Physiology Flashcards
What is autorhythmicity
When the heart is capable of generating electrical signals for rhythmic beating without an external stimuli
Where does the excitation originate normally
In pacemaker cells in the Sino-atrial node in the upper right atrium close to the SVC entrance
The SAN drives the heart in __________
Sinus rhythm
How is a normal cardiac excitation formed (3)
SAN cells generate spontaneous pacemaker potentials instead of having a stable resting membrane potential
This takes the membrane potential to a threshold where an action potential is created
This results in regular spontaneous action potentials forming
Causes of the spontaneous pacemaker potential (3)
Decrease in K+ efflux
Na+ influx - Funny current
Transient Ca2+ influx via T-type Ca2+ channels
What type of polarization is involved in the spontaneous pacemaker potential
Slow depolarization
Cause of rising phase of action potential
Activation of long lasting L-type Ca2+ channels causing Ca2+influx
What type of polarization is involved in the rising phase of pacemaker action potential
Depolarization
Causes of falling phase of action potential
Inactivation of L-type Ca2+ channels
Activation of K+ channels causing K+ efflux
What type of polarization is involved in the falling phase of pacemaker action potential
Repolarization
How does the cardiac excitation normally spread across the heart
Sino-atrial Node => Atrioventricular Node => Bundle of His => Left and Right branches => Purkinje fibres
Which parts of the heart have cell-to-cell spread of excitation (3)
From SAN through both atria
From SAN to AVN
Within ventricles
How does cell-to-cell current flow
Via gap junctions containing low resistance protein channels
AVN characteristics (4)
Located at base of right atrium above the junction of atria and ventricles
Only point of electrical contact between atria and ventricles
Small diameter
Slow conduction velocity
Importance of conduction delay in AVN
To ensure atrial systole precedes ventricular systole
How is the action potential on atrial and ventricular myocytes different from pacemaker cells (2)
The resting membrane potential remains at -90mV
There are 5 phases (phase 0 to 4) for myocytes but only phase 0,3 and 4 for pacemaker cells
Phase 0 (5)
Ventricular action potential is triggered via SAN impulses
Involves rapid activation of voltage-activated Na+ channels at a threshold potential (-65 mV) generating a Na+ conductance and an inward, depolarizing, Na+ current
This drives Vm towards the Na+ equilibrium potential (74mV)
Voltage-activated Na+ channels rapidly inactivate during depolarization and only recover upon repolarization
Overall influx of Na+ is dominant
Phase 1 (2)
Caused by rapid inactivation of Na current and activation of transient outward K+ current mediated via voltage-activated potassium channels
Overall efflux of K+ is dominant
Phase 2 (3)
A plateau occurs due to a balance of conductances between an inward depolarizing Ca2+ flow via voltage-activated L-type channels and an outward repolarizing K+ flow
During the plateau outward K+ current in phases 4 and 1 decreases
Voltage activated delayed rectifier K+ channels slowly open, generating the repolarizing current that increases with time
Phase 3 (3)
Occurs when outward K+ currents exceed inward Ca2+ current
This is due to Ca2+ L-type channels closing
Overall efflux of K+ is dominant
Phase 4 (4)
Membrane potential is steady at -90mV
It is close to equilibrium potential for K+ (-94 mV) due to K+ conductance via inward rectifier K+ channels - This forms an outward hyperpolarizing current
Membrane potential is not at Ek due to inward depolarizing leak Na+ conductance
Overall efflux of K+ is dominant
Sympathetic stimulation increases/decreases heart rate
Increases
Parasympathetic stimulation increases/decreases heart rate
Decreases
What is the continuous parasympathetic supply to the SAN and AVN
Vagus nerve
Function of vagal tone
Slows the intrinsic heart rate from 100 to 70 bpm
Normal heart rate
60 - 100bpm
Bradycardia
<60 bpm
Tachycardia
> 100 bpm
Vagal stimulation effect on heart rate
Slows heart rate via increase in AVN delay
