CVS Flashcards
What is afterload? And what is it roughly equivalent to?
The pressure in the wall of the left ventricle during ejection. Ie the load the heart must eject blood against.
Roughly equivalent to aortic pressure
What is preload?
The amount of stretch on the ventricles during diastole
What is preload related to?
End diastolic volume
What is total peripheral resistance?
The resistance to blood flow offered by all systemic vasculature
What happens to pressure as it reaches resistance?
The pressure drops
Constricting arterioles decrease pressure where and increase pressure where?
Decrease pressure in the venous side while increasing pressure on the arteriole side
What happens to pressures during vasodilation? (Peripheral resistance decreased)
Reduction in the arteriole side, increase in the venous side
What happens to the pressures if you increase peripheral resistance EG vasoconstriction
An increase in arteriole pressure and a decrease in venous pressure
If you increase cardiac output (SVxHR) but keep peripheral resistance the same what will happen to arteriole and venous pressures?
Increase in arteriole
Decrease in venous
If you keep the total peripheral resistance the same but decrease the cardiac output (SVxHR) what will happen to the venous and arteriole pressures?
venous pressure will increase and arteriole pressure decrease.
If a tissue needs more blood, what needs to happen?
Dilation of precapillary sphincters
If precapillary sphincters dilate what will happen to total resistance?
What does the heart need to do in response?
Reduction in total peripheral resistance
Heart needs to increase cardiac output to maintain BP.
How does the heart detect the fall in blood pressure due to something like dilation of a pre-capillary sphincter?
Baroreflex
What is cardiac output?
The amount of blood ejected in 1 minute. Stroke volume (end systolic volume-end diastolic volume) x HR
In ventricular filling, when should the ventricles stop filling ?
When they reach the pressure of the veins
What does the ventricular compliance curve describe?
With increased venous pressure, increased heart filling occurs.
The ventricular compliance curve can be increased and decreased in disease state. That can be problematic due to the association of this curve with what law?
Starlings law of the heart
What does starlings law of the heart state?
The more the heart is stretched (within reason) the greater the force of contraction
Starlings law of the heart is linked to what curve associated with the cardiac myocytes
Length tension curve of sarcomeres
In theory why does increased stretch increase contraction?
More exposed binding sites for the actin-myosin power stroke.
On top of the intrinsic control from stretch what other extrinsic factors can alter contractility?
Adrenaline and sympathetic stimulation
When aortic pressure increases as a result of an increase in total peripheral resistance what happens to heart filling?
Venous pressure reduces, thus a decrease in filling of the heart.
When we exercise total peripheral resistance falls. Explain why? And what happens next (dismissing sympathetic stimulation)
Heart and muscles require more oxygen therefore vasodilation.
A decrease in total peripheral resistance increases venous pressure.
More blood pushed back to heart and increased filling
Increased filling, increased stretch, increased cardiac output
Blood entering the right atria is from where?
Superior and inferior vena cava and coronary sinus
Blood leaving the right atria into the right ventricle, goes through what valve?
tricuspid
Blood leaves the right ventricle through what vessel and what valve
Pulmonary artery, Pulmonary valve
Blood from enters the left atria from where?
Pulmonary vein
Blood from the left atria reaches the left ventricle, passing through what valve
Mitral
Blood is ejected from the left ventricle through what valve and into what vessel
Aortic valve, into the aorta
What is seen on the left and right apical areas of the heart, closely wrapped around major vessels
Oracles
What causes a valve to open or close?
Pressure changes
What stops inversion of the mitral and tricuspid valves during systole?
Papillary muscles attached via chordae tondonae
What is the pressure roughly, in the left atrium
8-10mmHg
What is the pressure of the left ventricle roughly in systole and diastole
Systole 120 mmHg
Diastole 10 mmHg
What is the pressure in the right atrium roughly
0-4 mmHg
What is the pressure in the right ventricle during systole and diastole
Systole- 24mmHg
Diastole 4 mmHg
What is the pressure in the pulmonary artery during systole and diastole?
Systole- 24mmHg
Diastole 10mmHg
In what direction does the conduction system cause contraction. At a local myocytes level and globally in the ventricles
From inner to out, endocardial to epicardial
From the apex upwards
How many stages of the cardiac cycle are there?
7
The first stage of the cardiac cycle (usually thought of as) is atrial contraction;
What happens in regards to filling?
Final 10% of ventricle filled
During atrial contraction what position are the valves in?
tricuspid and mitral are open
Aortic and pulmonary are closed
What is the ventricle volume considered at the end of atrial contraction?
End Diastolic Volume
What follows atrial contraction?
Isovolumetric contraction
What heart sound is produced with isovolumetric contraction and why?
S1
Ventricle pressure exceeds atrial and causes closure of mitral and tricuspid valves
What happens to the volume of the ventricles with the s1 heart sound?
Volume stays the same (isovolumetric contraction)
What follows isovolumetric contraction?
rapid ejection
What is happening during the rapid ejection phase at both the ventricles and atria
The ventricle pressure exceeds the aorta, opening the aortic valve (same on other side) rapid decrease in ventricular volume
Blood is filling the atria
What follows rapid ejection?
reduced ejection
What is occurring, in relation to pressures in reduced ejection
A decline in ventricle pressure and a slow increase in atrial pressure
What follows reduced ejection?
Isovolumetric relaxation
What causes the aortic valve to close?
Brief backflow due to decreased ventricular pressure
What heart sound is produced when the ventricular pressure falls inducing back flow?
S2- closure of aortic valve
What volume does isovolumetric relaxation relate to?
end systolic volume
What follows isovolumetric relaxation?
Rapid filling
What happens in rapid filling, and what might be heard
Ventricular pressure below atrial so the mitral valve opens.
S3 can be heard sometimes
What is the final stage between rapid filling and atrial contraction? And what volume does it relate to?
Reduced filling
Ventricles reaching inherent relaxed volume (90%)
What is a typical stroke volume? What does that equate as?
80ml roughly
EDV-ESV
A heart at rest beat cycle lasts 0.9 seconds. How long is systole and how long is diastole?
.55 diastole
.35 systole
Which part of the cardiac cycle decreases with an increase in heart rate?
Duration of diastole
What does S1 represent
Closure of mitral valve
LUB
What does s2 represent?
Closure of aortic and pulmonary valve
DUB
What is S3 known as? And is it ever normal?
Ventricular Gallop
Normal in children
What causes heart sound s3 in an adult
A sudden deceleration of blood flow into the left ventricle
What does the prescence of s3 indicate
Congestive heart failure
what are some causes of aortic stenosis
Degenerate
Congenital
Rheumatic fever
What effect does aortic stenosis have on blood flow?
What is the resultant pressure change?
How does the body adapt to this?
Less blood through the aortic valve
Raises LV pressure
Hypertrophy of the left ventricle
What long term effect does having a hypertrophic left ventricle and aortic stenosis have?
Left sided heart failure
Angina (more tissue to perfuse)
Syncope
What effect can aortic stenosis have on RBC count? Why?
Decrease due to shearing forces inducing a microangiopathic haemolytic anaemia
What causes aortic valve regurgitation?
