Cardiovascular System 1-3 Flashcards
Why is a CVS important
- Means for transportation of nutrients and oxygen
3 layers of the heart
- Endocardium
- Myocardium – thick muscular layer
- Pericardium (3 layers)
Structure of pericardium
- Visceral layer of pericardium/ epicardium
- Pericardial cavity with 20 –50 mls of pericardial fluid
- Parietal layer of pericardium
- Fibrous pericardium - thick layer
Function of pericardium
- Fixes the heart in the mediastinum and limits its motion
- Prevents overfilling of the heart! = due to inextensible nature of fibrous pericardium
- (Implications in pericardial effusion = excess accumulation of fluid in pericardial cavity)
- Pericardial effusion can progress to stage where cardiac output I compromised = cardiac tamponade
- Lubrication – btw visceral and parietal layers
- Protection from infection – heart is close to lungs which is prone to infections
Innervation of pericardium
- Phrenic nerve (C3-C5) resposnible for somatic innervation of pericardium
- Originates from the neck and travels down thoracic cavity
- Common source of referred pain in pericarditis
Name the 2 Pericardial sinuses
—> little passageways in the pericardium
• Transverse
• Oblique
Transverse pericardial sinus
• Heart loops to bring primordial venous and arterial ends together – forming a primordial transverse pericardial sinus
Oblique pericardial sinus/ reflection
• Pulmonary Veins expand and pericardial reflection is carried out around them to form oblique pericardial reflection
Coronary circulation
- Oxygenated blood received on the right side of ‘ heart
- Supplies it round the body
- Oxygenated blood can’t diffuse into heart muscles – that is why we have coronary circulation
—> supply blood to myocardium
Coronary arteries
→ carries oxygenated blood to myocardium
–> end arteries
do not have sufficient overlap or anastomoses
If there is a block in the coronary artery = area supplied by the artery ischaemia
• Heart is very prone to ischaemia due to this
Coronary veins
→ take up deoxygenated blood from myocardium into right atrium
• All veins drain to coronary sinus (ig cardiac vein)→ right atrium
Aorta - coronary circulation
- Has opening of coronary arteries – which carries oxygenated blood to myocardium
- Coronary veins take up deoxygenated blood from myocardium into right atrium
Right coronary artery
- Supplies right atrium and right ventricle
- Arises from right side of aorta
- Arises from right cusp of aortic valve
- Flows along the coronary sulcus – passes through this groove
- Supplies right side of the heart
3 branches of right coronary artery
Sa nodal
Right marginal
Posterior descending
Sa nodal artery
- Arises from right coronary artery
* Supplies the sa node of heart
Right marginal artery
On the margin
• Goes all the way to the bottom
→ Supplies right ventricle and apex
• Also called the acute marginal artery as it forms an acute angle with the coronary sulcus
Posterior descending artery
• Right artery going all the way to the bottom down the back
- Supplies right and left ventricles and interventricular septum
- Also called as posterior interventricular artery – supplies both ventricles
Dominance
→ defined by which artery gives rise to posterior descending artery
3 types of dominance
Right dominant
Left dominant
Co-dominant
Right dominant
• Right dominance ~70-80%
Right dominance – PDA arising from right coronary artery
Left dominance
• Left dominance ~10%
Left dominance – PDA arising from left coronary artery
Co-dominant
• Defined by which artery gives rise to the PDA
• Co-dominant ~5-7%
Co dominant arise from both right and left coronary arteries
Left coronary artery
Arises from the left cusp of aortic valve
• Flows along the coronary sulcus
3 branches of left coronary artery
- Left anterior descending
- Left circumflex
- Left marginal
Left anterior descending artery
Supplies right and left ventricles and interventricular septum
•Also known as anterior interventricular artery
• Widow maker!! - common place of occlusion in myocardial infarction
Left circumflex artery
• Circumflex = curved or bent
- Arise from left coronary artery
- Supplies left atrium and left ventricle
Left marginal artery
- Also known as obtuse marginal artery
