cardiovascular module

boundaries of mediastinum

superior - superior thoracic inlet/aperture

lateral - lungs

inferior - inferior aperture

contents on trans-thoracic plane (7)

concavity of aortic arch

bifurcation of trachea

bifurcation of pulmonary trunk

azygos vein

thoracic duct

cardiac plexus

ligamentum arteriosum

great veins of thorax

svc

• azygos

• right brachiocephalic

  • internal jugular

  • subclavian

    • external jugular

    • axillary

• left brachiocephalic

  • internal jugular

  • subclavian

    • external jugular

    • axillary

aortic arch vessels

ascending

• coronary arteries

aortic arch

• brachiocephalic trunk

  • right common corotid

  • right subclavian

    • right internal thoracic

      • right anterior intercostal

    • axillary

• left common corotid

• left subclavian

  • left internal thoracic

    • left anteior intercostal

  • axillary

descending

• post. intercostal

pathway of phrenic nerve

c3-c5

posterior to corotid sheath, running on anterior scalene muscle

left - runs over left superior intercostal vein, then aorta

right - runs on right brachiocephalic vein, then svc

runs in front of hilum, between pericardium and parietal pleura, then pierces diaphragm

pathway of vagus nerve

runs in corotid sheath

left - under left superior intervostal vein, on aortic arch, behind hilum

right - on trachea, then oeosphagus

enters abdomen through oesophageal gap

right recurrent laryngeal nerve

a branch of the vagus nerve that loops under the right subclavian artery (brachiocephalic trunk) and ascends to the larynx, providing motor function to the vocal cords.

left recurrent laryngeal nerve

vagus nerve branch that loops around aortic arch

things to consider when selecting central vein for central line (6)

ease of access + user experience

other procedures occuring

risk of arterial puncture or pucnture of other structures

bleeding containment

infection risk

long term placement

phase 0 of fast response action potential

upstroke - external threshold triggers voltage gated Na+ channels → rapid depolarisation

phase 1 of fast response action potential

small repolarisation as iCl channel opens and itoK+ channel opens

phase 2 of fast response action potential

plateau - balance between inward iCa and outward iK1

phase 3 of fast response action potential

repolarisation - time and voltage dependent iK opens for efflux (triggered by depolarisation). iK1 remains open, iCa shuts

phase 4 of fast response action potential

resting potential - voltage dependent iK shuts, leaving iK1 open

differences of slow response action potential from fast response

mainly calcium upstroke, which is slower than Na+

higher resting potential at -60 mV

key features of pacemaker cells

mostly calcium upstroke, some sodium

intrinsic rise in resting potential

what drives rising potential in pacemaker cells

iK is mostly on

iCa - voltage gated

iF = sodium influx activated by hypoerpolarisation

how does psns change pacemaker rate

Ach opens iKAch → deeper hyperpolarisation

how does sns change pacemaker rate

NA increases opening of Ca2+ channels → faster rate of spontaneous depolarisation

measured potential in ecg depends on

actual magnitude of charges (depends on number of cells)

distance between dipole and recording electrodes

orientation of dipole and recording electrodes

main cell types in myocardium

cardiac fibroblasts

cardiomyocytes

endothelial cells

vascular smooth muscle cells

cardiac adipocytes

neurons

intercalated discs

at intercellular junctions, consisting of nexus/gap junctions, fascia adherns and macularadherens/desmosomes

ecm of myocardium

60% vascular

23% glycocalyx

7% connective tissue

6% empty space

4% collagen

l type calcium channels (DHPR)

carry inward calcium current → contributes to AP plateau and trigger for e-c coupling

activated by depolarisation, catecholamines

inhibited by dihydropyridines, low plasma calcium and sr calcium release

ryanodine receptors (RyR2)

in sr, regulated by caclium release from dhpr

myocyte relaxation proteins

sr - serca2a

sl - calcium atpase and ncx

mitochondrial uniporter

serca2a

in sarcoplasmic reticulum

regulated by phosphalamban

2 calcium for every atp

calsequestrin

buffers calcium in sr

35-40 calcium per calsequestrin molecules

ncx

sarcolemma sodium calcium exchange, every 3 na for 1 calcium

forward mode - calcium extrusion

• stimulated by low na+ (repolarisation) →leads to depolarisation due to na+ influx

