

Systole:

  • Physiological = isovolumic contraction, maximal ejection
  • Cardiological = M1 to A2 (between 1st and 2nd HS)

Diastole:

  • Physiological = diastole starts before A2 then isovolumic relaxation. After you get filling process
  • Cardiological = A2 to M1
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70
Q

What is preload and afterload? What can preload increase with?

A
  • Preload = load present before LV contraction has started (effectively load at end of diastole)
  • Afterload = load after ventricle starts to contract
  • Preload increases with a leaky mitral valve, blood can go back up the atrium, so on next beat the preload = normal + what went back into atrium. Ventricle needs to raise pressure in order to overcome resistance (volume that needs to be pumped), so ventricular wall thickens (hypertrophy)
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71
Q

What is Starling’s Law of the heart? What is the LV filling pressure?

A
  • Larger the volume of the heart, greater the energy of its contraction + amount of chemical change at each contraction.
  • LV filling pressure = difference between LA pressure and LV diastolic pressure
72
Q

What is the force-length interaction?

A

Decrease in length of sarcomere results in lower maximal force produced, e.g. cardiac sarcomere at 80% of its optimal length only has 10% of its maximal force. “All or none” - cardiac sarcomere has to function near upper limit of their maximal length

73
Q

What is the Frank and isovolumic contraction?

A
  • Heart can, during cycle, increase + decrease pressure even if volume fixed. Increasing diastolic heart volume leads to increased velocity + force of contraction = positive inotropic effect
74
Q

What do the terms contractillity, elasticity, compliance and diastolic distensibility mean?

A
  • Contractility = ability to increase its contraction velocity to achieve higher pressure independent of load
  • Elasticity = ability to recover normal shape after systolic stress
  • Compliance = relationship between change in stress + resultant strain (dP/dV)
  • Diastolic distensibility = pressure required to fill ventricle to same diastolic volume
75
Q

What is the pressure-volume loop?

A

Reflects contractility in end-systolic pressure volume relationship, while compliance is reflected at end diastolic pressure volume relationship

76
Q

What is haemostasis? What are the two types?

A
  • Haemostasis is the process to prevent + stop bleeding
  • Primary = platelet plug formation
  • Secondary = coagulation cascade
77
Q

What happens in vascular constriction? What is it mediated by?

A
  • Occurs when vessel is damaged
  • Opposing walls pressed together + walls become sticky allowing the vessel walls to be ‘glued together’ in small vessels (this acts to limit blood flow to the affected area)
  • Mediated by several factors (endothelin-1, neutral control)
78
Q

What is the platelet plug formation?

A

Platelets form blood clots. Platelet plug formation allows the bleeding to stop by closing the area.

79
Q

What happens in the platelet plug formation when endothelial cells lining the blood vessels are damaged? What happens when ADP and fibrinogen are released?

A
  • Endothelial cells lining blood vessels damaged, exposes collagen underneath
  • Healthy endothelial cells release Von Willebrand factors (VWF) that binds to exposed collagen
  • Platelets arrive and have VWF receptor. They bind to VWF. This slows down platelets + causes them to become active
  • Platelet activation causes platelets to change shape (smooth discoid to spiculated + pseudopodia) and causes them to express GbIIb/IIIa
  • Platelets contain 2 types of granules: electron dense granules + alpha granules. Electron dense granules release ATP, ADP, serotonin + calcium and produce energy needed for reactions. Alpha granules release fibrinogen, VWF, platelet derived growth factor + heparin antagonist and are used to create mesh work to capture other platelets
  • ADP released by electron dense granules and acts on P2Y1 + P2Y12 to cause platelet activation + amplification. Platelet activation results in increased expression of GbIIb/IIIa + they crosslink with other GbIIb/IIIa receptors on other platelets by binding to fibrinogen. Enables new platelets to bind to old ones = platelet aggregation = positive feedback
  • Fibrinogen releases by alpha granules + binds to GbIIb/IIIa receptors. Needs to be turned to fibrin.
  • Arachadonic acid can be converted to different products depending on COX enzyme. In presence of COX 1, converted to prostaglandin H2, then to thrombroxane A2. This activates prothrombin into thrombin. Thrombin turns fibrinogen into fibrin. Fibrin creates a network of mesh that captures other platelets
80
Q

What is the coagulation casacade?

A

Process of blood clotting, not be confused with platelet plug formation. Coagulation helps stabilise the plug. It ultimately converts soluble fibrinogen to fibrin which then forms a stable fibrin clot.

Vitamin K procoagulant factors: 1972. Factor 10, 9, 7 + 2

81
Q

Blood clots aren’t supposed to stay around forever. Which pathway breaks them down?