Aortic root dilation (leaflets pulled apart)
Valvular damage- endocarditis, rheumatic fever,
LV dilation
Myxomatous degeneration post heart attack
What is the main cause of mitral valve stenosis
Rheumatic fever (99.9%)
Where does pressure increase in Israel valve stenosis?
Left atria, venous system
What part of the heart is likely to become hypertrophic in mitral stenosis
The Right ventricle
What happens to the left atria in mitral valve stenosis
Left atria dilates
Where are some symtoms of mitral valve stenosis
Pulmonary oedema, dyspnoea, pulmonary HTN
How is MAP calculated?
Diastolic pressure + 1/3 of pulse pressure
OR
Cardiac output (stroke volume heart rate) x total peripheral resistance.
What is haemodynamic shock?
And what is circulatory shock?
- Acute condition of inadequate blood flow throughout the body
- A catastrophic fall in arterial pressure
In reference to the MAP, what can we stipulate shock can be a result of?
CO x TPR
Therefore a fall in either can result in shock
What is the bodies natural response to avoid shock?
Altering either TPR or CO
In a nutshell shock can be due to what 4 methods?
Cardiogenic
Mechanical
Hypovolaemia
Excessive vasodilation
What is cardiogenic shock?
A failure of the pumping action of the heart. Eg ventricle not fully emptying
What is mechanical shock?
An obstruction e.g ventricle cant fill
Is cardiac arrest part of haemodynamic shock?
No, but shock can progress to cardiac arrest
What is cardiac arrest
Unresponsiveness associated with lack of pulse
What is asystole
Loss of electrical and mechanical activity in the heart
What is PEA in the heart
Pulseless electrical activity
What is ventricular fibrillation?
When can it commonly occur?
What does it often lead to?
Uncoordinated electrical activity of the ventricles
Following MI, electrolyte imbalances and arrythmias
Cardiac arrest
What’s the difference between BLS and ALS
Basic- just compressions
Advances- defib
How does a defibrilator work?
Depolarises the cells into refractory period, giving time for coordinated activity to restart
Why is adrenaline given in shock
Increases cardiac output and peripheral resistance
In cardiogenic shock. Is the filling an issue?
No the heart fills but it doesnt pump correctly
In cardiogenic shock what clinical sign can sometimes be spotted? Why is this?
Raised JVP due to increased central venous pressure
What happens to arterial blood pressure in cardiogenic shock?
Decreases
In cardiogenic shock, what organ in particular suffers from a lack of perfusion? What clinical sign might occur?
Kidney
Oliguria (reduced urine output)
Is filling of the heart an issue in mechanical shock?
Yes, there is a restriction to filling
Give an example of something that can cause mechanical shock
Cardiac tamponade
Massive Pulmonary emobilsim
What happens to pressures in arterial and venous systems with mechanical shock?
Increase in venous, decrease in arterial
How would a massive PE cause mechanical shock?
If it occluded a large pulmonary artery so that the right ventricle cant fully empty
Back pressure increases venous pressure while decreasing arterial.
what is hypovolaemic shock commonly due to?
Haemorrhage
How much blood loss is likely to cause hypovoelemic shock?
20% upwards
In hypovolaemic shock what happens to venous and arterial pressures
Venous pressure falls, leading to arterial pressure to fall
What is the bodies response to hypovoelimic shock?
Baroreflex induces vasoconstriction, tachycardia, increased force of contraction (chrontropy and inotropy)
What is internal transfusion in shock?
A reduction in the capillary hydrostatic pressure causing a net movement of fluid into the capillaries
Given the physiology behind hypovoelemic shock what patient signs would be present?
Weak pulse, pale, tachycardia and cold
Aside from haemorrhage what else can cause hypovoelemia ?
Severe burns
Excessive diarrhoea or vomiting (due to loss of Na)
What is ‘shutdown’ in relation to tissue perfusion
Peripheral vasoconstriction reducing tissue perfusion
What can occur due to ‘shutdown’
Damage due to hypoxia
Local release of vasodilators causing further bp fall
Multi system failure
What longer term response aims to restore blood volume
RAAS and ADH
How long would a 20% loss of blood take to restore (given adequate salt and water intake)
3 days
What is normovoelemic shock?
A distributive shock caused by loss of resistance (vasodilation)
What can commonly cause a distributive shock?
Sepsis- toxic shock
How does toxic shock occur
Endotoxins released by circulating bacteria cause vasodilation.
Secondly capillaries become leaky in response
When is it septic shock?
When there is persisting hypotension that requires treatment to maintain DESPITE fluid resuscitation
What other common form of shock is distributive?
Not toxic/septic
Anaphylactic
What causes distributive shock in anaphylaxis?
Mast cells secrete histamine that cause massive vasodilation
What else occurs in anaphylactic shock (aside from mass vasodilation)
Bronchoconstriction and laryngeal oedema
What treatment is required in anaphylactic shock and why?
Adrenaline for its vasoconstrictive effects
What sets the resting membrane potential in a cardiac myocyte
K+ permeability
Why isn’t the cardiac myocytes resting potential equal to Ek
Due to small permeability to other ion species at rest
What is the result of an action potential in a cardiac myocyte
Calcium influx leading to contraction
A cardiac myocytes action potential has what additional stage when compared to a axon potential
Plateau following depolarisation
What is happening to a cardiac myocyte during diastole?
Maintains resting potential
What is the first stage of a cardiac action potential and what are the rough voltages
Opening of voltage gated sodium channels.
Depolarising the cell from -85 to +20mv
During the cardiac myocytes action potential what brings the voltage from +20mv to 0mv
Transient outward flow of K+
What is happening during the plateau phase of a cardiac myocytes
Opening of voltage gated calcium L type channels with opening of K+ channels
What occurs to bring the cardiac myocyte out of the plateau phase?
Inactivation of calcium channels.
What is special about the sinoatrial nodes electrical activity
It is spontaneously active, transmitting electrical impulses across the heart
Does the sinoatrial node have a resting membrane potential?
No, the most negative it will be is -60 (but slowly depolarising)
What is the pacemaker potential
Funny current. Slow depolarisation caused by influx of Na+
What channels are responsible for the funny current
Hyperpolarisation activated cyclic nucleotide gated channels (HCN)
Once the funny current reaches threshold what happens
L type calcium channels open to cause upstroke before voltage gated potassium channels open
HCN channels activate what messengers
Cyclic AMP and cyclic GMP
Why does the SA node set the rhythm
It’s cells are the quickest to depol
The SA node being \_\_\_\_ causes \_\_\_\_\_ 1 slow 2 failing 3. Quick 4. Random
- Bradycardia
- Asystole
- Tachycardia
- Fibrilation
What is the normal range for plasma levels of K
3.5-5.5 mmol
Why does plasma K have to be tightly controlled in relation to the heart
It’s levels are important for resting potential
In hyperkalemia what happens to the resting potential of the cell
It is less negative
Why is having a less negative RMP dangerous?
It can lead to Na channels remaining inactivated.