Parasympathetic neurotransmitter and acting receptor
ACh acting on muscarinic M2 receptors
Competitive inhibitor of ACh and its use
Atropine
Used in extreme bradycardia to increase heart rate
Effect of vagal stimulation on Pacemaker Potentials (4)
Cell hyperpolarises where its takes longer to reach threshold
Slope of Pacemaker Potential decreases
Frequency of AP decreases
Negative chronotropic effect
Which regions do the cardiac sympathetic nerves supply (3)
SAN
AVN
Myocardium
Sympathetic stimulation effects (3)
Increases heart rate
Decreases AVN delay
Increases force of contraction
Sympathetic neurotransmitter and acting receptor
Noradrenaline acting on β1 adrenoreceptors
Effect of noradrenaline on pacemaker cells (4)
Slope of Pacemaker Potential increases
Pacemaker potential reaches threshold quicker
Frequency of action potentials increases
Positive chronotropic effect
Cardiac myocytes characteristics (3)
It’s striated due to regular arrangement of contractile protein
No neuromuscular junctions
Electrically coupled by gap junctions
Importance of gap junction
Ensure each electrical excitation reaches all cardiac myocytes (All-or-none Law of the heart)
Importance of desmosomes (2)
Provide mechanical adhesion between adjacent cells
They ensure that tension developed by one cell is transmitted
Structure of striated muscle fiber (4)
Myofibrils => Actin (thin filaments) => Myosin (thick filaments) => Sarcomeres
How is muscle tension produced (2)
By ATP-dependent interactions - Sliding of actin filaments on myosin filaments
This causes the muscle to shorten and produce force
Is ATP required for both muscle contraction and relaxation
YES
Ca2+ in muscle contraction (3)
Triggers cross bridge formation
Released from sarcoplasmic reticulum
Release in cardiac muscle is dependent on the presence of extra-cellular Ca2+
Calcium Induced Calcium Release CICR mechanism (3)
Na+ ions enter T-Tubule
Triggers release Ca2+ ions
Ca2+ ions then attach to Ca2+ sensitive receptor in sarcoplasmic recticulum which opens channels releasing more Ca2+
Part of the stage 2 plateau phase
Steps of muscle contraction (7)
Sarcolemma is depolarized by action
potential that spreads along membrane and T-tubule
Ca2+ are released from sarcoplasmic reticulum
and bind to troponin and causing it to change shape
This causes tropomyosin proteins to move to a
different position exposing the binding site for myosin
Myosin binds with this site forming cross-bridges
Myosin heads tilt pulling actin filaments (power
stroke) towards centre of sarcomere
The heads hydrolyse ATP molecules, providing
enough energy for heads to let go of actin and return
to original position and bind again to exposed actin site
This process continues as long as binding sites are open
and ATP is in excess
Refractory period (2)
A period following an action potential where it is impossible to produce another action potential
It is protective for the heart in preventing generation of tetanic contractions in cardiac muscles
Stroke Volume (3)
The volume of blood ejected by each ventricle per heartbeat
equals to the End Diastolic Volume - End Systolic Volume
It is regulated by intrinsic and extrinsic (nervous and hormones) mechanisms
Changes in stroke volume are caused by
Changes in diastolic length or stretch of myocardial fibers
End Diastolic Volume (2)
Determines cardiac preload - The diastolic length/stretch of myocardial fibers
Determined by venous return to the heart
Frank-Starling Curve relationship
The more the ventricle is filled with blood during diastole (End Diastolic Volume), the greater the volume of ejected blood will be during the resulting systolic contraction (Stroke Volume)
Stretch and Ca2+ relationship (2)
Stretch increases affinity of troponin for Ca2+
Not for cardiac muscle as optimal length is achieved via muscle stretching (Frank-Sterling Mechanism)
What happens if venous return to right atrium increases (5)
EDV of right ventricle increases
SV into pulmonary artery increases due to Starling’s law
Venous return to left atrium increases
EDV of left ventricle increases
SV into aorta increases due to Starling’s law
Afterload definition and relationships (3)