- Forms obtuse angle with coronary sulcus
- Supplies left ventricle
Coronary arteries - name all right t left branches
3 branches of right coronary artery
• Sa nodal artery
• Right marginal artery
• Posterior descending artery
3 branches of left coronary artery
• Left anterior descending
• Left circumflex
• Left marginal
Great cardiac vein
• Drains the same cardiac territory supplied by the LCA
Middle cardiac vein
• Posterior surface of interventricular septum
Small cardiac vein
• Right margin of heart
3 blood vessel types
Artery
Vein
Capillary
Arteries
-> supply oxygenated blood to body
Pulmonary artery - takes deoxy blood from heart to lungs ‘
Veins
→ deoxygenated blood from tissues to heart
Pulmonary vein - oxy blood from lungs to heart
Capacitance vessels
Capillaries
• Exchange of nutrients
• Deoxygenated and oxygenated blood – gas exchange
• Reduced flow in capillaries = more efficient nutrient transfer
‘
3 main layers of blood vessels
- Tunica intimia
- Tunica media
- Tunica externa
Tunica intima
- Innermost lining of the blood vessel
- Lined by endothelium – damage to lining = clot formation
- In large arteries the internal elastic membrane , looks wavy (not in veins or arterioles) marks the outer boundary of the tunica intern
Tunica media
- Middle layer
- In arteries tunica media is the thickest layer - prominent
- Smooth muscle cells (SMC) supported by varying amounts of connective tissue (formed from elastic fibres)
- SMC contraction controlled by ANS (nervi vasorum), hormones, local chemicals
- Arteries have external elastic membrane, this is absent in the veins
Tunica externa / adventitia
• Outermost layer
• Blends into surrounding tissue and stabilises blood vessels
• In thick walled vessels: blood supply→ vasa vasorum (living cells require blood)
• Large arteries and veins contain vasa vasorum – provide nutrients to blood vessel
-arteries it is in tunica adventitia
Veins it is in tunica media
Differences in viewing arteries and veins
- Walls of arteries thicker than the veins
- In cross section arteries appear rounder than veins
- The endothelial lining of constricted arteries is thrown into folds and is pleated- due to elastic lamina in artery
3 vessels in arterial system
- Large elastic conducting arteries
- Medium Muscular (Distributing) Arteries
- Arterioles
Large elastic conducting arteries
- Largest, closest to the heart
- Aorta, pulmonary arteries – recieves large blood volume from left venticle
- Tunica media contains high density of elastic fibers – allows stretch
- Allows even flow of blood between systole and diastole
Medium muscular (distributing arteries)
- Distribute blood to skeletal muscles and internal organs
- More smooth muscle cells instead of elastic fibres
- Further away from heart – lower pressure – less elastic
- Muscular arteries branch
- Distribute blood to arterioles
Arteriole
-> regulates total peripheral resistance tpr, by vasoconstriction) dilation
- Tunica externa absent or very thin
- Tunica media: SMC
- Control blood flow between capillaries and arteries
- Called as resistance vessels
Capillaries -general structure
One layer of endothelium and its basement membrane
• Diameter of one RBC – very small
• Efficient exchange of nutrients
• For nutrient and gaseous exchange
3 types of capillaries
• Three types based on the size of the gaps between the endothelial cells
Continuous
Fenestrated
Sinusoid
Continuous capillary
- Most common
- Endothelial cells are continous
- Very small gap between cells but allows some passage using transport vesicles
- Allows exchange of small moldcules between plsma membrane and interstitial fluid
- in smooth , skeletal muscle and lungs
Fenestrated capillary
- Medium sized gaps
- Fenestrations in endothelial cells
- Allows large things to pass through but not rbc
- Present in kidneys, reabsorption small intestine
Sinusoid capillary
- Large gaps btw endothelaial cells
- Incomplete basememnt membrane – gaps
- Very Large gaps alllow passage of large molecules – plasma proteins and even cells
- Found in bone marrow, liver, spleen
Venous system
- Collect blood from tissues return it to heart
- Pressure much less than the arteries
- Walls are thinner and less elastic
