CVS physiology Flashcards
Local factors causing vasoconstriction
- Cold temperature
- Injured vessels ?secondary to Serotonin release
- Autoregulation (myogenic response)
Endothelial products causing constriction
- Endothelin 1
- Locally released platelet serotonin
- Thromboxane A2
Circulating hormones causing constriction
- Adrenaline (except skeletal muscle and liver)
- NA
- Ang II
- Circulating Na/K ATPase inhibitor
- ADH/ AVP
- Neuropeptide
Neural factors causing constriction
Increased discharge of noradrenergic vasomotor nerves
Local factors causing dilation
- Increased temperature
- Hypoxic
- Increased PCO2
- Lactate/ decreased pH
- Cells leaking K+ and osmolarity
- Cells burning energy (breakdown products of ATP eg. ADP, AMP, adenosine, phosphate)
- Histamine (released from damaged tissues)
Note that adenosine -> vasodilator in cardiac muscle, not skeletal
Endothelial products that cause dilation
- NO
- Kinins
- Prostacyclin
Circulating hormones that cause Dilation
Adrenaline in skeletal muscle and liver
CGRP-alpa
Substance P
Histamine
ANP
VIP
Neural factors that cause dilation
- Decreased discharge of noradrenergic vasomotor nerves
- Activation of cholinergic dilator fibres to skeletal muscle
What are the effects of long term autoregulation of local blood flow
- Body responds by increasing the size and number of blood vessels (via angiogenic factors)
- This is is stimulated by chronic rise in demand for O2
Name 3 angiogenic factors and their function
- Endothelial cell growth factors
- Fibroblast growth factor
- Angiogenin
Small peptides that cause new capillary loops to sprout from venules
Where is prostacyclin produced and what is its function
Endothelial and smooth muscle cells in blood vessels
- Inhibits platelet aggregation and promotes vasodilation thus increasing blood flow
- Promotes renin secretion by direct action on the JG cells or indirectly by reducing BP
How is thromboxane A2 made and what is its function
Derived from common precursor arachnidonic acid via COX pathway
Promotes platelet aggregation and vasoconstricton thus promoting plug formation
Describe the relationship between TXA and PGI2
Causes localised clot formation whilst maintaining distal blood flow
What happens if you give someone aspirin
Shifts balance towards PGI2 (i.e bleeding)
Produces irreversible inhibition of cyclooxygenase
What is another name for NO and where is it made
- Endothelium derived relaxing factor
- Made from arginine, crosses cell membrane readily, catalysed by NO synthase
What stimulates and inhibits release of NO
- Stimulated by products of platelet aggregation
- Inhibited by HB
What is the action of NO
- Vasodilation -> causes flow inducted dilation of large arteries
- Tonic release of NO is necessary to maintain BP
- Good in penile erection
- Vascular remodeling and angiogenesis
- Present in brain -> acting via cGMP (important for brain function)
- Important for cytotoxic activity of macrophages, including their ability to kill cancer cells
What are the 3 types of endothelin
1,2,3
Where is endothelin 1 made
Produced by endothelial cells, made fresh every time via transcription, with a half life of less than one minute
What stimulates and inhibits endothelin 1’s release
- Promoted by stretched wall, hypoxia, AngII, catecholamines, GF’s, insulin, oxidised LDL, HDL, thrombin
- Inhibited by NO, ANP, PGE2, prostacyclin
Actions of endothelin 1
- Potent vasoconstrictor, veins> arteriorles, particular effect on coronary artery vasoconstriction
- renovasoconstirction -> decrease RBF -> decrease GFR -> promote renin and aldosterone
- Positive chronotropic and inotropic
- Promote ANP
- Promote gluconeogensis
- Causes bronchoconstriction
- IV injection causes transient hypotension followed by sustained rise in BP (due to vasoconstriction)
What is the function of Kinins
- Increase permeability of capillaries