Initial excitability followed by potential inability to fire action potential
How can we treat hyperkalaemia in regards to preventing cardiac arrest
Calcium glauconate (makes heart more excitable) Insulin and glucose ( Insulin promotes K moving into the cell)
What effect does hypokalaemia have on action potentials?
Lengthens them and delays repolarisation
What is EAD and what can it result in
Early after depolarisations- VF
In contraction coupling what is the effect of depolarisation?
L type calcium channels open in t tubule
In contraction coupling, when calcium enters the cells what happens
Localised induced calcium release (in myocytes from sarcolemma and sarcoplasmic reticulum)
What does calcium bind to in contraction coupling
Troponin
When calcium binds to troponin what happens
Conformational change shifting tropomyosin revealing the actin binding site.
How is calcium returned back to normal level after contraction?
Most pumped back into sarcoplasmic reticulum via SERCAtpase, some out of the cell membrane via Na/C exchange and sarcolemma calcium atpase.
What nervous system co-ordinates the bodies response to exercise and stress?
ANS
What are the 2 divisions of the ANS
Sympathetic and parasympathetic
What is the main function of the ANS
Regulate physiological functions- HR, Body temp, BP
What activity of the ANS is increased with stress?
Sympathetic
When is parasympathetic ANS more dominant?
Under basal conditions
What receptor is found in the pupil of the eye to signal for dilation (contract radial muscle)
Alpha 1
The airways of the lungs have what receptors for sympathetic effect? What do they do in the lungs?
Beta 2
Relax
What receptor in the heart is there for sympathetic effect? What does it do?
Beta 1
Increase rate and force of contraction
Sweat glands have what 2 receptors for sympathetic effect? What do they do?
Alpha 1- localised secretion
Muscarinic 3- generalised secretion
What receptor in the pupil of the eye recieves parasympathetic stimulation? What does it do?
M3
Contraction (contracts sphincter muscle)
What receptor in the lungs recieves parasympathetic? What does it do?
M3
Contracts
What receptor in the heart recieves parasympathetic input? What’s the outcome?
M2
Decrease rate
If sympathetic drive to the heart increases, does that mean other sympathetically regulated activity is increased?
No different tissues independently regulate
BUT- on some occasions there is a more co-ordinated response
The ANS controls what in the cardiovascular system (4)
Heart rate
Force of contraction
Peripheral resistance of blood vessels
Amount of venoconstriction
What does the AND not do in the cardiovascular system
Initiate electrical activity
At rest the heart is normally under what influence?
Vagal
Parasympathetic dominating
The vagus nerve is what cranial nerve?
10 (x)
Where does the vagus nerve synapse?
Epicardial surface within walls of heart at SA and AV node
What do the post-ganglionic cells of the vagus nerve release?
ACh
What receptors does the vagus nerve act on? What 2 effects?
M2
Decrease rate
Decrease AV conduction velocity
Where do the postganglionic fibres of the sympathetic nervous input to the heart come from?
Sympathetic trunk
What does the sympathise trunk innervate?
SA, AV and myocardium
What do the sympathetic trunk nerves release?
Noradrenaline
What receptors does the sympathetic nervous system act on? And what are the effects (2)
Beta 1
Increase rate and increase force
Where is the cardiovascular centre in the brain
Medulla oblongata
What makes the funny current in the heart?
Turning on of a slow Na+ conductance
What sets the rhythm of the heart
AP firing in the SA node (sinus rhythm)
What effect does sympathetic activity heave on the funny current?
Increases the slope
How does the sympathetic nervous system increase the slope of the SA node funny current?
Beta 1 receptors
Gs protein
Increase cAMP
What effect does parasympathetic activity have on the funny current?
Decreases the slope
how does parasympathetic activity decrease the slope of the funny current in the SA node?
M2 receptors
- Gi- inhibits adenyl cyclase
- Ggamma- increases K+ conductance to cell.
How does noradrenaline acting on a B1 receptor increase the force of contraction?
Gs-> increase cAMP Activate protein kinase A Phosphoryalates calcium channels Intracellular calcium increases sarcoplasmic release. Increased contraction
Most arteries and veins have what receptors?
Alpha 1
Coronary and skeletal muscle vasculature have what receptors?
Beta 2
What allows for vasodilation to occur?
Vasomotor tone
Decreased sympathetic output to alpha 1 receptors results in what?
Vasodilation
Increased sympathetic output to alpha 1 receptors causes what?
Vasoconstriction
Circulating adrenaline has a higher affinity for what receptors?
Beta 2 compared to alpha 1
Circulating adrenaline having a higher affinity for beta 2 receptors compared to alpha 1 causes what?
Vasodilation of vessels with beta 2 (skeletal, myocardium, liver)
At very high levels of adrenaline in the body what does circulating adrenaline do?
Activate both beta 2 and alpha 1
How do beta 2 adrenoreceptors cause vasodilation
Increased cAMP->PKA-> potassium channels and inhibition of myosin light chain kinase-> relaxation
How does activation of alpha 1 receptors cause vasoconstriction?
Stimulates Ip3-> pip/dag-> increases calcium influx causing contraction.
What tissues produce more metabolites?
Active ones
What effect do local increases in metabolites have (eg adenosine, K+, H+, PCO2)
Strong vasodilator effects
What’s the most important for ensuring adequate perfusion of skeletal and coronary muscles?
Metabolites compared to beta 2 receptors
What receptors detect low pressure in the cardiac system?
Atrial receptors
Where are baroreceptors for the CVS system located?
Carotid sinus
Aortic arch
What is the baroreceptor reflex?
Increase MAP detected
Afferent to medulla
Efferent to heart and vessels
Vassolidation and bradycardia
What happens to barroreceptors when high BP persists
Re set to higher pressure
What are sympathomimetics?
Alpha adrenoreceptor and beta adrenoreceptor agonists
What are cholinergics?
Muscarinic agonists and antagonists
What sympathomimetic is used to restore function in cardiac arrest?
Adrenaline
What beta 1 agonist may be given in cardiogenic shock?
Dobutamine
What is salbutamol?
Beta 2 agonist
What is the action of a non selective beta1/2 antagonist like propranolol?
Slow heart rate and force of contraction (b1) Causes bronchoconstriction (b2)
What is used instead of a non selective b1/b2 antagonist ?
Selective b1 atenolol.
One cholinergic agonist and its use
Pilocarpine
Activator constrictor papillae
One cholinergic antagonist and its use?
Tropicamide
Dilate pupils
What is the short term regulator of blood pressure
Baroreceptors reflex
What does the baraoreceptor reflex adjust?
Sympathetic and parasympathetic input to the heart to alter cardiac output and TPR
Does the baroreceptor reflex have a sustained control on blood pressure
no
What is controlled in the long term management of blood pressure?
Sodium balance
How does controlling sodium balance alter blood pressure?
Controls the extracellular fluid volume
If you lower extracellular fluid what volume has been reduces?
Plasma volume
What are the four parallel neurohormonal pathways that control circulating volume (therefore bp)
Renin angiotensin aldosterone system
Sympathetic nervous system
Antidiuretic hormone
Atrial natriuretic peptide
Where is renin released from?
