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

- 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)

- 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

- 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

- 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

- 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

- 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

- 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

- 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

- Heart failure 

- Stroke 

- Cerebral haemorrhage 

- Chronic kidney failure 

- Hypertensive encephalopathy 

- Retinopathy 

- Peripheral vascular disease 

- Aortic aneurysm 

- LVF

- Myocardial infarction 

- Coronary heart disease 

- 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

Should be assessed by clinical history and physical examination:

- Brain

- Eyes

- Heart

- Kidneys

- Arteries

- 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

- 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⁺

- 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

- Venous pressure falls

- Cardiac output falls (Starling’s Law)

- Arterial pressure falls

- Detected by baroreceptors

- 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

- 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

- 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

- 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

- 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)

- 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)

- 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

- 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

- 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

- 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

- Low resistance shock (normovolaemic)

- Profound peripheral vasodilation -

I. Decrease in TPR

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

- 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

- 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