CVS Session 5 - Control Of BP, Hypertension And Circulatory Shock Flashcards Preview

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Flashcards in CVS Session 5 - Control Of BP, Hypertension And Circulatory Shock Deck (50):
1

Outline the regulation of blood pressure.

- Pressure = flow x resistance

I. Mean arterial BP = CO x TPR

II. CO = SV x HR - Both short and long term regulation

 

- Short term regulation – baroreceptor reflex

I. Adjust sympathetic and parasympathetic inputs to the heart to alter cardiac output.

II. Adjust sympathetic input to peripheral resistance vessels to alter TPR

2

Explain the baroreceptor reflex.

- The baroreceptor reflex works well to control acute changes in BP

- Produces rapid response to changes in BP

- Does not control sustained increases because the threshold for baroreceptor firing resets

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3

Explain the medium and longer term control of blood pressure. 

- Complex interaction of neurohumoral responses

- Directed at controlling sodium balance and thus extracellular fluid volume

- Plasma is part of the extracellular fluid compartment

I. Control of extracellular fluid volume controls plasma volume

II. Water follows Na+ therefore controlling total body Na+ levels controls plasma volume

4

Identify the four parallel neurohumoral pathways control circulating volume and hence BP.

  1. Renin-angiotensin-aldosterone system
  2. Sympathetic nervous system
  3. Antidiuretic hormone (ADH)
  4. Atrial natriuretic peptide (ANP)

5

Outline RAAS

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- Renin is released from granular cells of juxtaglomerular apparatus (JGA)

- Decreased circulating volume stimulates renin release:

I. Reduced NaCl delivery to distal tubule

II. Reduced perfusion pressure in the kidney causes the release of renin detected by baroreceptors in afferent arteriole

III. Sympathetic stimulation to JGA increases release of renin

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6

Briefly outline Angiotensen II Receptors. 

- Two types of Ang II receptors identified – AT1 and AT2

- Main actions via AT1 receptor

- G-protein coupled receptor

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7

Explain the action of aldosterone on the kidney.

AngII stimulates aldosterone release from the adrenal cortex

Actions of aldosterone:

- Acts on principal cells of collecting ducts

- Stimulates Na+ and therefore water reabsorption

- Activates apical Na+ channel (ENaC, Epithelial Na Channel) and apical K+ channel

- Also, increases basolateral Na+ extrusion via Na/K/ATPase

8

Outline the actions of ACE and bradykinin 

- Angiotensin converting enzyme and bradykinin

 

- The vasoconstriction effects of AngII are further augmented because ACE is also one of the kininase enzymes which breaks down the vasodilator bradykinin.

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9

Explain the action of inhibitors on ACE 

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10

Explain how the sympathetic nervous system control circulating blood volume and hence BP.

- High levels of sympathetic stimulation reduce renal blood flow

I.Vasoconstriction of arterioles

II. Decrease GFR – decrease Na+ excretion

- Activates apical Na/H-exchanger and basolateral Na/K ATPase in PCT

- Stimulates renin release from JGA

I. Leading to increased Ang II levels

II. Leading to increased aldosterone levels – increased Na+ reabsorption

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11

Explain how ADH controls BP. 

- Main role is formation of concentrated urine by retaining water to control plasma osmolarity – increases water reabsorption in distal nephron (AQP2)

 

- ADH release is stimulated by increases in

I.  Plasma osmolarity

II. Or severe hypovolaemia

 

- Also, stimulates Na+ reabsorption

I. Acts on thick ascending limb

II. Stimulates apical Na/K/Cl co-transporter

 

- Also, called arginine vasopressin - causes vasoconstriction

12

Outline how natriuretic peptides control BP 

- Atrial natriuretic peptide (ANP) promotes Na+ excretion

- Synthesised and stored in atrial myocytes

- Released from atrial cells in response to stretch

- Low pressure volume sensors in the atria

- Reduced effective circulating volume inhibits the release of ANP to support BP

I. Reduced filling of the heart

II. Less stretch

III. Less ANP released

13

Outline the actions of ANP. 