Granular cells of juztaglomerular apparatus (JGA)
What are 3 factors that stimulate renin release
Reduced NACL to distal tubule
Reduced perfusion pressure in kidney
Sympathetic stimulation to JGA increases renin release
Reduced perfusion in the kidney causing release of renin is detected by what?
Baroreceptors in afferent arteriole
Where are macula densa cells located?
Distal tubule
What can macula dense detect a change in?
NaCl delivery
Where does the sympathetic stimulation go in RAAS control?
Juxtaglomerular apparatus
What does renin do?
Convert circulating angiotensinogen to angiotensin 1
What happens to circulating angiotensin 1?
Angiotensin converting enzyme converts it into angiotensin 2
What are the 3 main effects of angiotensin 2?
Vasoconstriction
Na+ reabsorbtion
Aldosterone stimulation
Where does aldosterone come from?
Adrenal cortex
How many type of ang 2 receptors are there?
2
What receptor does ang 2 have its main action on?
AT1
What type of receptor is a AT1 receptor
G protein coupled for angiotensin2
Where are 5 sites of the AT1 receptor?
Arteriole Kidney Sympathetic NS Adrenal cortex Hypothalamus
Ang 2 stimulation to an AT1 receptor in the arterioles has what effect?
Vasoconstriction
Ang 2 stimulation to an AT1 receptor in the Kidney has what effect?
Stimulates Na+ reabsorbtion
Ang 2 stimulation to an AT1 receptor in the sympathetic nervous system has what effect?
Increased release of Noradrenaline
Ang 2 stimulation to an AT1 receptor in the adrenal cortex has what effect?
Aldosterone release
Ang 2 stimulation to an AT1 receptor in the hypothalamus has what effect?
Stimulates ADH release, increases thirst sensation
Where does aldosterone principlely act?
Cells of collecting duct
What are 3 actions of aldosterone on the cells of collecting ducts
Na+ reabsorbtion
Activate apical Na+ channel and apical K+ channel
Increase basolateral Na+ extrusion
What is the link between Angiotensin converting enzyme (ACE) and bradykinin?
ACE breaks down bradykinin
If ACE breaks down bradykinin what is the effect and why
Vasoconstriction because bradykinin is a vasodilator
Why do you get a dry cough when taking an ACE inhibitor
Accumulation of bradykinin (vasodilator) as no longer getting broken down
What are some examples of ACE inhibitor
Captopril, lisinopril, enalapril
High levels of sympathetic stimulation does what to renal blood flow?
Decreases it
Why does high levels of sympathetic stimulation reduce renal blood flow?
Vasoconstriction of arterioles
Why does decreased renal blood flow due to sympathetic stimulation increase blood pressure
Decreased glomerular filtration rate resting in decreased Na excretion
The sympathetic nervous system can directly stimulate renin release and reduce blood flow to the kidney, how else can it alter blood pressure?
Activate apical Na/H exchanger in proximal convoluted tubule
The 3 mechanisms of sympathetic stimulation on plasma volume control are?
Change arteriole flow to kidney
Stimulate renin release
Stimulate Na reabsorbtion in proximal convoluted tubule
What is the main role of ADH
Increase water reabsorbtion in distal nephron
What’s another name for ADH
Vasopressin
What is ADH release stimulated by?
Increases in plasma osmolality
Severe hypovolaemia
How does ADH act on Na+ reabsorbtion
Stimulates apical Na/K/Cl co-transporter in thick ascending limb
atrial natriuretic peptide does what to afferent arteriole?
Vasodilates
What effect does increased blood pressure have on GFR
Increases it
What effect does ANP have on sodium along the nephron?
It inhibits Na reabsorbtion
What system works in the opposite direction to RAAS, ADH, sympathetic stimulation in BP control
ANP
What can cause loss of sodium in urine? Neurohormonal control mechanism
ANP
What is loss of sodium in the urine called?
Natriuretic
What do prostaglandins act as a buffer against and why?
Buffer against excessive vasoconstriction (SNS, RAAS) because they are local vasodilators
What’s the effect of PGE2 on GFR
Enhances it and reduces Na reabsorbtion
What is dopamine formed from in the kidney?
Circulating L-DOPA
Where are dopamine receptors present in relation the the kidney?
Renal blood vessels
Cells of proximal convoluted tubule
Thick ascending loop TAL
What does dopamine cause in the kidney?
Vasodilation and increased renal blood flow
What does dopamine do to NaCl in the kidney? How?
Reduce reabsorbtion
Inhibits NH exchanger and Na/K in PCT and TAL
What are the 3 stages of hypertension
Stage 1,2 and severe
What is hypertensions main cause? 95% of cases
Unknown
If the cause of HTN is unknown what is it called
Primary HTN
What are some examples of secondary HTN
Renovascular disease, Chronic renal disease, Cushing
Primary hypertension is what?
Sustained blood pressure of a diastolic above 90 or a systolic above 140
How does renovascular disease cause secondary HTN
Reduced renal perfusion
Increased renin + RAAS activation
How does renal parenchymal disease cause secondary HTN
Na+ and water retention due to inadequate GFR
If the secondary HTN is due to an adrenal cause what is likely being secreted?
Aldosterone
What can HTN lead to?
Heart failure, MI, stroke, renal failure
What is the effect on afterload with HTN
Increased afterload
What can become damaged in HTN
Arterioles
I
If you have increased afterload what are 2 possible effects?
Left ventricular hypertrophy
Increased myocardial oxygen demand
If you have arterial damage, what are 2 possible effects?
Atherosclerosis, weakened vessels
How do you treat secondary HTN
Treat the cause
What are some non pharmacological treatments for HTN
Exercise
Diet
Reduced Na intake
Reduced alcohol intake
What pharmacological treatment for blood pressure affects the RAAS system
ACE inhibitors
What effects does ACE have?
Diuretic and vasodilatory
What is the purpose of an L type calcium channel blocker in HTN treatment?
Vasodilation
What vasodilator is primarily used to treat HTN
L-type calcium channel blocker
In principle what other vasodilator (not an L-type calcium channel blocker) can be used to treat HTN ? Why is it often not?
Alpha 1 receptor blocker
Can cause postural Hypotension
Why are beta blockers less commonly used in the treatment of HTN?
Beta blocker decrease sympathetic output which does lower bp but only used if other indicators eg previous MI
What else can be used tot treat HTN if you have an ACE inhibitor and an L type calcium blocker?
Diuretic
How does a diuretic lower BP
Inhibits Na/Cl cotransproter in distal tubule
What other diuretucis are there, that done have an effect on the distal tubule directly?
Aldosterone antagonist
Fluid collected from clotted blood is known as what
Serum
Fluid collected from unclotted blood is what?
Plasma
What is serum?
Plasma with clotting factors (in particular fibrinogen)
What is the most common cause of increased plasma viscosity
Multiple myeloma
What is an increase in RBC known as?
Polycythaemia
What is an increase in platelets known as?
Thrombocythaemia
What is an increase in white cells known as
Leukaemia
Polycythaemia, thrombocythaemia and leukaemia all result in what?