- Capacitance vessels (70% of total blood volume)
- Valves: infoldings of tunica intima = allow one directional flow of blood, prevent backflow
3 parts of venous system
Venules
Medium veins
Large veins
Venules
Collect blood from capillaries
- Resemble capillaries
- Endothelium, thin middle layer with few muscle cells and elastic fibers
- Very thin tunica externa made of connective tissue fibers
- Venules and capillaries are the primary sites of emigration of white blood cells to enter the tissue fluid
Medium veins
- Have all three layers
- Thin tunica media with few SMC
- Thick tunica externa
Large veins
- Have diameters greater than 10mm
- Have all three layers
- Thicker tunica externa
- Include superior vena cava, inferior vena cava
Blood flow and pressure
Pressure gradient maintains flow
• High pressure to low pressure – but resistance can hinder flow
Blood pressure equation
Change in pressure = cardiac output x total peripheral resistance
Cardiac output equation
• Cardiac output = heart rate x stroke volume
Cardiac output definintion
5L/min = normal value (amount of blood ejected by ventricles per minute)
Stroke volume definition
amount of blood ejected from ventricles per beat (approx 70ml/beat)
Velocity definition
- Flow per unit area
- Increasing velocity = increasing flow
- Decreasing velocity = increasing area
Velocity and flow and area
• Surface area of allll small arteries branches is larger than the surface area of just large artery
• Even though diameter of small artery is smaller than large artery
= surface area of all small arteries > large artery sa
Velocity = inversely proportionals to area
• High velocity = low area – large artery
• Low velocity = high area – small artery
Resistance definition
Total peripheral resistance
• Total resistance felt by blood flow as it passes around body
• Consider systemic circulation resistance (not pulmonary)
- Resistance = Pressure difference/ CO
- Resistance = Pressure difference/ Flow
Poiseuille’s Equation:
- resistance
- 𝑅 = 8𝑛𝑙 𝛱𝑟 4
* n= viscosity, l= length of the vessel, r= radius
Poiseuille’s Equation:
Viscosity
= fairly consitent for blood
Viscosity: Increased in
➢ Polycythemia (Increase in RBC)
➢ Dehydration – reduce water contwent
Viscosity: Decreased in
➢ Anaemia (Decrease in RBC)
Poiseuille’s Equation:
Length
Length: Increased with
➢ Weight
➢ Height
Poiseuille’s Equation:
Radius
- Arterioles tend to have the ability to change radius – that is why they are called resistance vessels
- Radius has profound affect on affecting reisstance
Radius: Increased in
➢ Vasodilation
Radius: Decreased in
➢ Vasoconstriction
Series vascular circuits
- All blood must pass through artery, arteriole, capillary, venule, vein
- All resistance adds up
- Total resistance is the sum of all the vessel resistances
Straight line
Parallel vascular circuits
- Capillaries – low radius, but resistance is very low (not high as expected)
- Capillaries branches are arranged in parallel = so resistance significantly decreases
- Lower resistance in parallel
- Arterioles are also parallel to eachother – but parallel to capillaries
- Arterioles have high resistance due to ability to change their radius
2 types of flow
Laminar
Turbulent -
Laminar flow
• Smooth and parallel in straight line
– Silent
– Velocity highest at the centre
– Low resistance
Occurs in most vessel except aorta
Turbulent flow
• All over the place
– Not silent
– High resistance
• Differences in properties allow blood pressure measurement
– in large arteries
– In diseased and narrowed arteries
Systolic blood pressure
Pressure in arteries during systole: 120 mmHg
Diastolic blood pressure
pressure in arteries during diastole: 80 mmHg
Pulse pressure
Systolic-diastolic (difference btw systole and diastole) blood pressure: 120-80: 40 mmHg
Mean arterial pressure
‘more weight to diastolic blood pressure because heart stays in diastole for longer)
• 2/3 DBP+ 1/3 SBP
• DBP + 1/3 PP
Pulse
- Expansion and recoiling of arteries creates pulse
- Pulse indicate heart rate
- Most readily measured at the radial artery, but can be measured at any of the pulse points shown
- Recorded as beats per minute
- Both the rate and the strength of the pulse are important clinically.