- Causes vasodilation of the afferent arteriole

- Increased blood flow increases GFR

- Also, inhibits Na+ reabsorption along the nephron

- Acts in opposite direction to the other neurohumoral regulators – causes natriuresis (loss of sodium into urine)

- If circulating volume is low ANP release is inhibited – this supports BP

14

What are prostaglandins?

- Act as vasodilators

- More important clinically than physiologically

- Locally acting prostaglandins (mainly PGE2) enhance glomerular filtration and reduce Na+ reabsorption

- May have important protective function

- Act as a buffer to excessive vasoconstriction produced by SNS and RAAS

- Important when levels of Ang II are high

15

What are the roles of Dopamine?

- Dopamine is formed locally in the kidney from circulating L-DOPA

- Dopamine receptors are present on renal blood vessels and cells of PCT & TAL

- DA causes vasodilation and increases renal blood flow

- DA reduces reabsorption of NaCl – Inhibits NH exchanger and Na/K ATPase in principal cells of PCT and TAL

16

What is hypertension and what causes it? 

- Hypertension: the sustained increase in blood pressure. 

 

- In around 95% of cases the cause is unknown – ‘essential’ or primary hypertension

 

- Where the cause can be defined it is referred to as secondary hypertension. Examples

I. Renovascular disease

II. Chronic renal disease

III. Hyperaldosteronism

IV. Cushing’s syndrome

 

- With secondary hypertension – important to treat the primary cause

17

What are the stages of hypertension? 

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18

Outline Primary hypertension. 

- Aka Essential hypertension

- No definable cause

I. Genetic factors – high BP tends to run in families

II. Environmental factors

III. Pathogenesis unclear

IV. Recent research suggests dysfunction of DA receptors

 

- Sustained elevation of BP

I. Diastolic pressure > 90mmHg

II. or Systolic pressure > 140mmHg

 

19

Outline the causes of Secondary Hypertension. 

- Only accounts for a small percentage of cases

- Identifiable pathological cause

- Can treat the primary cause

20

Explain Secondary hypertension: Renovascular disease.

- Occlusion of the renal artery (renal artery stenosis) causes a fall in perfusion pressure in that kidney

- Decreased perfusion pressure leads to increased renin production

- Activation of the renin-angiotensin-aldosterone system

- Vasoconstriction and Na+ retention at other kidney

21

Explain Secondary hypertension: Renal parenchyma disease

- Earlier stage may be a loss of vasodilator substances

- In later stage Na+ and water retention due to inadequate glomerular filtration – volume-dependent hypertension

22

Explain Secondary Hypertension: adrenal causes

- Conn's syndrome

I. Aldosterone secreting adenoma

II. Hypertension and hypokalaemia

 

- Cushing's syndrome

I. Excess secretion of glucocorticoid cortisol 

II. At high concentration acts on aldosterone receptors - Na+ and water retention

 

- Tumour of the adrenal medulla

I. Phaeochromocytoma

II. Secretes catacholamines (noradrenaline and adrenaline)

23

Explain the complications of hypertension. 

- Hypertension – the silent killer

- Although hypertension may be asymptomatic, it can have unseen damaging effects on – heart and vasculature – potentially leading to heart failure, MI, stroke, renal failure and retinopathy

24

Outline the general treatment of hypertension. 

- For secondary hypertension – treat primary cause

- Most cases no identifiable primary cause

- You can work out possible targets for treating hypertension from the following equations

I. BP = CO x TPR

II. BP = SV x HR x TPR

25

Outline the treatment of hypertension: non-pharmalogical approaches.

- Exercise

- Diet

- Reduced Na+ intake

- Reduced alcohol intake

- Lifestyle changes above can have limited effect

- Failure to implement lifestyle changes could limit the effectiveness of antihypertensive therapy

26

Outline the treatment of hypertension: targeting RAAS

- ACE inhibitors – prevent production of Ang II from Ang I

- Ang II receptor antagonists (AII antagonists)

- Ang II is a powerful vasoconstrictor, has direct actions on the kidney and promotes the release of aldosterone, thus leading to NaCl and H2O retention.

- Blocking production or action of Ang II has diuretic and vasodilator effects

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27

Explain the treatment of hypertension with vasodilators. 