A

Fibrinolytic pathway. Plasminogen - plasmin - fibrin breakdown

82
Q

What happens if low and high doses of aspirin are given? What does this do to the COX enzymes?

A
  • Low dose aspirin inhibits COX1, so less thrombroxane A2, so less aggregation
  • High dose aspirin inhibits both COX1 + COX2, reduction in aggregation
83
Q

Structure of the heart. Learn.

A
  • Semilunar valves = pulmonary + aortic valve
  • Veins carry blood to heart, arteries carry blood away, e.g. pulmonary vein (4) carries oxygenated blood back from lungs, pulmonary artery carries deoxygenated blood to lungs
84
Q

What is the mediastinum? What are the different areas?

A

Mediastinum = located between 2 pleural sacs. Divided into superior and interior via the sternal angle. The inferior mediastinum split into 3: anterior, middle (where heart + pericardium are) + posterior

85
Q

What are different layers of the heart?

A
  • Pericardium = double layered sac. Fibrous pericardium = outer layer. Serous pericardium = simple squamous epithelial layer. Parietal pericardium = lines fibrous pericardium, secretes fluid. Visceral pericardium (epicardium) = covers outer surface of heart
  • Epicardium = covers surface of heart + great vessels
  • Myocardium = muscular middle layer. Contain cardiac myocytes
  • Endocardium = innermost layer, made of epithelial cell layer, lines heart chambers + valves
86
Q

What are the coronary arteries? What is the coronary sinus?

A
  • Coronary arteries = transport oxygenated blood to heart muscle
  • Coronary sinus = delivers less-oxygenated blood to right atrium, as do superior + inferior vena cava
87
Q

What connects the trabeculated + smooth portion the right atrium? What is this the location of?

A
  • Crista terminalis
  • Location of SA node
88
Q

Explain the shape of the action potential graph.

A
  • 4 = resting potential (-90mV) = due to Na+/K+ ATPase (3 Na+ move out for 2K+ that move into cell) + Na+/K+ leak channels (100 K+ out for every K+ in, but Na+/K+ ATPase much more prominent)
  • 0 = rapid depolarisation = threshold reached (-70mV), leads to sodium gated fast channels opening. Na+ enters cells + depolarises for +20mV
  • 1 = partial repolarisation = K+ channels open + K+ leaves cell. Inflow of Na+ stops
  • 2 = plateau = voltage-gated Ca2+ channels open. Ca2+ moves in + counters K channels. Lasts approx. 200ms. Entry of Ca2+ into cell results in contraction of myocyte. Contraction of cardiac muscle longer than skeletal due to calcium channels that cause plateau. Less duration in atria than ventricles
  • 3 = repolarisation = K+ outflow and Ca2+ inflow stops until resting potential reached. Closure of Ca2+ channels, opening of more K+ channels
  • 4 = resting potential
89
Q

Desrcibe excitation-contraction coupling starting with the sinoatrial node.

A
  • SAN = determines heart rate. Hyperpolarisation results in Ca2+ entering which leads to depolarisation of cell
  • Atrioventricular node = wave of electrical activity spreads here. Only exit of of electrical impulse from atria to ventricle. Delays impulse to allow atria to contract + ventricles to fill
  • His-Purkinje system = rapid conduction into ventricles to allow coordinated ventricular contraction. Atrial impulse travels through myocyte so slow transfer of electricity then through large Bundle of His (large fibres with high permeability), leads to rapid spread of conduction in ventricles
90
Q

Does using the sympathetic and parasympathetic nervous system increase/decrease the heart rate? Which neurotransmitters bind to which receptors?

A
  • Sympathetic:
  • increases heart rate and force of contraction
  • norepinephrine binds to beta-1 receptors = increases calcium channel opening
  • slope of pacemaker potential = STEEPER = reaches threshold earlier = increased heart rate
  • Parasympathetic:
  • decreases heart rate
  • ACh acts on muscarinic-2 receptors = activates K+ channels and counters decay = hyperpolarises membrane
  • Also decreases calcium influx = decreases slope of pacemaker potential
91
Q

What do the terms absolute refractory period, effective refractory period, relative refractory period + excitability?

A
  • Absolute refractory period = no stimulus can generate an AP
  • Effective refractory period = large stimulus can generate an AP but it is too weak to conduct
  • Relative refractory period = large stimulus can generate an AP + it can conduct
  • Excitability = ability of myocardial cells to depolarise in response to incoming depolarising current
92
Q

What do arteries, arterioles and capillaries do in circulation?

