Week 1/2 - B(2) - Physiology 4 AND 5 - Kortokoff sounds, M.A.P/C.V.P, Baroreceptors, Postural Hypo, R.A.A.S/A.N.P/A.D.H Flashcards Preview

Year 1(B2) - Cardiology > Week 1/2 - B(2) - Physiology 4 AND 5 - Kortokoff sounds, M.A.P/C.V.P, Baroreceptors, Postural Hypo, R.A.A.S/A.N.P/A.D.H > Flashcards

Flashcards in Week 1/2 - B(2) - Physiology 4 AND 5 - Kortokoff sounds, M.A.P/C.V.P, Baroreceptors, Postural Hypo, R.A.A.S/A.N.P/A.D.H Deck (31)
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1
Q

What is the fashion in which bloods flows in normal arteries?

A

Laminar flow is the normal condition for blood flow throughout most of the circulatory system. It is characterized by concentric layers of blood moving in parallel down the length of a blood vessel.

2
Q

What is the definition of the * Systemic systolic arterial blood pressure * Systemic diastolic arterial blood pressure What should each pressure not exceed under resting conditions?

A

Systemic systolic arterial blood pressure * the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart contracts * pressure should not exceed 140mmHg under resting conditions Systemic diastolic arterial blood pressure * the pressure exerted by the blood on the walls of the aorta and systemic arteries when the heart relaxes * pressure should not exceed 90mmHg under resting conditions

3
Q

Blood flow in normal arteries in a laminar fashion Such laminar flow is not audible through a stethoscope - no sound is heard in a normal patent artery What equipment is used to measure the blood pressure and what are the sounds known as when using this equipment?

A

A sphygmomanometer and stethoscope are used to measure blood pressure The sphyg applies pressure (usually around the brachial artery) and this allows you to hear tubrulent blood flow and when the turbulence stops using a stethoscope The sounds heard are known as Korotkoff sounds

4
Q

There are a total of 5 Korotkoff sounds Why are no sounds heard when cuff pressure exceeds the peak systolic pressure?

A

No sound is heard when cuff pressure exceeds the peak systolic pressure because this will stop any blood flowing through the vessel. No sound heard because no blood flow.

5
Q

No sound is heard when cuff pressure exceeds peak systolic pressure. Initially the sphyg is pumped up until you cannot hear the blood flow any longer 30mmHg. When is the first sound heard and what is it known as?

A

Korotkoff soun 1 - peak systolic pressure When the cuff pressure is lowered slowly, the first Korotkoff sound is heard when we reach the peak systolic pressure (systemic systolic arterial blood pressure)

6
Q

What are Korotkoff sound 2 and 3?

A

When the pressure of the sphyg is between systolic and diastolic arterial blood pressure, Korotkoff sounds 2 and 3 are heard These are intermittent sounds due to turbulent blood flow arising because of the pressure

7
Q

What are the 4th and 5th pressure heard and why? Which is recorrded as the diastolic pressure?

A

The 4th sound heart is the last sound heard - the diastolic pressure It is the 5th Korotkoff sound that is recorded as the diastolic pressure as it is more reproducible - the point at which sounds disappears due to uninterrupted, smooth, laminar flow

8
Q

What is the main driving force of the blood around the systemic circulation? How is this calculated?

A

The main driving force for blood flow arises due to a pressure gradient between the aorta and the right atrium The RA pressure is close to zero so the main driving force for the blood is the mean arterial pressure Pressure gradient (between Aorta and RA) = Mean arterial pressure (MAP) minus Central venous (right atrial) pressure (CVP)

9
Q

Pressure gradient between Aorta and RA = MAP - CVP What is the approximate range or normal CVP is? Define what the MAP and what the approximate range of normal is?

A

Central venous pressure is normally approximately 3-8 mmHg Mean arterial pressure is the average arterial blood pressure during a single cardiac cycle which involves contraction and relaxation of the heart - normally approximately 70-105mmHg

10
Q

How is the MAP calculated? (remember the differences in length between systole and diastole) What is the approx mean arterial pressure for somebody who has a BP of 120/80?