- L-type Ca channel blockers

I. Reduce Ca2+ entry to vascular smooth muscle cells

II. Relaxation of vascular smooth muscle

 

- In principle, could also use α1 receptor blockers

I. Reduce sympathetic tone (relaxation of vascular smooth muscle)

II. Can cause postural hypotension

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28

Explain the treatment of hypertension with diuretics. 

- Thiazide diuretics – reduce circulating volume

- Inhibit Na/Cl co-transporter on apical membrane of cells in distal tubule

- Other diuretics e.g. aldosterone antagonists (spironolactone) will also lower BP  – not first line choice

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29

Explain the treatment of hypertension using beta blockers.

- Less commonly used to treat hypertension

- Blocking β1 receptors in the heart will reduce effects of sympathetic output – reduce heart rate and contractility

- Not used in hypertension alone

- Would only be used if there are other indications such as previous MI

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30

Identify some diseases attributable to hypertension (clue: all vascular). 

- Heart failure 

- Stroke 

- Cerebral haemorrhage 

- Chronic kidney failure 

- Hypertensive encephalopathy 

- Retinopathy 

- Peripheral vascular disease 

- Aortic aneurysm 

- LVF

- Myocardial infarction 

- Coronary heart disease 

31

Explain the effects of hypertension. 

- Increased afterload leads to:

i. LVF - heart failure

II. Increased myocardial oxygen demand - Myocardial ischaemia & Myocardial infarction

 

- Arterial damage leads to:

I. Artherosclerosis - Myocardial ischaemia & MI,  cerebrovascular disease (stroke), aneurysm, nephrosclerosis & renal failure, retinopathy

II.  Weakened vessels - cerebrovascular disease (stroke), aneurysm, nephrosclerosis & renal failure, retinopathy

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32

What are the target organs of clinical cardiovascular disease?

Should be assessed by clinical history and physical examination:

- Brain

- Eyes

- Heart

- Kidneys

- Arteries

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33

Outline Haemodynamic shock.

- Acute condition of inadequate blood flow throughout the body

- A catastrophic fall in arterial blood pressure leads to circulatory shock

Mean arterial BP = CO x TPR

- Shock can be due to fall in CO

- Or fall in TPR beyond capacity of the heart to cope

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34

Identify and define three different types of shock. 

Cardiogenic shock (pump failure) – ventricle cannot empty properly

- Mechanical shock (obstructive) – ventricle cannot fill properly

- Hypovolaemic shock – reduced blood volume leads to poor venous return

NB. Hypovolaemic shock can also result from severe burns and severe diarrhoea/vomiting and loss of Na+

 

35

Describe the characteristics of hypovolaemic shock

 

- Reduced blood volume

- Most commonly due to haemorrhage

- < 20% blood loss unlikely to cause shock

- 20-30% some signs of shock response

- 30-40% substantial decrease in mean aBP and serious shock response

- Severity of shock is related to amount and speed of blood loss

 

36

Explain what happens during a haemorrhage. 

- Venous pressure falls

- Cardiac output falls (Starling’s Law)

- Arterial pressure falls

- Detected by baroreceptors

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37

Explain what happens during the compensatory response.

- Increased sympathetic stimulation

- Tachycardia

- Increased force of contraction

- Peripheral vasoconstriction

- Venoconstriction

- Also, get some ‘internal transfusion’

- Increased peripheral resistance reduces the capillary hydrostatic pressure

- Net movement of fluid into capillaries

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38

Explain how peripheral vasoconstriction (shutdown) impairs tissue perfusion.

- Tissue damage due to hypoxia

- Release of chemical mediators – vasodilators

- TPR falls

- Blood pressure falls dramatically

- Vital organs can no longer be perfused

- Multi system failure

39

Outline hypovolaemia. 

- Longer term responses to restore blood volume

- Renin-angiotensin-aldosterone system

- Anti-diuretic hormone

- 20% blood volume loss – Restoration of body fluid volumes in about 3 days, if salt and water intake are adequate

- Patient has tachycardia, weak pulse, pale skin, cold, clammy extremities

 

40

What is pump failure and what are its potential causes?

- Acute failure of the heart to maintain cardiac output – pump failure

Potential causes:

I. Following myocardial infarction – damage to left ventricle

II. Due to serious arrhythmias

III. Acute worsening of heart failure

41

Describe the characteristics of cardiogenic shock.  

