Download Cardiogenic and Obstructive shock

Cardiogenic and Obstructive
Shock
Prakul Chanthong MD
Division of Cardiology, Department of Pediatrics
Faculty of Medicine, Siriraj Hospital
Mahidol University
Scenario
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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.
b.
c.
d.
Hypovolemic shock
Septic shock
Cardiogenic shock
Obstructive shock
• What is the appropriate management in this
case
a.
b.
c.
d.
NSS 20 ml/kg in 15 minutes
Broad spectrum antibiotic
Dopamine 10 microgram/kg/min
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
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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)
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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
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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
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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 child’s 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
Dobutamine
Epinephrine
Increase cardiac
contractility
Increase HR
Produce variable effects on
SVR
Phosphodiesterase
inhibitor
Milrinone
Reduce afterload
Improve coronary blood
flow
Improve contractility
Vasodilator
Nitroglycerine
Nitroprusside
Reduce afterload
Reduce venous tone
Vasopressors
Epinephrine
Norepinephrine
Dopamine
vasopressin
Increase SVR
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
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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 ...