- Chemotactic for leukocytes
- Relaxation of vascular smooth muscle - > through action of NO
- Contraction of visceral smooth muscle
What are the two types of kinins
Bradykinin and lysylbradykinin (kallidin)
Where are kinins made
Sweat glands, salivary glands, exocrine pancreas
How are kinins made
- Both types are formed by HMW and LMW kinongen after being chopped by kallikreins
- Tissue Kallikein acts on both HMWK and LMWK to form lysylbradykinin
- Plasma kallikrein splits of bradykynin
How are kinases inactivated
Kininase I or II (same as ACE)
Where is ANP located
Atrial muscles
What type receptors do ANP act on, how many are there
act via Guanylate cyclase and increasing cGMP
3 - A, B, C
What promotes ANP release
- Rise in CVP (hypervolemia, over infusion of N/saline)
- Increase in HR -> increase venous return
- Immersion of body in water
- Generally ANP will rise when aldosterone will fall
What reduces ANP release
- Anything that will reduce CVP (standing from supine, dehydration, blood loss etc)
What is ANP’s 5 actions
- Inhibits release of ADH -> water diuresis
- Increases GFR -> increases NA loss
- Inhibit release of renin -> reduce NA retention
- Lowers BP by inhibiting actions of several vasoactive substances
- May have a role in the brain of central control of BP (ANP and CNP)
What is serotonin derived from
Tryptophan
Where is Serotonin found
Platelets, Chromaffin tissue in gut, tissues in brain, in the retina
What is its action (serotonin)
- Constriction of some vessels
- Contraction of the ileum
- Potentiates the effects of NA
- May be involved in the vasospasm associated with migraines
- Acts as a central neurotransmitter
- NO effect on stimulation of cardiac muscle or secretion of saliva
- In brain - impact cerebral circulation
- May take part of local blood flow in intestinal tract
What inactivates Serotinin, what is the inactivated product called and where is it excreted
- Monoamine oxidase
- 5 hydroxyindoleacetic acid
- Excreted in urine
What is histamine derived from and where is it found
Histidine
Granules of basophils and mast cells
What stimulates release of histamine
Trauma
Allergic reactions
What is the function of histamine
- Dilate arterioles (powerfully)
- Increases capillary permeability
- Thus leading to local swelling in allergic and traumatic reactions
Who gets carcinoid syndrome?
1% of patients with carcinoids and 20% of those with widepsread mets
Clinical features of carcinoid syndrome
Flushing
Diaarhoea
Cramps
N + V
Cough
Wheezing
Dyspnoea
Nodular liver owing to hepatic mets
What are carcinoid tumours
Tumours arising from endocrine cells, mainly in GIT and lungs
What vasoactive substances are released in carcinoid syndrome
Serotonin
Bradykinin and kallikreins
Prostaglandin
Histamien
What do sympathetic fibres release and what is their function
- Release NA
- Increase HR and SV (therefore inotropic chronotropic)
- Constrict aterioles and veins (to appropriate organs)
- Inhibit effect of parasympathetics (from vagus) -> probably by release of neuropeptide Y
What happens when you cut sympathetic nerves
Blood vessels dilate
Function of parasympathetic nerves
Release Ach
Decrease HR
Function of atropine
Block effect of parasympathetics
What factors affect vasomotor area in Medulla (central control of BP)
- direct stimulation CO2, hypoxia
- excitatory input
· from cortex via hypothalamus
· from pain pathways & muscles
· from carotid & aortic chemoreceptors - inhibitory inputs
· from cortex via hypothalamus
· from lungs
· from carotid, aortic, and cardiopulmonary receptors
Where are the 4 baroreceptors located and what is their function
- carotid sinus & aortic arch receptors monitor the arterial circulation
- receptors in the wall of R) atrium monitor venous return
- receptors in wall of L) atrium monitor pulmonary circulation
Describe how these baroreceptors produce a response.