reverse mode - calcium entry

• stimulated by high Na+ (depolarisation) → contributes ap plataeu phase

surface anatomy of heart

right border = parasternal

left border = midclavicular

dermatomes for heart

t1-t4

transverse pericardial sinus

separates arteries from veins

oblique pericardial sinus

formed by reflection onto pulmonary veins of heart

how would heart look on x ray (normal)

right side = ascending aorta, right atrium, ivc

left side = aortic arch, left pulmonary vein, left auricle, left ventricle + apex

coronary arteries

right coronary artery

• sino atrial branch

• right marginal branch at inferior border

• ascends posteriorly to form av node branch

left coronary artery

• left circumflex branch that goes posteriorly

• left marginal branch along left border

• anterior interventricular banch

posterior descending interventricular branch

coronary sinus

where great and small cardiac veins drain, posterior

force of contraction is modulated by

dimensions of ventricle

rate of automaticity

neurotransmitters

inotropic drugs

frank-starling concept

increased in edv → increase in sv

due to stretch induced increase in cardiac contractility

biphasic response to stretch

rapid - overlap of contractile proteins and myofilament sensitivity

slow - increased calcium influx

factors increasing myofilament calcium sensitivity (6)

decreased acidity

increased sarcomere length

decreased catecholamines

decreased atp

increased caffein

decreased inorganic PO4

how does increasing heart rate affect force of contraction

less time for cytosolic calcium extrusion

more positive resting membrane poential leading to decreased sodium influx and calcium efflux via ncx

loads sr with calcium and amplitude of calcium transient increases

modulatoin of force via sympathetic nerves

increases sa node discharge rate

increases calcium influx

lusitropic - increases sr pump rate

decreases sensitivity of troponin for calcium

impact of beta agonists on force (5)

adenyl cyclase → increased cAMP → activates PKA → phosphorylates

TnI → decreased affinity of TnC

SL calcium channels → influx of calcium

phospholamban → increased sr calcium pump

ryr2 gating → increased sr calcium release

cardiotonic steroids

inhibits sodium pump → increases intracellular sodium → decreases calcium extrusion via ncx → increased sr calcium load

sympathomimetics

act via beta 1 receptors

bipyridines

act via phosphodiesterase, inhibits breakdown of cAMP

atherosclerosis definition

disease affecting innermost layer of large and medium sized arteries

appearing as plaques

tunica intima

endothelium separated by tight junctions → stops fluid from going into underlying tissue

scattered myointimal cells

basement membrane → gives firm anchor to endothelium

tunica media

vascular smooth muscle cell layers → generates basement membrane and regulates flow via contraction

elastic lamina layers

• separate in muscular, prominent in elastic

tunica externa

fibroblasts, leucocytes, nerves, lymphatics, blood vessels

positive risk factors of atherosclerosis

dyslipidaemia

cigarette smoking

hypertension

diabetes mellitus

negative risk factors of atherosclerosis

high levels of hdl cholesterol

moderate alcohol consumption

cardiovascular fitness

endothelial cell injury in atherosclerosis

cased by haemodynamics, chemical insults and cytokines

leads to altered permeability, adhesion of leukocytes and activation of thrombosis

leucocyte migration into developing plaque in atherosclerosis

circulate monocytes adhere to endothelium → differentiate into macrophages → ingest oxidised lipoproteins and turn into foam cells

smooth muscle cell activation and migration in atherosclerosis

activated by growth factors produced by endothelium, macrophages and platelets

proliferate and migrate into tunica intima

accelerated by failure of internal elastic lamina

lipoprotein entry and oxidation in atherosclerosis

lipoprotiens become oxidised in plaques

attracts monocytes

stimulates release of cytokines and growth factors → dysfunction and apoptosis in smooth muscle, macrophages and endothelium

unstable plaques in atherosclerosis

thin fibrous cap

high lipid content of necrotic core

inflammation

causes symptoms due to rupture, haemorrhage, thrombosis and dissection

three common clinical consqeuences of atherosclerosis

myocardial infarction

peripheral vascular disease

cebrovascular disease

sinus venarum

right receiving chamber on posterior wall, smooth

crista terminalis

boundary between atrium and auricle

musculi pectinati

muscle on auricle, parallel

conus arteriosus

smooth wall on right ventricle just before pulmonary valve cusps

reduces turbulence

trabeculae carneae

muscle within ventricles

cross-weaving for uniform contraction

septomarginal trabecula

moderator band, only on right ventricle

where to find first heart sound on surface

left hand, in fifth intercostal space

where to find second heart sound on surface

either side of sternum in second intercostal space

conduction system of heart

sa node → av node → av bundle at crux of heart → right and left bundle branches → subendocardial branches (purkinje fibres)

