Hypovolemic Shock Cardiogenic Shock Obstructive Shock: Prepared By: HO Tiviyah Mentor: DR Tiong Supervisor: DR Tham Min

HYPOVOLEMIC SHOCK
CARDIOGENIC SHOCK
OBSTRUCTIVE SHOCK
Prepared by: HO Tiviyah
Mentor: Dr Tiong
Supervisor: Dr Tham Min
HYPOVOLEMIC SHOCK
• The most common form of shock and to some degree is a
component of all other forms of shock.
• This is due to reduced circulating volume.
• Can be divided into two:
• Hemorrhagic
• Non-hemorrhagic
• Diagnosis is usually straight forward.
• S&S: thirst, muscle cramps, and/or orthostatic hypotension.
• Physical examination:
• dry mucous membranes, decreased skin turgor, and low jugular venous
distention.
• Tachycardia and hypotension can be seen along with decreased urinary output.
• Patients in shock can appear cold, clammy, and cyanotic
Hypovolemia- Etiology
Haemorrhagic
* trauma
* ruptured aortic aneurysm
* gastrointestinal bleed
Non haemorrhagic
* vomiting
* burns
* third space loss: Fluid loss into GIT or interstitial space, eg
bowel obstruction or pancreatitis
Pathophysiology
• Heart pumps well, but not enough blood volume to pump to the
systemic circulation
• Decreased preload due to intravascular volume loss
• Reduced stroke volume, resulting in reduced cardiac output
MAP = CO x TPR (total peripheral resistance)
CO = HR X SV
• The Baroreceptors sense reduced CO and lead to increased
systemic vascular resistance (SVR) in an effort to compensate.
• The vasoconstrictive mechanisms compensate for decreased
tissue perfusion by redirecting blood from the periphery to the
vital organs, thereby maintaining coronary, cerebral, and
splanchnic perfusion.
MAP = ↓CO x TPR
MAP = ↓CO x ↑ TPR
Compensatory mechanism
• vasoconstriction
• tachycardia
• venoconstriction
• tachypnea
• restlessness
• increased movement of interstitial fluid into capillaries
• increased secretion of vasopressin
• increased secretion of glucocorticoids
• increased secretion of renin and aldosterone
• increased secretion of erythropoietin
BRIEF MANAGEMENT : HYPOVOLEMIC SHOCK
• 1. ABC
• 2. Raise foot of the bed, unless cardiogenic
• 3. Fluid replacement : saline or colloid initially ;if
bleeding use blood
• 4. Monitor BP, CVP, urine output
• 5. Treat underlying causes
• 6. Correct electrolyte abnormalities
• The main problem is inadequate volume
• Unless cardiogenic shock is suspected, aggressive fluid
resuscitation with 1-2L of crystalloids should be started
while assessing for response and to repeat if necessary,
further resuscitation with colloids, pack cells or whole
blood may be appropriate
• Ensure adequate fluid resuscitation has taken place before
starting vasopressor support
• Give IV dopamine 5-20mcg/kg/min
• Add IV Noradrenaline 0.5-1.5mcg/kg/min if necessary
• Placement of central venous line may be necessary for guiding fluid
therapy
CARDIOGENIC SHOCK
• Cardiogenic shock is caused by decreased myocardial
contractility and inadequate systemic inflammatory
response to extensive myocardial damage
• Decreased cardiac output and evidence of tissue
hypoxia in the presence of adequate intravascular
volume
• Characterized by:
• persistent hypotension (systolic <80-90 / MAP<30
than baseline)
• Reduction in cardiac index (<1.8L/min/m2 without
support; <2.2L/min/m2 with support)
Causes
• MOST COMMON -> ACUTE STEMI with LV FAILURE

•
Others
• acute MR / ruptured septal wall
• Severe bradycardia
• Severe tachycardia ; eg AF
• Atrial and ventricular arrhythmia
• Aortic dissection
Pathophysiology
Signs and Symptoms
• Chest pain
• Palpitations
• Dyspnoea
• Nausea and vomiting
• Profuse sweating
• Confusion/disorientation
• Syncope
• Severe systemic hypotension
• Respiratory distress due to pulmonary congestion
Investigation
• ECG - to look for evidence of new ischemic changes

• CXR – worsening pulmonary congestion
• Emergency echo
• Elevated Lactate, reduce NaHCO3 – new or worsening acidosis
Prognosis
• GUSTO-Iib study shows mortality rate similar between STEMI

with CS and NSTEMI with CS
• Prognosis improved much if early successful reperfusion
therapy
MANAGEMENT
Management
• Position-supine
• Maintain SpO2 >90% or PO2>60
• Correct metabolic acidosis
• Sodium bicarbonate can be given if pH <7.2
• Fluid challenge
• IV fluid replacement should be guided by measuring pulmonary
capillary wedge pressure (PCWP) with right heart catheterisation.
Fluid can be given till PCWP of 18mmHg reached. If no signs of
LV failure or APO, empiric IV volume challenge of 250ml NS can
be given.
• If no invasive haemodynamic monitoring, small volume of 100ml
over 5-10mins can be given with strict monitoring of BP, PR,
peripheral perfusion and auscultation of lungs. If not responding
after 500cc-1L of fluid, start inotrope
Medications: (due to AMI)
• Aspirin
• Clopidogrel
• GP II b/IIIa inhibitor – improve outcome of NSTEMI
•
Withhold beta blocker, and other BP lowering medications
Inotrope
Noradrenaline
• Rapid recovery for circulatory support for cardiogenic shock
Dopamine
• At low dose, positive inotropic effects
• A higher dose (>10mcg/kg/min), it stimulates alpha adrenergic
receptors, causing vasoconstriction and increase peripheral
vascular resistance -> pulmonary capillary wedge pressure
increased
• Common side effect: tachyarrythmias
Specific Management
• STEMI- PCI or fibrinolytic

• NSTEMI- PCI/CABG; fibrinolytic not recommended
• Cardiac tamponade – pericardiocentesis
• Pneumothorax – needle thoracocentesis, chest tube
OBSTRUCTIVE SHOCK
Obstructive shock
• Inadequate cardiac output as a result of obstruction of

blood flow in the lungs or heart
Causes :
• tension pneumothorax
• pulmonary embolism
• cardiac tumour
• pericardial tamponade
Pericardial tamponade
Pericardial fluid collects
Intrapericardial pressure rises
Reduce ventricular filling
Impaired pumping ability of heart
Reduce cardiac output
Hypoperfusion
Shock
Pneumothorax
Air drawn into the pleural

space with each inspiration
The mediastinum is pushed

towards the contralateral hemithorax
Occlusion of vena cava
Causes cardiorespiratory arrest

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HYPOVOLEMIC SHOCK

• MOST COMMON -> ACUTE STEMI with LV FAILURE

• ECG - to look for evidence of new ischemic changes

• GUSTO-Iib study shows mortality rate similar between STEMI

• STEMI- PCI or fibrinolytic

• Inadequate cardiac output as a result of obstruction of

Pericardial fluid collects

Intrapericardial pressure rises

Reduce ventricular filling

Impaired pumping ability of heart

Reduce cardiac output

Air drawn into the pleural

The mediastinum is pushed

Occlusion of vena cava

Causes cardiorespiratory arrest

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