Increase whole blood viscosity
What is the effect on blood viscosity of raised levels f acute phase plasma proteins?
Minor changes in plasma viscosity
Name some acute phase plasma proteins
Fibrinogen
Complement
CRP
Raised acute phase plasma proteins are usually due to what?
Acute inflammation
A minor change in viscostiy of plasma can be a measure of what?
Inflammation
What marker is used to primarily measure inflammation ?
CRP
What is laminar flow?
Streamline flow with layers staying the same distance apart
What is happening to viscosity in laminar flow
Parabolic profile- the velocity of blood in the centre is greater than on the edges
What is turbulent flow?
When blood is continually mixing in the vessel
When can turbulent flow occur?
When flow is too great When it passes an obstruction Whe it makes a sharp turn When it passes over a rough surface When there is increased resistance to flow
What is the equation for pulse pressure?
Peak systolic pressure-end diastolic pressure
If our BP is 120/80 what is our pulse pressure?
40
What are the 4 stages of pulse pressure
Systolic uptake
Peak systolic pressire
Decline with diacrotic notch
Diacrotic run off
How is MAP estimated
Diastolic+ 1//3 of pulse pressure
E.g 120/80
80+ (1/3 of 40)= 93
A MAP below what level is dangerous and why?
Below 70
Organ perfusion is low
If peripheral resistance is high what can occur?
Retrograde flow
What 2 things can determine the feel of a pulse
The force that the left ventricle is able to eject blood at
The pulse pressure
In pulse strength what kind of things can alter the strength due to changing the left ventricle contraction force
LV failure
Aortic stenosis
Hypovolaemia
What is a strong pulse described as?
Bounding
What can bradycardia do to the feel of a pulse?
Widens pulse pressure leading to bounding pulse
What effect does low peripheral resitance have on diastolic pressure?
Low diastolic pressure
Vasodilation causes what in terms of resistance and diastolic pressure
Low resistance, low pressure
High peripheral resistance does what to diastolic pressure?
High diastolic pressure
Hot bath, exercise, pregnancy can all do what to peripheral resistance?
Lowers TPR
Lowering diastolic pressure eg exercise does what to pulse pressure
Increases it
What 4 systems can present with chest pain
Resp
Cardiac
GI
Msk
What are some examples of respiratory conditions that may present similar to an MI
Pneumonia
PE
What are some differences that a pneumonia presents with compared to an MI
Pain often slightly off to side
Can come with cough, temp and breathlessness
What differences would a patient who has a PE have to differentiate from MI
Pain sharp and well localised
Often worse with inspiration
Likely breathless
What are some examples of MSK pains that could be confused with MI?
Costochondiritis
Rib Fracture
What are some differences with having costochondiritis compared to an MI
Sharp well localised pain
Painful to palpate
What upper GI condition can present similar to an MI?
Reflux
How is reflux often described
Burning central pain
Worse on lying/ certain food
What 2 causes of chest pain related to the cardiac system are there?
Ischaemia
Pericarditis
What would an ischaemic cardiac pain present with?
Dull retrosternal pain/ heaviness
May be worse on exertion
May radiate to jaw, neck, shoulder, arm l>r
A patient with pericarditis would present with what symptoms?
Sharp retrosternal pain.
Can change with position (eased leaning forwards, worse lying flat)
Can worsen with deep breath/cough
Somatic cardiac pain refers to what structures?
Pleural sac, pericardial sac
How is somatic chest pain usually described?
Sharp, well localised, worse with cough/inspiration
What would visceral chest pain likely have as its source?
Heart or lung
Visceral pain is generally described how?
Dull, poorly localised and worse with exertion
What is pericarditis?
Inflammation of pericardium
Pericarditis is usually secondary to what?
Viral illness
What is the pathophysiological route of ischaemic heart disease
Atherosclerosis of coronary arteries
What are some non modifiable risk factors of IHD
Gender (male)
Age
Family history
What are some modifiable atherosclerosis risk factors?
Smoking, HTN, high cholesterol, diabetes, obesity, sedentary life
Is stable angina part of acute coronary syndrome?
No
What is stable angina?
Heart tissue ischaemia only occurs when metabolic demand of the cardiac muscle is greater than what can be delivered by coronary arteries.
What is essential for stable angina?
Relationship between rest and ease of symptoms
When is GTN spray able to relieve symptoms?
In stable angina
What does acute coronary syndrome encapsulate
UNstable angina
Myocardial infarction- STEMI/ NSTEMI
What is unstable angina?
When a stable angina plaque ruptures
If you have unstable angina and the plaque has ruptured, what will follow?
Platelet aggregation and thrombus formation leading to either partial or complete occlusion
What does an NSTEMI represent at a vessel level?
Partial occlusion of the vessel
Are there detectable enzymes with plaque rupture?
No, only once infarct is present
What is the main difference in history of a patient with acute coronary syndrome
Similar to stable angina but more intense and pain lasting longer
What clinical signs might differntiate stable angina from acute coronary syndrome?
Look unwell
Increased autonomic output- pale, nausea, sweating
Do you get heart murmurs with STEMI/NStemi
You can but not always
What are some key diagnostic tests when differentiating whether acute coronary syndrome is occurring
ECG
Blood test- troponin
What would you look at in an ECG when looking for acute cornonary syndrome
ST segment
T waves
Q wave
On an ecg what would you see with a STEMI
ST segment elevation
Hyperacute T waves
In unstable angina and NSTEMI what would you see on ECG
Patterns of ischaemia, ST depression, T wave flattened or inverted
What does a STEMI represent at a vessel level?
Complete occlusion of a vessel
How would you determine if the diagnosis was unstable angina or NSTEMI?
?
What is heart failure defined as
A state in which the heart fails to maintain adequate circulation the body needs despite adequate filling pressures.
Heart failure has a characteristic pattern of what?
Haemodynamic, renal, neural and hormonal responses
What is the primary cause of systolic heart failure?
IHD
What causes of non ischaemic heart disease can lead to heart failure?
HTN dilated cardiomyopathy Valvular issues Restrictive cardiomyopathy Hypertrophic cardiomyopathy
How is heart failure classed?
1-4
What is class 1 heart failure
No symptoms
What is class 2 heart failure?
Slightly limited physically but normal at rest
What is class 3 heart failure
Marked physical limitation but no symptoms at rest
What is class 4 heart failure.
Inability to carry out physical activity and may have symptoms at rest
What is the average cardiac output
5L/min
What is an average LV end systolic volume
75ml
What is an average LV end diastolic volume?
150
What is an average stroke volume
75ml
A normal ejection fracture is what?
50% upwards
What’s the normal weight of a heart?
330g
What 4 things does cardiac output depend upon?
Heart rate
Venous capacity (LV preload)
Aortic and peripheral impendence (afterload)
Myocardial contractility
What occurs in ventricular remodelling following acute infarction?
Initial infarct spreads. Cardiac tissue remodels and scars.
Wall thins to increase capacity
(Decreases cardiac output)
In heart failure what systems are activated
Neuro-hormonal: Sympathetic nervous system RAAS Natriuretic hormones ADH Endothelin Prostaglandins
What is the early compensatory response of the sympathetic nervous system to heart failure?