impact of sympathetic nerves on heart

increased hr, contraction, systemic bp and vasodilation of coronary arteries

impact of parasympathetic nerves on heart

decreased hr, systemic bp and vasoconstriction of coronary arteries

atrial fibrillation - no sinus conduction because no p wave

av node blocks

1 - long pr interval indiciating slowed av node conduction

2 - missing qrs complexes

3 - atria and ventricles contract indepedently

normal p wave duration

120ms

normal qrs width

120 ms

normal ventricular depolarisaion height

1mv

normal qt interval

350 - 440ms

reasons for decreased height of qrs

loss of muscle mass, increased fluid between electrodes and heart

elevation of st segment

indicates myocardial ischemia or infarction

often earliest recognised sign of acute mi

st depression

indicative of subendocardial ischemia

may be seen during abnormal exercise stress tests or with spontaneous angina pectoris

haemostasis

physiological response of blood vessel to injury

how do endothelium inhibit haemostasis

physically insulate tissue from blood

produce NO + prostacyclins → inhibits platelet activation

produce antithrombin → binds and inactivates thrombin

how does endothelium promote haemostasis (4)

produce endothelin → vasoconstriction

loss of barrier exposes underlying tissue → activates platelets and coagulation cascade

von willbrand factor → platelet adhesion to each other + ecm proteins exposed by vessel injury

thromboplastin → activates coagulation cascade

platelet promotion of haemostasis

activated by ecm proteins exposed when endothelium layer is damaged

secrete thromaxane a2, vasoactive amines and adp from granules → promote vasocontriction and platelet aggregation

coagulation cascade promotion of haemostasis

circulating zymogens sequentially activated

thrombin activated → cleaves fibrinogen into fibrin

thrombin also activates platelets

fibin + platelets → stable haemostatic plug

thrombosis

inappropriate activation of physiological mechanisms of haemostasis during life

consists of fibrin, platelets, trapped rbcs and wbcs

in both arteries and veins

virchow’s triad

factors causing thrombosis - endothelial injury, abnormal blod flow and hypercoagulability

artificial surfaces impact on thrombi

activates intrinsic coagulation cascade

bind pro inflammatory compliment cascade proteins

bind other proteins that may activate platelets

causes of turbulence in arteries

narrowing

aneurysms

infarcted myocardium

abrnomal cardiac rhythm

valvular heart disease

causes of stasis in veins

failure of right side of heart

immobillisation

compressed veins

varicose veins

blood viscosity

how does changes to blood flow cause thrombus

platelets come into contact with endothelium

impaired removal of pro-coagulant factors

impaired delivery of anti-coagulant factors

directly cause injury or activation of endothelium

atherosclerotic plaques → pro-coagulant

genetic causes of changes in blood constituents

deficiency of antithrombin III

deficiency of protein C

acquired causes for changes in blood constituent (6)

tissue damage

post-operative

malignancy

cigarette smoke → increased platelet activation

elevated blood lipids

oral contraceptives → increased clotting factors

physiological mechanisms to limit coagulation (3)

restriction to local site of injury

3 natural anticoagulants - antithrombins, protein c and s, tissue factor pathway inhibitor

fibrinolytic cascade → limits size of final clot through plasmin

emboli

intravascular mass carreid by blood flow from origin to distant site

can be thrombus, fat, air, bone marrow, debris, amniotic fluid

azygos system of veins

drains posterior thorax

main azygos vein connects with right superior intercostal, posterior intercostal on right side, acessory hemiazygous and hemiazygous on left

accessory hemiazygous may connect with left superior intercostal vein

left posterior intercostal veins come off hemiazygous veins

then lumbar inferiorly

thoracic duct

lymphatic structure from cisternal chyli in abdomen

drains into left subclavian vein, junction with left internal jugular vein with valve

upper oesophagus blood

subclavian a.→ inferior thyroid a. → inferior thyroid v. → brachiocephalic trunk

middle oesophagus blood supply

thoracic aorta to azygos vein

lower oesophagus blood

left gastric artery and left gastric vein

mean arterial pressure equation

diastolic pressure + 1/3 of pulse pressure