- Changes in rate and strength can indicate pathology
Measuring blood pressure
- Inflate cuff .120 mm Hg
- Stops blood supply so no sound in stethoscope
- Slowly decrease pressure to 120, so blood starts to flow through vessel
- Hear Korotkoff sound at systolic blood pressure
- Decrease bp to less than 80 bp – when last sound is heard = diastolic bp
Pericarditis
Swelling and irritation of thin sac like tissue surrounding heart
Cardiac tumponade
Extra fluid build up in space around heart
Apex beat
Impact of heart against wall in systole
5 th intercostal space
Vagus nerve
Parasympathetic nerve suppy to nerve
4 key components of the conducting system of the heart
Av node
Sa node
Bundle of his
Purkinge fibres
Phrenic nerve
Arise in neck c3-c5
- Sensory nerve supply of fibrous pericardium and parietal serous pericardium is
- right phrenic nerve
- left phrenic nerve
Also supply sensation to mediastinal and diaphragmatic pleura
Right phrenic nerve
Follows superior ivc and right border of heart
Descending vertically laterally to right atrium
Left phrenic nerve
Descends obliquely across arch of aorta and the anterior surface of heart related to left ventricle
Topic2
Cardiac cycle definition
sequence of alternating contraction and relaxation of the atria and ventricles with every heart beat = atria and ventricles contract and relax (mechanical), and some electrical events
Systolic phase summary
– Heart chambers are contracted (build pressures)
– Heart pumps the blood
-slightly shorter than diastolic pressure
Av and semilunar values closed
Diastolic phase summary
– Heart chambers are relaxed
– Heart fills with the blood
2/3 of each cardiac cycle
Av values
Atrioventricular values separate atria and ventricle
- tricuspid value separates right atrium and ventricles
- mitral value separates left atrium and ventricle
Values have papillary muscles connected to chorda tendinae to prevent reguirgitation
Semilunar valves
Separate ventricles from pulmonary and aortic circulation
- aortic valve
- pulmonary value
Sa node
pacemaker of the heart
• Specific cells found on base of superior vena cava form sa node
– Near the opening of the superior vena cava – SA node is able to contract faster than the rest of the heart tissue – Sets the pace of cardiac contraction – Pacemaker of the heart – The impulse is spread to the rest of the heart through conductive pathways
Passage of impulses
Sa node to Atria then av node then common bundle, bundle branches which supply ventrcles
5 cardiac cycle phases
- Atrial diastole
- Atria relaxes
- Atrial systole (Mid to late ventricular diastole)
- Early ventricular systole (Isovolumetric contraction)
- Mid to late ventricular systole (ventricular ejection)
- Early ventricular diastole (Isovolumetric diastole)
Atrial diastole
- –> atria relaxes
- —> Increase pressure
- All deoxygenated blood from body fills in RA
- All oxygenated blood from vein pools in LA
When Atrial pressure > ventricular pressure:
• AV valves open
• 70-80% blood moves into ventricles (without contraction, so flow is passive)
SA node fires impulse
• Results in atrial depolariasation
• Atria start to contract = start of atrial systole
Atrial systole (mid to late ventricular diastole)
–> increase atrium contraction due to sa node impulse
= increase atrial pressure
• Rest of the 20% of blood in atria is pushed into ventricles
—> when we are in atrial systole, ventricles are in mid to late ventricular diastole
• EDV – end diastolic volume = all blood is now in ventricles
• Approx 120ml
Clinical point
Atrial systole (mid to late ventricular diastole)
Patients who have problems with efficient atrial systole can still function normally.