A

Relaxation - diastole - is about twice as long as the contraction - systole MAP * = 2/3rd x diastolic + 1/3rd x systolic * = (2Diastolic + Sytolic) / 3 * eg (2x80 +120) /3 = 280 dividied by 3 * At a BP of 120/80 = the MAP is 93.3 mmHg

11
Q

What is the normal range of MAP again? What is the normal range of CVP again? What must the MAP be minimally to still perfuse the organs?

A

Normal MAP ranges from 70-105 mmHg Normal CVP (right atrial pressure) ranges from 3-8mmHg MAP of at least 60mmHg is needed to perfuse the coronary arteries, brain and kidneys

12
Q

How can MAP be calculated using the cardiac output? Define cardiac output and how it is calculated?

A

MAP = cardiac output x systemic vascular resistance (total peripheral resistance) Cardiac output is the volume of blood pumped by each ventricle of the heart per minute To calculate this, must know the volume pumped by each ventricle heart per beat and how may beats per minute * Therefore, CO = Stroke volume (SV) x Heart rate (HR)

13
Q

Mean arterial pressure * = Cardiac output x Systemic vascular resistance * Stroke volume x Heart rate x Systemic vascular resistance What is systemic vascular resistance? What are the major resistance vessels?

A

Systemic vascular resistance is the sum of resistance of all vasculature in the systemic circulation Major resistance vessels are the arterioles

14
Q

What is vessel resistance proportional and inproportional to?

A

Vessel resistance to blood flow - * directly proportional to the blood viscosity and vessel length * inversely proportional to the radius of the blood vessel to the power of 4 (this is the poiseulle equation)

15
Q

MAP = CO x SVR = HR x SV x SVR How does the autonomic nervous system affect the MAP State for both * parasympathetic (effect on heart) and * sympathetic (effect on heart, arterioles and veins)

A

Parasympathetic - Heart - decrease HR, decrease CO, decrease MAP Sympathetic - Heart - Increase HR & contractile force (SV) –> increase CO, increase MAP Arterioles -vasoconstriction, increase SVR, increase MAP Veins - vasoconstriction, increase venous return, increase EDV, increase SV, increase CO, increase MAP

16
Q

How is the regulation of mean arterial blood pressure controlled in short and long term?

A

In short term, the barorecetpor reflex controls the MAP In long term, it is through controlling the blood volume

17
Q

What is the function of the baroreceptors and where are they? Is this a type of positive or negative feedback mechanism?

A

Baroreceptors are mechanoreceptors located in the carotid sinus and in the aortic arch. Their function is to sense pressure changes by responding to change in the tension of the arterial wall. It is negative feedback - therefore increase in stretch will cause receptors to signal the medulla to lower MAP (vice versa if decrease in stretch in carotid)

18
Q

Describe how baroreceptor reflex acts in a person who stands up? What can dysfunction cause?

A

Normally when a person stands from a lying position, the venous return to heart decreases - due to effect of gravity (meaning decrease in EDV, SV, CO and MAP) * Reduction in stretch sensed by baroreceptors - medulla signaled * Vagal tone is decreased (increased HR, CO and MAP * Sympatehtic is increased - increases MAP via heart rate, contractile strength and venoconstriction * Returns MAP to normal Baroreceptor dysfunction can cause postural hypotension due to failure for short term blood pressure control

19
Q

Baroreceptor dysfunction can cause postural hypotension due to failure for the short term blood pressure control What are the causes and symptoms of postural hypotentsion? (orthostatic hypotension)

A

Causes incude Age related Medications eg antihypertensives Certain diseases eg Addison’s Hypovolaemia Symptoms Light headedness Syncope (fainting)

20
Q

How is a diagnosis of orthostatic hypotension confirmed?

