Shock is a medical condition in which the blood perfusion to the tissues decreases, resulting in cellular injury and inadequate tissue function. It is a life - threatening condition signified by rapid heart rate, hypotension (low blood
pressure), weak pulse, and sign of poor end -organ perfusion (i.e., low urine output, confusion, or loss of consciousness).
Shock alters the mental state of the patient and is a state of medical emergency. A state of shock increases lactate metabolism as it leads to anaerobic metabolism.
Mortality rate in a patient with shock is quite high, even though optimal treatment is provided in an ICU.
2.1.2. Treatment for Cardiovascular Shock
The treatment of cardiovascular shock involves:
1) Primary Therapy: This therapy aims at correcting the cause (i.e., haemorrhage, infection, myocardial infarction, and anaphylaxis), and
2) Secondary Therapy: This therapy aims at correcting the associated hemodynamic disturbance. The following drugs are employed for their hemodynamic effects:
1) Sympathomimetic amines,
2) α-adrenoceptor blocking agents,
3) Corticosteroids,
4) Oxygen,
5) Cardiac glycosides,
6) Glucagon, and
7) Dextrans.
2.1.2.1. Sympathomimetic Amines
Sympathomimetic amines act via β1-adrenoceptors in the heart,
- and β2-
adrenoceptors in the blood vessels, and dopamine receptors in the cerebral,
coronary, mesenteric, and renal vascular beds. Patients with shock resulting from
decreased circulating volume of blood should be given either blood or plasma
volume expanders. They may later be given sympathomimetic agents for the
improvement of tissue perfusion.
Mechanism of Action
Either one or more mechan ism of action of sympathomimetic amines helps to
maintain the perfusion of vital organs (brain, heart, and kidney), and other
visceral organs:
1) Increased Myocardial Contractility: Sympathomimetic amines increase the cardiac output in case of adequate venous return.
2) Constriction of the Capacitance: Sympathomimetic amines contract the vessels or venules to prevent venous pooling.
3) Dilation of Resistance: Sympathomimetic amines dilate the a rterioles either by affecting or constructing the resistance vessels in non-vital organs.
Adverse Reactions
Restlessness, headache, pallor, dizziness, precordial pain, and palpitation are the adverse effects of therapeutic doses of sympathomime tic amines. As a result of overdosage, convulsions, cerebral haemorrhage, and tachyarrhythmia resulting in fatal ventricular arrhythmias are induced.
Prolonged Administration of Vasoconstricting Sympathomimetic Amines:
When these agents (especially, nor-adrenaline) are administered for a long time, a strong constriction of the post
-capillary sphincter occurs due to decreased plasma volume. As a result, the capillary pressure is increased , leading to loss of fluids through the capillary walls. Also, a decrease in renal blood flow and glomerular filtration rate is seen. Thus, a condition of marked tissue hypoperfusion and irreversible shock usually results.
Prolonged Administration of Large Doses of Nor -Adrenaline: When largedoses of nor -adrenaline are administered for a long time, necrosis of theintestines, liver and kidneys, haemorrhage, focal myocarditis, intravascularplatelet aggregation, and subepicardial haemorrhage occur.
If the sympathomimetic amines are suddenly withdrawn aftera prolonged therapy, recurrent and profound hypotension occurs; thus, the therapy should be discontinued gradually with appropriate fluid replacement.
Examples of Drugs
Nor-adrenaline, adrenaline, dopamine, and the synthetic compounds
like
isoprenaline, metaraminol, and dobutamine , are some of the sympathomimetic amines employed in the treatment of shock. Mephentermine, methoxamine, and phenylephrine are the s ympathomimetic amines preferred as pressor agents during anaesthesia. Some of these drugs are discussed below:
1) Nor-Adrenaline: It increases the perfusion pressure and cardiac output in patients with shock who have very low peripheral vascular resistance. Hence, it is employed in patients suffering from low peripheral resistance shock.
However, it should not be administered in patients with shock syndrome, characterised by high peripheral resistance and low or normal blood pressure.
This is because in such patients, nor-adrenaline further induces vasoconstriction, resulting in loss of plasma volume via capillaries and a further worsening of kidney function.
2) Adrenaline: Administration of this drug increases the cardiac output ,decreases the renal blood flow
, and increases t he Total Peripheral
Resistance (TPR). Adrenaline is employed in the management of anaphylactic shock.
