Blood Pressure Control and Haemodynamic Shock

Question 1

Pressure = flow X resistance, so what are the equations for cardiac output and blood pressure?

Answer 1

CO = SV X HR and BP = CO X TPR

Question 2

What controls the blood pressure in the short term and briefly, how?

Answer 2

Baroreceptors reflex adjust sympathetic and parasympathetic inputs inputs to the heart to alter cardiac output and adjust sympathetic input to peripheral resistance vessels to alter TPR.

Question 3

Baroreceptors reflex:
Nerve endings in the ______ ______ and ______ of the _______ are sensitive to stretch - more stretch when increased _________ _________. Afferents pathways lead to the ________ _________ ________ in the medulla.

Answer 3

Carotid sinus
Arch of the aorta
Arterial pressure
Cardiac control centre

Question 4

What is a limitation of the baroreceptors reflex in terms of controlling blood pressure?

Answer 4

It works well to control acute changes and is fast acting, but won’t control a sustained increase, because the threshold for baroreceptors firing resets.

Question 5

After the baroreceptors reflex, what controls BP medium/long term?

Answer 5

Complex interactions of neurohormonal responses - control Na+ balance and thus extracellular fluid volume (water follows sodium).

Question 6

4 pathways control the circulating volume and so blood pressure, what are they?

Answer 6

1. Renin angiotensin aldosterone system (RAAS)
2. Sympathetic nervous system
3. Antidiuretic hormone (ADH/vasopressin)
4. Natriuretic peptides

Question 7

Where is renin produced and in which situations is it released?

Answer 7

Renin is produced in granular cells of juxtaglomerular apparatus (JGA) if: reduced delivery of NaCl to the distal tube, reduced kidney perfusion (detected by baroreceptors in afferent arterioles) or if JGA receives sympathetic stimulation.

Question 8

Which proteins does renin get involves once it’s been released and how?

Answer 8

Renin catalysts the reaction of Angiotensin –> Angiotensin I and ACE (Angiotensin converting enzyme) converts this to Angiotensin II.

Question 9

Where does Angiotensin act and what are its functions?

Answer 9

Causes vasoconstriction and stimulates Na+ reabsorption at the kidneys and stimulates the release of aldosterone from the adrenal cortex. Receptors: AT1 are GPCRs and do main actions as above and increase NA release (+ve fb) and increases thirst at the hypothalamus (stimulates ADH release).
There is also AT2.

Question 10

What does aldosterone do, once Angiotensin II has stimulated its release from the adrenal cortex?

Answer 10

Acts on principal cells of collecting ducts, stimulating Na+ (and therefore H2O) reabsorption, activates apical Na+ channels (ENaC - epithelial) and apical K+ channels and increases basolateral Na+ extrusion via NaKATPase (high levels mean slightly low K+ levels).

Question 11

How does ACE further augment the vasoconstriction affect, after having increased the levels of Ang II?
What affect can ACE inhibitors sometimes have as a result of this?

Answer 11

ACE breaks down the vasodilator bradykinin into peptide fragments.
ACE inhibitors e.g. Ramipril, Captopril, cause a bradykinn build up and so a dry cough.

Question 12

Sympathetic nervous system:
High levels of sympathetic stimulation ______ renal blood flow (vasoconstriction arterioles and decreases GFR, so reduced Na+ __________ - stimulates granule cells of afferent arterioles to stimulate the reabsorption from ____), activates _______ NHX, ____________ NaKATPase in proximal convoluted tube and stimulates ______ release from JG cells (increases Ang and Ald levels).

Answer 12

Reduce
Excretion
PCT
Apical
Basolateral 
Renin

Question 13

What is diuresis?

Answer 13

The loss of salt and water through the kidney.

Question 14

What is the function of ADH (aka arginine vasopressin)?