A

Postural hypotension is confirmed by a drop in blood pressure after standing for 3 minutes when previously lying flat * drop in systolic blood pressure of >20mmHg * or a drop in diastolic blood pressure >10mmHg

21
Q

What is the non-pharmacological management of orthostatic hypotension? What is the pharmacoogical management? (1st and 2nd line)

A

Non pharmacological management - eliminate causative factors eg antihypertensives if possible Make sure when standing up not to move away from chair too quickly Pharmacological management Fludricortisone - essentially a synthetic version of aldosterone from the kidneys - increases sodium and ater retention 2nd line - sympathomimetics eg midodrine (alpha 1 agonist - arteriolar vasoconstriction)

22
Q

As said previously, the long term regulation of MAP is down to controlling the blood volume - controlling the extracellular fluid volume What are the two main factors affecting extracellular fluid volume? What are the three hormones that act as effectors to regulate these factors and therefore regulate the ECF volume?

A

Two main affectors affecting the ECF volume are sodium /water excess or defecit The three hormones important in regulating this are: Renin-Angiotensin -Aldosterone System (RAAS) Atrial natriuretic peptide (ANP) Antidiuretic hormone (vasopressin) (ADH)

23
Q

The extracellular fluid is equal to the plasma volume + the interstitial fluid volume What is the interstitial fluid?

A

The interssitial fluid is the fluid which bathes the cells and acts as the go-between the blood and body cells

24
Q

Leads discuss the role of the RAAS (renin-angiotensin-aldosterone-system) Where is renin released and what does it stimulate? What is renin also known as? What converts angiotensin 1 and where is it produced?

A

Renin (eg angiotensinogenase) is released from the kidneys and converts angiotensinogen (produced in the liver) to angiotensin 1 Angiotensin 1 is then converted to angiotensin 2 by ACE (angiotensin converting enzyme) which is produced primarily by the pulmonary vascular endothelium

25
Q

What are the three functions of angiotensin II ie what does it cause and what does it stimulate the release of? What is the function of the homrone released due to angiotensin II?

A

Angiotensin II causes Systemic vasoconstriction - therefore increases SVR, which increases MAP Also stimulates thirst and ADH release - contributing to plasma volume increase Stimulates the releases of aldosterone from the adrenal cortex - main cause of plasma volume increase due to sodium and water retention

26
Q

What receptor does angiotensin II bind to, to exert its effects?

A

Angiotensin to binds to angiotensin type 1 receptors mainly to exert its effects

27
Q

What is the rate limiting step for the RAAS system? Where is this substance released from?

A

The rate limiting step for the RAAS system is the renin secretion which is released from the granular cells of the juxtaglomerular apparatus in the kidneys Juxtaglomerular appaatus * Macula densa * Granular cells * Extraglomerula mesangial cells

28
Q

The Renin angiotensin aldosterone system is regulated by mechanisms which stimulates Renin release from the granular cells of the juxtaglomerular apparatus in the kidney. What are these mechanisms which stimulate renin release?

A

Renal artery hypotension - caused by decreased systemic blood pressure Stimulation of the renal sympathetic nerves Decreased Na+ concentration in the renal tubular fluid (that passes between the afferent and efferent arteriole to the glomerulus) sensed by the macula densa cells of the juxtaglomerular apparatus

29
Q

What does ANP stand for,? Where is it released from and in response to what? And what does it cause?

A

Atrial natiuretic peptides are released from the heart atria (as well as other organs) in response to cardiac distension (hypervolaemia) * They cause excretion of salt and water in the kidneys therefore reducing blood volume & pressure * Decreases renin release - deceases Na/water retention, decreases BP * Acts as a vasodilatior - decreases SVR and BP Natriuetric peptides provide a counter-regulation to RAAS

30
Q

What does ADH stand for and what is it also known as? Where is it produced, stored and what stimulates its release?

A

ADH - anti-diuretic hormone - aka vasopressin It is synthesised in the hypothalamus and stored in the posterior pituitary gland Its secretion is stimulated by reduced ECF volume or by increased ECF osmolality (main stimulus)

31
Q

What is the role of ADH?

A

ADH Acts in the kdiney tubules to increases reabsorption of water (conserves water –> increase uring concentration) (increases ECF and PV increasesing CO and BP) ADH also acts on blood vessels causing vasoconstriction - increases SVR and BP

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