A
  • Arteries = low resistance, media contain elastic + smooth muscles which cushions systole
  • Arterioles = total arteriolar resistance = total peripheral resistance. Determined by local, neural + hormonal factors. Role in determining arterial pressure + in distributing flow to tissue organs. TPR (total peripheral resistance), vascular smooth muscle determines radius. VSM contracts, decrease in radius, increase in resistance + flow. VSM relaxes, increase in radius, decrease in resistance + flow
  • Capillaries = large area, slow flow + allows time for nutrient/waste exchange. Interstitial fluid/plasma determines ECF distribution. Flow determined by arteriolar resistance + pre-capillary sphincter
93
Q

What do veins and lymphatic do in circulation?

A
  • Veins = low resistance, valves to prevent backflow. Skeletal muscle = contraction of muscle + squeezing blood back to heart. Respiratory pump = inhalation, pushing down of diaphragm leads to increased abdominal pressure. Sympathetic = vasoconstriction. Frank-Starling mechanism - increased volume = increased contraction.
  • Lymphatics = excess fluid/proteins filtered from capillaries, return of interstitial fluid to Cv system. Unidirectional flow aided by lymph vessels, respiratory pump + skeletal muscle
94
Q

What are the equations for cardiac output, blood pressure, pulse pressure and mean arterial pressure? What do the terms stroke volume, heart rate, end-diastolic volume, ejection fraction and end-systolic volume mean?

A
  • Cardiac output = heart rate x stroke volume. It is the amount of blood ejected by each ventricle per minute. Any factor that affects SV or HR affects cardiac output
  • Blood pressure = CO x total peripheral resistance
  • Pulse pressure = systolic - diastolic pressure
  • Mean arterial pressure = diastolic pressure - 1/3 PP
  • Stroke volume = volume of blood ejected by each ventricle with each beat
  • Heart rate = heart beats per minute
  • End-diastolic volume = volume of blood in each ventricle at end of diastole
  • Ejection fraction = percentage of end-diastolic volume ejected with each beat. SV/EDV
  • End-systolic volume = volume of blood remaining in each ventricle at end of systole
95
Q

What is the Frank-Starling mechanism?

A
  • The force of contraction is directly proportional to initial length of muscle fibre WITHIN PHYSIOLOGICAL LIMITS
  • LV systolic volume increases as ventricles get stretched due to increased volume in diastole
  • Stroke volume increases as end diastolic volume increases
  • Increased EDV = increased stretch of muscle fibres = increased interaction between thick + thin filaments = increased force of contraction
96
Q

What is the oxygen dissociation curve? Which factors affect it?

A
  • Oxygen dissociation curves show the relationship between oxygen levels (partial pressure) and amount of oxygen bound to Hb in red blood cells (% saturation)
  • As CO2 or H+ increases, binding affinity of Hb for O2 decreases
97
Q
A

1 - G

2 - H

3 - F

4 - C

5 - J

98
Q
A

1 - B

2 - E

3 - F

4 - D

5 - H

99
Q
A
100
Q
A

1 - B

2 - C

3 - H

4 - A

5 - G

6 - J

101
Q
A

1 - C

2 - E

3 - J

4 - H

5 - D

6 - A

7 - B

102
Q

What does an ECG show? What do the squares show?

A
  • An ECG shows changes in voltage over time + not action potentials. It records the overall change in voltage overtime + not individual sections of the heart.
  • Produces graph of voltage against time. Small square across = 40ms, so big square = 200ms. One small square up = 0.5mV.
103
Q

What do the different parts of an ECG represent? How long should they last?

A
  • P wave = atrial depolarisation (SAN, smaller as atria has less muscle). Mitral valve open, blood moves from A to V
  • QRS complex = ventricular depolarisation = quicker because of specialised fibres portrayed peak. Length between start of P wave + start of QRS wave due to delay at AV node. ISOVOLEMIC CONTRACTION. Aortic valve opens.
  • ST segment = interval between depolarisation + repolarisation
  • T wave = ventricular repolarisation. Aortic valve stops
  • P wave = 60-80ms
  • PQ/PR interval = 120-200ms
  • QRS complex = 80-120ms
  • QT interval = 350-440ms in males, 350-460ms in females
  • ST segment = 100-120ms
  • T wave = 120-160ms
104
Q

What is the difference between an electrode and a lead?

A
  • Electrode = physical connection to a patient in order to measure potential at that point. 10 electrodes = 12 lead ECG
  • Lead = graphical representation of electrical activity in a particular ‘vector’
105
Q

What are the bipolar leads? Where are they put?