- if too much volume increased wall stretch (+) afferent fibres pass via glossopharyngeal & vagus nerves to medulla end in nucleus tractus solitarius (NTS)
- inhibits the tonic discharge of vasoconstrictor nerves
- excites the vagal innervation of the heart, producing vasodilation, a drop in BP, bradycardia & decrease CO
What happens to the baroreceptor reflex in chronic hypertension
Mechanism is rest to maintain elevated rather than normal BP
What 6 things increase HR
- reduced CO ( decreased activity of baroreceptors in arteries, LV,a nd pulmonary circulation)
- reduced venous return (increased activity of atrial stretch receptors)
- hypoxia, exercise, fever, inspiration
- emotions, e.g. excitement, anger, painful stimuli
- hormones, e.g. adrenaline, thyroid hormones
- Bainbridge reflex
What things decrease HR
- Increased CO (Increased activity of baroreceptors in arteries, LV & pulmonary circulation)
- Increased venous return
- Emotion, e.g. fear, grief, expiration
- NA
- Stimulation of pain fibers in trigeminal nerve
- Raised ICP
Describe the law of circulation
- In general, HR & BP go hand in hand
- Things that increase HR also increases BP
- Things that reduce HR also reduces BP - if they can in opposite direction then something is seriously wrong
- Increase HR, reduce BP shock
- Reduce HR, increased BP raised ICP
What is coronary flow at rest
250ml/min (5% of CO)
What is the oxygen extraction fraction of coronary arteries at rest
70%
When does coronary flow occur
During diastole when myometrium is relaxed and pressure is low
Why does coronary flow reduce in tachycardia
Because diastole is shorter
Where does no coronary flow occur in systole and what implication does this have
Sub-endocardial portion of LV
Leaves it prone to ischaemic damage (most common site for MI)
What impact does heart failure have on coronary flow
Rise in venous pressure, reduces flow because it reduces effective coronary perfusion pressure)
(Coronary perfusion pressure is Aortic distolic pressure - LVEDP and in HF you get an increase in LVEDP)
What key changes occur during exercise with respect to coronary flow
Oxygen extraction 100%
Flow increases 5-6x
Increase in flow is limited if there is proximal stenosis
What 2 receptors are located on coronary arterioles
- Alpha adrenergic (vasoconstriction)
- Beta adrenergic (vasodilation)
What happens to coronary vessels if you inject NA
- stimulated both A and B adrenergic receptors
- Naturally wants to constrict coronary vessels
- But actually dilates them instead. This is because it increases HR, CO and SBP -> accumulation of vasodilator metabolites
- I.e the direct effect of NA on the heart is vasoconstriction but clinically it indirectly causes vasodilation
What would happen if you gave someone NA + a betablocker
Would take away the chronotropic and inotropic effects of beta receptors, so sole effect would be vasoconstriction
What impact does stimulation of vagal fibres have on coronary flow
Dilates the coronary vessels
What happens if you inject adrenaline
- HR and CO increase
- SBP increases
- DBP and TPR decrease
(widening of pulse pressure)
How does NA cause coronary vasodilation
Produces vasodilator metabolites as a result of increased myocardial activity
What happens if you inject NA
- Increase SBP and DBP
- TPR increases
- HR and CO decrease
What 5 factors influence CEREBRAL blood flow
- ICP
- MAP at brain level
- MVP at brain level
- Local constriction and dilation of cerebral arterioles
- Viscosity of blood
How is normal blood flow maintained in the brain
- Autoregulation (maintains arterial pressure of 65-140)
- Cerebral metabolism remains constant
Why does ICP cause HTN and bradycardia
CO2 accumulates which stimulates the vasomotor centre
Describe fetal circulation
- Blood from mum -> baby via umbilical vein (80% oxygenated)
- Ductus venosus diverts blood from liver to IVC (67% as now mixed with IVC blood from legs)
- Foramen ovale directs blood to LA (diverts the lung)
- LA to LV -> aorta -> head (65% oxygenated)
- Blood from SVC ends up in RA then RV. Blood in RV goes to pulmonary artery.
