Hypervolemia and Hypertension (W1 15/11) Flashcards Preview

Case 3: Hypertension > Hypervolemia and Hypertension (W1 15/11) > Flashcards

Flashcards in Hypervolemia and Hypertension (W1 15/11) Deck (25)
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1

LO: What is the physiological basis of auto-transfusion?

LO: What are the compensatory mechanisms active in haemorrhage and shock?

LO: What are the compensatory mechanisms active in hypertension?

These are the LO's dodo brain.

2

What does haemorrage mean?

An escape of blood from a ruptured blood vessel.

3

How much of blood can a healthy, young person lose before BP control mechanisms start to fail, and thus shock occurs?

30%

4

What is shock, as a physiological response?

Shock is an acute/severe failure of the cardiovascular system to provide the tissues with nutritional blood flow, and leading to reduced removal of waste products of metabolism.

5

Name the four types of shock?

Hypovolaemic

Anaphylactic

Cardiogenic

Septic

(H.A.C.S)

6

Describe hypovolaemic shock.

  • It is the most commen types of shock.
  • This type of shock is caused by insufficient circulating volume, which could be due to heamorrage or loss of fluid through vomitting or diarrhoea.
  • Also can be caused by severe burns.
  • Symptoms of haemorragic shock include:
  1. Cold skin: due to constriction of the peripheral blood vessels.
  2. Clammy skin due to activation of the sympathetic NS, releasing adrenalin, which activates sweat glands.
  3. Pale: due to ishaemia of the cells,
  4. Rapid and shallow breathing due to sympathetic nervous system stimulation and acidosis.

  5. Progressive fall in systolic and diastolic blood pressure

  6.  Cyanosis in nail beds, lips, and ear lobes

  7. Hypothermia due to decreased perfusion and evaporation of sweat

7

Name five causes of shock

(1)        Heart attack

(2)        Severe or sudden blood loss from an injury or serious illness

(3)        Large drop in body fluids, such as following a severe burn or severe vomiting and/or diarrhea

(4)        Blood poisoning from major infections

(5)        Exposure to extreme heat or cold for too long

8

How can shock cause death?

One of the key dangers of shock is that it progresses by a positive feedback mechanism. Poor blood supply leads to cellular damage, which results in an inflammatory response to increase blood flow to the affected area. This is normally very useful to match up blood supply level with tissue demand for nutrients. However, if enough tissue causes this, it will deprive vital nutrients from other parts of the body. Additionally, the ability of the circulatory system to meet this increase in demand causes saturation, and this is a major result, of which other parts of the body begin to respond in a similar way; thus, exacerbating the problem. Due to this chain of events, immediate treatment of shock is critical for survival

9

Describe cardiogenic shock.

  • It is non-heamorrhagic shock
  • Due to a decrease in the contractions/contractile ability of the myocardium.  Heart fails to circulate blood efficiently to the tissues. 
  • Can be caused by cardiac tamponade (fluid accumulation around heart (caused by pericarditis), prevents normal filling of heart) myocardial infarction, pulmonary embolism (obstructs outflow from heart).
  • Symptoms: weak or absent pulse, arrhythmia, often tachycardia

10

Describe Septic Shock.

  • Shock caused by overwhelming bacterial infection. If enough tissue causes an inflammatory response and blood is diverted to them, it will deprive vital nutrients from other parts of the body. Other parts of the body begin to respond in a similar way; thus, exacerbating the problem. 
  • Major cause - endotoxin release by microorganisms especially gram negative bacteria.
  • Blood ‘pools’ or redistributes in veins (relative hypovolaemia) and this leads to a decrease in arterial BP and perfusion

  • In septicaemic shock, bacterial infection induces overproduction of nitric oxide (NO) by inducing the expression of the NO-producing enzyme called iNOS (i = inducible). NO causes vascular smooth muscle to relax and therefore lowers BP

  • AKA type of distributive shock

  • Common conditions that predispose to sepsis:
  1.          Diabetes
  2.          Cirrhosis
  3.          Post natal (after giving birth)
  4.          Post abortion infections

11

Describe Anaphylactic Shock

  • Blood ‘pools’ or redistributes in veins (relative hypovolaemia) and this leads to a decrease in arterial BP and perfusion

  • AKA distributive shock

  • Anaphylactic shock is caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes histamine release, leading to over production of NO, causing widespread vasodilation, leading to hypotension and increased capillary permeability.

12

How does increased NO production in endothelial cells causes smooth muscle relaxation?

As in the case of septic and anaphylactic shock.

  • It raises cGMP levels in smooth muscle cells.
  • The cGMP mechanism works by (google this)

13

What happens when BP falls in shock?

Compensatory mechanisms come into play. But, if these mechanisms are not sufficient to restore blood pressure and BP keeps falling,turns into refractory shock which can become irreversible and death will ensue.

