Physiology Creator: Cameron McCloskey Flashcards
True or False: Bachmann’s bundle is located in the left atrium.
True
The SA node fires at a rate of?
60-100pbm
Where does excitation originate in the heart?
SA node
What causes the rising phase of the action potential (depolarisation) in SA node cells?
Opening of Ca++ channels, resulting in Ca++ influx
On an EKG the P-wave represents what area of the heart?
Atrial contraction mid to late ventricular diastoly
What gives rise to pacemaker potential?
A
Decrease in K+ efflux
Slow Na+ influx
What causes the falling phase of the action potential (repolarisation) in SA node cells?
Opening of K+ channels, resulting in K+ efflux
Where is the SA node located
Upper right atrium (close to SVC entry)
Summarise the phases of the SA node action potential
A
Pacemaker potential: decreased K+ efflux, slow Na+ influx
Rising phase: Ca++ influx
Falling phase: K+ efflux
When the heart is controlled by the SA node, it is said to be in what type of rhythm?
Sinus rhythm
Which structure in the heart does NOT propagate action potentials?
The annulus fibrous
AV node cells are large and slow to conduct. True/False?
False
They are small and slow to conduct
which structure is propagation of the action potential the fastest in the heart?
c. The bundle of His
In which structure is propagation of the action potential the slowest in the heart?
b. The AV node
What is the pacemaker potential due to? 3charges
- Increase in funny current 2. Background current of potassium influx (Ib) 3. Transient Ca2+ influx
which structure in the heart is there a plateau in the cardiac action potential?
e. The ventricular myocardium
what is intercalated discs
is a combination of bundles of gap and desmosome junctions
Why is AV nodal delay present?
A
To allow time for atrial systole to precede ventricular systole
what is (1) Funny 𝑵+channels (𝑰𝒇)
These channels are open when the cell is at rest Allows more slow movement of Na+ to move into cell making inside of cell + + Allows less slow movement of K+ to move out of cell making inside of cell
How calcium in the cell is shunted back into the sarcoplasmic reticulum during repolarisation ?
- Into SR: ATP dependent Ca++/H+ exchanger. Na+/ Ca++ exchanger via secondary active transport
- Out of cell: ATP dependent Ca++/H+ exchanger. Na+/ Ca++ exchanger via secondary active transport
What happens when the pacemaker potential reaches threshold?
L-type calcium channels open allowing for calcium influx
What are the 2 main causes of the falling phase in a nodal action potential?
- Inactivation of L-type calcium channels - This reduces the inward flow of calcium ions, which contributes to depolarization, and starts to decline during the falling phase.
- Activation of outward potassium channels - This leads to an efflux of potassium ions out of the cell, resulting in repolarization of the membrane potential during the falling phase.
So, to summarize, the falling phase in a nodal action potential is due to both the inactivation of L-type calcium channels and the activation of outward potassium channels.
What permits the spread of excitation between myocardial cells?
Gap junctions
Where is the AV node located?
At the base of the right atrium just above the atrium/ventricular junction
What is the purpose of the AV node?
To allow conduction to spread to the ventricles from the atria
What attribute of the AV node allows for heart contraction coordination?
It has a low conduction velocity allowing there to be delay between atrial and ventricular contraction
What is the bundle of His?
This is a bundle of nerve fibres which carries the impulse from the AV node to the ventricles where the impulse passes upwards via Purkinje fibres in the ventricles
What is the resting potential of a myocardial cell?
-90mv
In a myocardial action potential, what is phase 0
Rapid depolarisation from -90mv to +20mv due to Na+ influx
Which type of channels are phosphorylated by stimulation of the SNS?
a. L- type Ca++ channels
In a myocardial action potential, what is phase 4
Resting membrane potential is achieved (-90mv)
The PSNS can affect the contractility of the heart. a. True b. False
False
only nodes
During the relative refractory period APs can be
triggered.
True
The SNS has a positive chronotropic action. a. True/ false
True
In a myocardial action potential, what is phase 3
Closure of Ca2+ channel influx and K+ efflux begins
In a myocardial action potential, what is phase 2
L-type Ca2+ channel influx
In a myocardial action potential, what is phase 1
Closure of Na+ channels and transient K+ channels
What is the plateau phase and what causes it?