The resistance in which the heart is pumping
If afterload increases initially the heart is unable to eject the full SV so EDV increases
If increased afterload continues to exist ventricular hypertrophy occurs to overcome resistance
Stimulation of sympathetic nerves increases/decreases contraction force
Increases - Positive Inotropic effect
Sympathetic stimulation on ventricular contraction (5)
Peak ventricular pressure rises Rate of pressure change during systole increases Decreases systole duration Rate of ventricular relaxation increases Duration of diastole decreases
Sympathetic stimulation on ventricular contraction on a Frank-Starling Curve (2)
Since peak ventricular pressure increases, EDV increases too
This shifts the curve to the left
How do negative inotropic agents on ventricular contraction look like on a Frank-Sterling Curve (2)
Shifts curve to the right
Example is heart failure
Effect of parasympathetic nerves on ventricular contraction (2)
Very little innervation of ventricles by vagus - Little direct effect on SV
Vagal stimulation has influence on heart rate NOT contraction force
Adrenaline and noradrenaline released from adrenal medulla on SV (2)
Have inotropic and chronotropic effect
Effects minor compared to noradrenaline from sympathetic nerves
Cardiac Output (3)
The volume of blood pumped by each ventricle per minute
Equals to Stroke Volume * Heart rate
A resting healthy adult has an cardiac output of normally 4900ml
When are the heart sounds produced, the types and the valves involved
When the valves close
S1 - Tricuspid and Mitral (Lub)
S2 - Pulmonary and Aortic (Dub)
What is the Cardiac Cycle
Refers to all events that occur from the beginning of one heart beat to the beginning of the next
At a heart rate of 75 beats/min what are the duration of ventricular diastole and ventricular systole respectively
Around 0.5 and 0.3 seconds
Events during the Cardiac Cycle (5)
Passive Filling Atrial Contraction Isovolumetric Ventricular Contraction Ventricular Ejection Isovolumetric Ventricular Relaxation
Passive Filling Events (5)
Pressure in atria and ventricles close to zero
AV valves open so venous return flows into ventricles
Aortic pressure is 80 mmHg and aortic valve is closed
Similar events occurs in right ventricle and pulmonary artery but pressure is much lower
Ventricles become 80% full
Atrial Contraction Events (3)
P-wave indicates atrial depolarization
Atria contracts between P-wave and QRS
Upon atrial contraction completion the end diastolic volume reaches 130ml and the end diastolic pressure is a few mmHg in a resting healthy adult
Isovolumetric Ventricular Contraction Events (5)
Ventricular contractions begins after QRS - Indicates ventricular depolarization
Ventricular pressure rises steeply exceeding the atrial pressure where the AV valves shut
This produces the first sound - Lub
Aortic valve remains shut where no blood enters or leaves ventricle
This produces tension around a closed volume
Ventricular Ejection Events - Part 1 (4)
When ventricular pressure exceeds aorta/pulmonary artery pressure the semi-lunar valves open - This is a silent event
Stroke Volume is ejected by each ventricle leaving the End Systolic Volume
Stroke volume is approximately 70ml
Aortic pressure rises
Ventricular Ejection Events - Part 2 (5)
T-wave indicates ventricular repolarization
The ventricles relax and pressure decreases
Once the pressure falls below the aortic/pulmonary pressure the semi-lunar valves shut
This produces the second heart sounds - Dub
The valve vibration produces the dicrotic notch in aortic pressure curve
Isovolumetric Ventricular Relaxation (4)
Closure of semi-lunar valves signal the beginning of this process
The AV valves shut
The tension decreases around a closed volume
When ventricular pressure falls below atrial pressure the AV valves open - This is a silent events where a new cycle begin
S1 heart sound indicates what
The beginning of systole
S2 heart sound indicates what
The beginning of diastole
Locations of auscultation of heart valves (4)
Aortic - Right 2nd intercostal space lateral to sternum
Pulmonary - Left 2nd intercostal space lateral to sternum