• as atrial systole only pushes out remaining 20% of blood
Edv
end diastolic volume = all blood is now in ventricles
• Approx 120ml
Early Ventricular systole (isovolumetric contraction)
—> SA Node signals/ impulses reach ventricles
* Ventricles begin to contract * Av valves close shut as ventricular pressure > atrial pressure = to prevent backflow of blood * AV valves closed→ S1 or lub sound or 1st heart sound
S1 heart sound cause
Closure of av valves in early ventricular systole (isovolumetric contraction)
Isovolumetric contraction –
blood can’t go anywhere, valves are closed and no contraction
Mid to late ventricular systole
—> pressure in ventricle > pressure in aorta/ pressure in outflow tracts (pulmonary artery/ aorta)
• Semi lunar valvues open up - av values close • All blood is ejected into outflow tract = rapid ejection phase = huge amount of blood pumped int outflow tract
• Some blood remains in ventricles: End systolic volume (ESV)
End systolic volume (ESV)
amount of blood remaining in ventricles after ventricle systole
Stroke volume - cardiac cycle
- SV = amount of blood being pumped out per beat
* Stroke volume SV = EDV – ESV
Ventricular diastole (isovolumeitric relaxation)
—> when we are in atrial systole, ventricular are in mid to late ventricular diastole
At this same time atria is in systole all relaxing to fill with blood
• Ventricles start to relax * Semi lunar valves close to prevent backflow * Semilunar valves closed→ Dub sound/2nd heart sound/ S2
Isovolumetric relaxation phase
n early ventricular diastole
• All blood is pumped into outflow tract
• Semi lunar valves close
• Atrioventricular valves close = S 2 heart sound
• Ventricles are slowly relax
• But there is no change in blood movememnt as valves are closed in very early ventricular diastolic phase
Wiggers diagram
2.1 b notes
Wiggers diagram - atrial systole
What is seen
A wave
P wave
Wiggers diagram - atrial systole
A wave
Atrial pressure rises due to atrial systole
Wiggers diagram - atrial systole
Pwave
P wave in an ecg signifies onset of atrial depolarisation
Wiggers diagram - isovolumetric contraction (early ventricular systole)
What is seen
C wave
QRs complex in ecg
Wiggers diagram - isovolumetric contraction (early ventricular systole)
C wave
Closing of mitral value causes c wave in atrial pressure curve
Wiggers diagram - isovolumetric contraction (early ventricular systole)
Qrs complex of ecg
Signifies onset of ventricular depolarisation
Wiggers diagram - mid to late ventricular systole (rapid ejection)
What is seen
X descent
Wiggers diagram - mid to late ventricular systole (rapid ejection)
X descent
Atrial pressure initially decreases as atrial base is pulled downward as ventricle contracts
Wiggers diagram - mid to late ventricular systole ( reduced ejection)
What is seen
T wave of ecg
V wave
Wiggers diagram - mid to late ventricular systole ( reduced ejection)
T wave
Ventricular repolarisation detected by t wave of ecg
Wiggers diagram - mid to late ventricular systole ( reduced ejection)
V wave
Atrial pressure gradually rises due to the continued venous return from lungs
Wiggers diagram - early ventricular diastole ( isovolumetric relaxation )
Dicrotic notch
Dicrotic notch in aortic pressure curve caused by value closure
2 types of valve defects
Stenosis
Regurgitation
Stenosis basic definition
valve doesn’t open enough or properly, obstructs normal blood flow
Regurgitation basic definition
• Valvuar regurgitation/ insufficiency / incompetence = valve doesn’t close properly, causes leakage of blood, backflow
2 types of stenosis
Aortic valve stenosis
Mitral valve stenosis
2 types of regurgitation
Mitral valve regurgitation (left atrioventricular valve)
Aortic valve regurgitation
Aortic valve stenosis - definition
- Less blood passes through valve
- Increases left ventricle pressure
- = left ventricle hypertrophy (push harder to pass blood through narrow valve opening, increased ventricle muscle mass)
Aortic valve stenosis _ causes
- (degenerative) Age = calcified ends of valves over time/ fibrosis
- Congenitial causes (born with) = some may have a bicuspid valve formation rather than the tricuspid structure
- Chronic rheumatic fever = where antibodies released to deal with strep infection have an autoimmune effect –> inflammation and commissural fusion of leaflets
Aortic valve stenosis - effects
Left sided heart failure
• Lead to syncope
• Angina = lack of sufficient blood supply to the heart
• Microangiopathic hemolytic anaemia = force blood through narrow valve at hight pressure can damage rbcs