- Heart fills, but fails to pump effectively

- Central venous pressure (CVP) may be normal or raised

- Dramatic drop in arterial BP

- Tissues poorly perfused

I. Coronary arteries may be poorly perfused – exacerbates problem

II. Kidneys may be poorly perfused – reduced urine production (oliguria)

42

When would one start to consider cardiac arrest?

- Unresponsiveness associated with lack of pulse

- Heart has stopped or has ceased to pump effectively

- Asystole (loss of electrical and mechanical activity)

- Pulseless Electrical Activity (PEA)

- Ventricular fibrillation (uncoordinated electrical activity)

I. Most common form of cardiac arrest

II. Often following MI / electrolyte imbalance

III. Or some arrhythmias (eg long QT and Torsades de Pointes)

43

How does one manage cardiac arrest?

- Basic life support – chest compression and external ventilation 

- Advanced life support

I. Defibrillation

II. Electric current delivered to the heart

III. Depolarises all the cells – puts them into refractory period

IV. Allows coordinated electrical activity to restart

 

- Adrenaline

I. Enhances myocardial function

II. Increases peripheral resistance

44

Describe the characteristics of mechanical shock in terms of cardiac tamponade. 

- Cardiac tamponade

I. Blood or fluid build-up in pericardial space

II. Restricts filling of the heart

III. Limits end diastolic volume

IV. Affects left and right sides of heart

 

- High central venous pressure

- Low arterial blood pressure

- Heart attempts to beat – continued electrical activity

45

Describe the characteristics of mechanical shock in terms of pulmonary embolism. 

- Massive pulmonary embolism (PE)

 

- Embolus occludes a large pulmonary artery

I. Pulmonary artery pressure is high

II. Right ventricle cannot empty

III. Central venous pressure high

IV. Reduced return of blood to left heart

V. Limits filling of left heart

VI. Left atrial pressure is low

VII. Arterial blood pressure low

VIII. Shock

IX. Also: chest pain, dyspnoea

46

How might an embolus reach the lungs? 

- Typically, due to deep vein thrombosis

- Portion of thrombus breaks off

- Travels in venous system to right side of the heart

- Pumped out via pulmonary artery to lungs

- The effect of this will depend on the size of the embolus

47

Describe the characteristics of distributive shock. 

- Low resistance shock (normovolaemic)

- Profound peripheral vasodilation -

I. Decrease in TPR

II. Blood volume constant, but volume of the circulation has increased

48

Describe the characteristics of anaphylactic shock. 

- Severe allergic reaction (anaphylaxis)

I. Release of histamine from mast cells – other mediators

II. Powerful vasodilator effect – fall in TPR

III. Dramatic drop in arterial pressure - Increased sympathetic response - ­ CO increased but can’t overcome vasodilation

IV. Impaired perfusion of vital organs

V. Mediators also cause bronchoconstriction and laryngeal oedema – difficulty breathing

 

- Patient will have

I. Difficulty breathing

II. Collapsed

III. Rapid heart rate

IV. Red, warm extremities

 

- Acutely life threatening

- Adrenaline – Vasoconstriction via action at α1 adrenoceptors

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49

Describe the characteristics of septic (toxic) shock. 

- Sepsis – serious life-threatening response to infection, can lead to septic shock

 

- Endotoxins released by circulating bacteria

I. Profound inflammatory response (excessive)

II. Causes profound vasodilation

III. Dramatic fall in TPR

IV. Fall in arterial pressure

V. Impaired perfusion of vital organs

VI. Also - capillaries become leaky (reduced blood volume)

VII. Increased coagulation and localised hypo-prefusion

 

- Persisting hypotension requiring treatment to maintain blood pressure despite fluid resuscitation.

 

- Decreased arterial pressure

I. Detected by baroreceptors

II. Increased sympathetic output

III. Vasoconstrictor effect overridden by mediators of vasodilation

IV. Heart rate and stroke volume increased

 

- Patient has

I. Tachycardia

II. Warm, red extremities initially BUT later stages of sepsis – vasoconstriction – localised hypo-perfusion

 

50

Describe the general feature of management of the various types of shock.

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