3) Dopamine: Renal and mesenteric blood flow is increased by this drug due to its action on dopamine receptors. Dopamine causes stimulation of the heart via activation of β-receptors. It increases the cardiac output and renal blood flow. It does not affect the TPR. It successfully treats oliguric patients having either low or normal peripheral vascular resistance. Dopamine can also be combined with α-blocking agent in a vasoconstricted patient. It is used in the treatment of cardiogenic, septic and traumatic shock.
4) Isoprenaline: It exerts its action by a β-adrenergic activity. It acts on the heart and the periphery. It does not cause vasoconstriction in the kidneys (unlike adrenaline). It is helpful in patients with shock who have a high
peripheral vascular resistance.
5) Metaraminol: Its haemodynamic actions are similar to those of nor-adrenaline. However, its duration of action is longer than that of nor-adrenaline.
6) Dobutamine: It is a newly synthesised synthetic catecholamine that exerts its actions by acting primarily on β1-receptors. It targets the cardiac β1- receptors, and thus its action on β2- and -receptors are less pronounced. Its
action on - and β2-receptors of blood vessels are not much efficient, and thus have comparatively fewer vascular effects.
Dobutamine is employed in patients with severe CHF, and in those who have undergone cardiac surgery as a short-term therapy. It increases the cardiac output as efficiently as isoprenaline. Its adverse effects in the form of
tachycardia and arrhythmias are fewer as compared to those associated withthe use of isoprenaline.
2.1.2.2. α-Adrenoceptor Blocking Agents
The α-adrenoceptor blocking agents are used to reduce the intense vasoconstriction caused by the reflex release of nor -adrenaline (from the adrenergi c nerves) and catecholamines (from the adrenal medulla) as a result of shock.
Advantages of α-adrenoceptor blocking agents are:
1) The harmful effect of vasoconstriction on microcirculation in tissues is avoided.
2) Rapid administration of intravenous fluid is enabled such that the central
venous pressure is not increased.
3) The occult plasma volume deficit is unmasked.
However, hypotension may be seen as an adverse effect of these agents,particularly in patients with myocardial insufficiency. Therefore, therapy constituting -blockers should be followed by adequate replacement of fluids.
Thus, tissue perfusion is markedly improved.
The most commonly employed α-adrenoceptor blocking agent is phenoxybenzamine. It is a life -saving drug in patients with surgical shock or trauma. It causes an intense re-distribution of blood flow and plasma volume. For
this effect, it needs to be administered intravenously in a dose of 1mg/kg of body weight diluted well in 500ml of glucose (5%). In 30 minutes , the complete effect of the drug is seen. It has duration of action of several hours. It exerts its action in the form of a non-competitive inhibitor at the -receptor. Phentolamine is another -blocking agent having a shorter duration of action Pressor drugs reverse the effect of this drug because they competitively inhibit the action of phentolamine at the α-receptor. Either dopamine or nor-adrenaline
is simultaneously administered along with the -blockers to counteract the vasoconstriction produced. Any of these drugs do not affect the cardiac stimulant action of the -blockers.
2.1.2.3. Corticosteroids
The useful effects of corticosteroids in states of shock are not completely understood. Their efficacy is also controversial. The sensitivity to endotoxin may be decreased when corticosteroids are administered in cases of septic shock.
However, this increases the chances of infection, while increasing the probability of bacteraemia. A high dose of corticosteroids are administered in a patient with shock as they bring the following responses:
1) A positive inotropic effect,
2) Decreased peripheral resistance,
3) Stabilisation of lysosomes,
4) Preservation of integrity of small vessels, preventing leakage from microcirculation, and
5) Decreased adhesiveness of the platelets.
It is suggested that microcirculation is improv ed by all these effects that accountfor a combination of increase in cardiac output, vasodilatation and protection of cells from the damaging effects of proteases (by lysosomal membrane stabilisation). Although no suggestion relating to their advantageous effects in patients with shock has been reported. Yet, administration of corticosteroids in large doses has been established to decrease the formation and liberation of cardio-depressant elements from tissues due to their property of lysosomal membrane stabilisation. This property of corticosteroids also accounts for other cellular effects that protect the cells from damage against hypoxia.
2.1.2.4. Oxygen
Maintenance of adequate oxygen exchange requires positive pressure ventilation. Also, the concentration of gases in blood should be monitored frequently to avoid
toxicity of oxygen.
Advantages of supplemental oxygen in shock patients are:
1) Cardiac output is increased by the supplementation of oxygen, and
2) Oxygenation of the tissues can be improved significantly.
Supplementation of oxygen in patients with shock is of immense importance in:
1) Conditions of arterial hypoxaemia (usually seen in cardiogenic shock),
2) Conditions of dyspnoea or cyanosis, and
3) When arterial PO2 falls below 60mm Hg.
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