Maintained during phase 2 of a myocardial AP. Due to Ca2+ influx through L-type channels. Maintains peak AP
How does the sympathetic system affect heart rate?
Increases
How does the parasympathetic system affect heart rate?
Decreases
What is vagal tone?
Continuous influence of the vagus nerve on SA node lowering heart rate to normal levels
What is the normal range for heart rate?
60-100bpm
What is the term for low heart rate (<60bpm)?
Bradycardia
What is the term for high heart rate (>100bpm)?
Tachycardia
On which receptors does acetylcholine from the vagus nerve act?
Type 2 Muscarinic
What type of drug is atropine and what may it be used for?
Competitive acetylcholine inhibitor Treats bradycardia by speeding up heart rate
What three effects does sympathetic stimulation have on the heart?
- Increase HR 2. Decrease AV node delay 3. Increases contractile force
Noradrenaline from the sympathetic system acts on which receptors in the heart?
B1
What is a chronotropic effect?
Something which influences heart rate e.g. positive chronotropic increases HR
In an ECG what does the P wave represent?
Atrial depolarisation
In an ECG what does the QRS complex represent?
Ventricular depolarisation
In an ECG what does the T wave represent?
Ventricular repolarisation
In an ECG what does the PR interval represent
AV node delay
In an ECG what does the ST segment represent?
Ventricular systole
In an ECG what does the TP interval represent?
Diastole
How long does the cardiac cycle normally last?
lasts about 0.8 seconds or 800
What 5 events comprise the cardiac cycle?
- Passive Filling 2. Atrial Contraction 3. Isovolumetric ventricular Contraction 4. Ventricular Ejection 5. Isovolumetric ventricular Relaxation
Describe passive filling
Pressure in atria is slightly higher than ventricles allowing for passive filling of ventricles with blood
Passive filling accounts for what percentage of ventricular filling?
80%
Describe how atrial contraction contributes to ventricular filling
The final 20% of ventricular filling is achieved by atrial conraction
Describe isovolumetric ventricular contraction
Ventricular pressure rises past atrial pressure upon contraction cause AV valves to close. Semilunar valves remain close so pressure builds around a closed volume
Describe ventricular ejection
Ventricular pressure exceeds aortic/pulmonary valve pressure causing ejection of stroke volume
What is the end systolic volume?
This is the amount of blood left behind in the ventricles after contraction
How is stroke volume calculated?
SV = EDV - ESV
When do the semilunar valves close?
When ventricular pressure falls after contraction?
What causes the first hearts sound?
Closing of AV valves during isovolumetric ventricular contraction
What causes the second heart sound?
Closing of semilunar valves after ventricular ejection
What causes the dicrotic notch in the pressure curve?
Valve vibration
What does isovolumetric ventricular relaxation involve?
The closing of aortic and pulmonary valves
What causes the third heart sound (S3)?
Occurs after 2nd heart sound - due to acceleration and deceleration of blood into the ventricles - can signify cardiac disease
What causes the fourth heart sound (S4)?
Occurs shortly before the first heart sound - due to rapid blood flow into less compliant ventricles (usually left) causing turbulence
Where are the S3 and S4 heart sounds best heard?
Apex
Where is the aortic area?
2nd intercostal space Right parasternal
Where is the pulmonary area (for the valve )?
2nd intercostal space Left parasternal
Where is the tricuspid area which rib intercostal space
4th intercostal space Left parasternal
Where is the mitral area?
5th intercostal space Left parasternal
For which two reasons does arterial pressure never fall to zero?
- Contraction of arterial and arterioles muscle 2. Retraction of elastic fibres
What is blood pressure?
Hydrostatic (outward) pressure exerted on vessels by blood flow
What is the upper limit of blood pressure before treatment?
140/90mmHg
What is the term used to describe blood flowing without turbulence?
Laminar blood flow
What are Korotkoff sounds?
There are 5 and they are heard when blood pressure is taken
At which Korotkoff sound is diastolic pressure measured and why?
5
At sound 5, the change is more easily heard as any sound heard changes to silence
Technically the fourth Korotkoff sound is where diastolic pressure occurs
What drives blood circulation?