Tricuspid - Left 4th intercostal space lateral to sternum
Mitral - Left 5th intercostal space mid-clavicular line (Same as the apex beat)
How does arterial pressure not fall to zero during diastole
Due to elastic recoil from the elastic fibers in the arteries
The Jugular Venous Pulse occurs
After right arterial pressure waves
What is blood pressure
The outwards hydrostatic pressure exerted by the blood on blood vessel walls
What is Systolic Arterial Blood Pressure and its normal value
The pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts
It should not normally reach or exceed 140 mmHg under resting conditions
What is Diastolic Arterial Blood Pressure (2)
The pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes
It should not normally reach or exceed 90 mm Hg under resting conditions
Definition of hypertension
Clinic blood pressure of 140/90 mmHg or higher and day time average of 135/85 mmHg or higher
What is pulse pressure and its normal range
The difference between systolic and diastolic blood pressures
Normal range is between 30-50 mmHg
Physiologic basis for
Indirect Measurement of Arterial Blood Pressure (4)
Blood flows in a laminar fashion which is not audible through a stethoscope
Upon external pressure exceeding the systolic pressure the flow is blocked and no sound is produced
But if the external pressure is in between systolic and diastolic pressure the flow becomes turbulent whenever blood pressure exceeds cuff pressure
This is audible through a stethoscope
What does the first Korotkoff sound indicate
Peak systolic pressure
What do the fifth/last Korotkoff sound indicate
Minimum diastolic pressure
What is Mean arterial Blood Pressure (MAP)
The average arterial blood pressure during a single cardiac cycle involving heart contraction and relaxation
MAP formulas (3)
=[(2* diastolic pressure) + systolic pressure]/3
=Diastolic Blood Pressure + 1/3 Pulse Pressure
=Cardiac output * Systemic Vascular Resistance
Why do you multiply the diastolic pressure by 2 when calculating for MAP
The duration of diastole is twice as long as systolic
Normal arterial Blood Pressure
<140 Systolic
<90 Diastolic
Normal Range of Mean arterial Blood Pressure
70-105 mmHg
Minimum MAP to perfuse coronary arteries, brain and kidneys
60 mmHg
What is Systemic Vascular Resistance/Total Peripheral Resistance
The sum of resistance of all vasculature in the systemic circulation
Which blood vessels have the most Systemic Vascular Resistance
Arterioles
Baroreceptors of Short-term Regulation of Mean arterial Blood Pressure (2)
Carotid baroreceptors around carotid sinus
Aortic baroreceptors around aortic arch
Control centre of Short-term Regulation of Mean arterial Blood Pressure
Medulla
Baroreceptors Reflexes in the Prevention of Postural Hypotension - When a normal person stands up from lying (6)
Venous return to heart decreases due to gravity
MAP decreases transiently
Firing rate of baroreceptors decreases
Vagal tone of heart decreases and sympathetic tone increases
This increases HR and SV then SVR via arterioles as main site
This increases venous return and stroke volume correcting the MAP fall
The increase in SVR amongst healthy people results in
An increase in DBP
Postural Hypotension cause
Results from failure of Baroreceptor responses to gravitational shifts in blood when moving from horizontal to vertical position
Postural (Orthostatic) Hypotension risk factors (5)
Age related Medications Certain diseases Reduced intravascular volume Prolonged bed rest
Postural Hypotension positive result
Indicated by a drop within 3 minutes in systolic pressure of at least 20 mmHg (with or without symptoms) and diastolic pressure of at least 10 mmHg (with symptoms)
Postural Hypotension Symptoms (5)
Those of cerebral hypoperfusion - lightheadedness, dizziness, blurred vision, faintness and falls
Baroreceptors only respond to acute changes in blood pressure (True/False)
TRUE
How is MAP in the long-term
Via control of blood volume
Total body fluid equals to
2/3 of intracellular fluid + 1/3 extracellular fluid
Extracellular fluid volume equals to
Plasma Volume + Interstitial Fluid
How is the Blood Volume and MAP controlled
