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Cardiogenic shock
Presented by
Rashmimala Pradhan
Associate Prof.
SNC SOA DTU
Cardiogenic shock
• Syndrome of inadequate tissue perfusion
associated with normal circulating BV, and low
cardiac output.
• Symptoms: dyspnoea, poor exercise
tolerance, confusion, sweating, PND.
• Signs: tachycardia, cold skin, high JVP, added
heart sounds, engorged liver, peripheral
oedema.
ASSESSMENT
Assess for:
– Blunt trauma to the chest
– Cardiac tamponade
– Cardiac dysrhythmias
Core Skills Treat for Shock 28
– Myocardial infarction
– Cardiac contusion
CONT…
Assess for
– Tachycardia
– Muffled heart sounds
– Engorged neck veins with hypotension
– Dyspnea
– Edema in feet and ankles
Etiologies
Mechanical complications of MI:
– Papillary Muscle Rupture!!!!
– Ventricular aneurysm
– Ventricular septal Rupture
• Other causes:
– Cardiomyopathies
– tamponade
– tension pneumothorax
– arrhythmias
– valve disease
Pathophysiology
Impaired pumping ability of LV leads to…
• Decreased stroke volume leads to…..
• Decreased CO leads to …..
• Decreased BP leads to…..
• Compensatory mechanism which may lead to
…
• Decreased tissue perfusion !!!!
Impaired pumping ability of LV leads to…
Inadequate systolic emptying leads to ...
Left ventricular filling pressures (preload) leads
to...
Left atrial pressures leads to ….
Pulmonary capillary pressure leads to …
Pulmonary interstitial & intra alveolar edema
!!!!
CLINICAL FEATURES
Abnormal heart sounds
• Murmurs
• Pathologic S3
• Pathologic S4
Pericardial tamponade
– muffled heart tones, elevated neck veins
• Tension pneumothorax
– JVD, tracheal deviation, decreased or absent
unilateral breath sounds, and chest
hyperresonance on affected side
MANAGEMENT
Goal of management :
• Treat Reversible Causes
• Protect ischemic myocardium
• Improve tissue perfusion
• Optimizing pump by:
– Increasing myocardial O2 delivery
– Maximizing CO
– Decreasing LV workload (Afterload)
COLLABORATIVE MANAGEMENT
Limiting/reducing myocardial damage during
Myocardial Infarction:
• Increased pumping action & decrease workload
of the heart
– Inotropic agents
– Vasoactive drugs
– Intra-aortic balloon pump
– Cautious administration of fluids
– Transplantation
• Consider thrombolytics, angioplasty in specific cases
OPTIMIZING PUMP FUNCTION:
– Pulmonary artery monitoring is a necessity !!
– Aggressive airway management: Mechanical
Ventilation
– Judicious fluid management
– Vasoactive agents
• Dobutamine
• Dopamine
OPTIMIZING PUMP FUNCTION (CONT)
– Morphine as needed (Decreases preload,
anxiety)
– Cautious use of diuretics in CHF
– Vasodilators as needed for afterload reduction
– Short acting beta blocker, esmolol, for
refractory tachycardia
Therapy of low Stroke Volume
• Drugs to move point back down curve: e.g..
GTN(nitro glycerin), diuretics, head-up posture
• Drugs to improve contractility: I.v.
inotropes, amrinone, ACE inhibitors
• Drugs to prevent fluid retention: ACE
inhibitors, diuretics.
Dopamine
• Dopamine receptor activation at low doses-
”splanchnic dilation” (2-5 mcg/kg/min)
• Beta receptor activation-increase cardiac
output (5-10 mcg/kg/min)
• Alpha receptor activation-vasoconstriction
(>10 mcg/kg/min)
Dobutamine
• primarily a beta 1-receptor agonist (cardiac
stimulation), but it also has mild beta 2 effects
(vasodilation)
• causes a dose-dependent increase in stroke
volume
• decrease in cardiac filling pressures
• an alkaline pH inactivates catecholamines such as
dobutamine
• Dose 2-20 mcg/kg/min
Dobutamine
Dobutamine is the preferred inotropic agent for
the acute management of low output states due
to systolic heart failure. Because dobutamine
does not usually raise the arterial blood
pressure, it is not indicated as monotherapy
in patients with cardiogenic shock.
Norepinephrine
• Alpha-receptor agonist that promotes
widespread vasoconstriction
• administration of any vasoconstrictor agent
carries a risk of hypoperfusion and ischemia
involving any tissue bed or vital organ
• Dose 8-12 mcg/min
?