Increase contractility, vasoconstriction and tachycardia
What is the long term change of the sympathetic nervous system in response to heart failure?
Down regulation of beta andergenic receptors
Noradrenaline induces cardiac hypertrophy.
Up regulation of RAAS
What component of the RAAS causes organ damage in response to heart failure?
Angiotensin 2
What organs are damaged from the upregulation of RAAS in heart failure by angiotensin 2?
Heart- LV hypertrophy, fibrosis and remodelling
Vascular- atherosclerosis, vascular hypertrophy
Kidney- decrease in glomerular filtration rate and increase in proteinuria leading to renal failure
What are sensitive markers for heart failure?
Natriuretic hormones
How do natriuretic hormones respond to up-regulation of RAAS in heart failure?
Atrial stretch causes release of ANP/BNP
Constriction of afferent arterioles to kidneys.
Decreases NA reabsorbtion and inhibits RAAS
What happens to sodium levels in heart failure? Why?
Excess NA retention due to RAAS up regulation
Why is RAAS activated in heart failure?
Reduced renal blood flow
SNS induction of renin from macula densa
What peptides act to balance the effects of RAAS in heart failure (NA+ and H20 balance as well as vascular tone)
Natriuretic peptides
Why do we get hyponatraemia in heart failure?
Excess H20 retention due to excess NA retention
Normally what would hyponatraemia do to ADH (vasopressin) what happens in heart failure? What’s the outcome?
Normally it would inhibit ADH release
In heart failure its stimulated
Causes more H20 retention and increased systemic resistance
What is a poor prognostic sign in heart failure? Why is it being secreted?
Endothelin
Secreted as a renal vasoconstrictor
Why does heart failure lead to oedema?
Increased capillary hydrostatic pressure
What is oedema?
Excessive fluid within tissues interstitium/ intracellular
Why does vascular endothelium have increased arterial resistance in heart failure?
Due to SNS
RAAS
Reduced NO
Increased endothelin
What does increased arterial resistance in heart failure result in systemically?
Cachexia
Renal failure
Anaemia (due to less EPO from kidneys)
What is used to treat anaemia associated with heart failure?
EPO (less produced by kidneys)
Heart failure with normal LV function is known as what?
Heart failure with a preserved ejection fracture
What is the issue with heart failure with a preserved ejection fraction?
Diagnosis is more difficult but mortality is similar
What are some clincal signs of right sided heart failure?
Raised JVP Dyspnoea Hepatic enlargement Ascites Pleural effusion
What are some signs of left sided heart failure?
Fatigue, exertional dysponoae, Orthopnea, gallop rhythm.
What are signs of chronic heart failure?
Pulmonary congestion, venous congestion, dependent oedema
What are some symptoms of chronic heart failure?
Dyspnoea, lethargy, Orthopnea
Where is JVP visualised?
Between 2 heads of Sternocleidomastoid
What is CRT (sacubitril)
Drug that delivers 2 active molecules in salt complex.
One enhances vasorelaxation
One inhibits AT1 receptors
In the viscous circle of heart failure, what is the overlapping cause
A decrease in cardiac output and stroke volume
In the viscous circle of heart failure. Once you have decreased cardiac output and stroke volume. What 2 (main things occur) how are they linked?
There is neurohormonal activation
There is decreased renal perfusion
Decreased renal perfusion additionally increases neurohormoal activation
IN the viscous circle of heart failure, when you have decreased renal perfusion following a decrease in cardiac output and stroke volume, how does that perpetuate a further fall in CO and SV?
There is an increase in sodium and water retention (due to decreased perfusion) this increases blood volume and therefore preload on the heart. This leads to further ventricular dilation and wall stress
In the viscous cycle of heart failure, once you have decreased CO and SV that leads to neurohormoal activation. What primary effects occur and how does that perpetuate further decreases in CO and SV
Increased neurohormoal activation increases systemic vascular resistance. Increased outflow resistance further impairs the LV function thus decreaseing CO and SV
What underpins the treatment of heart failure?
Overactivation of RAAS and SNS
What is prescribed to mange the overactivation of the SNS in heart failure
Beta blockers
What is prescribed to manage the overactivation of RAAS in heart failure
RAAS inhibitors- ACE, ARB, MRA
In what direction to ventricles depolarise
Endocardium to epicardium
What node has the fastest rhythm, what is it?
SA node 60-100
What is the AV node continuous with
Bundle of HIs
How can depolarisation reach the ventricles
Only through the bundle of HIS
Where do the right and left bundle branches lie?
Sub endochrondrially in the IV septum
What is the purkinje fibres role?
Allow rapid spread of depolarisation through ventricular myocardium
4 meters per second
If depolarising waves are heading towards a lead. What will happen?
Positive complex
If depolarising waves are heading away from a lead, what will happen?
Negative complex
If repolarisation waves are heading towards a lead what will be seen?
Negative complex
If repolarising waves are heading away from a lead, what will be seen?
Positive complex
What can change the size of complex on ECG ?
Size of signal, direction (if straight at electrode larger deflection)
When can you see SA node depolarisation on an ECG
You cant see it as its too small, but assume its directly before start of P wave
What does the P wave represent
The spread of depolarisation across the atria
What happens on an ECG as the depol reaches the AV node
There is an isoeletric flat line where no activity is detected
Other than the AV node delay, what else contributes to the isoelectric flat line following a P wave
The spread through the fibrous ring and bundle of HIS
What direction is the Q wave seen in lead 2 and why?
Downward deflection due to oblique depolarisation in the septum
What does the R wave represent?
Depol spreading towards the apex
What can give a larger R wave
Cardiac hypertrophy
What is the S wave caused by
Depolarisation away from lead 2 to base of heart
How is repolarisation seen on ECG
As a t wave, upwards as it is moving away
How many views of the heart does an ECG give you
12
How many chest leads?
6
How many limb views? What are they
AVR, AVL, 1,2,AVF, 3
What views look at the inferior heart?
2,3,AVF
What leads look at the left side of the heart
1 AVL
What do V1/2 chest leads look at?
Right ventricle and septum
What do v3/4 chest leads look at
Apex and anterior wall of ventricles
What do V5/6 chest leads look at
Left ventricle
What is one second on ECG paper
5 large squares, 25 small ones
1 large square is how many seconds
0.2
1 small square is how many seconds
0.04
How many boxes is the pr interval
3-5
How many boxes is the QRS
3
Abnormal rhythms on ECG are due to what (2)
Abnormal impulse formation
Abnormal conduction
Supraventricular rhythms can arise from where?
Sinus node
Atrium
Av node
Ventricular rhthms arise from where?
Ventricle only
Supraventricular rhythms will always have normal what?
Normal ventricular depolarisation
Normal narrow QRS complex
Ventricular rhythms demonstrate what changes?
Longer depolarisation
Wide and bizarre QRS complexes (dependent on foci)
What are 3 ventricular rhythms
Ventricular premature beats
VT
VF
What ECG changes are seen with an atrial beat
The p wave doesnt have perfect round shape
What ECG changes are seen in an AV junctional beat? What different AV junction beats are there?