The pressure gradient between aorta and right atrium
How is mean arterial blood pressure (MABP) calculated? (3)
- MABP = (2 x diastolic + systolic)/3
- MAP = 1/3 (systolic – diastolic) + diastolic
- MABP = CO x TPR
What is the pulse pressure?
This is the difference between systolic and diastolic pressure
What is the range for MABP?
70 - 105mmHg
What is the minimum requirement of MABP to perfuse organs?
60mmHg
What can happen is MABP is too high?
Damage to organs, vessels and extra strain is placed on the heart
What is TPR?
Total peripheral resistance
The sum of all the resistances in systemic and peripheral circulations
What are the main resistance vessels and what eveidence is there for this?
Arterioles
The blood pressure drops the most after entering these vessels
What effect does parasympathetic stimualtion have on the cardiovascular system?
- Decreases heart rate
- Decreases cardiac output
- Decreases MABP
What effects does sympathetic stimulation have on the cardiovascular system?
- Increase heart rate
- Increase contractile strength
- Increase cardiac output (increased stroke volume)
- Increase MABP
What are baroreceptors?
Pressure receptors
Where is the control centre located for baroreceptors?
The medulla
What are the effectors for the baroreceptors?
The heart and blood vessles
Where are the two groups of baroreceptors located?
- Aortic arch
- Carotid sinus (bifurcation)
Which cranial nerves allow signals to be sent from baroreceptors to the brain?
9 and 10
(IX and X)
(Glossopharyngeal and Vagus)
How do blood vessles “react” to increased carotid sinus afferent nerve fibre firing?
Vasodilate
How do blood vessles “react” to cardiac vagal nerve efferent nerve fibres?
Vasodilation
Explain the process baroreceptors go through when a person stands up quickly after lying down
- Venous return decreased due to a drop in blood pressure
- Firing rate of baroreceptors decreases
- Vagal tone of the heart decreases as the sympathetic system increases heart arte and stroke volume to attempt a blood pressure increase
- Sympathetic constrictor tone increases TPR which increases venous return and stroke volume correcting the low MABP and increasing it
What happens to the baroreceptor response when blood pressure is maintained over a long period of time?
The baroreceptor response is designed tor respond to acute changes.
The response sets a new baseline value to an acute change, if this change is mainatined it will become the new “normal”
How is MABP controlled long term?
Blood volume
Total body fluid is made up of which two components?
- Extracellualr volume
- Intracellular volume
What two components make up extracellular fluid volume?
- Plasma volume
- Interstitial fluid volume
What happens in order to balance a fall in plasma volume?
Compensatory mechanisms shift fluid from the interstitial fluid volume
Blood volume and MABP are controlled by mechanisms regarding ____________ _____ ______
Extracellular Fluid Volume
(ECFV)
Which two main factors affect ECFV?
- Water excess or deficit
- Na+ excess or deficit
Which three systems are involves in regulating ECFV?
- Renin Angiotensin Aldosterone system
- Atrial Naturiuretic Peptide
- Antidiuretic Hormone (Vasopressin)
How does the RAAS regulate MABP?
By regulating TPR and plasma volume
Where is renin produced and what is its function?
Kidneys (juxtaglomerular apparatus)
Stimulates formation of angiotensin I in the blood from angiotensinogen (from liver)
What happens to angiotensin I?
It is converted to angiotensin II by angiotensin converting enzyme (ACE, produced in pulmonary vascualr endothelium)
What does angiotensin II stimulate?
- Release of aldosterone from adrenal cortex
- Causes systemic vasoconstriction increasing TPR
- Stimulates thirst and ADH release (contributes to increasing plasma volume)
What does aldosterone do?
Acts on kidneys to increase sodium and water retention to increase plasma volume and hence MABP
What can stimulate renin release form the juxtaglomerular apparatus in the kidneys?
- Renal artery hypotension
- Stimulation of renal sympathetic nerves
- Decreased [Na+] in renal tubuar fluid (sensed my macra densa)
What are the macra densa?
Can detect [Na+] in renal tubular fluid
Specialised renal tubules composed of extraglomerular mesangial and granular cells (which release renin)
What is atrial natriuretic peptide (ANP) and when is it released?
Atrial myocytes synthesise a 28-amino acid peptide (ANP)
Released in response to atrial distension (stretch) in hypervolaemic states
What does ANP do?
