Tag: cardiac output

In order to understand how to care for a patient in shock, we must first understand the pathophysiology of shock, as well as how to assess, diagnose, and manage it through appropriate nursing interventions. The most common types of shock are the Hypovolaemic Shock, Cardiogenic Shock, and Septic Shock. Throughout this blogpost we will be looking in detail at the definition, classification, and pathophysiology of shock.

What is Cardiac Output?

Cardiac Output (CO) is the volume of blood ejected from the heart over 1 minute. In adults, normal Cardiac Output is between 4-6L/min.

Cardiac Index (CI) is a haemodynamic parameter related to the cardiac output from the left ventricle in 1 minute to body surface area (BSA). In adults, normal Cardiac Index should be between 2.5-4L/min/m2.

Stroke volume (SV) is the volume of blood pumped out of the left ventricle during each systolic cardiac contraction.

Mean Arterial Pressure (MAP) is the average arterial pressure throughout one cardiac cycle, systole, and diastole.

Systemic Vascular Resistance (SVR) is the resistance in the circulatory system which affects the blood pressure and the flow of blood. SVR is also a component of cardiac function, eg. vasoconstriction leads to an increased SVR.

Formulas:

Cardiac Output (CO) = Heart Rate (HR) X Stroke Volume (SV)

Cardiac Index (CI) = Cardiac Output (CO) / Body Surface Area

Mean Arterial Pressure (MAP) = Cardiac Output X Systemic Vascular Resistance (SVR)

Cardiac Output Determinants

• HEART RATE – influenced by both the sympathetic and parasympathetic system, as well as by intrinsic regulation
• STROKE VOLUME – determined by cardiac preload (PL), afterload (AL), and cardiac contractility (CC).

Preload determinants

Preload (PL) is the stretching force exerted on the ventricle by the blood contained within at the end of diastole.

The Starling’s Law of the Heart indicates that increased volume returned to the heart causes an increase in Cardiac Output, however, following a certain increase in volume returned causes a decrease in Cardiac Output.

Preload determinants include:

• VOLUME OF BLOOD RETURNED TO LEFT VENTRICLE – influenced by venous return, total blood volume, and atrial kick
• LEFT VENTRICLE COMPLIANCE (stretching ability) – influenced by the stiffness and thickness of the muscle wall

Examples: in Hypervolaemia, preload is too low, whilst in Congestive Heart Failure, preload is too much.

Afterload Determinants

Afterload (AL) is the resistance (a.k.a. Systemic Vascular Resistance SVR) that the heart must overcome to push blood into the systemic circulation.

An increase in Afterload causes an increase in the required effort and oxygen demand by the heart, eg. vasoconstriction increases Systemic Vascular Resistance, total blood volume and viscosity.

To reduce the heart’s workload we can provide therapeutic nursing management, including the administration of vasodilators.

Cardiac Contractility Determinants

Cardiac Contractility (CC) is the force by which the heart contracts. CC is determined by:

• VENOUS RETURN – Starling’s Mechanism
  • STIMULATION OF THE SYMPATHETIC NERVOUS SYSTEM
  • INCREASE IN INTRACELLULAR CALCIUM (Ca++) – such as after use of Digoxin
  • PHARMACOLOGICAL INTERVENTIONS – eg. administration of Inotropes

Shock Definition

Shock can be defined as an acute widespread process of impaired tissue perfusion resulting in cellular, metabolic and haemodynamic changes, causing an imbalance between cellular oxygen supply and demand. Shock leads to death if not controlled in time.

Normal tissue perfusion requires:

• adequate blood volume
• adequate cardiac pump
• effective circulatory system

Impairment of any of the above, thus, impairment in normal tissue perfusion, may lead to SHOCK…

Impaired oxygen perfusion causes:

1. inadequate blood flow reaching the tissues
2. inadequate delivery of oxygen and nutrients to the cells
3. cell starvation due to oxygen and nutrient deprivation
4. cell death
5. multiple organ failure
6. death

Classification of Shock

Shock can be classified into 3 different types. Whilst the management of shock varies based on the type of shock it is, the resulting effect of all 3 types of shock is the same – decreased tissue perfusion.

Hypovolaemic Shock

Hypovolaemic shock is the most commonly occurring type of shock, which is also easily reversible if treated in a timely manner. Features of a hypovolaemic shock include:

• loss of circulating or intravascular volume
• impaired tissue perfusion
• inadequate delivery of oxygen and nutrients
• may be caused by relative and absolute hypovolaemia, or loss of blood or other fluids

Cardiogenic Shock

• impaired ability of the heart to pump blood as it should (left or right ventricle dysfunction), causing systemic hypoperfusion and tissue hypoxia
• may be caused by cardiac injury (eg. cardiac tamponade), cardiopulmonary arrest, following cardiac surgery, dysrhythmias (severe tachycardia or bradycardia), myocardial tissue necrosis following a Myocardial Infarction, or structural problems (eg. valvular damage or regurgitation, pulmonary embolus, acute myocarditis, papillary muscle rupture, intracardiac tumour, and congenital defects
• compensatory mechanisms may worsen the situation…eg. reduced cardiac output due to myocardium death causes increased contractility which further increases the heart’s workload and oxygen demand; reduced blood pressure causes the release of catecholamines which leads to vasoconstriction, subsequently leading to a further increase in cardiac workload and oxygen demand

Distributive Shock

• impaired distribution of circulating blood volume
• vasodilation
• capillary leaks

Distributive Shock is further sub-classified into 3 other types of shock:

SEPTIC SHOCK:

While sepsis is defined as a life-threatening organ dysfunction caused by dysregulated host response to infection, a septic shock is defined as a subset of sepsis in which underlying circulatory, cellular and metabolic abnormalities and profound enough to substantially increase the risk of mortality.

