Circulatory shock (circulatory failure): causes, symptoms, diagnosis, treatment

By Cristiano Antonino On Jul 7, 2022

Circulatory shock, an overview. Since the ultimate purpose of the blood circulation is to supply oxygen and other vital nutrients to the body’s organs, circulatory insufficiency occurs when this function is not performed effectively

Circulatory insufficiency or shock occurs when the blood circulation is unable to meet the metabolic demands of vital organs such as the brain, heart, kidney and so on. In simple terms: tissues need more blood nourishment than the body can provide, and tissue that is not adequately nourished risks necrosis, i.e. death.

Necrosis of vital tissue can lead to irreversible damage and death of the patient.

Although there are many parameters that indicate the presence of suboptimal circulation (e.g. arterial hypotension), the condition of shock is only present when signs of vital organ dysfunction are evident (e.g. sensory abnormalities, reduced urine output).

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Causes and risk factors of circulatory shock

The causes that can lead to circulatory shock are many and can involve various systems, particularly – but not exclusively – the circulatory system.

Circulatory shock may be the consequence of inadequate cardiac contractility, or insufficient vascular tone (inadequate afterload) or hypovolaemia (inadequate pre-load).

For example, myocardial infarction can cause inadequate cardiac contractility, which can lead to shock, in this case referred to as ‘cardiogenic’.

Sepsis (infection in the bloodstream), on the other hand, can cause vasodilatation with reduced afterload and circulatory shock termed ‘septic’.

Haemorrhage, trauma or surgery with secondary dehydration can cause significant hypovolaemia (reduction in circulating blood volume), and this can precipitate hypovolaemic shock if the circulating blood volume is inadequate to cope with the body’s metabolic demands.

However, the loss of more than 20-25% of circulating blood mass is required for such conditions to occur.

Other causes of shock include those pathologies that lead to obstruction of blood flow (e.g. massive pulmonary embolism causing an increase in the afterload of the right ventricle and inadequate preload of the left ventricle), and those that alter myocardial contractility through a restriction of heart function (e.g. constrictive pericarditis and pericardial tamponade).

The most complex forms of shock are those caused by maldistribution of blood flow

This category of circulatory failure includes septic shock, toxic shock, anaphylactic shock and neurogenic shock.

In each of these conditions, there is a decrease in perfusion to vital organs secondary to the loss of peripheral resistance resulting from vasodilation and hypotension.

Of these different types of shock secondary to insufficient vascular tone, the most common form is septic shock: it results in a syndrome affecting the heart, vascular system and most body organs.

Although the most common cause of septic shock is infections caused by gram-negative bacteria, a large number of microorganisms can cause this syndrome through the release of toxins into the bloodstream.

The role of metabolism is an important point to consider when assessing patients with circulatory failure.

Indeed, any condition that increases the metabolism of these patients has the potential to increase the incidence and severity of shock.

For example, fever increases oxygen consumption and may, therefore, lead to circulatory shock in patients with marginal cardiac function.

Classification of circulatory shock

Shock is classified into two major groups: that which is caused by a decrease in cardiac output and that which is caused by a decrease in total peripheral resistance.

Each type includes several subgroups:

1) Decreased cardiac output shock

Cardiogenic shock
myogenic
from myocardial infarction
from dilated cardiomyopathy;
mechanical
from severe mitral insufficiency;
from interventricular septal defects;
from aortic stenosis;
from hypertrophic cardiomyopathy;
arrhythmic.
Obstructive shock;
pericardial tamponade;
massive pulmonary thromboembolism;
atrial myxoma (tumour of the heart);
ball thrombus (spherical thrombus intermittently occluding a heart valve, often the one connecting the left atrium of the heart with the left ventricle, i.e. the mitral valve);
Hypertensive PNX (hypertensive pneumothorax).
Hypovolaemic shock;
haemorrhagic hypovolaemic shock (hypovolaemia is caused by copious internal or external blood loss);
non-haemorrhagic hypovolaemic shock
from severe dehydration
from gastrointestinal leakage;
from burns;
from renal damage;
from diuretic drugs;
from hyposurrenalism;
from fever;
from profuse sweating.