- Pulmonary artery -> aorta via the ligamentum arteriosum (i.e bypassing the lungs as alveoli filled with fluid) then down to the trunk and body (60%)
- i.e better oxygenated blood goes to the head
- From the aorta -> umbilical arteries -> placenta (55% of CO)
- Venous blood only 26% saturated
What 3 things close in the fetal circulation at birth
- Umbilical vein (ductus venosus shuts off)
- Fetal lung expands, generating intrathoracic negative pressure; blood start to flow into the lungs and returning into LA;
therefore pressure in LA rises (closure of foramen ovale) - Aortic pressure increases (closure of ductus arteriosus)
What are the 4 features of a congenital ventricular septal defect
- a pan systolic murmur
- increased pulmonary blood flow
- possible late RVF
- possible late pulmonary hypertension
What are the most important factors that maintain high blood flow in skeletal muscle during exercise
Local mechanisms
- Fall in PO2
- Accumulation of vasodilator metabolites (this is the most important of the 2)
What other factors contribute to maintaining high blood flow in skeletal muscle
- some decrease in tonic vasoconstrictor discharge (reduced constrictor tone in the arterioles) may be involved
- the ‘muscle pump’ in exercising muscle, improves venous return, lowers venous pressure, & helps increase blood flow
What happens to blood flow in resting muscle after sympathectomy and after exercise and what does this mean
blood flow in the resting muscle doubles after sympathectomy but once exercise has commenced, there is no difference in flow
in normal & sympathectomised muscle.
Thus the most important factor increasing blood flow through an active muscle is local action of metabolites on vessels of the muscle
Describe the pathway of electrical activity in the heart
- SA node
- 3 atrial internodal pathways (anterior, middle, posterior)
- AV node
- Bundle of HIS
- R) and L ) bundle branches (septum activated from Left to right)
- Purkinje fibres
- Apex to base to reach end of purkinje system then from endocardium to epicardium
Which fibres traverse the fibrous cardiac skeleton
Bundle of his
Function of purkinje fibres
Convey electrical excitation to ventricular muscle
Where is the SA node
Wall of RA below SVC
What are the last parts of the heart to be depolarised
- pulmonary conus
- top part of interventricular septum
- basal, posterior parts of LV
Speed of SA node depolarisation
- within node 0.05m/s
- spread to atrial muscle 0.3m/s
- through internodal pathway 1m/s
Where is the AV node located
- Posterior wall R) atrium, behind tricuspid vave
What is AV conduction speed and why is it slow
- Conduction through it is slow 0.05m/s
- Delay of 0.1 to 0.13s
- This delay allows completion of atrial systole before ventricles begin to contract
- Slow because small size of fibres, low resting membrane potential & paucity of gap junction
Outline parasympathetic activity on the SA and AV nodes
- Vagus nerve releases Ach at SA and AV node
- in SA node Ach binds to M2 muscarinic receptors (+) G protein opens up special K+ channels hyperpolarisation of membrane so that it takes longer for cell to reach threshold therefore reduce HR
- similar effects delay transmission through AV node as well
- so net effect of vagal parasympathetic on SA & AV node reduce HR & delay AV nodal conduction
Effect of sympathetic innervation on SA/AV node
- acting on SA node & AV node increase HR and increase transmission
- NA binds to B1 receptors, which causes an increase in cellular cAMP increased permeability of sarcolemma to Na & Ca
ions in addition to a more steeply sloping prepotential cells reach threshold more quickly
Synchronisation of heart beat (5 steps)
- RA systole precedes LA systole
- LV contracts before RV
- RV ejection begins before LV ejection (since pulmonary arterial pressure is lower than aortic pressure)
- during inspiration, the aortic valve closes slight before pulmonic valve
- during expiration, the pulmonary & aortic valves close at the same time
ECG manifestations of wolf parkinson white syndrome
- Short PR
- Wide slurred QRS complex
- Normal PJ interval
- Paroxysmal atrial trachycardia
Two tacchycardias associated with WPW
- AF (life threatening as can progress to VT/VF)
- AVRT (initiated by premature atrial beat)
What block is associated with atrial flutter and why
- almost always a/w 2:1 or greater AV block because in adults, AV node cannot conduct > 230/min
Describe the pattern of atrial flutter (rate and shape)
sawtooth pattern, 200-350/min
How can you slow ventricular rate in atrial flutter
Carotid sinus pressure
What is the most common re-entry pathway associated with atrial flutter
in the most common form of this arrhythmia, there is a large counterclockwise circus movement in RA
