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Cardiogenic and Obstructive

Shock
Prakul Chanthong MD
Division of Cardiology, Department of Pediatrics
Faculty of Medicine, Siriraj Hospital
Mahidol University
Scenario

A 1 week-old infant
BW 3 kg
Feeding intolerance for 1 days
Past History : maternal G1P1, NL, BW 3.2 kg
Physical Examination
Temp 37.6 C, HR 180/min, RR 70/min, BP 40/20
mmHg
Dyspnea with subcostal and intercostal retraction
Poor skin perfusion
Capillary refill 5 sec
Normal S1, Single S2
No murmur
Abdomen : soft, liver 3 cm below RCM
Physical Examination
Temp 37.6 C, HR 180/min, RR 70/min, BP 40/20
mmHg
Dyspnea with subcostal and intercostal retraction
Poor skin perfusion
Capillary refill 5 sec
Normal S1, Single S2
No murmur
Abdomen : soft, liver 3 cm below RCM
What is the most likely diagnosis?
a. Hypovolemic shock
b. Septic shock
c. Cardiogenic shock
d. Obstructive shock
What is the appropriate management in this
case
a. NSS 20 ml/kg in 15 minutes
b. Broad spectrum antibiotic
c. Dopamine 10 microgram/kg/min
d. PGE 0.05 microgram/kg/min
Cardiogenic shock
Inadequate tissue perfusion resulting from
myocardial dysfunction
Caused by
Pump failure (poor contractility)
CHD
Arrhythmia
Common causes of cardiogenic shock
CHD
Myocarditis
Cardiomyopathy
Arrhythmia
Sepsis
Poisoning or drug toxicity
Myocardial injury
Pathophysiology
Cardiogenic shock characterized by
Decreased cardiac output
Marked tachycardia
High SVR

Preload Contractility Afterload

Variable Decreased Increased


Compensatory increase in SVR
Increase HR and LV afterload
Decrease SV
Increase venous tone (RA) and pulmonary
capillary pressure (LA)
Renal fluid retention
Pulmonary edema
Signs of cardiogenic shock
Assessment Finding
Breathing Tachypnea
Increase respiratory effort

Circulation Tachycardia
Normal or low BP, narrow pulse pressure
Weak or absent peripheral pulse
Delayed capillary refill
Signs of CHF
Cyanosis
Cold, pale, diaphoretic skin
Change in mental status
Oliguria
Increased respiratory effort often
distinguishes cardiogenic shock from
hypovolemic shock.
Hypovolemic shock is characterized by
quite tachypnea
Obstructive shock
A condition of impaired CO caused by physical
obstruction of blood flow
Type of obstructive shock
Cardiac tamponade
Tension pneumothorax
Ductal-dependent CHD
Massive pulmonary embolism
Physical obstruction low CO, inadequate
tissue perfusion, increase SVR
Early presentation indistinguishable from
severe hypovolemic shock
PE signs of systemic or pulmonary venous
congestion
Increased respiratory effort, cyanosis, vascular
congestion
Cardiac tamponade
Accumulation of fluid, blood, air in pericardial
space
Increased intrapericardial pressure
Impede systemic and pulmonary venous return
Reduce ventricular filling
Decreased CO
Common causes
Penetrating trauma
Cardiac surgery
Inflammatory disease
Signs
Diminished heart sound
Pulsus paradoxus
Distended neck vein
Diagnosis
Echocardiogram
ECG
Tension pneumothorax
Continuous leaking of air and accumulate in pleural
space
Increase pleural pressure
Compression of lung and mediastinum structures
Impair venous return
Decrease cardiac output
Cardiac arrest
Distinguishing signs
Hyperresonance on the affected side
Diminished breath sounds on affected side
Distended neck veins
Tracheal deviation toward contralateral side
Rapid deterioration
Ductal-Dependent Lesions
Generally present in the first week of life
Left ventricular outflow tract obstruction (ductal
dependent for systemic blood flow)
Coarctation of aorta
Interrupted aortic arch
Critical aortic stenosis
HLHS
Signs of LVOT obstructive lesions
Rapidly progressive deterioration in systemic
perfusion
CHF
Preductal VS postductal differential cyanosis
Absence of femoral pulses
Rapidly deterioration in mental status
Respiratory failure with signs of pulm. edema
Massive pulmonary embolism
Total or partial obstruction of PA or its branches
May lead to pulmonary infarction
Relatively rare in children
Results
Ventilation/perfusion mismatch
Systemic hypoxia
Increased PVR RV failure, low CO
Impaired LV filling low CO
Rapid fall in end-tidal CO2
Management
Goal
Reverse perfusion abnormalities
Improve balance between perfusion and tissue
metabolic demand
Restore organ function
Prevent cardiac arrest
The longer the interval between the
precipitating event and the start of
resuscitation, the poorer the outcome
Warning signs
Marked tachycardia
Absent peripheral pulse
Weakening central pulse
Cold distal extremities with very prolonged
capillary refill
Narrowing pulse pressure
Altered mental status
Hypotension (late finding)
Treatment
Optimizing oxygen content of the blood
Improving volume and distribution of cardiac
output
Reducing oxygen demand
Correct metabolic derangement
Optimizing oxygen content of the blood
Administration of a high concentration of oxygen
Transfusion - if Hb is low
Using CPAP or PEEP or other airway interventions to
correct V/Q abnormalities
Improving volume and distribution of cardiac
output
Based on the type of shock
Reducing oxygen demand and O2 consumption
Factors increased O2 demand
Increase work of breathing assisted ventilation
Fever - antipyretics
Pain and anxiety analgesics and sedatives
Correct metabolic derangement
Hypoglycemia
Hypocalcemia
Hyperkalemia
Metabolic acidosis
Therapeutic End Points
Normal pulses (no differential between central and
peripheral pulse)
Capillary refill <2 sec
Warm extremities
Normal mental status
Normal blood pressure
Urine output > 1ml/kg/hr
Decreased serum lactate
Reduced base deficit
Venous oxygen saturation > 70%
General management of shock
Positioning
Oxygen administration
Vascular assess
Fluid resuscitation
Monitoring
Frequent assessment
Ancillary studies
Pharmacologic support
Subspecialty consultation
Monitoring
Pulse oximetry oxyhemoglobin saturation
Heart rate
Blood pressure and pulse pressure
Mental status
Temperature
Urine output
Frequent assessment
Evaluate trends in the childs condition
Determine response to therapy
Plan the next management interventions
Ancillary studies
Identify the etiology and severity of shock
Evaluate the organ dysfunction secondary to
shock
Identify metabolic derangements
Evaluate the response to therapeutic
interventions
Pharmacologic support
Class Drug Effect
Inotropes Dopamine Increase cardiac
Dobutamine contractility
Epinephrine Increase HR
Produce variable effects on
SVR
Phosphodiesterase Milrinone Reduce afterload
inhibitor Improve coronary blood
flow
Improve contractility
Vasodilator Nitroglycerine Reduce afterload
Nitroprusside Reduce venous tone