2) Shock from decreased total peripheral resistance (distributive shock)

septic shock (with the variant ‘toxic shock’)
allergic shock (also called ‘anaphylactic shock’);
neurogenic shock;
spinal shock.

Pathophysiology of circulatory shock

The majority of organs are affected by the consequences of circulatory failure.

Reduced cerebral perfusion initially leads to decreased cognitive functions and vigilance, and subsequently to the onset of a comatose state.

In response to inadequate blood circulation, reduced diuresis is observed in the kidneys, while the skin typically becomes cold and clammy as peripheral circulation is reduced in an attempt to preserve blood flow to vital organs.

Shock can also alter the coagulation system and lead to the appearance of disseminated intravascular coagulation (DIC), a complex problem of medical interest that results in haemorrhages caused by the consumption of platelets and clotting factors.

In circulatory failure, the lungs are also affected, but the circulatory problem is influenced by the type of shock present.

In fact, when the cause is contractile insufficiency of the left ventricle (reduced contractility), blood stagnates in the pulmonary circulation causing pulmonary oedema, this condition is therefore known as congestive heart failure.

In contrast, when shock is due to loss of vascular tone or hypovolaemia, the pulmonary consequences are minimal, except in severe cases where pulmonary hypoperfusion leads to adult respiratory distress syndrome (ARDS).

Symptoms and signs of circulatory shock

Shock usually leads to a similar clinical picture in most patients, regardless of its aetiology.

Patients in shock usually present with arterial hypotension, tachypnoea and tachycardia.

Peripheral pulses are typically weak or ‘stringy’ as a result of reduced systolic ventricular output.

Signs of organ dysfunction are also present and include oliguria (reduced urine output), sensory changes and hypoxaemia.

Following the release of epinephrine, which causes peripheral vasoconstriction in an attempt to compensate for hypotension, the skin often appears cold and sweaty.

In severe forms of shock, metabolic acidosis is often observed, an indication of the activation of anaerobic metabolism secondary to the lack of oxygen supply to peripheral tissues.

This metabolic alteration is often (but not always) accompanied by a reduction in mixed venous blood oxygen tension (PvO2) and an increase in serum lactate, which is the end product of anaerobic metabolism.

The reduction in PvO2, on the other hand, occurs because the peripheral tissues extract more oxygen than normal from the blood flowing through them at low speed to compensate for the reduction in cardiac output.

In patients in shock, evaluation of serum electrolytes is useful, as significant alterations in them (e.g. hypokalemia) can contribute to impaired cardiovascular conditions and can be easily corrected.

The evaluation of electrolytes is also useful in the calculation of the anion gap, which makes it possible to highlight the occurrence of lactic acidosis secondary to the production of lactic acid of anaerobic origin.

To calculate the anion gap, the value of chlorine (Cl-) and bicarbonates (HC03) must be added together and the value of sodium (Na+) subtracted from this sum.

Normal values are 8-16 mEq/L. In patients in shock, values above 16 mEq/L indicate that the shock is more severe and causes lactic acidosis.

In patients with insufficient peripheral vascular tone (e.g. septic shock, toxic shock) fever or hypothermia and leucocytosis are typically present.

Since patients with maldistribution shock show peripheral vasodilatation, their extremities may remain warm and pink despite poor blood supply to vital organs.

Haemodynamic monitoring of patients with septic shock in the hyperdynamic phase shows an increase in cardiac output, a reduction in peripheral vascular resistance and a low or normal PCWP

The PaO2 of patients with septic shock may, therefore, be normal despite inadequate peripheral tissue oxygenation.

The normality of this parameter in septic shock patients is probably due to reduced peripheral oxygen utilisation and the presence of peripheral arteriovenous shunts.

In the later stages, then, the myocardium often undergoes functional depression so that cardiac output tends to decrease.

Patients with hypovolemic shock, on the other hand, typically present with poor perfusion in the extremities, which causes the appearance of slow capillary refill, peripheral cyanosis and cold fingers.