Causes release of water and Na+ in urine.
The system reduces MABP and causes vasodilatation and reduced renin release.
This is a counter regulatory mechanism for RAAS
What is ADH?
Anti-diuretic hormone (vasopressin)
A peptide hormone
Where is ADH produced?
Precursor formed in hypothalamus and stored in posterior pituitary
What will stimulate ADH secretion?
Reduced ECFV or increased extracellular fluid osmolarity
What monitors plasma osmolarity?
Osmoreceptors
How does ADH function?
Acts on kidney tubules to increase water reabsorption allowing for increased blood volume and MABP.
It will stimulate vasoconstriction to increase TPR and MABP
What is shock?
An abnormality of the circulating system resulting in inadequate tissue perfusion
What is the pathway for shock?
- Inadequate tissue perfusion
- Inadequate tissue oxygenation
- Anaerobic metabolism
- Waste product build up
- Cellular failure and death
Which two factors are essential for there to be adequate tissue perfusion?
Adequate cardiac output and blood pressure
Which three factors can affect the stroke volume?
- Preload
- Myocardial contractility
- Afterload
What is the preload?
The preload is the amount of blood in the ventricles before systole - it is the EDV
What is afterload?
This is the amount of blood left in the ventrciles after systole - provides resistance for contracting heart muscle during the next contraction
Why does hypovolaemic shock occur?
Loss in blood volume
Why does hypovolaemic shock lead to inadequate tissue perfusion?
- Loss in blood volume
- Venous return/EDV reduced
- Stroke/cardiac volume reduced
- Blood pressure lowered
- Inadequate tissue perfusion
In response to hypovolaemic shock, which way does the Frank-Starling curve shift and why?
To the right
Decreased EDV (sub-optimal fibre length) hence stroke volume is reduced
What is cardiogenic shock?
Occurs when the heart cannot pump enough blood around the body due to decreased cardiac contractility
How does cardiogenic shock lead to inadequate tissue perfusion?
- Decreased contractility
- Decreased stroke volume
- Decreased cardiac output
- Reduced blood pressure
- Inadequate tissue perfusion
How does cardiogenic shock affect the Frank-Starling curve?
Shifts very far to the right - more than heart failure alone
What is obstructive shock?
Due to increased intrathoracic pressure which decreases venous return
(e.g. pneumothorax)
Why does tissue perfusion become inaqequate in obstructive shock?
- Decreased venous return and EDV
- Decreased stroke volume
- Decreased cardiac output
- Reduced blood pressure
- Decreased tissue perfusion
What does neurogenic shock involve?
Loss of sympathetic tone causing massive vasodilatation
Why does neurogenic shock lead to a lack in tissue perfusion?
- Massive vasodilatation
- Reduced venous return and EDV
- Reduced stroke volume
- Reduced cardiac output and blood pressure
- Inadequate tissue perfusion
What is vasoactive shock?
The release of vasoactive mediators causing massive vasodilatation and increased capillary permeability
Why is capillary permeability a relevant factor to vasoactive shock?
This can lead to a decreased blood volume and cause hypovolaemic shock
How does vasoactive shock lead to inadequate tissue perfusion?
- Massive vasodilatation
- Decreased venous return and EDV
- Decreased stroke volume and cardiac output
- Lowered blood pressure
- Inadequate tissue perfusion
How should shock be treated?
- ABCDE approach
- High flow oxygen - makes most of tissue perfusion that does occur
- Increase blood volume
- Use of positive inotropes e.g. adrenaline for anaphylaxis
- In septic shock, vasopressors can be used to cause mass vasoconstriction and increase MABP
What are the two main causes of hypovolaemic shock?
- Haemorrhage (trauma, surgery etc.)
- Vomiting, diarrhoea, excessive sweating (decreases ECFV)
How is haemorrhagic shock characterised?
Tachycardia - baroreceptor reflex
Small volume pulse - cardiac output is lowered
What is the myogenic (Bayliss) effect?
This involves the control of vessel dilatation/constriction to ensure blood flow remains constant when there is fluctuating blood pressure
It prevents damage to areas such as the brain
What are the first vessels to arise from the aorta?
Right and left carotid arteries
Where does coronary venous blood primarily drain?