Via extracellular fluid volume
Main factors affecting extracellular fluid volume (2)
Water excess or deficit
Na+ excess or deficit
Hormones Which Regulate Extracellular Fluid Volume (3)
Renin-Angiotensin- Aldosterone System - RAAS Natriuretic Peptides – NPs Antidiuretic Hormone (Arginine Vasopressin) - ADH
Role of The Renin-Angiotensin-Aldosterone System
Regulates plasma volume, SVR and hence the MAP
Renin role (2)
Released from kidneys
Stimulates formation of angiotensin I in the blood from angiotensinogen produced by the liver
How is Angiotensin I is converted to angiotensin II
By Angiotensin converting enzyme (ACE) produced by pulmonary vascular endothelium
Roles of Angiotensin II (3)
Stimulates the release of Aldosterone from the adrenal cortex
Causes systemic vasoconstriction - increases SVR
Stimulates thirst and ADH release
What is aldosterone and its function
Its a steroid hormone
It acts on kidneys to increase sodium and water retention increasing plasma volume
What is the rate limiting step for RAAS
Renin secretion from the juxtaglomerular apparatus in the kidney
Mechanisms which stimulate renin release (3)
Renal artery hypotension caused by systemic hypotension
Stimulation of renal sympathetic nerves
Decreased Na+ concentration in renal tubular fluid sensed by macula densa
Natriuretic Peptides (NPs) characteristics and roles (6)
Peptide hormones synthesised by heart
Released in response to cardiac distension or neurohormonal stimuli
They cause salt and water excretion decreasing blood volume and blood pressure
They decrease renin release decreasing blood pressure
Act as vasodilators decreasing SVR and blood pressure
Provides a counter regulatory system for the RAAS
Types of natriuretic peptides are released by the heart (2)
Atrial Natriuretic Peptide (ANP)
Brain-type Natriuretic Peptide (BNP)
Atrial Natriuretic Peptide (ANP) characteristics (2)
A 28 amino acid peptide synthesised and stored by atrial myocytes
Released in response to atrial distension (hypervolemic states)
Brain-type Natriuretic Peptide (BNP) characteristics and uses (3)
A 32 amino acid peptide synthesised by heart ventricles and brain
BNP is first synthesised as prepro-BNP which is then cleaved to pro-BNP (108 amino acids) and finally BNP
Serum BNP and the N-terminal piece of pro-BNP (NT-pro-BNP, 76 amino acids) can be measured in patients with suspected heart failure due to longer half-life
Antidiuretic Hormone (ADH) characteristics and roles (4)
Is synthesised by the hypothalamus and stored in the posterior pituitary
Secretion is stimulated by reduced extracellular fluid volume, increased extracellular fluid osmolality and increased plasma osmolality
Acts in kidney tubules to increase water absorption - This increase extracellular and plasma volume hence cardiac output and blood pressure
Also acts on blood vessels to cause vasoconstriction increasing SVR and blood pressure - More significant in those with hypovolaemic shock
Plasma osmolality indications and monitoring (2)
Indicates relative solute-water balance
Monitored by osmoreceptors mainly in the brain close to hypothalamus
What is shock
An abnormality of the circulatory system causing inadequate tissue perfusion and oxygenation
Stages of shock (5)
Inadequate tissue perfusion => Inadequate tissue oxygenation => Anaerobic respiration => Accumulation of metabolic waste products => Cellular failure
Adequate tissue perfusion depends on
Adequate blood pressure and cardiac output
Hypovolaemic Shock stages (6)
Loss of blood volume => Decreased venous return => Decreased end diastolic volume => Decreased stroke volume => Decreased cardiac output and blood pressure => Inadequate tissue perfusion
Cardiogenic Shock definition
Sustained hypotension due to decreased cardiac contractility
Cardiogenic shock stages (4)
Decreased Cardiac Contractility => Decreased stroke volume => Decreased cardiac output and blood pressure => Inadequate tissue perfusion
Cardiogenic shock example
Acute myocardial infarction
Tension Pneumothorax:
Obstructive Shock
stages (6)
Increased intrathoracic pressure => Decreased venous return due to change in pressure gradient => Decreased end diastolic volume => Decreased stroke volume => Decreased cardiac output and blood pressure => Inadequate tissue perfusion
