Cardiogenic Shock and Pulmonary Edema

Cardiogenic Shock and Pulmonary Edema

Cardiogenic Shock and Pulmonary Edema

Marysol I. Dalisay, MDMarysol I. Dalisay, MD

Cardiogenic ShockCardiogenic Shock


• Systemic hypoperfusion – Severe depression of the cardiac index

{<2.2 (L/min)/m2}– Sustained systolic arterial hypotension

(<90 mmHg)– Despite a elevating filling pressure

{pulmonary capillary wedge pressure (PCWP) <18mmHg}

– Associated with in-hospital mortality rates >50%

• Systemic hypoperfusion – Severe depression of the cardiac index

{<2.2 (L/min)/m2}– Sustained systolic arterial hypotension

(<90 mmHg)– Despite a elevating filling pressure

{pulmonary capillary wedge pressure (PCWP) <18mmHg}

– Associated with in-hospital mortality rates >50%


• Circulatory Failure:– Caused by primary myocardial failure

• Secondary to – Acute MI – most common– Cardiomyopathy– Myocarditis– Cardiac tamponade

• Circulatory Failure:– Caused by primary myocardial failure

• Secondary to – Acute MI – most common– Cardiomyopathy– Myocarditis– Cardiac tamponade

IncidenceIncidence

• Leading cause of death of patients hospitalized with MI

• Shock associated with ST elevation MI and less common with non-ST elevation MI

• Complicating CS– LV Failure - 80% of the cases– MR, VSR, RV failure, free wall rupture,

tamponade - others

• Leading cause of death of patients hospitalized with MI

• Shock associated with ST elevation MI and less common with non-ST elevation MI

• Complicating CS– LV Failure - 80% of the cases– MR, VSR, RV failure, free wall rupture,

tamponade - others

PathophysiologyPathophysiologyMI

Myocardial DysfunctionSystolic Diastolic

↓Cardiac output↓ Stroke volume

↓Hypotension↓Systemic perfusion

↓Coronary perfusion pressure

↓Compensatory vasoconstriction

IschemiaProgressive Myocardial

Death

Death

↑LVEDPPulmonary Congestion

Hypoxemia

Patient ProfilePatient Profile

• Increased risk of CS– MI– Older age– Female– Sex– Prior MI– DM– Anterior MI location– Reinfarction soon after MI

• 2/3rd of patients with CS – Flow limiting stenoses in all 3 major coronary artery– 20% have left main coronary artery stenosis

• Rarely occur in the absence of significant stenosis– LV apical ballooning/Takutsubo cardiomyopathy– Often in response to sudden severe emotional stress

• Increased risk of CS– MI– Older age– Female– Sex– Prior MI– DM– Anterior MI location– Reinfarction soon after MI

• 2/3rd of patients with CS – Flow limiting stenoses in all 3 major coronary artery– 20% have left main coronary artery stenosis

• Rarely occur in the absence of significant stenosis– LV apical ballooning/Takutsubo cardiomyopathy– Often in response to sudden severe emotional stress

TimingTiming

• Present on admission– 1/4th of patients – CS complicating MI– 1/4th – rapid thereafter within 6hours of MI

onset

• Present on admission– 1/4th of patients – CS complicating MI– 1/4th – rapid thereafter within 6hours of MI

onset

Clinical FindingsClinical Findings

• Chest pain• Dyspnea• Appear pale• Apprehensive• Diaphoretic• Mentation altered• Pulse – weak and rapid (90 -110)• Severe bradycardia• SBP reduced (<90mmHg)

– With narrow pulse pressure (<30mmHg)• Tachypnea, Cheyne-Stokes respiration, Jugular

Venous Distention

• Chest pain• Dyspnea• Appear pale• Apprehensive• Diaphoretic• Mentation altered• Pulse – weak and rapid (90 -110)• Severe bradycardia• SBP reduced (<90mmHg)

– With narrow pulse pressure (<30mmHg)• Tachypnea, Cheyne-Stokes respiration, Jugular

Venous Distention

Clinical FindingsClinical Findings

• Precordium– Quiet, weak apical pulse

• S1 usually soft, S3 gallop present• Systolic murmur in Severe MR and VSR• Rales• Oliguria is usually common

• Precordium– Quiet, weak apical pulse

• S1 usually soft, S3 gallop present• Systolic murmur in Severe MR and VSR• Rales• Oliguria is usually common

