Cardiogenic ShockCardiogenic Shock

Samuel Cloud, DO, FACEP

Assistant Professor of Emergency Medicine

University at Buffalo

Samuel Cloud, DO, FACEP

Assistant Professor of Emergency Medicine

University at Buffalo

A CaseA Case

• A 72 yo male is brought to the ED from the countryside with fatigue and dyspnea for 2 days.

• Has been a smoker for 50 years.• No other medical history is known.• Is agitated upon presentation and is unable

to give any history.

A CaseA Case

• Vitals upon arrival: HR 135, BP 90/60, RR>40, SpO2 62% on room air.

• Thin male in respiratory distress using accessory muscles for respiration.

• Moist cool skin.• Tachycardic heart rate (? gallop).• Diffuse rales upon pulmonary exam.

A CaseA Case

Cardiogenic ShockCardiogenic Shock

• Cardiogenic shock is the worst manifestation of decompensated heart failure.

• It is defined as systolic blood pressure less than 90 with a severe reduction in the cardiac index (<2.2 L/min/m2) with adequate or elevated filling pressures (pulmonary capillary wedge pressure >15 mm Hg).

PathophysiologyPathophysiology

• As the stroke volume falls the systemic vascular resistance increases via elevation of endogenous vassopressors such as angiotensin II and norepinephrine.

• This leads to decreased tissue blood flow. • This decreased blood flow is especially

dangerous for the heart as it leads to more myocardial ischemia and then further declines in cardiac function.

PathophysiologyPathophysiology

• The SHOCK trial found that patients had widely variable calculated systemic vascular resistance, and some patients had low systemic vascular resistance despite being on vasopressors.

• It is likely that the tissue ischemia causes release of cytokines similar to septic shock which leads to vasodilation of the blood vessels instead of vasoconstriction.

PathophysiologyPathophysiology

• These patients are immunocompromised. Most are intubated, so they can also develop sepsis which can contribute to their hypotension.

• In the SHOCK trial 13% of patients with cardiogenic shock also developed sepsis.

EtiologyEtiology

Non-myocardial infarction (MI) causes of cardiogenic shock include:

• End-stage cardiomyopathy.• Myocarditis.• Severe aortic or mitral stenosis.• Acute aortic valve insufficiency (from aortic

dissection).• Left atrial myxoma.

EtiologyEtiology

Non-MI causes of cardiogenic shock include: • Myocardial contusion, traumatic chordae

tendineae rupture or traumatic pericardial tamponade.

• Septic shock with myocardial depression.• Hypertrophic cardiomyopathy causing

ventricular outflow obstruction.

EtiologyEtiology

• The most common cause of cardiogenic shock is myocardial infarction (MI) with acute left ventricular failure.

• It is most common with an anterior MI.• Patients who have had a previous MI and

have reduced systolic function already are more likely to develop cardiogenic shock from a new MI.

EtiologyEtiology

• Most patients have severe three vessel coronary artery disease.

• Autopsy studies of patients who have died of cardiogenic shock due to an acute MI demonstrate that at least 40% of their left ventricles are infarcted (old and new infarctions).

EtiologyEtiology

• The next most common cause of cardiogenic shock is right ventricular infarction.

• MI can also cause mechanical issues that can precipitate or worsen cardiogenic shock.

• Inferoposterior infarction can lead to rupture or severe dysfunction of the papillary muscles causing acute mitral regurgitation.

EtiologyEtiology

• Anterior and inferior infarctions can lead to interventricular septum rupture and acute left to right shunting of blood.

• Left ventricular wall rupture following MI causes acute cardiogenic shock from tamponade as can a hemorrhagic pericardial effusion following MI.

• Patients who have pre-existing valvular disease such as severe aortic stenosis are at increased risk of cardiogenic shock if they also then have an MI.

EtiologyEtiology

• Severe sinus bradycardia from an inferior MI, or complete heart block due to an anterior MI can worsen cardiogenic shock.

• Rapid atrial fibrillation/flutter or ventricular arrhythmias can worsen or precipitate cardiogenic shock.

• Use of beta-blockers, calcium channel blockers, nitrates, or morphine in a patient with cardiogenic shock can worsen it.

EtiologyEtiology

• A rare but increasingly recognized cause of cardiogenic shock is stress-induced cardiomyopathy. It is also called takotsubo cardiomyopathy or broken heart syndrome.

• It is caused by severe stress, often in post-menopausal woman.

EtiologyEtiology

• Stress-induced cardiomyopathy presents as a patient with chest pain, ST elevation MI with elevated troponins.

• When they are taken to the cardiac catheterization suite they are typically free of significant coronary artery disease and they have “apical ballooning” found on left ventriculography.

• Almost all patients recover with in a few weeks.

Japanese Octopus Cage (Takotsubo)Japanese Octopus Cage (Takotsubo)

EtiologyEtiology

• Etiology of cardiogenic shock from the SHOCK registry:

• Left ventricular failure in 79%• Severe mitral regurgitation in 7%• Ventricular septal rupture in 4%• Right ventricular failure in 2%• Tamponade in 1.7%• And “other causes” 7%-prior severe valvular

disease, excess beta blocker or calcium channel blocker use.