Coronary sinus
In the coronary circulation, what are the two main areas for occulusion?
- Left carotid
- Left anterior descending
The coronary circulations have many special adaptions. List 4
- High capillary density
- High basal flow
- High oxygen extraction (75% vs normal 25%)
- Intrinsic and extrinsic control mechanisms for blood flow
Decribe 3 intrinsic mechanisms that confer special adaptions to the coronary circulation
- Decreased PO2 causes vasodilatation
- Metabolic hyperaemia (increased blood flow) ensure blood flow meets demand
- Adenosine (from ATP) is a potent vasodilator
Noradrenaline acts on which type of receptors in coronary arterioles?
Alpha 1
The vasoconstricting effect of the sympathetic system is avoided by opposing factors that promote vasodilatation, what are these factors?
- Increased CO (due to increased HR/SV)
- Increased adenosine due to cardiac work
- Decreased PO2 due to increased work
- Increased metabolites (K, PCO2, H) due to increased metabolism
- Increased circulating adrenaline
Why does the majority of blood flow in the coronary arteries occur during diastole?
The arteries are compressed during systole
The brain is supplied by which two artery types?
- Carotid arteries
- Vertebral arteries
A stoke can be caused by a _______ but also __________.
Thrombosis
Haemorrhage
Special adaptions of the cerebral circulation include?
- Autoregulation - Bayliss effect
- Direct sympathetic stimulation has little effect
- The brain does not participate in baroreceptor reflexes
Increased PCO2 in the brain causes what?
Cerebral vasodilatation
Decreased cerebral PCO2 causes what?
Cerebral vasoconstriction
Why does hyperventilation cause fainting?
PCO2 is reduced so cerebral vasoconstriction occurs
This limits blood flow to the brain
The process by which (sympathetic) vasoconstrictor effects is termed what?
Functional symptholysis
How is cerebral perfusion pressure calculated?
CPP = MABP - ICP
(ICP = intracranial pressure)
How can intracranial pressur be increased?
Haemorrhage, tumour, and other factors introducing more material into the confined cranial space
What forms the blood brain barrier?
The tight intercellular junctions formed between cerebral capillaries
The blood brain barrier allows ______ _______ and ______ to cross but not ___________ substances
Carbon dioxide and oxygen
Hydrophilic subtances
How does glucose pass the BBB?
Via specific carrier molecules
How is the pulmonary circulation resistant to oedema?
Absorptive forces exceed filtrative forces
How is skeletal blood flow increased during exercise when the sympathetic system induces vasoconstriction?
- Local metabolic hyperaemia overcomes the sympathetic vasoconstrictor activity
- Circulating adrenaline acts on B2 adrenergic receptors
- Increased cardiac output contributes to increased muscular blood flow
Describe the action of the skeletal muscle pump
- Large veins lie between skeletal muscle
- The contraction of skeletal muscle aids blood flow
- Valves present backflow of blood
What causes varicose veins?
The failure of venous valves leading to the pooling of blood in the lower limbs
What are:
a) The major capacitance vessels
b) the major resistance vessels
a) Veins
b) Arterioles
Which factors can affect the stroke volume?
- Pre-load
- Myocardial contractility
- Afterload
Total peripheral resistance is mostly controlled by what?
Vascualr smooth muscle in walls of arterioles
Resistance to blood flow is directly proportional to what?
- Blood viscocity
- Blood vessel length
Resistance to blood flow is inversely proportional to what?
The radius of blood vessels
Vascualr smooth muscle is innervated by sympathetic nerve fibres. This utilises which neurotransmitter and which receptor?
Normadrenaline on alpha receptors
What is vasomtor tone and what causes it?
The state of vascular smooth mucle always being contracted
This is due to tonic discharge of noradrenaline
Where are two regions of the body where the parasympathetic system has influence over blood vessels?
- Penis
- Clitoris
Adrenaline has what effect when it binds to beta 2 receptors?
Vasodilatation
(of skeletal muscle and cardiac arterioles)
Angiotensin II can have what effect on arteries?
Vasoconstriction
Intrinsic mechanisms of vascular smooth muscle include which two factors?