Laboratory FindingsLaboratory Findings

• ↑WBC count with left shift• Renal function – normal

– BUN and Crea rise progressively

• ↑↑Hepatic transaminases – Liver hypoperfusion

• Anion Gap acidosis and ↑Lactic Acid– Poor tissue perfusion

• ABG – hypoxemia and metabolic acidosis– Compensated by respiratory alkalosis

• ↑↑↑Cardiac markers, creatinine phosphatase, MB fraction

• ↑↑↑Troponin I and T

• ↑WBC count with left shift• Renal function – normal

– BUN and Crea rise progressively

• ↑↑Hepatic transaminases – Liver hypoperfusion

• Anion Gap acidosis and ↑Lactic Acid– Poor tissue perfusion

• ABG – hypoxemia and metabolic acidosis– Compensated by respiratory alkalosis

• ↑↑↑Cardiac markers, creatinine phosphatase, MB fraction

• ↑↑↑Troponin I and T

ElectrocardiogramElectrocardiogram

• Q waves• >2mm ST elevation• LBBB• More than ½ are anterior• Global ischemia due to severe left

main stenosis– Severe >3mm ST depression in multiple

leads

• Q waves• >2mm ST elevation• LBBB• More than ½ are anterior• Global ischemia due to severe left

main stenosis– Severe >3mm ST depression in multiple

leads

Chest RoentgenogramChest Roentgenogram

• Pulmonary vascular congestion & pulmonary edema– Absent in 1/3rd of patients

• Heart size– Normal during 1st MI– Enlarged when occur with previous MI

• Pulmonary vascular congestion & pulmonary edema– Absent in 1/3rd of patients

• Heart size– Normal during 1st MI– Enlarged when occur with previous MI

EchocardiogramEchocardiogram

• Should be obtained promply• Left to right shunt – VSR• Proximal aortic dissection with AR or

tamponade – visualized• Pulmonary embolism

• Should be obtained promply• Left to right shunt – VSR• Proximal aortic dissection with AR or

tamponade – visualized• Pulmonary embolism

Pulmonary Artery Catherization

Pulmonary Artery Catherization

• Generally recommended for measurement of filling pressures and cardiac output to confirm the diagnosis and optimize use of IV fluids, inototrophic agents and vasopressors.

• Equalization of right and left sided filling pressure suggest cardiac tamponade as the cause of CS

• Generally recommended for measurement of filling pressures and cardiac output to confirm the diagnosis and optimize use of IV fluids, inototrophic agents and vasopressors.

• Equalization of right and left sided filling pressure suggest cardiac tamponade as the cause of CS

Left Heart Catherization and Coronary Angiography

Left Heart Catherization and Coronary Angiography

• Measurements of LV pressure, definition of coronary anatomy and Left ventriculography– Provide useful information – Indicated with CS complicating MI

• Measurements of LV pressure, definition of coronary anatomy and Left ventriculography– Provide useful information – Indicated with CS complicating MI

Acute Myocardial Infarction

Acute Myocardial Infarction

General MeasuresGeneral Measures

• Initial therapy– Aimed at maintaining the adequate

systemic and coronary perfusion by raising systemic BP with vasopressors and adjusting volume status to a level that ensures optimum LV filling pressure

– Systolic BP (90 mmHg) or mean BP (>60mHg) and PCWP (20 mmHg)

– Hypoxemia and acidosis must be corrected– Ventilatory support

• Initial therapy– Aimed at maintaining the adequate

systemic and coronary perfusion by raising systemic BP with vasopressors and adjusting volume status to a level that ensures optimum LV filling pressure

– Systolic BP (90 mmHg) or mean BP (>60mHg) and PCWP (20 mmHg)

– Hypoxemia and acidosis must be corrected– Ventilatory support

VasopressorsVasopressors

• Norephinephrine– Potent vasoconstrictor– Inotropic stimulant – Increases myocardial myocardial O2

consumption– Reserved for CS with refractory hypotension– Dosage: 2-4 µg/min

• Dosage of 15µg/min higher – unlikely beneficial

• Norephinephrine– Potent vasoconstrictor– Inotropic stimulant – Increases myocardial myocardial O2

consumption– Reserved for CS with refractory hypotension– Dosage: 2-4 µg/min

• Dosage of 15µg/min higher – unlikely beneficial

VasopressorVasopressor

• Dopamine– Low doses (≤2 µg/kg/min)

• Dilates the renal vascular beds

– Moderate doses (2-10 µ/kg/min)• Positive chronotrophic and inotrophic effects

– β-adrenegic receptor stimulation

– Higher doses• α-adrenegic receptor

• Dopamine– Low doses (≤2 µg/kg/min)