Answer 14

Its main role is to form concentrated urine by retaining water to control plasma osmolarity (increases water reabsorption in distal nephron).
Also stimulates Na+ reabsorption (via apical NaKCl transporter on thick ascending limb).
Can cause vasoconstriction.

Question 15

When is ADH released?

Answer 15

When dehydrated - plasma osmolarity increased or severe hypovolaemia.

Question 16

ANP synthesised and stored in atrial myocytes is released in response to stress (low pressure volume sensors), how does it act on blood pressure?

Answer 16

Promotes Na+ excretion. Reduced effective circulating volume inhibits the release of ANP to support BP. ANP causes vasodilation of afferent arterioles - increased blood flow means increases GFR, inhibiting Na+ reabsorption along the nephron - it acts in the opposite direction to other neurohormonal regulators.

Question 17

What do Prostaglandins do?

Answer 17

They are vasodilators, acting locally to enhance the Glomerular Filtration Rate and reduce Na+ reabsorption - important when levels of Ang II are high, as they act as a buffer to SNS/RAAS vasoconstriction.

Question 18

Where and how is dopamine formed where does it act, to do what?

Answer 18

Dopamine is formed locally in the kidney from circulating L-DOPA. Receptors are present on renal blood vessels, PCT (proximal convoluted tube) cells and TAL (thick ascending limb). It causes vasodilation and increased renal blood flow and reduces the reabsorption of NaCl (inhibits NHX and NaKATPase in principal cells).

Question 19

When someone’s arterial blood pressure is too high, they may get hypertension, what is it and what are the different types?

Answer 19

A sustained increase in BP: Stage 1 (mild) => 140/90mmHg, Stage 2 (moderate) => 160/100mmHg and severe is equal to or over 180 systolic or 110 diastolic mmHg.

Question 20

95% hypertension cases are essential/primary, what is the difference between primary and secondary hypertension?

Answer 20

Primary hypertension is with an unknown cause. Essential hypertension , may be due to genetic factors, environmental, unclear pathogenesis, dysfunction of DA receptors.
Secondary is when cause can be defined, where it’s important to treat the underlying cause (only a small percentage of cases).
Both have either a systolic pressure of equal to/over 140mmHg or diastolic 90mmHg.

Question 21

How is hypertension self perpetuating?

Answer 21

Over time, high blood pressure causes arteries to stiffen.

Question 22

Renovascular disease is an example of a cause of secondary hypertension, what does it do?

Answer 22

Renal artery stenosis (occlusion) causes a fall in perfusion pressure, so increased renin production (RAAS) leading to vasoconstriction and Na+ reabsorption at the kidney.

Question 23

How does Renal parenchyma disease cause secondary hypertension?

Answer 23

In the early stages there may be some loss of vasodilator substances and at a later stage, sodium and water retention due to inadequate GFR (then volume dependent high BP).

Question 24

What are the adrenal causes of secondary hypertension?

Answer 24

Conn’s syndrome - aldosterone secreting adenoma (leading t hypertension and hyperkalaemia).
Cushing’s syndrome - excess secretion of glucocorticoid cortisol (at high concentrations acts on aldosterone receptors).
Tumour of adrenal medulla - pheochromocytoma secretes catecholamines.

Question 25

Hypertension may be asymptomatic, but it can have damaging effects on the heart and vasculature, leading to which conditions in the long term?

Answer 25

Myocardial infarction, stroke, renal failure and retinopathy. A rise in BP increases mortality.

Question 26

Hypertension effects on CVS:
Hypertension leads to increased ___________ so left ventricular hypertrophy and failure, plus increase myocardial ________ demand, so _________ and MI, also arterial damage, so _________ vessels and atherosclerosis, both leading to cerebrovascular disease/stroke, aneurysm, nephrosclerosis and ______ failure and retinopathy.

Answer 26

Afterload
Oxygen
Ischaemia
Weakened
Renal

Question 27

Interventions can save lives, how would you work out what to do to lower blood pressure?