A
  • Bipolar leads measure potential difference between two electrodes
  • Forms a triangle between both wrists and left leg. Left + right arm and left leg.
106
Q

What are unipolar leads? What are the first 3?

A
  • Measures potential difference between an electrode (positive) + a combined reference electrode (negative)
  • aVR (right arm), aVL (left arm) + aVF (left leg). Bisect the angles of the triangle. Combine two electrodes as reference, all positive
107
Q

The first 6 are all limb leads. What are the unipolar chest leads?

A
  • V1 = R. of sternum 4th intercostal space
  • V2 = L. of sternum 4th intercostal space
  • V3 = Inbetween V2 + v4
  • V4 = R. of sternum 5th intercostal space
  • V5 = 5th intercostal space anterior axillary line
  • V6 = 5th intercostal space midaxillary line
108
Q

What are the general patterns of the P wave, QRS complex and T wave?

A
  • P wave always positive in all leads except for aVR (-ve). This is because impulse goes from r. atrium to l. atrium. From aVR, this is basically moving away, so it’s -ve
  • QRS complexes. V1 + V2 more anterior + when conduction goes down ventricle, l.v. has more muscle + it locates posteriorly, so peak is -ve because it’s going away. As you come more lateral (V3-V6) the QRS because +ve as more anterior
  • T wave positive in all leads except aVR for same reason
109
Q

What are the components of blood pressure?

A
  • Autoregulation (smooth muscles, stretching results in them contracting = immediate auto regulation). Intrinsic = brain, heart + skin (highly regulated). Extrinsic = temperature via hypothalamus
  • Local mediators
  • Humoral mediators
  • Baroreceptors
110
Q

What are the definitions of these terms:

  • Cardiac output
  • Stroke volume
  • Heart rate
  • End-diastolic volume
  • Ejection fraction
  • End-systolic volume?
A
111
Q

What are some major vasoconstrictors?

A
  • Local:
  • Endothelin-1 (released by endothelium in response to damage, slows blood flow)
  • Hormonal:
  • Adrenaline
  • Angiotensin II
  • ADH
  • Medulla:
  • Pressor region
112
Q

What are some major vasodilators?

A
  • Local:
  • NO
  • Lactic acid
  • Hypoxia (systemic only, vasoconstrictor in pulmonary system)
  • Bradykinin (causes release of NO + prostacyclin)
  • Prostaglandins (specifically prostacyclin)
  • Hormonal:
  • Adrenaline
  • ANP
  • Medulla:
  • Depressor region (works by inhibiting the pressor region)
113
Q

What are baroreceptors? What are primary and secondary baroreceptors? What are cardiopulmonary baroreceptors?

A
  • Baroreceptors = pressure sensors. Play a key role in short-term regulation of blood pressure, blood volume and H2O, RAAS + Na+ are long-term factors in blood pressure control.
  • Primary (arterial) = carotid sinus + aortic arch, secondary = vein, myocardium + pulmonary vessels.
  • Increased BP sensed by baroreceptors, increased firing rate, increase in parasympathetic stimulation + decrease in sympathetic stimulation. This results in decreased CO + TPR. BP = CO x TPR, so BP decreases.
  • Cardiopulmonary baroreceptors = atria, ventricles + pulmonary artery. When stimulated, decreased vasoconstrictor, so decreased BP. Decreased release of angiotensin, aldosterone + vasopressin leads to fluid loss = key in blood volume regulation
114
Q

What are chemoreceptors?

A
  • Chemoreceptors = chemosensitive regions in medulla
  • High PaCO2 = vasoconstriction, increased peripheral resistance + increased BP
  • Low PaCO2 = low medullary tonic activity, so low BP (similar changes with increased and decreased pH)
  • Pa02 has less of an effect on the medulla
115
Q

Are the key central effectors peripheral or central?

A

Peripheral, e.g. blood vessels, heart + kidney (fluid balance). Peripheral = very sensitive to PO2 decrease and PCO2 +pH increase, increased sympathetic outflow = increased TPR. Decreased PO2 decreases parasympathetic output to heart, increases HR, increases CO. Central = most sensitive to CO2 + pH, less so to O2. Increased firing leads to sympathetic outflow = increased TPR

116
Q

What supplies the SA node?

A
  • In 60% it’s the right coronary artery
  • In 40% it’s the left coronary artery
117
Q

What supplies the AV node?

A
  • 70% RCA only
  • 20% RCA & LCA
  • 10% LCA
118
Q

What are the branches of the right coronary artery? What do these supply?

A
119
Q

What are the branches of the left coronary artery? What do these supply?

A
120
Q

Diagram you should learn

A
121
Q

What is the first branch of the aorta?