- Chemical factors
- Physical factors
These allow for matching between blood flow and metabolic need
Intrinsic controls are able to _________ the extrinsic controls for vascular smooth muscle contraction
Override
Give three examples of humoral agents which can cause vasodilatation
- Histamine
- Bradykinin
- Nitric oxide
How is nitric oxide produced?
Produced by vascular endothelium from L-arginine by action of nitric oxide synthase
When will nitric oxide be released?
- It is always released by tonic discharge
- Endothelial stress (e.g inside the heart endocardium layer)
- Receptor activation
How does nitric oxide exert its effect?
Diffuse into smooth muscle cells and activate cGMP - a secondary messenger
This allows for smooth muscle relaxation
Give 4 examples of humoral agents which can stimulate contraction of smooth muscle?
- Serotonin
- Thromboxane A2
- Leukotrienes
- Endothelin
Of the two, endothelial vasoconstrictors or vasodilators, which one contributes to vascular health and which does the opposite promoting thrombosis, inflammation and oxidation?
Vasodilators - vascular health
Vasoconstrictors - negative impact on vascular health
Name a physical factor responsible for the intrinsic control of vascular smooth muscle contraction
Temperature
How does increased atrial pressure impact stroke volume?
Increases stroke volume
EDV increases leaving to a lerger stoke volume
Name factors which aid venous return
- Skeletal muscle pump
- Respiratory pump
- Increased blood volume
- Increased atrial pressure
- Increased venomotor tone
What happens to the Frank-Starling curve during exercise?
It shift to the left
Ventricular pressure, SV and EDV rise
Heart failure causes the Frank-Starling curve to shift to the what?
Right
The p wave in an ECG represents which phase of the cardiac cycle?
Rapid filling phase
What is end systolic volume?
Amount of blood left in the LV after it contracts
Atrial contraction is triggered by:
Atrial depolarisation by Sa nodde
How much blood is present in the ventricles during passive filling
70-80%
what is heart’s septum ?
wall separating the right and left sides of the heart
Pulmonary circulation loop
Systemic loop
SVC
IVC
veins transport oxygenated blood to the heart and pulmonary arteries transport deoxygenated blood to the lung.
from the heart to the aorta to the rest of the body
- big superior vena cava
- big inferior vena cava
120/ 80 mmHg
- 120 systolic contract sound lub
- 80 diastolic relaxes sound dub
What are the two moments where a new action potential cannot be generated?
A
Plateau phase (Na channels in closed state)
and
—-repolarisation (K channels open, thus membrane cannot depolarise)
general purpose of refractory period
Preventing tetanic contraction of the heart
What is meant by end diastolic volume (EDV)?
A
Volume of blood remaining in each ventricle following diastole.
Its determined by Venous return
Describe the Frank-Starling Law of the Heart
A
The greater the EDV (as a result of more venous return), the greater the stroke volume will be during systole
What is meant by positive inotropic effect?
A
Force of contraction increases (due to sympathetic stimulation)
only in sympathetic
Normal cardiac out put is equal to
5L/ beat
Positive chronotropic agents
Factors which .Increase heart rate include
What is the similatory and differences between isoproterenol and atropine
Both are chronotropic agents Isoproterenol is selective Beat 1 agonist Atropine M2 antagonist thus Both increase HR
What is atrial bainbridge reflex
Increase increase positive chrontropic agent
Factors effect preload , contractility and after load
What’s the differences between elastic arteries and muscular arteries
4 features Character Diameter Structure Function. Aorta and renal artery
What is is special about Arterioles
High resistance vessels
What is the 4 specialties of vein that help them push blood against gravity
Veins made of thin tunica media large lumen 1. Valves of tunica interna 2. Muscular milking 3. Respiratory pump 4. Sympathetic tone
What is varicose veins
Twist which cause enlargement of blood vessels due to back flow
Which layer of blood vessels is under vasomotor tone
Tunic media
What is the Stimulators vasoconstriction of tunic media
Angiotensin II Norepinephrine and epinephrine Vasopressin (ADH) Endothelin
What is the stimulators vasodilator of tunic media
Nitricnoxide and Prostaglandin Arterial natriuretic peptide Increase cellular activity Decrease oxygen Increase CO2 Increase proton (H+ )
What is the vasa vasorum (vessels on vessels )
Small system of blood vessel that nourish the tunica extern supply blood to tunica media and adventitia
What do the EDV and ESV depend on
EDV is pre pumped volume in ventricle base on venous return and stretchy myocardium ESV post pumped volume in ventricle base on contractility and afterload Therefore the factors which effect STROKE VOLUME are 1. Preload , 2. contractility and 3. Afterload.