IncidenceIncidence

• Cardiogenic shock occurred in 5-9% of cases of MI in the 1970’s and 1980’s.

• According to recent studies cardiogenic shock now occurs in 5% of ST-elevation MI.

• This is likely due to early cardiac catheterizations and revascularization.

• Cardiogenic shock occurs in 2.5% of non-STEMI (NSTEMI).

Clinical ManifestationsClinical Manifestations

• The classic presentation is a patient with altered mental status, tachypnea, tachycardia, rales, cool extremities and oliguria.

• The SHOCK registry proved this isn’t always the case.

• One-third of patients did not have pulmonary edema upon presentation and 5.2% did not have hypotension upon presentation despite having other signs of hypoperfusion (cool extremities, etc.)

Onset of ShockOnset of Shock

• Most patients develop cardiogenic shock after they are admitted to the hospital from the emergency department.

• In the GUSTO-I trial only 0.8% of patients with MI had cardiogenic shock upon hospital arrival.

• In the SHOCK trial the median time to onset of shock was 5.5 hours.

Onset of ShockOnset of Shock

• Seventy five percent of patients developed cardiogenic shock within 24 hours of the onset of their MI.

• Some patients can have delayed cardiogenic shock for up to a week.

DiagnosisDiagnosis

• A focused clinical exam will enable one to diagnose cardiogenic shock at the bedside usually.

• Pay careful attention to the cardiac exam.• Are they tachycardic or bradycardic?• Do they have a laterally displaced point of

maximal impulse indicating cardiomegaly?• Do they have valvular murmurs?• Are their heart sounds muffled?

DiagnosisDiagnosis

• Make sure to check the blood pressure in more than one extremity to confirm it is truly low.

• An EKG is also critical in the management of cardiogenic shock since most cases are caused by an acute MI.

• Cardiac catheterization should be performed as early as possible in patients having an acute MI.

DiagnosisDiagnosis

• Echocardiography should also be done as soon as possible to evaluate for ejection fraction, look for tamponade, interventricular septum rupture and assess for valve abnormalities.

DiagnosisDiagnosis

• Swan-Ganz catheters have fallen out of favor in the US and are rarely used any longer.

• They are only recommended when patients have persistent hypotension despite adequate resuscitation.

DiagnosisDiagnosis

• Intra-arterial pressure monitors are recommended by the ACC/AHA for patients who have blood pressures less than 80, patients in persistent shock, and patients who are receiving vassopressor or inotropic agents.

TreatmentTreatment

• As with any critically ill patient follow the A,B,C’s: airway, breathing, and circulation.

• If the patient has depressed mental status intubate them.

• If they are having moderate trouble breathing you may consider continuous positive airway pressure (CPAP) initially.

• If they are in mild respiratory distress apply a non-rebreather facemask for high flow oxygen.

TreatmentTreatment

• Start 2 large bore peripheral IV’s, or insert an intra-ossious line or central line if they have difficult IV access or if they immediately require vasopressors.

• Place them on a heart monitor and keep a defibrillator nearby.

• Do not use morphine, nitrates or loop diuretics in hypotensive patients.

TreatmentTreatment

• Vasopressors: Norepinephrine or high-dose dopamine are first line agents in cardiogenic shock.

• Vasopressors should be used in the lowest possible dose for hypotensive patients.

• Inotropic agents: Dobutamine has beta 1 and some beta 2 agonist activity. It can exacerbate hypotension and is used in combination with a vasopressor and not in patients with severe hypotension.

TreatmentTreatment

• Virtually all patients with an acute MI should have a cardiac catheterization and revascularization with either angioplasty and stent placement or coronary artery bypass grafting (CABG) as soon as possible.

• The SHOCK trial proved this strategy was superior to medical support and thrombolysis.

TreatmentTreatment

• The greatest benefit of this strategy were patients under the age of 75.

• Overall 20 patient lives were saved per 100 patients treated at 6 months with the early invasive treatment strategy versus thrombolysis and medical support.

TreatmentTreatment

• Thrombolytic therapy can prevent cardiogenic shock if given early enough in a patient with a large MI, but once cardiogenic shock has occurred its effectiveness declines.

• A large prospective study did show that thrombolytic therapy combined with IABP use decreased hospital mortality compared with IABP alone or thrombolysis alone for patients with acute MI complicated by cardiogenic shock.

TreatmentTreatment

• In many patients with cardiogenic shock in the US, especially those with acute MI, intraaortic balloon pump counterpulsation (IABP) is used to temporarily reduce a patient’s afterload.

• Short-term left ventricular assist devices can also be used in patients with acute MI and refractory shock. The data is mixed about how effective they are and patients are at risk for major bleeding and infection.

Tandem Heart DeviceTandem Heart Device

Thank you!Thank you!

• Questions?