A

It’s not the brachiocephalic trunk. It’s actually the coronary artery

122
Q

What does the phrenic nerve innervate? Where does the right phrenic nerve pass into the diaphragm?

A

Diaphragm. Right phrenic nerve passes through diaphragm at IVC opening (T8). ‘C3, 4 + 5 keep diaphragm alive’ as phrenic nerve originates from C3,4 + 5

123
Q

How long should the cardiac cycle last?

A

0.8 s. Systole = 0.3s, diastole = 0.5s. 60/0.8 = 72 bpm average

124
Q

What does the force of contraction in the muscles depend on?

A

Depends on the concentration of cystolic Ca2+. Amount of Ca2+ returned to ECF and SR at end of contraction = amount that entered cytosol during excitation

125
Q

What are is the mean arterial pressure? What are the equations?

A
  • Mean arterial pressure = average pressure during cardiac cycle
  • MAP = diastolic + (1/3*systolic-diastolic)
  • MAP = 2/3 diastolic + 1/3 systolic
  • MAP = CO * TPR
126
Q

Which factors affect stroke volume?

A

Preload, myocardial contractility and afterload

127
Q

Why does an increase in heart rate not necessarily mean a proportionate increase in cardiac output? Also, does does vagal and sympathetic stimulation increase or decrease the heart rate?

A

Duration of diastole shortens, so ventricles have less time to fill, so EDV doesn’t increase as much as expected. Vagal (parasympathetic) stimulation decreases HR (ACh acts on muscarinic-2 receptors), sympathetic stimulation increases HR (noradrenaline binds to beta-1 receptors)

128
Q

What is the pacemaker potential? What are the 3 main stages?

A

In the pacemaking cells of the heart, e.g. sinoatrial node, pacemaker potential is the slow, positive increase in voltage across the cell’s membrane.

  • Phase 0 = opening of voltage-gated Ca2+ channels, depolarisation due to influx of Ca2+
  • Phase 3 = closure of Ca2+ channels, opening of voltage-gated K+ channels, repolarisation due to efflux of K+
  • Phase 4 = closure of K+ channels, Na+ in via HCN channels, Ca2+ in via T-type channels
129
Q

What is the pacemaker potential controlled by?

A
  • Sympathetic stimulation (increases heart rate + force of contraction)
  • Parasympathetic (Vagal) stimulation (decreases heart rate)
130
Q

What are the 3 main phases of the pacemaker potential?

A
  • Phase 0 = opening of voltage-gated Ca2+ channels, depolarisation due to influx of Ca2+
  • Phase 3 = closure of Ca2+ channels, opening of voltage-gated K+ channels, repolarisation due to efflux of K+
  • Phase 4 = closure of K+ channels, Na+ in via HCN channels, Ca2+ in via T-type channels. Automacity of SA node is due to SPONATANEOUS DIASTOLIC DEPOLARISATION (Phase 4) because of the always open HCN Na+ channels = pacemaker potential, technically there isn’t a resting membrane potential but a restless one
131
Q

What is the primary pacemaker?

A

Primary pacemaker = SA node. Others, e.g. AV node are pacemakers but slower

132
Q

Vasoconstriction increases blood pressure, but what happens to the flow?

A

Decreases flow to that region as blood is shunted to other lower resistance areas

133
Q

In chronic hypertension, what happens to baroreceptors and hence the firing rate?

A

Baroreceptors reset to regulate elavated blood pressure. Firing rate of baroreceptors decreases in response to chronic hypertension. Medullary cardiovascular centres also adapt to elevated pressure = new normal

134
Q

What is the carotid sinus innervated by?

A

Glossopharyngeal nerve

135
Q

What type of cells is the endocardium comprised of?

A

Endothelium cells

136
Q

Define cardiac output and give the equation. What factors affect cardiac output?

A
  • CO = SV x HR, amount of blood output by the heart every minute
  • Any factor that affects stroke volume and/or heart rate affects cardiac output
137
Q

Which vessels provide the most to TPR?

A

Arterioles

138
Q

How long is the cardiac cycle?

A

0.8s, systole 0.3s + diastole 0.5s

139
Q

What does the 5th aortic arch become?

A

Nothing

140
Q

What is the most external structure in the artery?

A

Adventitia

141
Q

What is the effect of increased central venous pressure on stroke volume (in normal individual)?

A

Increases SV - because this would increase preload

142
Q

What phase of the action potential of a cardiac myocyte is shown by the T wave on an ECG?

A

Phase 3; rapid depolarisation of contractile cells

143
Q

Does the medullary pressor region send impulses via the sympathetic or parasympathetic route?