Factors effect after load
Increase vascular resistance in systemic circulation Diastolic hypertension Thrombus
Bruit can be heard with stethoscope when ?
There is narrow lumen due to either plaque / thrombus .
Mumurs can be heard with stethoscope when
There is valve stiffing or the heart muscles
Korotkoff sounds
Sounds heard when measuring blood pressure via ausculatory method
How RAAS is stimulated in during hypotension
- Decrease sympathetic stimulation on JG cells of the glomerulus 2. Decrease plasma electrode level by macula densa cells in distal converting tube 3. Decrease blood pressure which detect by renal Baroreceptors.
Angiotensin II action pathway
- Act on adrenal cortex increase secretion of aldosterone 2. Act of posterior pituitary glands increase secretion of ADH 3. Act on hypothalamic thirst centre increase WATER absorption 4. Act in the kidney causes Na , Cl amd H2O reabsorption
What there factors stimulate ADH real see from the posterior pituitary glands
- Increase angiotensin II plasma concentration 2. Decrease in blood plasma low H2O 3. LWO Na concentration in the glomerular filtration
In general kidney will retain 😋 Na when
when activated by aldosterone
When we want to inhibit noradrenaline mediated effect of vascular constriction what type of drug is mostly used to block action of noradrenaline
Alpha blockers e.g phentolamine this because most alpha blockers are located in blood vessels and when activated will cause vasoconstriction
A 40 year old lady was running for the bus. As a result of the additional sympathetic output to her heart, positive inotropy and chronotropy would be observed in her left ventricle. What changes would you expect to occur with respect to her left ventricle?
Increased sympathetic output increases both the force (inotropy) and rate (chronotropy) of contractions, which results in increased pressure when the heart contracts (systolic pressure), stroke volume (amount of blood ejected), stroke work (work done by ventricles to eject blood) and heart rate, as the heart is working much harder. As more blood is ejected from the heart, it is logical that both the end-systolic and diastolic volumes will decrease
In aortic pressure tracings, an incisura or dicrotic notch is seen at the end of systole.
What is the cause of this dicrotic notch?
At the end of the systole, ejection of blood from the left ventricles has just ended, such that the pressures in aorta just exceed the pressure in the left ventricle. As a result, the aortic valves close, which causes a slight backflow of blood into left ventricles. There is hence a slight temporary decrease in the aortic pressure, which is what the incisura or dicrotic notch refers to
Adeno(S)ine = (S)lowing down, At(R)opine = make the heart (R)apid
Depolarisation during an action potential is primarily caused by which gate channel
Influx of sodium through voltage-gated ion channels
NOT
ligand-gated ion channels do not play a primary role in the depolarization phase of the action potential. Ligand-gated ion channels open in response to the binding of specific molecules or ligands to the receptor sites on the channel protein, but they are not directly involved in generating the action potential.
The “funny” current is activated by [blank] rather than depolarisation.
A
Hyperpolarisation
How to measure the P-R interval
from the beginning of the P wave to the beginning of QRS complex
ST segment is where
Ventricule systoly coccur
the sympathetic stimulation cause what to the slop of pacemaker potential
It increases it Make it sharper
in cornonry artery surgery
internal mammary artery can be used as graft
If a patient had aggressive CPR what should be avoided
throumbolysis
during passive filling the artries and ventricules is close to zero
True
difference between first degree heart block and sinus bradycardai
First-degree heart block is a delay in the transmission of electrical impulses from the atria to the ventricles, which results in a prolonged PR interval on an ECG. Sinus bradycardia is a slower than normal heart rate due to a decrease in the firing rate of the sinoatrial node, with a normal rhythm and PR interval on an ECG.
The additional heart sound heard on examination in this patient occurs in late diastole, just before the first heart sound.
S4
Evaluation of sections of the myocardium demonstrates evidence of apple green birefringence with polarised light. What is the most likely diagnosis?
Amyloidosis
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