• Dilates the renal vascular beds

– Moderate doses (2-10 µ/kg/min)• Positive chronotrophic and inotrophic effects

– β-adrenegic receptor stimulation

– Higher doses• α-adrenegic receptor

VasopressorVasopressor

• Dobutamine– Synthetic sympathomimetic amine– Positive inotropic– Positive chronotropic activity

• Minimal– At low doses (2.5 µg/kg/min)

• Moderate– At higher doses

• Dobutamine– Synthetic sympathomimetic amine– Positive inotropic– Positive chronotropic activity

• Minimal– At low doses (2.5 µg/kg/min)

• Moderate– At higher doses

Aortic CounterpulsationAortic Counterpulsation

• Intraaotric Balloon Pumping (IABP) System– Capable of augmenting both arterial diastolic

pressure and cardiac output– A sausage shaped balloon is introduced

percutaneously into the aorta via femoral artery– In contrast with vasopressors and inotropic

agents, myocardial O2 consumption is reduced– Usuful in stabilizing measure in patients with CS

prior to and during cardiac catheterization and percutaneos coronary intervention (PCI) or prior to urgent surgery

– CI: AR, Aortic Dissection

• Intraaotric Balloon Pumping (IABP) System– Capable of augmenting both arterial diastolic

pressure and cardiac output– A sausage shaped balloon is introduced

percutaneously into the aorta via femoral artery– In contrast with vasopressors and inotropic

agents, myocardial O2 consumption is reduced– Usuful in stabilizing measure in patients with CS

prior to and during cardiac catheterization and percutaneos coronary intervention (PCI) or prior to urgent surgery

– CI: AR, Aortic Dissection

Reperfusion-Revascularization

Reperfusion-Revascularization

• Rapid establishment of blood flow in the infarct-related artery is essential in the management of CS and forms the centerpiece of management.

• Shock Trial• Early revascularization with PCI or CABG is a

class I recommendation for patients age <75 years with ST elevation or LBBB MIwho develop CS within 36hrs of MI and who can be revascularized within 18hrs of development of CS.

• Older patients who are suitable candidates for aggressive care should also be offered early revascularization.

• Rapid establishment of blood flow in the infarct-related artery is essential in the management of CS and forms the centerpiece of management.

• Shock Trial• Early revascularization with PCI or CABG is a

class I recommendation for patients age <75 years with ST elevation or LBBB MIwho develop CS within 36hrs of MI and who can be revascularized within 18hrs of development of CS.

• Older patients who are suitable candidates for aggressive care should also be offered early revascularization.

PrognosisPrognosis

• Wide range of expected death rates– Independent risk factors

• Advanced age• Depressed cardiac index• Ejection fraction• BP• More extensive coronary artery disease• Renal insufficiency

• Wide range of expected death rates– Independent risk factors

• Advanced age• Depressed cardiac index• Ejection fraction• BP• More extensive coronary artery disease• Renal insufficiency

Shock Secondary to Right Ventricular Infraction

Shock Secondary to Right Ventricular Infraction

• Accounts for 3% of CS complicating MI• Salient features:

– Absent pulmonary congestion– High right atrial pressure– RV dilatation and dysfunction– Mildly or moderately depressed LV function– Predominance single-vessel proximal right coronary artery

occlusion• Management

– IV fluid administration • To optimize atrial pressure (10-15mmHg)

– Avoidance of excess fluid– Symphatomimetics– IABP– Early reestablishment of infarct – arterial flow

• Accounts for 3% of CS complicating MI• Salient features:

– Absent pulmonary congestion– High right atrial pressure– RV dilatation and dysfunction– Mildly or moderately depressed LV function– Predominance single-vessel proximal right coronary artery

occlusion• Management

– IV fluid administration • To optimize atrial pressure (10-15mmHg)

– Avoidance of excess fluid– Symphatomimetics– IABP– Early reestablishment of infarct – arterial flow