A

Sympathetic - to the heart

144
Q

What structure electrically insulates the ventricles from the atria?

A

Fibro-granular rings around the AV valve

145
Q

What is blood composed of?

A
  • Cellular component (45%):
  • Erythrocytes (99.1%)
  • Leukocytes (neutrophils, eosinophils, basophils, monocytes + lymphocytes) + platelets (0.9%)
  • Plasma component (55%):
  • Proteins (albumin + carrier proteins, coagulation factors, immunoglobins)
  • Water
146
Q

What are the two types of transfusions? What is cross matching?

A
  • Types:
  • Homologous (emergency transfusion)
  • Autologous (self-tranfusion)
  • Cross matching = test to see if donor’s blood is safe for recipient, recipient serum mixed with donor’s blood. If blood not safe, transfusion reaction (rejection)
147
Q

Extra facts to learn about embryology for SBA and spotter.

A
  • Heart appears in 3rd week (starts beating ~day 23)
  • Constriction of ductus arteriosus > ligamentum ateriosum 10-15 hours after birth
  • Obstetrical climbing = constriction of umbilical vein > ligamentum teres
  • Increased L atrial pressure + decreased R atrial pressure due to first breath causes foramen ovale to close > fossa ovalis
  • Ductus venous constricts > ligamentum venosum shortly after birth
148
Q

Which factors affect cardiac output? Which factors affect stroke volume? Which factors affect preload and afterload?

A
  • CO = SV x HR
  • SV affected by preload, afterload and contractility
  • Preload = ventricular wall stress at end of systole = EDV. EDV determines force of contraction due to stretch of myocardial wall - based on Frank-Starling law, where stroke volume depends on force of contraction (increased EDV = increased stretch of myocardium = increases length of overlapping filaments = increased force of contraction = increased stroke volume. After max. stretch reached, little overlap between actin + myosin, lots of unbound myosin heads, decreased force of contraction, decreased volume)
  • Preload affected by atrial contractility, venous return, ventricular compliance, valvular resistance, heart rate
  • Afterload = ventricular wall stress during systole, amount of resistance ventricles must overcome during systole, indirectly proportional to SV (unlike preload)
  • Afterload affected by valvular diseases, aortic pressure and SVR/TRP
149
Q

What is the path of the action potential?

A
  • Excitation initiated in SA node, spreads atria and AV node
  • Impulse CANNOT spread directly from atria to ventricle, only through AV node
  • AV nodal delay = 0.1ms, helps ventricles to completely fill before entering systole
  • AV node -> Bundle of His -> Bundle branches -> Purkinje fibres
150
Q

What is blood pressure? What are the different types of pressure?

A
  • Blood pressure = pressure exerted by blood on a given vessel surface area. Delta P = Pi (MAP) - Pf (CVP).
  • Types or pressure:
  • Systolic pressure (point when LV pressure during ejection = aortic pressure during ejection
  • Diastolic pressure = pressure caused by recoiling of arteries during diastole
  • Pulse pressure = SP - DP
  • Mean arterial pressure
151
Q

What is resistance? Which factors affect it?

A
  • Physical/mechanical pushback of blood
  • Factors affecting resistance:
  • Viscosity
  • Vessel length
  • Vessel radius
152
Q
  • What is a universal plasma donor?
  • What ion is responsible for major depolarisation in nodal cells?
  • What is serum?
  • What enzyme is responsible for clot breakdown?
  • Which of the following clotting factors are not vitamin K dependent?
    a) X

b) II
c) IV
d) VII
- Which protein can be a measure in the blood as a sign for myocardial infarctions?
- Which type of vessel is responsible for the total peripheral resistance for the system circulation?
- Which cranial nerve receives input from aortic arch baroreceptors?

  • Which of these is not a factor of cardiac preload?
    a) Venous return

b) Atrial contractility
c) TPR
d) Heart rate

A
  • AB+. O- is the universal blood donor
  • Ca2+ as nodal cells
  • Plasma without clotting factors
  • Plasmin
  • C
  • Troponin T
  • Arterioles have highest resistance to blood flow
  • X - Vagus
  • C
153
Q

Which sentence best describes the relationships of BP & SVR with the parasympathetic nervous system?

A. Parasympathetic nerves decrease peripheral blood vessel diameter thereby decreasing systemic vascular resistance and decreasing blood pressure.

B. Parasympathetic nerves decrease peripheral blood vessel diameter thereby increasing systemic vascular resistance and increasing blood pressure.

C. Parasympathetic nerves do not have a major influence on peripheral blood vessel diameter as blood vessels do not have parasympathetic innervation.