Where is the QT interval measured, how long is it normally, what does it correspond to and is it prolonged in hypokalemia
- from start of QRS complex to end of T wave about 0.35-0.42sec
- corresponds to electrical systole
- is NOT prolonged in hypokalemia
What does the QT interval represent
- indicates period of ventricular depolarization & repolarization
- Corresponds to eletrical systole
Describe QT interval relationship with HR
Inverse relationship
Is QT prolonged with hypokalemia
No
What is systolic pressure
Peak pressure in ventricles during contraction
What is diastolic pressure
lowest pressure in ventricles during relaxation
pulse pressure
systolic - diastolic
MAP
diastolic + 1/3 of pulse pressure
How long does isometric ventricular contraction last
0.05 seconds
Which part of the cardiac cycle has the most rapid pressure change per unit time
Isometric contraction of L) ventricle
What is the pressure in the LV during systole and diastole
120/80
What is the pressure in the RV during systole and diastole
25/12
What is the pressure in the RV when the aortic valve closes
15
EDV
150ml
SV
70-90ml
ESV
EDV - SV = 130-80 = 50ml remains in each ventricle at end of systole
EF
SV/EDV
~65% very important in evaluating index of ventricular function
7 Phases of the cardiac cycle
- Atrial contraction (0.1 seconds)
Systole 0.3 seconds
2. Isovolumetric ventricular contraction
3. Rapid ventricular ejection
4 Reduced ejection
Diastole (0.4 seconds)
5 Isovolumetric ventricular relaxation
6 Rapid ventricular filling
7 Reduced ventricular filing
Describe the first step of the cardiac cycle
Atrial contraction
- Starts with firing of SA node, corresponds with P wave.
- Atria contract
-Pressure within atria increases
- Blood is pumped into ventricle
- Increase in right atrial pressure
- Slight increase in ventricular volume and pressure
-
Describe the second step of the cardiac cycle
Isovolumetric contraction
- QRS complex
- ventricular depolarisation followed by contraction
- Ventricular contraction represented by R wave
- When LV pressure exceeds LA, AV valves close (fist heart sound)
- Ventricles contract with a rapid rise in LV pressure
- Volumes stay the same.
- Once pressure in ventricle exceeds aorta/pulmonary the AV valves open
Describe the third step of the cardiac cycle
Rapid ventricular ejection
- Sudden ejection in large volume of blood in the first third of systole
- ST segment (period between ventricular depolarisation and re-polarisation)
Describe the 4th step of the cardiac cycle
Reduced ventricular ejection
- Ventricular pressure decreases (T wave) as ventricle relaxes
- Blood flow due to inertia not contraction.
Describe the 5th step of the cardiac cycle
Isovolumetric ventricular relaxation
- Start of diastole is marked by the dicortic notch on the arterial pressure wave form. (Occurs when aortic pressure exceeds ventricular pressure, and blood starts to flow backwards into the heart).
- AV valves close (aortic closes before pulmonary)
- Now all the valves are closed, atria are filling with blood.
Describe the 6th step of the cardiac cycle
Rapid ventricular filling
- Occurs when ventricular pressure is lower than atrial
- AV valves open
- ventricles rapidly fill with blood
Describe the 7th step of the cardiac cycle
Reduced ventricular filling (distasis)
- ventricles get 90% of blood between this and step 6)
What impact do inotropes have on cardiac function
- Increase contractiltiy therefore increase SBP
- reduce afterload and preload
- Increase CO
- Increase EF
Give 4 examples of inotropes
Catecholamines
Dopamine
Digoxin
Glucagons (in high doses)
Describe the molecular pathways of the 4 inotropes
Increased intracellular cAMP influx of Ca stronger contraction
1. adrenaline & NA act on B1 receptors (+) adenylyl cyclase increased cAMP
2. Dopamine, when injected, stimulates heart via B1 receptors as above
3. glucagons increases formation of cAMP in cardiac muscles
4. xanthines (caffeine, theophylline) these inhibit the breakdown of cAMP
* digoxin due to their inhibitory effect on Na-K ATPase in myocardium influx of Ca
Name 3 negative inotropes
- hypercapnia, hypoxia and acidosis
- heart failure
- drugs, e.g. beta-blockers, Ca channel blockers, barbiturates, and many anaesthetics
How is CO calculated
SV x HR
What is CO
Amount of blood pumped by each ventricle per minute
What is resting CO related to
Surface area
What is CI
CI = CO/SA (square meter) varies between 2 to 5
What conditions do not effect CO
- sleep
- moderate changes in environmental temp
What conditions increase CO
- anxiety & excitement (50-100%)
- eating (30%)
- exercise (up to 700%)
- high environmental temp
- pregnancy
- adrenaline
What conditions decrease CO
- Sitting or standing form lying position (20-30%)
- Rapid arrhythmias
- Heart disease
Explain starlings Law
Increasing venous return (i.e EDV) increases SV and CO.