Vasopressors Epinephrine Increase SVR


Norepinephrine
Dopamine
vasopressin
Management of cardiogenic shock
Cardiogenic shock condition of inadequate
tissue perfusion resulting from myocardial
dysfunction
Venous congestive, cardiomegaly suggestive
of cardiac etiology
Main objective
To improve the effectiveness of cardiac function
and output by
Increasing the efficacy of ventricular emptying
Decrease metabolic demand
The most effective way to increase stroke
volume reduce afterload rather than giving
inotropic agent
Specific management
Cautious fluid management and monitoring
Laboratory and nonlaboratory studies
Phamacologic support
Cautious fluid management and monitoring
CXR cardiomegaly adequate intravascular
volume
History of inadequate preload cautious fluid
bolus may be given with frequently assess of
respiratory function
Consider establishing central venous assess
Index of preload status
Access for multiple infusions
Monitoring of central venous saturation
Laboratory and nonlaboratory studies
Laboratory
Assess - impact of shock on end organ
function
ABG matabolic acidosis, adequacy of oxygenation and
ventilation
Hb concentration adequate O2 carrying capacity
Serum lactate, central venous saturation adequacy of
cardiac output
Laboratory and nonlaboratory studies
Nonlaboratory
Study Use
CXR Cardiac size, pulmonary vascular markings,
pulmonary edema, pulmonary pathology

ECG Arrhythmia, myocardial injury, drug toxicity

Echocardiogram May be diagnostic, CHD, ventricular wall


motion, valvular dysfunction, preload
Pharmacologic support
Diuretic pulmonary edema, systemic venous
congestion
Vasodilator milrinone
Reducing metabolic demand critical
component
Ventilatory support
Antipyretics , analgesia, sedation
Drug therapy to increase cardiac output
Vasodilator
Inotropes
Phosphodiesterase inhibitor
Specific treatment considerations
Administer fluid resuscitation cautiously
Give 5-10 ml/kg isotonic crystalloid infusion
Deliver slowly (over 10-20 min)
Administer supplementary oxygen, consider need
for BiPAP or mechanical ventilation
Assess for pulmonary edema
Be prepared to assist ventilation
Obtain expert consultation early
Management of obstructive shock
Obstructive shock
Cardiac tamponade
Tension pneumothorax
Ductal dependent CHD
Massive pulmonary embolism
Management of obstructive shock
Early presentation may resemble
hypovolemic shock
Initial approach may include administering a
fluid challange (10-20 ml/kg)
Main objective of treatment
Correction of the cause of obstruction to CO
Restoration of tissue perfusion
Cardiac tamponade
Accumulation of fluid, blood or air in
pericardial space
Resulting in
Impaired systemic venous return
Impaired ventricular filling
Reduced cardiac output
Favourable outcome depend on
Urgent diagnosis
Immediate treatment
May improve with fluid administration
Pericardiocentesis
Echocardiography
Fluoroscopy
Tension pneumothorax
Immediate needle decompression
Inserting an 18-20 gauge over the-needle catheter
3rd rib in midclavicular line
Chest tube placement
Ductal-Dependent lesions
CHD generally present in the first week of life
Continuous infusion of PGE1
Other management
Ventilatory support
Consult with appropriate specialist
Echocardiography
Inotrope improve myocardial contractility
Judicious fluid administration
Correction of metabolic derangements
Pulmonary embolism
Oxygen
Ventilatory assistance
Fluid therapy if poor perfuse
Confirm diagnosis echocardiogram, CT, angiography
Anticoagulant definitive treatment patient is not
in shock
Thrombolytic severe CVS compromise
Without immediate management, patients
with obstructive shock often progress rapidly
to cardiopulmonary failure and cardiac arrest
Thanks for your
attention ...