Aortic valve stenosis - murmur
mumur between s1 and s2 heart sound due to increased ressistance to flow
• Crescendo-decrescendo murmur
Aortic valve regurgitation - definition
Blood flows back into left ventricle during diastole
• Valve leaflets don’t close properly
Aortic valve regurgitation - causes
- Aortic root dilation (dilation of valve leaflets)
* Valvular damage (endocarditis – infammation of endocardium, rheumatic fever)
Aortic valve regurgitation - effects
- Increased blood backflow = increases blood volume in left ventricle = increase stroke volume on next cardiac cycle
- Diastolic pressure decreases
- = higher pressure difference between systole and diastole – causes bounding pulse (head bobbing, Quinke’s sign = flushing red to pale white in nail bed)
- Left ventricular hypertrophy = increased LV pressure
Aortic valve regurgitation - murmur
- Early decrescendo diastolic murmur
* Bouncring red line after s2 phase, due to movement and backflow of blood
Mitral valve regurgitation - definition
Blood flows back into left atrium
Myxomatous degeneration can weaken tissue leading to prolapse
—> papillary muscle and chordae tendineae - normally pull leaflets of mitral valve taught to keep valve closed in systole
= when these prolapse - regurgitation
Mitral valve regurgitation - causes
- Damage to papillary muscle after heart attack
- Left sided heart failure, leads to left ventricle dilation which can stretch valve
- Rheumatic fever can lead to leaflet fibrosis which disrupts seal formation
Mitral valve regurgitation - effects
—> some blood leaks back onto left atria after systole
• Increases preload as more blood enters
• More blood then enters ventricle in next heart cycle
• Can cause left ventricule hypertrophy
Mitral valve regurgitation - murmur
–> holosystolic murmur – due to flow of blood through partilally open mitral valve, lasts the duration of systole
Mitral valve stenosis - definition
Mitral value is narrowed, does not open properly so it blocks blood flow
Mitral valve stenosis - causes
• Rheumatic fever
• Commissural fusion of valve leaflets
• Harder for blood to flow from left atria to ventricle
Increase in left atria blood pressure as it can’t properly expel its blood volume
Mitral valve stenosis - effects
• LA dilation
○ Atrial fibrilation –> increase rsik of thrombus formation and stroke
○ Oessophagus compression–> problems swallowing, dyshpagia
• Pulmoary odeoma
• Dyspnea
• Pulmonary hyertension
Rv hypertrophy =
Mitral valve stenosis - murmur
Snap and diastolic rumble
Jugular venous pulse
- Bedside indicator of right heart function
- No structures impede observed pressure ways
- Observable fluctuations over sternacleidomastoid muscle SCM = distinct ways – for right heart
Points to note on jugular venous pulse profile
Graph on 2.1 c
A- back pressure on IVC due to atrial contraction (largest)
• Pressure wave that reverberates back up to jugular vein
C- tricuspid valve closure (valve between ra and rv)
x – ventricular contraction
V – atrial filling
Y – tricuspid valve opening anf venticular filling
Heart sounds + cause
1 = closure of mitral and tricuspid values 2= closure of aortic and pulmonary valves 3= sometimes present from filling of left ventricle
Why do we increase cardiac output
• Maintain blood pressure
○ Blood pressure = cardiac output x TPR (total peripheral resisstance)
○ Increase bp bring down cardiac output
• Supply should meet demand
Chronotrophic agent
anything that effects heart rate
Tachycardia
High heart rate > 100
Bradycardia
Heart rate below 60 bpm
Average heart rate
• Average heart rate in healthy adult is 60-80bpm
positive chronotropic agents
Things that increase heart rate
- sympathetic nervous system (Epinephrine/norepinephrine)
- Hormones (T3, T4) = increase metabolism
- Body temperature (increase)
- Increased Ca2+ levels (more action potentials)
- Hypoxia and hypercapnia
- Age
How does • sympathetic nervous system (Epinephrine/norepinephrine) increase heart rate
○ heart –> baroreceptors –> medulla —> sympathetic nervous system –> epinephrine/norepinephrine –> stimulate SA and AV nodes
• Hypoxia and hypercapnia
Impact on heart rate
○ Hypoxia = low oxygen in tissues
○ Hyercapnia = high co2
○ Both are due to problems in lungs, detected by chemoreceptors –> brain –> increase respiratory rate –> increase heart rate
Factors that decrease heart rate
negative chronotropicagents
• Parasympathetic nervous system (Acetylcholine)
• Hyperkalaemia (Increased K+ levels) Impact action potentials