Sarcomeres stretch increasing myosin actin binding with a greater strength of contraction.
Explain the frank starling curve
Describes the relationship between EDV and SV.
Increse EDV and get increased SV to a point. If sarcomeres get lengthened too much actin and myosin cant bind and SV reduces.
Things shift curve up (i.e increase SV for a given EDV). Inotropes
What decreases EDV
- reduced ventricular compliance (e.g. MI, infiltrative disease)
- pericardial effusion
- reduced venous return to heart, e.g. standing
What increases EDV
- Stronger atrial contraction
- negative intrathoracic pressure during inspiration
- increased venous return to heart, e.g. muscle pumps during exercise, increase in blood volume, venous tone, negative thoracic pressure
What paramaters are reduced in a failing LV
- ejection fraction
- rate of rise of pressure (dP/dt) at the commencement of systole
- stroke-volume at a given filling pressure
- systolic shortening of myocardial fibres
What is pre load
The degree to which the myocardium is stretched before it contracts.
EDV: volume load created by blood entering ventricles at end of diastole before contraction.
Establishes sarcomere length
What is after-load
- Amount of resistance ventricles must overcome during systole
- Establishes degree, speed of sarcomere shortening, ventricular wall stress
What factors influence CO
- Heart rate (sympathetic and parasympathetic innervation)
- SV (increases when strength of contraction increases without an increase in fibre length which occurs with sympathetic innervation)
- Pre load and after load
What makes cardiac function worse in AS
- increased pressure gradient across the aortic valve
- increased reflux through the aortic valve
- increased aortic systolic pressure
- rapid HR
What features occur in someone with AS and do these improve with surgery
Features of pressure overload
- Hypertrophy
- Fibrosis
- Vascualr insufficiency
- Changes in myosin isoform expression
- Cardiac status improves post-operatively but features of pressure overload do not.
Give 4 reasons for oedema occurring
- increased filtration pressure (pushing force) arterial dilation, venular constriction, increased venous pressure
- decreased osmotic pressure (pulling force) low proteins, proteins leak into interstitial space
- increased capillary permeability histamine, bradykinin, substance P, etc…
- inadequate lymph flow, e.g. lymph obstruction
In what patients does increased interstitial fluid production occur
- extensive thermal burns
- irreversible shock
- major deep vein thrombosis
- acute hypoalbuminaemia
Define Bernoullis principle
The greater the velocity of flow in a vessels, the lower the lateral pressure distending its walls.
When a vessel is narrowed, the velocity of flow in the narrowed portion increases and the distended pressure decreases.
When fluid flows through the narrow portion of a tube - the kinetic energy of flow is increased as the velocity increases and the potential energy is reduced. Consequently the measured pressure is lower than it would have been at that point if the tube had not been narrowed.
What is the basis of Bernoullis principle
Kinetic energy and pressure energy can be interconverted so that total energy remains unchanged.
What is potential/ pressure energy
Pressure exerted laterally against walls of the vessel
What is total energy of a blood vessel
The sum of kinetic and potential energies
What two ways can pressure drop in the arterial system and are they reversible
- Pressure drop due to overcoming resistance. This is irreversible as energy is lost by heat dissipation.