The P wave becomes inverted (depol heading upwards)
High, middle or low AV junctiona beats
The shape of a ventricular rhythm will dependent on what?
The foci of the beat
What is lead 2 usually best for looking at?
P waves
Rhythm
What are some key ECG changes with AF
No p waves just wavy baseline
Impulses arrive at AV node rapidly and irregularly
Some are conducted to ventricles and form normal QRS
In AF what is the pulse and heart rate described as
Irregularly irregular
What is the reason fo AF
Multiple atrial foci chaotically impulsing
What does the atria do in AF
Quiver rather than contracts
What is an AV conduction block (both its lay name and what it is)
Heart block
A delay or failure of conduction of impulse from atrium to ventricles via AV node or bundle of HIS
What are causes of AV conduction blocks
acute MI
Degenerative
What different types of heart block are there
First degree
Second degree: mobitz type 1 and type 2
Third degree aka complete heart block
What rhythm develops in complete heart block
Ventricular escape rhythm
What ECG changes are seen in first degree heart block
PR interval prolonged over 5 small squares
Normal QRS
What’s happening in first degree heart block
Slow conduction in av node and bundle HIS
What is 2nd degree mobitz type 1? What phenomenon is happening
Wenkebach phenomenon
There is progressive lengthening of the PR interval until one P is no conducted.
What is seen on the ECG of 2nd degree type 2 heart block?
Sudden non-conduction of a beat (dropped QRS), normal PR interval
What is the risk of 2.2 heart block
High risk of progressing to CHB
What is happening in 3rd degree heart block?
The impulses from the atria cant reach the ventricle. Results in ventricular pace maker taking over
What is seen on ECG of 3rd degree heart block
Dissociation of P- QRS
Very slow QRS complex that are usually wide
What rate does a ventricular escape rhythm normally run at
30-40bom
What are the clincal implications of 3rd degree heart block
HR often too slow to maintain BP
Urgent pacemaker needed
What is seen on ECG with a ventricular ectopic beat?
Wide QRS in a different shape
Why is the QRS wider in ventricular ectopics
Slower depolarisation
What’s ventricular tachycardia defined as?
Run of 3+ ventricular ectopics
What is VT described as?
A broad complex tachycardia
What’s dangerous about VT
Persistent VT at high risk of VF
What’s occurring in VF
Abnormal chaotic, fast chaotic ventricular depol
Impulses from numerous ectopic sites
What’s the clincal outcomes of VF
There’s no coordinated contraction, no cardiac output and therefore cardiac arrest
Where are changes of ischaemia or MI seen
In the leads that are facing the area
I want to look at the inferior aspect of the heart, what leads should i look at
2,3, AVF
I want to look at the lateral aspect of the heart, what leads should i look at
1, AVL, V5, V6
I want to look at the septum, what leads should i look at
V1, V2
I want to look at the anterior heart, what leads should i look at
V3,4
What heart muscle is the most vulnerable
Sub-endocardial (furthest away from coronary )
When is ‘flow’
Diastole
Why does exercise decrease myocardial perfusion
Diastole is shorter with rapid heart rate, there is less time for blood flow.
What do leads facing an area of reduced myocardial perfusion show?
ST segment depression and T wave inversion
When are ischaemic changes seen on ECG
May only be during exercise but with severe lumen reduction seen at rest
What is reduced myocardial perfusion caused by
Coronary atherosclerosis
What is seen acutely in the ECG of unstable angin/ NSTEMI
T wave inversion or
ST depression
What is seen weeks after unstable angina or NSTEMI on ecg
St and t waves normal
No Q waves
If a muscle injury extends the full thickness from endocardium to epicardium, what is the result?
STEMI
What is a STEMI due to?
Complete occlusion of lumen by thrombus
What is seen on ECG of a STEMI
ST segment elevation in leads facing area
What happens in a stemi if perfusion is not re-established?
Muscle necrosis
In the days that follow a STEMI, what ECG changes are seen
T wave inverts, Q wave deepens.
After weeks it normalises other than the deep Q wave
What does a pathological q wave look like
Over 1 small square wide
A depth more than 1/4 of the r wave
What do pathological q waves indicate
Necrosis
What happens to the resting membrane potential in hyperkalaemia
Less negative
What happpens to the RMP in hypokalaemia
More negative
What ECG changes are seen in early hyperkalaemia (7)
High t waves
What ecg changes are seen with a serum potassium of 10
VF
What ecg changes are seen in hyperkalaemia with a serum potassium of 8
Prolonged PR interval
Depressed ST segment
High T wave
What ecg changes could be seen with a serum potassium of 3.5
Low t waves
What ecg changes could be seen with a serum potassium of 2.5
Low t wave, low st segment
The overall direction of spread of the ventricular depolarisation is called what
Cardiac axis
Where is the normal cardiac axis
Down to the left
-30 to +90
What is a left axis (less than -30) deviation associated with
Conduction block of anterior branch left bundle
Inferior MI
LVH
What is a right axis deviation (+90) associated with
RVH
Cardiovascular drugs can alter what? (Some drugs alter more than one of these aspects)
Circulating blood volume
Peripheral resistance and blood flow
Force the heart contracts at
Rate and rhythm of the heart
What is Atrial flutter?
Atrial chambers beat too fast and are out of sync with the ventricles- usually due to circular organised motion
The difference between flutter and fibrilation is that flutter is regular
What is atrial fibrilation
Disorganised contactions of the atria, irregularly irregular
What are the two types of tachycardia?
Supraventricular and ventricular
What are some potential causes of tachycardia?
Ectopic pacemaker activity
Afterdepolarisations
AF/AFL
Re-entry loops
What are 2 causes of ectopic pacemaker activity?
1, damaged myocardium that depolarises spontaneously
2, latent pacemaker region activated due to ischaemia that dominates over the SA node
What do afterdepolarisations cause?
Tachycardia following triggered activity
What is sick sinus syndrome
Sinus bradycardia due to an intrinsic issue to the SA node causing slow depolarisation
Other than sick sinus syndrome what else can cause a sinus bradycardia?
Beta blockers and calcium channel blockers
Conduction block at AV node or bundle of HIS
What is triggered activity?
Delayed after depolarisation
Early after depolarisation
What is a delayed after repolarisation and when is it more likely to happen?
Action potential straight after RMP has resumed
More likely to happen if intracellular calcium is too high
What is early after depolarisation? When is it more likely to occur?
As the cell is returning to RMP another action potential occurs potentially leading to oscillation
More likely to happen when action potential is prolonged
Do re-entrant mechanisms occur in the normal heart? Do they occur when a complete block of conduction has occurred?
No, No
Re-entrant depolarisations occur when there is incomplete unidirectional damage
What is a re-entrant loop? What can it cause?
When a circular loop occurs of action potential that isn’t being stopped by cells in refractory period
Can cause:
AF in atria
Av nodal re-entry
Accessory pathway between atria and ventricles, wolf Parkinson white syndrome
What are the 5 basic methods/classes of drugs used to treat arrythmias?