. • Decreased Ca2+ levels
How does • Parasympathetic nervous system (Acetylcholine) impact heart rate
○ heart –> baroreceptors –> medulla —> sympathetic nervous system –> acetylcholine –> stimulate SA and AV nodes
3 factors affecting stroke volume
• Preload
○ Stretch of the ventricles
• Contractility
• Afterload
Stroke volume - preload
–> • Amount of stretch of the ventricles in diastole (before pumping out blood) = end-diastolic volume (EDV)
Factors that alter pre load
- Venous return
- Skeletal muscle pump
- Respiratory pump
- Venous tone
- Gravity
Venous return + pre load (edv)
○ Blood being brought back into atria (oxygenated or deoxygenated)
○ Increase venous return = increase preload
Skeletal muscle pump + pre load (edv)
○ Used to pump blood back to heart,
○ More skeletal muscle pump = more contraction
Increase venous return, edv and stroke volume
Respiratory pump + pre load (edv)
○ Inspiration = increase thorax volume = decrease thorax pressure
○ Push diaphragm down in inspiration = increase abdominal pressure = increased venous return - due to suction like effect pulling blood from venous system to heart
Venous tone + pre load (edv)
○ Veins have sympathetic supply, that may tell them to constrict, when veins constrict all blood is pushed up = increased venous return
Gravity + pre load (edv)
○ When person stands up blood turns to pool into legs = decrease venous return slightly
Stroke volume- contractility
Frank starling curve
- Increasing venous return leads to increased left ventricular end diastolic pressure (LVEDP) and volume (‘increased preload’).
- This causes an increase in stroke volume, so that the extra blood is pumped out of the ventricle
- Shows more end diastolic volume = more stroke volume or less end diastolic volume = less stroke volume
→ stroke volume of heart increases in response to an increase in volume of blood in vessels
Inotropic agent
anything that affects contractility
Factors that increase the contractility (Positive inotropic)
• Sympathetic nervous system (Epinephrine/norepinephrine)
○ Impact myocardium, muscle contraction
○ Bind to beta adrengeric receptors in myocardium
* Hormones (T3/T4), glucagon * Drugs -
- increase calcium ion influx during action potential
Factors that decrease the contractility (negative inotropic)
• Beta blockers
○ Blocking the beta adrenergic receptors
• Ca2+ channel blockers ○ Blocking calcium entering cells that is needed by troponin for muscle contraction (refer to FBS) • Increase in K+, Na+, H+
Stroke volume - afterload
—> Afterload: The amount of resistance that needs to be overcome by the ventricles to pump blood to aorta
• Resistance ventricles feel when pushing blood into aorta
Increase in afterload decreases stroke volume (negative relationship)
Factors that increase afterload:
• Semilunar valve damage ‘’
○ Any problem with valves = resistance = increased afterload
• Increased vascular resistance ○ Heart has to push further = increase afterload
Factors that decrease afterload:
• Decreased vascular resistance
○ Decrease afterload
Aortic sinuses
Where deoxygenated blood from heart drains
Trabecular carnae
Ridges in the ventricles
Atrial appendages (auricles)
Hold back blood as ventricles pump
Remnants of fetal atria
Relieve high pressure by increasing atrial capacity at times of stress
Topic 3
Stages of embryology of the heart
Blastulation (week 1) Gastrulation (week 2) Neurulation (week3) Development of heart (week 3) Heart tube Looping of the heart ( 22nd - 23rd day) Septation of the heart (27 th day) Formation of av valves (week 4) Formation of interatrial septum Formation of intravenericular septum Formation of inflow tracts to right atrium Formation of outflow tracts
Blastulation
Oocyte → zygote =cleavage) → morulla → blastocyst
Blastocyst structure
Inner cell mass (embryoblast) Outer cell mass (trophoblast) - cytrotrophoblast - Syncytiotrophoblast = placenta
Gastrulation week 2)
- Inner cell mass differentiates – into 2 discs
• Epiblast
• Hypoblast - Pre chordal plate forms –> where epiblast and hypoblast fuse together
- Formation of primitive groove (made from epiblast cells proliferation)
- formation of 3 germ layers
• Cells near primitive groove start to migrate into the groove down into the hypoblast layers
- endoderm, mesoderm, ectoderm
Neurulation (week 3)
- Formation of notochord
—> near primitaive groove more cells migrate down and form the tube = notochord - Notochord pushed into mesoderm layer
- Formation of neural groove
• Neural fold closes and is pushed down into mesoderm