- Conversion of potential to kinetic energy (reversible as vessel is able to widen out again)
What are the 4 types of shock
- Hypovolemic shock
- Distributive shock
- Cardiogenic shock
- Obstructive shock
Causes of hypovolemic shock
- bleeding, trauma, surgery
- burns
- fluid loss due to vomiting & diarrhoea
Causes of distributive shock
(marked vasodilation, vasogenic or low resistance shock)
- fainting (neurogenic shock)
- anaphylaxis
- sepsis also cause hypovolemic shock due to increased capillary permeability with loss of fluid into tissue
Causes of cardiogenic shock
(inadequate CO by the diseased heart)
- MI, arrhythmia’s
- CCF
Obstructive shock
(Obstruction to flow)
- tension pneumothorax
- pulmonary embolism
- cardiac tamponade, cardiac tumours
What is hypovolemic shock characterised by
low CVP, low CO, and high peripheral resistance
What are the 6 compensatory reactions activated by bleeding.
- vasoconstriction, venoconstriction
- tachycardia, tachypnea (thoracic pumping)
- restlessness increased skeletal muscle pumping (in some cases)
- increased movement of interstitial fluid into capillaries
- increased secretion of
* NA and Adrenaline
* Vasopressins
* Glucocorticoids
* Renin & aldosterone
* EPO - increased plasma protein synthesis
What causes systolic heart failure
Caused by IHD, myopathy, severe volume or pressure overload from valve pathology
Describe the pathophysiology of systolic heart failure
- Systolic heart failure is impaired ventricular contractility (Loss of inotropy).
- Causes a downwards shift in frank starling curve.
- This results in a reduction in SV and a compensatory increase in EDV (i.e preload)
- Preload increases because ESV increases (essentially the volume left over is added to the venous filling pressure)
- If preload did not increase, the decline in stroke volume would be even greater for a given loss of inotropy
- However, the increase in EDV is not as big as the increase in ESV therefore SV and EF decrease.
Describe the pathophysiology of diastolic heart failure
- ventricular compliance is reduced from extreme myocardial hypertrophy
What cardiac parameters are effected in systolic heart failure
- Increased EDV (dilated ventricle)
- Reduced SV (weak ventricular contraction)
- Reduced EF
- Increased ESV
How does the heart respond in systolic failure
- Hypertrophy
- Increased sympathetic discharge
- Increased secretion of renin and aldosterone (Na and water retention, this is due to reduced renal perfusion, this initially increases contractility by increasing venous return and preload)
What are the causes of diastolic heart failure
- ventricular compliance is reduced from extreme myocardial hypertrophy, e.g. hypertrophic subaortic stenosis,
longstanding severe hypertension, restrictive cardiomyopathy, AS
How does the heart respond in to diastolic heart failure
- the stiff ventricle requires increased diastolic filling pressure
- EF initially maintained, but elasticity of myocardium is reduced decreased filling inadequate SV hypertrophy, Na
& water retention
Outline the difference between cardiac failure with diastolic dysfunction and failure with systolic dysfunction
- ejection fraction reduced in systolic failure; initially maintained in diastolic failure
- myocardial wall thickness loose and dilated in systolic; bulky in diastolic
- EDV increased in SHF, reduced in DHF
- ESV increased in SHF, reduced in DHF
What mechanism is similar between systolic and diastolic heart failure
Diastolic filling pressure (ventricualr diastolic pressure)
What does the brodie-trendelenburg test include
- the patient reclines with the leg elevated to empty the veins
- the superficial veins are compressed in the thigh
- the patient then stands while the veins are observed
- rapid filling on standing of the superficial veins below the knee during the phase of compression indicates incompetent leg & ankle perforators
- Brodie-Trendelenburg test can sometimes be additionally useful in detecting incompetent lower leg & ankle perforators, which indicate severe dysfunction of the venomuscular pump
What are the 4 things that happen when you are upside down/negative gravitation is acting on the body
- increased CO
- increase cerebral arterial pressure
- ecchymoses around the eyes
- mental confusion
What occurs to venous pressure in the head when you stand.
- Generally veins above the heart have a tendency to collapse on standing.
- However the dural venous sinuses are very rigid and do not as they have very rigid walls. Therefore the pressure in them remains sub-atmospheric if lying or standing.
- This increases the further the distance from the top of the collapsed neck veins (superior saggital sinus can be -10mmhg)
- Dural sinus pressure is not constantly negative -> element of positional
