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Flashcards in Session 12 Deck (25):

What is meant by 'Shock'?

Used to describe acute circulatory failure with either inadequate or inappropriately distributed tissue perfusion, resulting in generalised lack of oxygen supply to cells.



How might inadequate tissue perfusion come about?


Acute condition of inadequate blood flow throughout the body

A catastrophic fall in arterial blood pressure leads to circulatory shock

  • Cardiogenic shock: inability og the heart to eject enough blood e.g. in ischaemic cardiac damage
  • Mechanical shock: due to a restriction on the filling of the heart e.g. cardiac tamponade, or obstruction to blood flow through the lungs e.g. pulmonary embolism
  • Hypovolaemic shock: due to loss of circulating fluid volume (e.g. haemorrhage)
  • Normovolaemic (distributive) shock: due to uncontrolled falls in peripheral resistance (e.g. in sepsis of anaphylaxis)


What could poor regional perfusion be due to?

Arterial occlusion: peripheral artery disease, coronary artery disease

Venous congestion: varicose veins, deep vein thrombosis


Describe Peripheral Vascular Disease in Veins

Veins contain ~70% if blood volume at any one time

Capacitance vessels have thin walls, low pressure, valves which prevent wrong direction of flow, external compression by skeletal muscle – musculovenous pump

Superficial vessels drain into deep vessels via perforating veins. If valves are incompetent, blood can go from deep veins to superficial veins --> varicose veins


Explain about Deep Vein Thrombosis

Commonly occur in calf veins, popliteal, femoral, iliac

Tender swollen calves

Risk of pulmonary embolism – chest pain, breathlessness

If there is a large PE resulting in occlusion, that can cause shock



What are varicose veins, and what can they lead to?

dilated, torturous superficial veins

Can be asymptomatic or lead to venous ulcers (chronic sores)


Explain about Coronary Artery Disease

atheromatous plaque, partially occluding coronary artery

Ischaemic heart disease

>70% occlusion – compromised blood flow when O2 demand increases and blood flow through LCA largely during diastole (shortens when HR increases --> limiting blood flow to LCA)

90% occlusion: ischaemia at rest



Discuss Ischaemic Heart Disease - Angina

Central chest pain – radiates to neck and left arm

Brought on by exercise, relieved by rest (stable angina)

Investigated with exercise stress test: 12-lead ECG, heart rate and blood pressure monitored whilst patient exercises on treadmill. Starts gently and increases in levels of exercise intensity

Test is positive if there is chest discomfort or ECG changes

Treatment: nitrates (main effect venodilation, reducing preload), β-blockers (reducing workload – contracts less hard, slower) and calcium channel antagonists reduce workload


Explain about Unstable Angina

Rapid onset pain at rest: severe central – radiates less

Disruption of atherosclerotic plaque and thrombus formation

Limited duration and extent of obstruction

May be ST depression and/or T wave inversion

No detectable necrosis (cardiac enzymes and troponin not elevated)



Explain about a STEMI

Acute severe central chest pain (crushing)

Radiating to neck, left shoulder and arm

Not relieved by rest

Be aware some patients do not experience pain

Strong sympathetic reaction: sweating, pallor due to sympathetic vasoconstriction

Rupture of atheromatous plaque – formation of thrombus (inappropriate clot: thrombus detaches or propagates along coronary artery and blocks it. Necrosis (death) of myocardial tissue

STEMI necrosis of full thickness of myocardial wall

NSTEMI more limited – ST depression and inverted T waves

ECG changes are most obvious in leads viewing the damaged myocardium


What biomarkers would you look for in a STEMI?

Specific cardiac troponin isoforms - TnI and TnT

Creatine Kinase MB


Explain about Cardiac Arrest

Unresponsiveness associated with lack of pulse


Heart has stopped or ceased to pump effectively


Asystole (loss of electrical and mechanical activity)


Ventricular fibrillation (uncoordinated electrical activity)


Most common form of cardiac arrest


May occur following MI or electrolyte imbalance or some arrhythmias (e.g. long QT and Torsades de Pointes)


Torsades de Pointes is a distinctive polymorphic ventricular tachycardia in which the QRS amplitude varies and the QRS complexes appear to twist around the baseline – associated with a prolonged QT interval, may degenerate into sustained ventricular tachycardia or ventricular fibrillation


Basic life support: chest compression and external ventilation


Advanced life support: defibrillation – electric current delivered to the heart, depolarises all the cells – puts them into refractory period. Allows coordinated electrical activity to restart

Adrenaline – enhances myocardial function, increases peripheral resistance


Essentially what can shock be due to?