Answer 27

Use the BP equations or treat the underlying cause of secondary hypertension.

Question 28

Describe some non-pharmacological treatments for hypertension.

Answer 28

Exercise, diet - reduced Na+ and alcohol intake - lifestyle changes have limited effect, but failure to implement them could limit antihypertensive therapy effectiveness.

Question 29

How do ACE inhibitors work?

Answer 29

Prevent Angiotensin II being formed, but can lead to a dry cough.

Question 30

How do Angiotensin II receptor agonists exert their effect?

Answer 30

Blocking has antidiuretic and vasodilator effects, since Angiotensin II would otherwise powerfully vasoconstrict and have direct action on the kidneys and promote aldosterone release, leading to sodium and water retention.

Question 31

Describe some vasodilators.

Answer 31

L-type Ca2+ channel blockers, which relax vascular smooth muscle. You could also use alpha-1 receptor blockers to reduce sympathetic tone, but this may cause postural hypertension (falls in the elderly).

Question 32

Describe the action of some diuretics.

Answer 32

Thiazides diuretics reduce circulating volume, by inhibiting the Na+Cl- cotransporter on the apical membrane of cells in the distal tube.
Aldosterone antagonists have some diuretic effects.

Question 33

When are beta blockers used for hypertension and why?

Answer 33

There are used less commonly and not just for hypertension alone - need other indicators e.g. Previous MI. They block beta-1 receptors in the heart, reducing the effect of sympathetic output to reduce HR and contractility.

Question 34

Why is control of arterial blood pressure important?

Answer 34

To ensure tissue perfusion and avoid hypertension.

Question 35

How do you work out mean arterial BP? E.g. If systolic pressure is 120mmHg and diastolic is 80mmHg.

Answer 35

2/3 diastolic pressure + 1/3 systolic pressure.
Or diastolic + 1/3 pulse pressure (difference between systolic and diastolic).
2/3 80= 53.3
1/3 120 = 40
So 93.3.

Question 36

What is haemodynamic shock?

Answer 36

An acute condition of inadequate blood flow throughout the body. A catastrophic fall in BP leads to circulatory shock - result of fall of CO or TPR.

Question 37

What is cardiogenic shock?

Answer 37

Haemodynamic shock from a fall in CO - pump failure, caused by damage to the left ventricle following an MI, serious arrhythmias or acute worsening of heart failure. The heart fills, but fails to pump effectively.

Question 38

How does cardiogenic shock affect CVP, blood pressure and perfusion?

Answer 38

Central venous pressure may be normal (or raised with blood pressure) and there’s a dramatic drop in blood pressure. Tissues are poorly perfumed including those to the coronary arteries, which exacerbates the problem and to the kidneys, resulting in oliguria - reduced urine production.

Question 39

What is cardiac arrest and what are the different types?

Answer 39

Unresponsiveness associated with a lack of pulse - the heart as stopped or ceased to pump effectively. Either:
Pulseless Electrical Activity (PEA) - dissociation of electrical and mechanical activity,
Ventricular Fibrilation - uncoordinated electrical activity, most common often following MI, electrolyte imbalance or some arrhythmias. May become … Asystole - loss of electrical and mechanical activity.

Question 40

What are BLS and ALS? Why may adrenaline be administered?

Answer 40

Basic life support involves chest compression and external ventilation.
Advanced life support involves defibrillation with an electrical current delivered to the heart, which depolarises all cells and puts them into the refractory period allowing coordinated electrical activity to restart.
Adrenaline enhances myocardial function and increases peripheral resistance.

Question 41

How is mechanical shock caused by cardiac tamponade and what are the effects of this on pressure etc?

Answer 41

A type of haemodynamic shock caused by decreased CO. There’s cardiac tamponade with blood built up in the pericardial space, which restricts filling and so limits end diastolic volume, affecting the left and right sides.
There’s a high CVP and a low BP.
The heart attempts to beat, so there is still electrical activity.