D. Parasympathetic nerves increase peripheral blood vessel diameter thereby increasing systemic vascular resistance and increasing blood pressure.

E. Parasympathetic nerves increase peripheral blood vessel diameter thereby decreasing systemic vascular resistance and decreasing blood pressure

A

C. There is no parasympathetic innervation of blood vessels

154
Q

Which sentence best describes the relationships of SVR & BP with the sympathetic nervous system?

A. Sympathetic nerves increase peripheral blood vessel diameter thereby increasing systemic vascular resistance and increasing blood pressure.

B. Sympathetic nerves increase peripheral blood vessel diameter thereby decreasing systemic vascular resistance and decreasing blood pressure.

C. Sympathetic nerves decrease peripheral blood vessel diameter thereby increasing systemic vascular resistance and increasing blood pressure.

D. Sympathetic nerves decrease peripheral blood vessel diameter thereby decreasing systemic vascular resistance and decreasing blood pressure.

E. Sympathetic nerves do not influence peripheral blood vessel diameter and have no effect on systemic vascular resistance and blood pressure.

A

C

155
Q

Match the following questions to the most appropriate vessel:

Occlusion is most likely to result in a fatal heart attack

A. Right main coronary artery

B. Right circumflex artery

C. Left circumflex artery

D. Left anterior descending artery

E. Left main coronary artery

A

E. Occlusion of the left main coronary artery - it supplies the largest area of heart muscle via its many branches including the left circumflex and LAD

156
Q

Which nerve innervates the pericardium?

A. Phrenic nerve

B. Internal Thoracic nerve

C. T2-T4 intercostal nerves

D. Medial Pectoral nerve

E. Vagus nerve

A

A

157
Q

If the end diastolic volume (EDV) in the average healthy person’s left ventricle is 120mls, what would you expect the end systolic volume (ESV) to be?

A. 50mls

B. 100mls

C. 70mls

D. 10mls

E. 0mls

A

A. Normal stroke volume = 70mls, so 120 - 70 = 50mls

158
Q

Which of these following statements is correct?

A. Atrial systole corresponds to closure of the tricuspid valve

B. Atrial contraction occurs before the P-wave on ECG

C. Ventricular systole corresponds to closure of the pulmonary valve

D. Ventricular volume increases during ventricular systole

E. For part of the cardiac cycle, both atrial and ventricular diastole occur together

A

E. A. Atrial systole opens the tricuspid valve
B. P wave precedes atrial contraction
C. Ventricular systole opens the pulmonary valve
D. Ventricular volume decreases during systole
E. Both atria and ventricles are in diastole during the isovolumetric ventricular relaxation phase of the cardiac cycle.

159
Q

Consider the pressure changes within the heart and decide which pressure is most affected in the following situation:

(Left ventricular end-diastolic pressure, left atrial end-systolic pressure, left ventricular end-systolic pressure, mean aortic pressure, left atrial end-diastolic pressure)

i) Increase in this signifies left heart failure
ii) Increase in this indicates mitral valve stenosis

A

i) Left ventricular end-diastolic pressure
ii) Left atrial end-systolic pressure

160
Q

What is the purpose of the Ductus Arteriosus in the foetal cardiovascular system?

A. Allow blood to bypass the foetal systematic circulation by shunting it from the Aorta to the Pulmonary Artery.

B. Allow blood to bypass the foetal systemic circulation by shunting it from the Left Atrium to the Right Atrium.

C. Allow blood to bypass the foetal lungs by shunting it from the Pulmonary Artery to the Aorta

D. Allow blood to bypass the foetal lungs by shunting it from the Right Atrium to Left Atrium.

E. Allow blood to bypass the foetal Liver by shunting maternal blood to the Inferior Vena Cava.

A

C

161
Q

Cardiac Output is calculated from…

A. heart rate x mean blood pressure

B. stroke volume x systemic resistance

C. heart rate x stroke volume

D. mean blood pressure x systemic resistance

E. mean blood pressure x stroke volume

A

C

162
Q

Pulmonary oedema in the presence of a normal central venous pressure is a sign of:

A. right heart failure

B. biatrial failure

C. left heart failure

D. biventricular failure

E. respiratory failure

A

C. A raised central venous pressure is a reflection of right sided heart failure. Respiratory failure can lead to right heart failure.
Left sided heart failure causes and increase in pulmonary pressure leading to pulmonary oedema.