Shock can be due to fall in CO or fall in TPR beyond capacity of the heart to cope


Fall in cardiac output could be due to mechanical (pump cannot fill), pump failure or loss of blood volume

  • Cardiogenic shock (pump failure) – ventricle cannot empty properly
  • Mechanical shock (obstructive) – ventricle cannot fill properly
  • Hypovolaemic shock – reduce blood volume leads to poor venous return

Fall in peripheral resistance could be due to excessive vasodilation


Explain about Cardiogenic Shock

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

Following myocardial infarction: damage to left ventricle

Or due to serious arrhythmias (profound tachycardia orbradycardiaresulting in a drop in arterial pressure)

Acute worsening of heart failure

Central venous pressure (CVP) may be normal or raised; heart fills but fails to pump effectively

Dramatic drop in arterial BP

Tissues poorly perfused – coronary arteries which exacerbates problem, kidneys which leads to reduced urine production (oliguria) and brain which leads to loss of consciousness, confusion and dizziness


Explain about Mechanical Shock caused by Cardiac Tamponade

Blood or fluid build up in pericardial space (so heart is not able to expand)

Restricts filling of the heart – limits end diastolic volume

Affects left and right sides of heart

High central venous pressure

Low arterial blood pressure (ventricles can’t fill properly – not able to pump properly)

Heart attempts to beat – continued electrical activity


Explain about Mechanical Shock caused by Pulmonary Embolism

A massive pulmonary embolism occluding a large pulmonary artery could lead to circulatory shock

Pulmonary artery pressure is high

Right ventricle cannot empty

Central venous pressure is higher

Reduced return of blood to left heart – due to occlusion of pulmonary artery

Limits filling of left heart

Left atrial pressure is low

Arterial blood pressure is low


Also chest pain, dyspnoea


Explain about Hypovolaemic Shock


Reduced blood volume


Most commonly due to haemorrhage

~5L in an average 75kg man

<20% of blood loss unlikely to cause shock

20-30% some signs of shock response

30-40% substantial decrease in mean arterial blood pressure and serious shock response

Severity of shock is related to amount and speed of blood loss – worse if blood loss is rapid (more likely to go into shock with a smaller amount of blood loss if loss is rapid)

When there is a haemorrhage, venous pressure falls, cardiac output falls (Starling’s Law), arterial pressure falls and this is detected by Baroreceptors.

The compensatory response is increased sympathetic stimulation, tachycardia, increased force of contraction (due to increased contractility), peripheral vasoconstriction and venoconstriction (increases venous pressure --> increases return to heart)

Increased peripheral resistance due to peripheral vasoconstriction leads to internal transfusion, reducing the capillary hydrostatic pressure which increases THE NET MOVEMENT OF FLUID INTO THE CAPILLARIES.

Signs and symptoms of Hypovolaemic shock: tachycardia, weak pulse, pale skin and cold, clammy extremities

Apart from haemorrhage, hypovolaemic shock can also result from severe burns, severe diarrhoea or vomiting and loss of Na+


What can occur in Hypovolaemic Shock if treatment isn't given?


Decompensation can occur if treatment isn’t given


Peripheral vasoconstriction (shutdown) impairs tissue perfusion

Tissue damage due to hypoxia

Release of chemical mediators – vasodilators which overcome sympathetic vasoconstriction effect

TPR falls

Blood pressure falls dramatically

Vital organs can no longer be perfused

Multi-system failure


Explain about Distributive Shock

Low resistance shock (normovolaemic – no change in blood volume); shock occurs because of fall in TPR

Profound peripheral vasodilation results in a catastrophic drop in TPR. Blood volume is constant but volume of the circulation has increased

Toxic shock

Anaphylactic shock



Explain about Toxic Shock


Endotoxins released by circulating bacteria cause:


Profound vasodilation

Dramatic fall in TPR

Fall in arterial pressure

Impaired perfusion of vital organs

Also – capillaries become leaky but which reduces blood volume


Decreased arterial pressure: detected by Baroreceptors leading to increased sympathetic output. Vasoconstrictor effect overridden by mediators of vasodilation. Heart rate and stroke volume increased

Patient has tachycardia and warm, red extremities because of vasodilation however later stages of toxic shock - vasoconstriction


Explain about Anaphylactic Shock


(severe allergic reaction – anaphylaxis)


Release of histamine from mast cells (and other mediators such as prostaglandins, leukotrienes and cytokines) has a powerful vasodilator effect – fall in TPR

This results in a massive drop in arterial pressure which via the baroreceptor reflux, leads to an increased sympathetic response – leading to increased CO but can’t overcome vasodilation

Impaired perfusion of vital organs

Mediators also cause bronchoconstriction and laryngeal oedema – difficulty breathing

Patient will have difficulty breathing, collapse, rapid heart rate and red, warm extremities

Acutely life-threatening

Treatment: adrenaline – vasoconstriction via action at α1 adrenoceptors – works on β2 normally to cause vasodilation but in high enough concentration binds to α1 adrenoceptors to cause vasoconstriction to try and increase venous return to the heart and therefore increase cardiac output


Give an overall summary of shock


Explain about Hypertension

sustained increased in arterial blood pressure

Arterial BP > 140/90 mmHg


CO = SV x HR

Regulation of blood pressure at three sites:

  • Kidneys (regulates blood volume which alters SV)
  • Heart regulates CO through altering rate and force of contraction
  • Vasculature regulates TPR


What are the consequences of hypertension?


Long standing hypertension --> left ventricular hypertrophy (risk of heart failure)


Risk of arterial disease


  • Coronary arteries – MI, angina
  • Cerebrovascular system – stroke
  • Renal vasculature – kidney failure
  • Aorta



Explain about treatment of hypertension


Non pharmacological: e.g. weight loss, exercise, reduced salt intake


Pharmacological: diuretics, vasodilators, ACE inhibitors – vasodilation, reduced blood volume

Beta blockers