 

14

What are decompensatory mechanisms?

See decompensatory mechanisms in

B & L, Chapter 31, pp 509-511.

Or

BB. Chapter 25 p 608. Irreversible shock

15

How does the body respond to haemorrage?

When a haemorrage happens, the blood volume decreases, venous return is decreased, so cardiac output is also decreased due to the starling mechanism. This means arterial blood pressure falls. This is detected by baroreceptors. If local blood flow falls, you get stanant hypoxia (less oxygen to tissues  resulting from slow peripheral circulation). This is detected by chemoreceptors and activates sympathetic activity to be increased.

16

What is the body's immediate response to haemorrage?

  • Sympathetic activity is increased: heart rate increases, vasoconstriction of arterioles and veins by vasopressin/ADH
  • There is reduced renal perfusion as the renin-angiotensin system is activated: 
  1. Juxta-glomerular cells (they are specialized smooth muscle cells mainly in the walls of the afferent arterioles, and some in the efferent arterioles, that deliver blood to the glomerulus) convert prorenin, already in the blood, into renin).
  2. Renin now converts angiotensinogen into angiotensin 1.
  3. Angiotensin 1 is converted into angiotensin 2 by angiotensin converting enzyme.
  4. Angiotensin 2 is a vasocontrictor. It causes blood vessels to narrow so BP increases.
  5. Angiotensin 2 also stimulates the release of aldosterone from adrenal cortex.
  6. Aldosterone causes more sodium and water to be reabsorbed into the blood, to increase blood volume.
  7. The activation of the renin-angiotensin system also results in reduced urine volume, increased venous return volume, increased  cardiac output, increased BP.

17

What is the body's intermediate response to haemorrage?

  • Vasoconstriction causes capillary pressure to fall.
  • Sympathetic NS causes glucagon to become glucose and enters blood, increasing blood osmolarity.
  • Capillaries absorb water from the interstitial space because a osmotic gradient is created by the activation of the sypathetic NS. This increases blood volume and BP.

18

Describe hormonal regulation to increase BP

  • Baroreceptors in the kidney respond to decrease in perfusion pressure by increasing the rate of renin secretion. 
  • Renin converts angiotensinogen into angiotensin
  • Angiotensin 1 is converted into angiotensin 2 by angiotensin converting enzyme. 
  • Angiotensin 2 is a vasoconstrictor. It causes blood vessels to narrow so BP increases.
  • Angiotensin 2 also stimulates the release of aldosterone from adrenal cortex.Aldosterone causes more sodium and water to be reabsorbed into the blood, to increase blood volume.

  • Baroreceptors in the arch of the aorta and corotid sinuses (nerve in the neck) detect decrease BP too. They send a message along the sympathetic nerves to the pituitary to release ADH and the adrenal medulla to release epinephrine.

  • ADH causes vasoconstriction and increased water reabsorbtion into the blood.

  • Epinephrine causes stroke volume and heart rate and vasoconstriction to increase.

  • Overall BP increases.

19

What is hypertension a result of?

An in-balance in the long term regulation of either CO or Total Peripheral Resistance (or both).

 

20

In roughly what percentage of the population is hypertension found?

30%

21

What would be considered a hypertensive BP for anyone under 50?

Any BP greater than 140/90 is hypertensive for under 50 aged people.

22

What do hypertensives have a higher risk of?

Myocardial infarction, strokes and renal failure.

High BP damages lining of blood vessels- the endothelial cells. This leads to a number of proliferative responses including atherosclerosis.

23

What does essential hypertension refer to?

Hypertension without a known cause. Accounts for more than 95% of cases.

24

What are the possible causes of secondary hypertension?

  1. Renal artery stenosis (most common cause) or aortic stenosis
  2. Hyperaldosteronism
  3. Phaeochromocytoma- catecholamine secreting tumour
  4. Medications – for e.g. steroid medicines, the contraceptive pill
  5. Pregnancy -  can cause pre-eclampsia – this can be serious and harm baby

25

Name the four types of treatment for hypertension?

  1. Behaviour Modification: stop smoking, change diet to low-fat, low-salt, include fruit and vegetables, less alcohol, less stress, less coffee, and less weight.
  2. Take Peripheral Dilators: they reduce total peripheral resistance(widen blood vessels) and therefore lower BP. Examples: 

    (i)ACE inhibitors (e.g. ramipril) or angiotensin-II receptor antagonists (e.g. candesartan)

    (ii)Calcium-channel blockers (eg. amlodipine)

  3. Increase fluid loss: diuretics (e.g.      bendroflumethiazide). These will lower blood volume through fluid loss and decrease BP . Have to monitor blood electrolytes especially K+
  4. Give alpha and beta-adrenergic receptor antagonists (blockers). Beta blockers like atenalol reduce cardiac output, so reduce BP. Alpha blockers lower total peripheral resistance so lower BP.