163
Q

Severe pulmonary hypertension is a cause of

A. biventricular failure

B. right heart failure

C. biatrial failure

D. left heart failure

E. isolated septal hypertrophy

A

B

164
Q

Shortness of breath, severe peripheral oedema and ascites after a heart attack indicates:

A. right heart failure

B. left heart failure

C. biventricular failure

D. biatrial failure

E. isolated septal hypertrophy

A

C

165
Q

Describe the normal pathway of conduction through the heart. Where;

A = Sino Atrial Node (SAN)
B = Bundle of his
C = Contraction of the atria
D = Purkinje fibres
E = Atrio Ventricular Node (AVN)
F = Contraction of the ventricles
  • E, C, A, D, B, F
  • A, C, E, D, B, F
  • A, E, C, B, D, F
  • E, C, A, B, D, F
  • A, C, E, B, D, F
A

A, C, E, B, D, F

166
Q

Which artery most frequently supplies the AVN?

A. Left coronary artery

B. Right coronary artery

C. Left circumflex artery

D. Posterior descending artery

E. Left anterior descending artery

A

B. The RCA supplies the area above including both SA & AV nodes. The LAD supplies most of the area below the AV conducting system, the His-Purkinje system.

167
Q
  • What percentage of blood is fluid and cellular?
  • What is the name for the process of red blood cell formation?
  • What is the hormone responsible for white blood cell production?
  • Name all the cells in the immune system that have a kidney bean shaped nucleus.
  • Why does a neutrophil have a multilobed nucleus?
  • Why are basophils highly granular?
  • What’s the difference between a monocyte and a neutrophil?
A
  • 45% cellular, 55% fluid
  • Erythropoeisis
  • Granulocyte-macrophage colony-stimulating factor
  • Eosinophils and monocyte - macrophages and neutrophils are multilobed not classed as kidney bean shaped
  • Allows it to wrap around the invader
  • Contains lots of histamine
  • Monocytes can divide into macrophages + dendritic cells whilst neutrophils can’t + and neutrophils have a multilobed nucleus whilst monocytes have a kidney bean shaped nucleus
168
Q
  • What chromosome is Rh found on?
  • If someone is Rh positive, do they have Rh antigens or not?
  • Is ABO a peptide or carbohydrate antigen?
  • Which blood group is the universal donor? Which blood group is the universal receiver?
  • Can A+ give to AB-?
A
  • Chromosome 1
  • Yes
  • Carbohydrate
  • Universal donor is O-, universal recipient is AB+
  • No, positive can’t give to negative
169
Q

What is the speed of blood flow determined?

A
  • Arteriolar resistance
  • Number of open precapillary sphincters
  • Cardiac output (thus stroke volume + heart rate)
170
Q

What happens to blood pressure from arteries to capillaries to veins? How about blood velocity?

A
  • Blood pressure falls from arteries to capillaries to veins
  • Blood velocity falls from arteries to capillaries then increases from capillaries to veins
171
Q

Is blood flow the fastest in the centre of the lumen? How about blood flow at the edges? What happens to laminar flow during contraction?

A
  • Blood flow through centre of lumen flows fastest
  • Blood flow at edges is slowest (due to increased friction)
  • Contraction = less blood in centre, so decreased speed, so less flow. Contraction causes turbulence = disrupts laminar flow
172
Q

Key equations:

A
  • Cardiac output = heart rate x stroke volume
  • Blood pressure = cardiac output x TPR
  • Pulse pressure = systolic - diastolic pressure
  • Mean arterial pressure = diastolic pressure + 1/3 pulse pressure
  • Ohm’s law: flow = pressure gradient / resistance
173
Q

What are the Korchoff sounds?

A
  • Lub = atrioventricular close
  • Dub = semilunar close
  • 3rd heart sound = passive filling of ventricles
  • 4th heart sound = ventricular hypertrophy
174
Q

What do the terms positively chronotropic and ionotropic mean? How about negatively?

A
  • Positively chronotropic = heart rate increases
  • Positively ionotropic = contraction force increases.
  • Adrenaline + noradrenaline = more adenyl cyclase = more cyclic AMP = more Na+ + Ca2+ channels activated = threshold met sooner = more frequent firing
  • Negatively chronotropic = heart rate decreases
  • Negatively ionotropic = contraction rate decreases
  • Acetylcholine = less adenyl cyclase = less cyclic AMP = less Na+ + Ca2+ channels activated = threshold met later = less frequent firing
175
Q

What structures make up the right and left heart borders?

A
  • Right heart border = superior + inferior vena cava, right atrium
  • Left heart border = right ventricle, left atria + left pulmonary artery
176
Q

What do the terms inotropic and diastolic distensibility mean?

A
177
Q
A

Phase 1 (17 decks)

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