In this type of patients, haemodynamic monitoring shows reduced cardiac filling pressures (low CVP and PCWP), low cardiac output and high systemic vascular resistance.

In hypovolaemic shock, reduced diuresis is also observed as the kidneys attempt to conserve body fluids.

Diagnosis

The diagnosis of shock is based on various tools, including:

anamnesis;
objective examination;
laboratory tests;
haemochrome;
haemogasanalysis;
CT SCAN;
coronarography;
pulmonary angiography;
electrocardiogram;
chest X-ray;
echocardiogram with colordoppler.

Anamnesis and objective examination are important and must be performed very quickly.

In the case of an unconscious patient, the history can be taken with the help of family members or friends, if present.

On objective examination, the subject with shock often presents pale, with cold, clammy skin, tachycardic, with reduced carotid pulse, impaired renal function (oliguria) and impaired consciousness.

During diagnosis, airway patency should be ensured in patients with impaired consciousness, the subject should be placed in the anti-shock position (supine), and the casualty should be covered, without sweating, to prevent lipotimia and thus further aggravation of the shock state.

In shock, the electrocardiogram (ECG) most frequently shows tachycardia, although it is possible to show abnormalities in cardiac rhythm when coronary perfusion is inadequate.

When this occurs, ST-segment elevation or T-wave inversion, or both, are possible.

When considering the use of vasopressor drugs for the correction of hypotension, it is therefore necessary to assess the presence of ST-segment elevation and T-wave changes on the ECG, findings that may suggest the heart’s poor tolerance to the stretching caused by the vasopressor-induced increase in afterload.

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Treatment in circulatory shock

The treatment of patients in shock consists of a few general aids.

Oxygen therapy allows the treatment of hypoxaemia and maximises the efficiency of blood circulation.

Oxygen may initially be necessary at high concentrations (above 40%), especially in the presence of pulmonary oedema.

Endotracheal intubation is, on the other hand, necessary when the patient’s sensorium is depressed to such an extent that the possibility of endotracheal aspiration is feared.

Mechanical ventilation is often indispensable in the treatment of patients in shock, in order to reduce the oxygen consumption of the respiratory muscles and the demands on the circulatory system, as well as in the treatment of respiratory insufficiency.

Mechanical ventilation is most useful when rapid normalisation (e.g. septic shock) of clinical conditions is not likely and in the presence of respiratory failure.

Finally, the use of positive end-expiratory pressure (PEEP) may be necessary when the PaO2 is less than 60 mmHg with a FiO2 greater than 0.50.

Careful monitoring of the patient in the intensive care unit (ICU) is also very important.

Therefore, it is necessary to place a pulmonary artery catheter in order to carefully assess the cause of the circulatory problem and monitor the patient’s response to medical therapy.

In general, the pulmonary artery catheter is used when measurements of pulmonary pressure, cardiac output or PO, mixed venous, are required to assess the patient and his response to therapy.

In patients in hypovolaemic shock, rapid reintegration of circulatory volume (volaemia) plays a crucial role.

As a general rule, fluid replenishment is necessary whenever systolic blood pressure is below 90 mmHg and there are signs of organ dysfunction (e.g. sensory abnormalities).

When the patient has lost large amounts of blood, the ideal treatment is to replenish the volaemia using blood, but if there is no time to cross-test the blood to be infused, circulatory support can be provided by administering a plasma-expander (e.g. normal saline, hydroxyethyl starch) until definitive treatment is available.

The administration of antibiotics and plasma-expander is, however, essential for the treatment of patients suffering from septic shock.

In this case, the potential source of infection should also be sought, which may include the points of

of surgical approach, wounds, permanent catheters and drainage tubes.

Volume expansion may also be useful in this type of shock to increase arterial pressure, thus filling the void created by peripheral vasodilatation secondary to sepsis.

Vasopressor drugs such as dopamine or norepinephrine improve hypotension by partially reversing the vasodilation caused by sepsis, stimulating cardiac contractility and thus increasing cardiac output.

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