Neurogenic Shock: Distributive Shock stages (5)
Loss of sympathetic tone to blood vessels and heart => Venous and arterial vasodilation => Decreased venous return, SVR and heart rate => Decreased cardiac output and blood pressure => Inadequate tissue perfusion
Vasoactive Shock: Distributive Shock stages (5)
Release of vasoactive mediators => Venous and arterial vasodilation - Increased capillary permeability => Decreased venous return and SVR => Decreased cardiac output and blood pressure => Inadequate tissue perfusion
Obstructive shock examples (3)
Cardiac temponade Pulmonary embolism Severe aortic stenosis
Neurogenic shock example
Spinal cord injury
Vasoactive shock examples
Septic shock
Anaphylactic shock
Treatment of shock (7)
ABCDE approach High flow oxygen Volume replacement - EXCEPT in cardiogenic Inotropes for cardiogenic shock Chest drain for tension pneumothorax Adrenaline for anaphylactic shock Vasopressors for septic shock
Causes of hypovolaemic shock (2)
Haemorrhage - Trauma, surgery
Non-haemorrhage - Vomiting, diarrheoa, excessive sweating
Compensatory mechanisms can maintain blood pressure until
> 30% of blood volume is lost
How is cerebral blood flow regulated
By the myogenic response where if MAP rises resistance vessels automatically constrict to limit flow and vice versa
Resistance to blood is proportional to _________ and inversely proportional to ___________
Blood viscosity and length of blood vessel;
The radius of blood vessel to the power 4
The resistance to blood flow is controlled by
Vascular smooth muscles through changes in the radius of arterioles
What Chemical local metabolites causes vasodilation and metabolic hyperaemia (6)
Decreased local PO2 Increased local PCO2 Increased local [H+] (decreased pH) Increased extra-cellular [K+] Increased osmolality of ECF Adenosine release
Local humoral agents causing vasodilation (3)
Histamine
Bradykinin
Nitric Oxide
Nitric oxide implications (4)
Continuously made by vascular endothelium from amino acid L-arginine through Nitric Oxide Synthase (NOS)
Has short life for few seconds
Stress on vascular endothelium causes release of calcium and activation of NOS
NO diffuses into adjacent smooth muscle cells activating cGMP that acts as second messenger for signalling smooth muscle relaxation
Local humoral agents causing vasoconstriction (4)
Serotonin
Thromboxane A2
Leukotrienes
Endothelin
Properties of endothelial produced vasodilators (3)
Anti-thrombotic
Anti-inflammatory
Anti-oxidants
Sheer stress mechanism (2)
Arteriole dilation causes sheer stress in arteries upstream to make them dilate
This increases blood flow to metabolically active tissues
Factors influencing venous return (4)
Venomotor tone
Skeletal muscle pump
Blood volume
Respiratory pump
Venomotor tone (3)
Venous smooth muscle are supplied with sympathetic nerve fibres
Stimulation give venous constriction
Increased venomotor tone increases venous return, SV and MAP
Respiratory pump (3)
In inspiration intrathoracic pressure decreases and intraabdominal pressure increases
This increases pressure gradient for venous return creating a suction
Increasing rate and depth of breathing increases venous return
Acute CVS responses to exercise (5)
Sympathetic activity increases
CO increases due to SV and HR increasing
Sympathetic vasomotor nerves causes vasoconstriction in kidneys and gut reducing flow
Metabolic hyperaemia overcomes vasomotor drive causing vasodilation in skeletal and cardiac muscle increasing blood flow in proportion to metabolic activity
Increase in CO increases BP but SVR and DBP decreases, increasing the pulse pressure
Chronic CVS responses to exercise (6)
Reduction in sympathetic tone and noradrenaline levels
Increased parasympathetic tone to the heart
Cardiac remodeling
Reduction in plasma renin levels
Increased vasodilator and decreased vasoconstrictor release from endothelial
Decreased arterial stiffening
What is Transient Loss of Consciousness (TLOC)