THANK YOU

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Cardiogenic shock

  • 1. Cardiogenic shock Presented by Rashmimala Pradhan Associate Prof. SNC SOA DTU
  • 2. Cardiogenic shock • Syndrome of inadequate tissue perfusion associated with normal circulating BV, and low cardiac output. • Symptoms: dyspnoea, poor exercise tolerance, confusion, sweating, PND. • Signs: tachycardia, cold skin, high JVP, added heart sounds, engorged liver, peripheral oedema.
  • 3. ASSESSMENT Assess for: – Blunt trauma to the chest – Cardiac tamponade – Cardiac dysrhythmias Core Skills Treat for Shock 28 – Myocardial infarction – Cardiac contusion
  • 4. CONT… Assess for – Tachycardia – Muffled heart sounds – Engorged neck veins with hypotension – Dyspnea – Edema in feet and ankles
  • 5. Etiologies Mechanical complications of MI: – Papillary Muscle Rupture!!!! – Ventricular aneurysm – Ventricular septal Rupture • Other causes: – Cardiomyopathies – tamponade – tension pneumothorax – arrhythmias – valve disease
  • 6. Pathophysiology Impaired pumping ability of LV leads to… • Decreased stroke volume leads to….. • Decreased CO leads to ….. • Decreased BP leads to….. • Compensatory mechanism which may lead to … • Decreased tissue perfusion !!!!
  • 7. Impaired pumping ability of LV leads to… Inadequate systolic emptying leads to ... Left ventricular filling pressures (preload) leads to... Left atrial pressures leads to …. Pulmonary capillary pressure leads to … Pulmonary interstitial & intra alveolar edema !!!!
  • 8. CLINICAL FEATURES Abnormal heart sounds • Murmurs • Pathologic S3 • Pathologic S4
  • 9. Pericardial tamponade – muffled heart tones, elevated neck veins • Tension pneumothorax – JVD, tracheal deviation, decreased or absent unilateral breath sounds, and chest hyperresonance on affected side
  • 10. MANAGEMENT Goal of management : • Treat Reversible Causes • Protect ischemic myocardium • Improve tissue perfusion • Optimizing pump by: – Increasing myocardial O2 delivery – Maximizing CO – Decreasing LV workload (Afterload)
  • 11. COLLABORATIVE MANAGEMENT Limiting/reducing myocardial damage during Myocardial Infarction: • Increased pumping action & decrease workload of the heart – Inotropic agents – Vasoactive drugs – Intra-aortic balloon pump – Cautious administration of fluids – Transplantation • Consider thrombolytics, angioplasty in specific cases
  • 12. OPTIMIZING PUMP FUNCTION: – Pulmonary artery monitoring is a necessity !! – Aggressive airway management: Mechanical Ventilation – Judicious fluid management – Vasoactive agents • Dobutamine • Dopamine
  • 13. OPTIMIZING PUMP FUNCTION (CONT) – Morphine as needed (Decreases preload, anxiety) – Cautious use of diuretics in CHF – Vasodilators as needed for afterload reduction – Short acting beta blocker, esmolol, for refractory tachycardia
  • 14. Therapy of low Stroke Volume • Drugs to move point back down curve: e.g.. GTN(nitro glycerin), diuretics, head-up posture • Drugs to improve contractility: I.v. inotropes, amrinone, ACE inhibitors • Drugs to prevent fluid retention: ACE inhibitors, diuretics.
  • 15. Dopamine • Dopamine receptor activation at low doses- ”splanchnic dilation” (2-5 mcg/kg/min) • Beta receptor activation-increase cardiac output (5-10 mcg/kg/min) • Alpha receptor activation-vasoconstriction (>10 mcg/kg/min)
  • 16. Dobutamine • primarily a beta 1-receptor agonist (cardiac stimulation), but it also has mild beta 2 effects (vasodilation) • causes a dose-dependent increase in stroke volume • decrease in cardiac filling pressures • an alkaline pH inactivates catecholamines such as dobutamine • Dose 2-20 mcg/kg/min
  • 17. Dobutamine Dobutamine is the preferred inotropic agent for the acute management of low output states due to systolic heart failure. Because dobutamine does not usually raise the arterial blood pressure, it is not indicated as monotherapy in patients with cardiogenic shock.
  • 18. Norepinephrine • Alpha-receptor agonist that promotes widespread vasoconstriction • administration of any vasoconstrictor agent carries a risk of hypoperfusion and ischemia involving any tissue bed or vital organ • Dose 8-12 mcg/min
  • 19. ?