SHOCK

Aminath Shafa RN MSN

• ↓ Cardiac output/ ineffective circulating blood volume Decreased
perfusion  cellular hypoxia = Shock

• Oxygen delivery < Oxygen demand

↓perfusion  Cell death  Organ Failure  Death

Types
• Cardiogenic Shock (MI, Arrhythmia, Cardiac tamponade, Pulmonary
embolism, ventricular rupture etc)

• Hypovolemic Shock (Fluid loss; hemorrhage, vomiting, diarrhea, burn

etc)

• Distributive Shock (Sepsis, Superantigen, Burn)

 Pathophysiology
↓perfusion

Anerobic respiration

Lactic acid + ↓ATP

Metabolic acidosis

Cell death
Common Clinical manifestations of Shock
• Dyspnea End organ damage
• Tachypnea • Syncope
• Tachycardia • Confusion
• Hypotension • Lethargy
• Pale skin • ↓ Urine output
• Sweating • Cold, clammy skin
• ST elevation
Type Pulse pressure Volume
Cardiogenic Narrow High
Hypovolemic Narrow Low
Distributive Wide Low
 Cardiac Output
• Amount of blood that the heart pumps per minute (4 to 8 L/min)
• How to determine Cardiac output?
• CO= HR x SV (stroke volume)
• SV= amount of blood pumped by LV with each beat (50 -100ml)
• SV= EDV-ESV
• EDV (end-diastolic volume): the total amount of blood the ventricle hold
at the end of its load
• ESV (end systolic volume): The amount of blood that remain inside the
ventricle after contraction
 Stroke volume
• Is determine by 3 factors which can be manipulated by medication to
alter the stroke volume increasing the cardiac output

Contractility Preload Afterload

Force of the contraction of
the heart muscle
↑ force ↑ blood eject
Degree of stretch at the end
of ventricular filling
↑ stretch ↑ force of
contraction
The resistance that ventricle
has to overcome involving 2
component
• Vascular pressure
• Valvular damage
Stages
of
Shock
Body’s Normal Compensatory mechanism in
Shock
Activated with decreased CO and BP
Sympathetic Nervous Renin Angiotensin Aldosterone
system mechanism
• Vasoconstriction • Vasoconstriction Fluid retention increases
increasing afterload increasing the after load the workload
• Chronotrophic affect • Fluid retention
increasing the heart rate increasing the workload
• Inotropic effect
increasing the force of
contraction
 General Diagnostic findings in Shock

• Complete blood count (blood cell count)

• ↑ lactate • ↑ Troponin

• ↓pH (acidosis) • ↓SPO2

• Altered renal function test • ↓oxygen level in arterial blood

• Altered liver function test • Culture

General Complications in Shock

• Multi organ failure ; damage to your liver, kidneys, Brain from lack of

oxygen, which can be permanent

• If not treated, death

Cardiogenic Shock
• Also known as pump failure

• Cardiogenic shock is the inability of the heart to maintain cardiac output

necessary to meet body needs

• Most often caused by a severe heart attack

• Rare condition

• Mortality rate high

• Quick action and assessment to reduce morbidity and mortality rate

 Causes
• Diastolic dysfunction (valvular dysfunction)
• Systolic dysfunction (issues with contraction)
• Arrhythmia
• Structural failure (LV failure)

Low cardiac output  Low perfusion

 Management of Cardiogenic shock
Temporary support
• Mechanical ventilation/oxygen support
• Vasopressors
• Inotropic agents along with Nitrate vasodilator
• Beta blockers to stop SNS
• ACE inhibitor/ Angiotensin receptor blocker to block the angiotensin system
• Aldosterone antagonist to stop aldosterone activity
• Specific measure
• Fibrinolysis: Thrombolytics
• Revascularization of coronary arteries; percutaneous coronary intervention (PCI)/
coronary artery bypass grafting (CABG)
• Cardiac transplantation
 Medical management …
Assistive devices
• Intra-aortic balloon pump: improves the diastolic and lowers the end-
systolic pressure without affecting the mean blood pressure
• Percutaneous left ventricular assist device: augments cardiac output

General measures (manage reversible causes)

• Hypoxia
• Hyperkalemia
• Hypothermia
• Arrhythmias
• Hyperglycemia
Hypovolemic Shock
• 5L of blood in an average adult

• ↓ fluid volume(15% or more) in blood

• ↓ venous return to heart
• ↓ Preload
• ↓Stroke volume
• ↓cardiac output
• ↓ perfusion

Symptoms of shock vary on the level of fluid loss

 Causes
• Relative hypovolemic shock: INSIDE fluid shift from intravascular
system fluid/ blood collection/ leaking inside the body
• Internal bleeding
• Severe burn injury
• Massive vasodilation (sepsis)
• Fracture of long bone (femur)
• Absolute hypovolemic shock: OUTSIDE fluid shift from intravascular
system fluid leaves the body
• Massive bleeding
• Vomiting
• Diarrhea
• Sweating (endocrine disorder)
Staging Volume loss
Management of Hypovolemic shock
• Stop external bleeding
• Fluid replacement along with
• Vasopressor
• Replacement of blood cell, with blood transfusion
• Inotropic support
Distributive Shock
• ↑ inflammatory mediators  Abnormal vasodilation (especially in
venous system) + ↑ Capillary permeability  venous blood pooling &
vascular leakage

• ↓ pressure in the blood vessels

Causes
Distributive shock occurs, when the fluid/blood moves away from the
heart leading to not having enough blood to pump
• Sepsis
• Anaphylactic
• Neurogenic
• Spinal
• Burns trauma
Medical Management
• Fluid resuscitation
• Antibiotics/ septic shock
• Vasopressors
• Inotropes

General measures (manage reversible causes)

Hypothermia
Coagulopathy
Acidosis
 Reference
• Buerke M, Lemm H, Dietz S, Werdan K. Pathophysiology, diagnosis, and treatment
of infarction-related cardiogenic shock. Herz. 2011;36(2):73-83.
doi:10.1007/s00059-011-3434-7
• Robbins and Cotran pathologic basis of disease (Ninth edition.). Philadelphia, PA:
Elsevier/Saunders. Kumar, Vinay, Abul K. ... Philadelphia, PA: Elsevier/Saunders, 2015
• Delgado, S.A. (2017). Manual of Critical Care Nursing: Nursing Interventions and
Collaborative Management, 7th edition. Critical care nurse, 37 1, 81 .
• Windecker S. Percutaneous left ventricular assist devices for treatment of patients
with cardiogenic shock. Curr Opin Crit Care. 2007;13(5):521-527.
doi:10.1097/MCC.0b013e3282efd5bc