A state of real or apparent loss of consciousness with loss of awareness characterized by amnesia for the period of consciousness, loss of motor control, loss of responsiveness and a short duration
Causes of TLOC (4)
Head trauma
Syncope
Epileptic seizure
TLOC mimics - Psychogenic pseudo-syncope
What is syncope
Transient loss of consciousness due to cerebral hypoperfusion characterized by rapid onset, short duration and spontaneous complete recovery
Types of syncope (3)
Reflex Syncope
Orthostatic hypotension -Orthostatic syncope
Cardiac Syncope
Reflex syncope (5)
Refereed to all types of syncope
Neural reflexes causes cardioinhibition by vagal stimulation decreasing HR and CO
And/or vasodepression through sympathetic activity to blood vessels where vasodilation causes decreased SVR, SV and CO
This causes MAP to decrease
If fall of MAP is of sufficient severity to affect cerebral perfusion, this causes a transient period of hypoperfusion resulting in syncope
Types of reflex syncope (3)
Vasovagal syncope
Situational syncope
Carotid Sinus syncope
Vasovagal syncope - VVS (6)
Most common type of syncope
Faint is triggered by emotional distress (pain, fear) or orthostatic stress
Associated with typical prodrome (pallor, sweating, nausea)
Averted by horizontal gravity neutralization or leg crossing increasing venous return
Main risk in VVS is risk of injury
Treatments are hydration, avoid triggers, education, reassurance
Situational syncope (3)
Faint during or immediately after a specific trigger (cough, micturition, swallowing)
Treatments is treating cause of possible (cough), lie patient down during episode, avoid dehydration and excessive alcohol
Some cases require permanent cardiac pacing
Carotid Sinus syncope - CSS (5)
Triggered by mechanical manipulation of neck
More common in elderly males
Associated with conditions like carotid artery atherosclerosis
May occur after head or neck surgery or radiation
Cardiac permanent pacing is required
Cardiac Syncope (2)
Caused by cardiac event resulting in sudden decrease of CO
Causes are arrhythmias, acute MI, structural cardiac disease (aortic stenosis), pulmonary embolism, aortic dissection
Evaluation of patient presenting with TLOC involves (3)
Careful history
Physical examination including orthostatic BP
12-lead ECG
Features indicating a cardiac syncope (5)
Syncope during excretion or when supine
Presence of structural cardiac abnormality or CHD
Family history of sudden young death
Sudden onset palpitations immediacy followed by syncope
ECG findings of arrhythmic syncope
Adaptations of Coronary Circulation (4)
High capillary density
High basal blood flow
High oxygen extraction
Only supplied by increasing coronary blood flow
Intrinsic Mechanisms of Coronary Blood Flow (3)
Decrease in partial pressure of O2 causes vasodilation
Metabolic hyperaemia matches flow to demand
Adenosine from ATP is a potent vasodilator
Extrinsic Mechanisms of Coronary Blood Flow (3)
Coronary arterioles supplied by sympathetic vasoconstrictor nerves but due to over-ridden by metabolic hyperaemia because of increased heart rate and stroke volume
So sympathetic stimulation causes vasodilation despite functional sympatholysis
Circulating adrenaline activates Beta-2 adrenergic receptors causing vasodilatation
Most of coronary blood flow and myocardial perfusion occurs
In diastole when subendocardial vessels from left coronary artery are not compressed
Special Adaptations of Cerebral Circulation (5)
Basilar and carotid arteries anastomose to form Circle of Willis
Major arteries arise from circle of Willis where perfusion is maintained even if one artery is occluded
Auto regulation of blood flow guards against changes in flow if MAP changes within 60 - 160mmHg
Direct sympathetic stimulation has very little effect - Baroreceptor reflex is negligible
Increase in partial pressure of CO2 causes vasodilation and vice versa - This is why hyperventilating causes collapse
Relationships of auto regulation in cerebral blood flow (2)
If MAP increases, resistance vessels constrict limiting blood flow and vice versa
MAP below 50mmHg causes confusion, fainting and damage
Effect of Intracranial Pressure (ICP) in Cerebral Blood Flow (4)
Normal intracranial pressure is 8-13mmHg