• microorganism entry into the patient’s body
• dysregulated host response characterised by excessive peripheral vasodilation, causing maldistribution of blood volume, over-perfused peripheral areas and under-perfused central areas
• is the major cause of admission in the critical care setting

Septic Shock may originate from the community (>80% of cases) or during a stay in a healthcare facility.

ANAPHYLACTIC SHOCK:

• severe antigen-antibody reaction causing histamine release
• signs & symptoms include vasodilation, hypotension, bradycardia, increased capillary permeability, bronchospasm, laryngeal oedema, and stridor

NEUROGENIC SHOCK:

• disruption of sympathetic nerve activity below the level of a spinal cord injury or disease
• signs & symptoms include vasodilation, hypotension, bradycardia, warm dry skin, and loss of thermoregulation

Obstructive Shock

• obstructive shock is often classified with cardiogenic shock
• obstructive shock is mechanical obstruction which impedes the heart from generating adequate cardiac output
• examples of obstructive shock include Tension Pneumothorax, Pericardial Tamponade and Pulmonary Embolus

The Pathophysiology of Shock

Initial Stage

Within the initial phase of shock, effects are very subtle and at cellular level. An increase in serum lactate indicates metabolic acidosis due to cells switching from aerobic to anaerobic respiration.

1. Decrease in Cardiac Output
2. Decrease in tissue perfusion
3. Cells switch from aerobic to anaerobic respiration
4. Accumulation of Lactic Acid
5. Lactic Acidaemia (Low pH)
6. Cellular Damage

Compensatory Stage

During the compensatory stage of shock, the patient’s body attempts to improve tissue perfusion through neural, chemical, and hormonal compensation, mediated by the sympathetic nervous system.

NEURAL COMPENSATORY MECHANISMS

• increased Heart Rate and Cardiac Contractility
• arterial and venous vasoconstriction
• circulation lessens within the peripheries and becomes more focused on vital organs perfusion

CHEMICAL COMPENSATORY MECHANISM

• chemoreceptors detect acidosis and stimulate hyperventilation so more Carbon Dioxide is exhaled

HORMONAL COMPENSATORY MECHANISMS

Hormonal compensatory mechanisms aim to increase the blood pressure to cause an increase in tissue perfusion.

• the anterior pituitary gland is stimulated, causing secretion of ACTH (Adrenocorticotropic Hormone), which then stimulates the adrenal cortex to produce glucocorticoids (glucagon), which causes an increase in blood glucose level
• the adrenal medulla is also stimulated, causing the release of adrenaline and noradrenaline, which result in vasoconstriction, leading to an increased Blood Pressure and increased Heart Rate
• renin response is activated, which facilitates the conversion of Angiotensinogen into Angiotensin II; this conversion causes vasoconstriction, release of aldosterone (which leads to sodium retension), and release of antidiuretic hormone (ADH) by the posterior pituitary gland (which leads to water retention)

SYMPTOMS EXPERIENCED DURING THE COMPENSATORY PHASE:

• cold, clammy skin
• drop in urine output
• tachycardia
• tachypnoea
• hyperglycaemia

Progressive Stage

• compensatory mechanisms start failing
• shock cycle continues indefinitely
• anaerobic respiration causes energy exertion within the cells
• cells are unable to function, and irreversible damage occurs (Mitochondria become unable to use oxygen for the production of energy, and Lysosomes release digestive enzymes which then cause further cellular damage)
• utilisation of the limited oxygen delivered into the cells becomes problematic

During the progressive stage, organ systems start to fail…

• Myocardial Hypoperfusion causes decreased Cardiac Output leading to ventricular failure, enabling shock to progress further
• Decreased Cerebral Blood Flow causes CNS dysfunction, causing failure of the sympathetic nervous system, failure of the thermoregulation mechanism, cardiac and respiratory depression, and altered mental status
• Impaired Coagulation leading to microclot formation, which may cause Disseminated Intravascular Coagulation (DIC)
• Renal Vasoconstriction & Hypoperfusion causes decreased urine output and increased creatinine, which may also lead to Acute Tubular Necrosis (ATN)
• GastroIntestinal Tract Hypoperfusion causes decreased peristalsis (decreased bowel sounds), release of Gram-negative bacteria (which worsens shock), and liver hypoperfusion due to deranged LFTs
• Pulmonary Vasoconstriction along with microemboli, parenchymal inflammation, and alveolar oedema all lead to respiratory failure (Acute respiratory distress syndrome ARDS)

SYMPTOMS EXPERIENCED DURING THE PROGRESSIVE PHASE:

• electrolyte imbalance
• metabolic acidosis
• respiratory acidosis
• peripheral oedema
• tachycardia
• arrhythmias
• hypotension
• pallor
• cool clammy skin
• altered level of consciousness
• reduced bowel sounds

Refractory Stage

In the final stage of shock, the patient becomes unresponsive to treatment, experiences multiple organ failure, eventually leading to death.

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