Question 42

How is mechanical shock caused by PE and what are the effects of this on pressure etc?

Answer 42

A massive pulmonary embolism may involve the embolus occluding a large pulmonary artery, so the pressure’s high and the right ventricle can’t empty, so there’s a high Central Venous Pressure, with reduced return to the left ventricle limiting filling, left atrium pressure low, arterial BP low leading to shock, pain and dyspnoea.
The effect depends on the size of the embolus.

Question 43

What is hypovolaemic shock and how extreme does the situation need to be to result in it?

Answer 43

Reduced blood volume, often caused by haemorrhage. <20% blood lost, means shock is unlikely, 20-30% some signs of shock response and 30-40% involves a substantial decrease in mean arterial BP and a serious shock response - severity related to amount and speed of loss.

Question 44

What happens to the body after haemorrhage?

Answer 44

Venous pressure falls, CO falls, arterial BP falls - monitored by baroreceptors. The compensatory response increases sympathetic stimulation, leading to tachycardia, an increased force of contraction, peripheral vasoconstriction and venoconstriction.
Also some internal transfusion with increased TPR reducing capillary hydrostatic pressure - net movement of blood - think of Starling’s Law.

Question 45

How will a patient who has hypovolaemic shock from haemorrhage present? What else may cause this?

Answer 45

Tachycardia, weak pulse, pale skin and cold, clammy extremities.
It may also result from severe burns, diarrhoea, loss of sodium and vomiting.

Question 46

With hypovolaemic shock, what is the Danger of Decompensation?

Answer 46

Peripheral vasoconstriction impairs perfusion, leading to tissue damage from hypoxia, so release of chemical mediators, which are vasodilators decrease total peripheral resistance, blood pressure falls and vital organs are no longer perfumed, leading to multi-system failure.

Question 47

After haemorrhage etc, what is the long term response to restore blood volume and how long does this take?

Answer 47

Neurohormonal: RAAS and ADH. If salt and water intake is adequate, 20% blood volume loss should be restored in 3 days.

Question 48

What is distributive shock?

Answer 48

Low resistance/normo-volaemic profound peripheral vasodilation, decreasing total peripheral resistance. The 2 types are toxic/septic shock and anaphylactic shock.

Question 49

What is toxic/septic shock?

Answer 49

Serious, life threatening response to infection, consisting of a profound inflammatory response and vasodilation. A fall in BP means decreased perfusion to vital organs and leaky capillaries decrease the blood volume as well as increased coagulation and localised hypoperfusion.

Question 50

How is toxic shock treated and what does the body do in response?

Answer 50

Persisting hypotension requires treatment to maintain blood pressure, despite fluid resuscitation. Decreased arterial blood pressure is detected by baroreceptors leading to an increased sympathetic output, but the vasoconstriction effect is overridden by vasodilation, HR and SV are increased.

Question 51

How would a patient with toxic shock present?

Answer 51

Tachycardia, warm red extremities initially, but in later stages of sepsis vasoconstriction and localised hypoperfusion stop this.

Question 52

What happens in anaphylactic shock, briefly?

Answer 52

Severe allergic reaction triggers release of histamine (and other mediators) from mast cells, with powerful vasodilator effects.

Question 53

What are the effects of the mediators and responses in anaphylactic shock?

Answer 53

A fall in TPR, means a drop in arterial BP, so an increased sympathetic response increases CO, but it can’t overcome the vasodilation, leading to impaired perfusion of the vital organs.
Mediators can also cause bronchoconstriction and laryngeal oedema, leading to difficulty breathing.

Question 54

How would a patient with anaphylactic shock present and what should be done to help them?

Answer 54

Difficulty breathing, collapsed, tachycardic, red warm extremities. Acutely life threatening.
Adrenaline should be given to vasoconstriction via action at alpha-1 adrenoreceptors (in Epipen).