- Drugs that block voltage sensitive sodium channels
- Antagonists of beta adrenoreceptors
- Drugs that block K channels
- Drugs that block calcium channels
- Adenosine (not 1-4)
What is an example of a drug that is used to treat arythmia that blocks voltage sensitive Na channels?
How does it stop arythmia?
When is it used clinically?
Lidocaine
Blocks Na channels in open or inactive state- preferentially damaged depolarised tissue as these fire automatically.
Used post MI if patient has signs of VT
What drug in antiarythmia treatment is a beta blocker?
How does it have its affect?
What does it treat?
When is it used?
Propranolol
Blocks beta 1 decreasing sympathetic input by decreasing the slope of pacemaker potential in SA node.
Prevents supraventricular tachycardia, slows rate in AF
Also used following MI to decrease work of heart
Also prevents ventricular arythmia
Also used in myocardial ischaemia
Potassium channel blockers are generally not used to treat arythmia due to arythmia causing effect, what drug is the exception and when is it used?
Amioderone, treatment on Wolff Parkinson white and can also suppress ventricular arythmia post MI
What drug treats arythmia by blocking calcium channels?
How does it work?
Veramipril
Decreases slow of AP at SA node, decreasing AV nodal conduction and decreasing force of contraction
What is Adenosines mode of action? How can it be used in short spells of time?
Acts on A1 receptors at AV node enhancing K conduction and hyperpolarising cells to terminate re-entrant SVT
Has a short half life
What are the two drug methods in treating heart failure, which one is predominantly used?
- Using positive inotropy to increase cardiac output
2. Drugs that reduce the work of heart (predominant use)
What is DIgoxin an example of?
How does it work? (Channel change and nerve change)
What’s the result?
When would it be used in Heart failure?
Cardiac glycoside
Channel- blocks Na/K atpase, leading to increase Na inctracelluar, which leads to less Na/Ca out of cell. Ca stores increase within the cells increasing force of contraction
INcrease vagal nerve activity- slowing AV conduction
Decrease HR and INcrease contraction force
Used when arrythmias like AF are also present in HF
What is Dobutamine and when is it used?
Beta adrenonergic agonist used in cardiogenic shock or acute but reversible heart failure
What 3 drug classes are predominantly used in heart failure treatment
ACE inhibitor
Beta blocker
Diuretics
What effect does anACE initiator have i reference to decreasing work load for a heart failure patient?
Decrease vasomotor tone thus decreasing afterload
Decrease blood volume which reduces preload
When does angina occur?
What is it due to?
How do you want to treat it ? Generally
When oxygen supply doesnt meet demand of heart (no myocytes death)
Due to narrowing of coronary arteries
Reduce the work load of heart and improve blood supply
Briefly explain how the following drug classes will help with myocardial ischaemia
Beta blocker
Calcium channel antagonist
Glycerol trinitrate
Beta blocker- decreased work by decreases sympathetic
Calcium channel antagonist- decrease AV node conduction and chronotropy
Glyceryl nitrate- venodialtion , collateral coronary dilation
How do organic nitrates cause dilation of vessels?
React with thiols in smooth muscle to give NO release
NO activate gunylate cyclase which increases cGMP which lowers inreacellular calcium causing relaxation
What heart conditions come with an increased risk of thrombus
AF
Acute MI
Mechanical prosthetic heart valves
What are some anticoagulants? And general site of action
Heparin inhibits thrombin
Warfarin inhibits vitamin K
Digabatran-oral thrombin inhibitor
Aspirin- antiplatelte
What is HTN associated with?
What are some resultant drugs used for this?
Increased blood volume (due to Na and water retention) or increased TPR
ACE inhibitor- lower blood volume, and TPR
Calcium channel blocker- selective for smooth muscle
Diuretic
Beta blocker and alpha 1 antagonist not routinely used
What is pericardiocentesis?
Procedure to remove blood/fluid from pericardial sac
What heart sound would you hear with pericarditis?
Friction rub
Later effusion would result in soft distant heart sound
What’s the physiological range for CVP
3-8mmHg
What mechanism maintains the right and left eject the same volume over a minute?
Frank starling mechanism
What does ASKME refer to in relation to JVP pressure?
The JVP pulse pressure changes Atrial contraction Systole Klosed tricuspid Max atrial filling Emptying of atria
What is coarction of the aorta?
Narrowing of the aorta where the ductus arteriosis was
Decreased peripheral pulses as a result
What makes up the tetralogy of fallot
Overriding aorta
Pulmonic stenosis
VSD
RVH
What cardiac issues is down syndrome associated with?
VSD and ASD
What heart sound is heard with a patent ductus arteriosus?
Long crescendo following S2
What would the physiological effects of poisoning by using a acetylcholinesterease inhibitor be?
AUtonomic- increased saliva and pancreatic juices, decrease HR and BP, pupil constrict
NMJ- paralysis due to NMJ blockade
Brain- initial increase with convulsions followed by depression
What’s an acetylcholinesterase?
Breaks down Ach in cleft of NMJ
What would be the most life threatening aspect of Achestersase inhibitor??
Paralysis of resp muscles (requires ventilation)
What is the treatment for ACh-esterase inhibitors poison?
Atropine- muscarinic receptor agonist
2 sites of baroreceptors
Carotid sinus
Aortic arch
Sympathetic stimulation does what to HR and TPR
Increase x2
In cardiac tamponade what happens to CVP?
Pulm pressure?
LA pressure?
CO?
CVP increases as heart cant fill causing back fill
Pulm pressure increases as blood cant enter LA
LA pressure increases due to compression
CO falls
If a 70kg man loses 1.25L of blood what is the loss?
What will be the sequence of events in falling pressures
25% loss Decreased venous return Decreased EDV Decreased SV Decreased CO Decreased BP
How can circulating volume be increased after haemorrhage
- Blood
2. Crystalloid fluid
Fluid resuscitation uses what?
Crystalloid fluid
What are some mediators of anaphylaxis
Histamine Lekotrines Prostaglandins Cytokines Kinins
In anaphylaxis what will the hands and pulse feel like?
Warm hands, strong bounding pulse
In haemorrhage what will the hands and pulse feel like
Cold and thready
Why does someone with COPD or asbestosis often have creamy secretions? Why do they change with infection
Constant prescence of neutrophils/macrophages due to chronic inflection change in colour with infection as new cell types enter
Why is nausea associated with cor pulmonale
Hepatomegally compressing stomach
An increase in HB in hypoxia due to cor pulmonale is good and bad why
Increased O2 capacity
Increased viscosity
In MI what would happen to blood Co2 levels as CO is increased
Initial decrease due to high RR
Then an increase as gas exchange impaired
Why give aspirin post MI
Decreased risk of further clots
What is a recommended treatment for STEMI (under 12 h)
Percutaneous coronary intervention to reurfuse
What is unstable angina?
Thrombosis on top of atheromatous plaque that doesnt completely occlude vessel but causes iscaemia
What would a loud systolic murmur and strong apex beat likely be?
Aortic stenosis with LVH