Cerebral Perfusion Pressure (CPP) = Mean Arterial Pressure (MAP) - ICP
Increasing ICP decreases CPP and cerebral blood flow
Conditions which increase ICP can lead autoregulation failure of cerebral blood flow
Why does the blood brain barrier impermeable to ions, catecholaines and proteins
It protects neurones from fluctuating levels of substances in blood
Special Adaptations of Pulmonary Circulation (3)
Pulmonary capillary pressure is low (8-11 mmHg) compared to systemic capillary pressure (17-25 mmHg)
Absorptive forces exceed filtration forces - Protects against pulmonary oedema
Decreased oxygen causes vasoconstriction of pulmonary arterioles - Diverts blood to poorly ventilated areas
Skeletal muscle blood flow during exercise (3)
Metabolic hyperaemia overcomes sympathetic vasoconstrictor activity
Circulating adrenaline causes vasodilatation
This increases CO increasing skeletal muscle blood flow
What are varicose veins
Blood pools in lower limbs when venous valves become faulty
Why don’t varicose veins lead to decreased CO
Due to chronic compensatory increase in blood volume
Blood flow in capillaries is dependent on
Contractile state of terminal arterioles
Precapillary sphincters function
Regulate flow in tissues to be slow for adequate time for exchange
Transport across capillary wall (4)
Lipid soluble substances like O2 and CO2 pass through endothelial cells
Small water soluble substances like ions, glucose and amino acids pass through pores
Exchangeable proteins are moved across by vesicular transport
Plasma proteins cant cross capillary wall
Transport mechanism across capillary wall (2)
Fluid movement follows pressure gradient (bulk flow)
Movement of gases and solutes follow Fick’s law of diffusion
Transcapillary fluid flow (4)
Flow is passively driven by pressure gradient across capillary wall
It is ultra filtration
Net Filtration Pressure (NFP) = Forces favouring filtration - forces opposing filtration (Starling forces)
A Filtration coefficient (Kf) also affect net fluid filtration
Forces favouring filtration (2)
Capillary hydrostatic pressure - About 35 mmHg
Interstitial fluid osmotic pressure (Negligible to other forces)
Forces opposing filtration (2)
Capillary osmotic pressure - About 17 mmHg
Interstitial fluid hydrostatic pressure (Negative in some tissues and negligible too)
Why are Interstitial fluid osmotic pressure and Interstitial fluid hydrostatic pressure negligable
Mainly due to plasma proteins which usually do not leave capillary wall
NFP formula
= (Capillary hydrostatic pressure + Interstitial fluid osmotic pressure) - (Capillary osmotic pressure + Interstitial fluid hydrostatic pressure)
Starling forces favour (2)
Filtration at arteriolar end
Reabsorption at venular end
Starling forces in pulmonary capillaries (4)
Pulmonary resistance is 10% of systemic circulation
Pulmonary hydrostatic pressure is low (8 -11 mmHg)
Capillary osmotic pressure is at 25 mmHg
Efficient lymphatic drainage removes filtered fluid preventing interstitial fluid accumulation
Oedema definition
Accumulation of fluid in interstitial space
Pulmonary oedema consequence
Diffusion distance increases where gas exchange compromised
Oedema causes (4)
Raised capillary pressure
Reduced plasma osmotic pressure
Lymphatic insufficiency
Changes in capillary permeability
Raised capillary pressure (2)
Due to arteriole dilatation or increased venous pressure Causes LVF (pulmonary oedema), RVF (peripheral oedema like ankle and sacral) and prolonged standing predisposes to swollen ankles
Reduced plasma osmotic pressure (3)
Normal level is 65-80 g/L
Oedema if < 30 g/L
Causes are malnutrition, protein malabsorption, excessive renal excretion of protein, hepatic failure
Lymphatic insufficiency (2)
Due to lymph node damage
Filariasis - Elephantiasis (Parasites blocking lymphatics)
Changes in capillary permeability (2)
Due to inflammation
Histamine increases protein leakage
Left ventricular failure in relation to pulmonary oedema (4)
Accumulation of fluid in interstitial and intraalveolar lung spaces
Identified by varying SOB degree
May be crepitations in auscultations of lung bases
CXR shows haziness in perihilar region