Mitral RegurgitationMitral Regurgitation

• May complicate MI and result in CS• Occurs most often on the first day with

a second peak several days later• Diagnosis confirmed by echo-Doppler• IABP is recommended• Dobutamine – raise cardiac output• Mitral valve surgery – definitive

therapy

• May complicate MI and result in CS• Occurs most often on the first day with

a second peak several days later• Diagnosis confirmed by echo-Doppler• IABP is recommended• Dobutamine – raise cardiac output• Mitral valve surgery – definitive

therapy

Ventricular Septal DefectVentricular Septal Defect

• Shunting of blood from the left to the right ventricle

• Opening of interventricular septum• Management and timing similar to MR

with IABP and surgical correction

• Shunting of blood from the left to the right ventricle

• Opening of interventricular septum• Management and timing similar to MR

with IABP and surgical correction

Free Wall RuptureFree Wall Rupture• Dramatic complication of STEMI • Occur during the first week after the onset of symptoms• Higher incidence

– First infaction– History of HPN– No history of angina pectoris – Relatively large Q-wave infarct

• Clinical presentation– Sudden loss of pulse and BP– Lost of consciousness– Sinus rhythm on ECG (PEA)

• Myocardium continues to contract but blood flow goes into the pericardium

• Cardiac tanponade ensues• Fatal• Management

– Urgent pericardiocentesis– Surgical repair

• Dramatic complication of STEMI • Occur during the first week after the onset of symptoms• Higher incidence

– First infaction– History of HPN– No history of angina pectoris – Relatively large Q-wave infarct

• Clinical presentation– Sudden loss of pulse and BP– Lost of consciousness– Sinus rhythm on ECG (PEA)

• Myocardium continues to contract but blood flow goes into the pericardium

• Cardiac tanponade ensues• Fatal• Management

– Urgent pericardiocentesis– Surgical repair

Acute Fulminant MyocarditisAcute Fulminant Myocarditis

• Can mimic acute MI with ST deviation or bundle branch block and marked elevation of cardiac enzymes

• Causes in CS – 15% cases• Patients – younger• Do not have typical ischemic chest pain• ECG – global LV dysfunction• Management

– Same as CS complicating acute MI but does not need coronary revascularization

• Can mimic acute MI with ST deviation or bundle branch block and marked elevation of cardiac enzymes

• Causes in CS – 15% cases• Patients – younger• Do not have typical ischemic chest pain• ECG – global LV dysfunction• Management

– Same as CS complicating acute MI but does not need coronary revascularization

Pulmonary EdemaPulmonary Edema

DiagnosisDiagnosis

• Rapid onset of dyspnea at rest• Tachypnea• Severe hypoxemia• Rales and Wheezing – airway

compression• HPN – release of endogenous

cathecholamines

• Rapid onset of dyspnea at rest• Tachypnea• Severe hypoxemia• Rales and Wheezing – airway

compression• HPN – release of endogenous

cathecholamines

DiagnosisDiagnosis

• Echocardiography– May identify systolic or diastolic ventricular

dysfunction and valvular lesions

• Brain natriuretic peptide levels– Support heart failure as the etiology of acute

dyspnea with pulmonary edema.

• Swan-Ganz Catheter– Measurements of PCWP– Helps to deifferentiate high pressure (cardiogenic)

from normal pressure (noncardiogenic)

• Echocardiography– May identify systolic or diastolic ventricular

dysfunction and valvular lesions

• Brain natriuretic peptide levels– Support heart failure as the etiology of acute

dyspnea with pulmonary edema.

• Swan-Ganz Catheter– Measurements of PCWP– Helps to deifferentiate high pressure (cardiogenic)

from normal pressure (noncardiogenic)

ManagementManagement

• Oxygen therapy• Positive-Pressure Ventilation

– Improve oxygenation and cardiac function and reduce the need for intubation

– Mechanical ventilation with positive end-expiratory pressure• Decrease preload and afterload• Redistribute lung water from the intraalveolar

to the extraalveolar space • Increase lung volume to avoid atelectasis

• Oxygen therapy• Positive-Pressure Ventilation

– Improve oxygenation and cardiac function and reduce the need for intubation

– Mechanical ventilation with positive end-expiratory pressure• Decrease preload and afterload• Redistribute lung water from the intraalveolar

to the extraalveolar space • Increase lung volume to avoid atelectasis

Management – Reduction of Preload


• The quantity of extravascular lung water is related to both the PCWP and intravascular volume status.

• Diuretics– Loop diuretics – furosemide, bumetanide, torsemide– Effective even in the presence of hypoalbuminemia,

hyponatremia, and hypocloremia– Furosemide – venodilator that can reduce preload

rapidly• Diuretic of choice (≤0.5mg/kg)

• The quantity of extravascular lung water is related to both the PCWP and intravascular volume status.

• Diuretics– Loop diuretics – furosemide, bumetanide, torsemide– Effective even in the presence of hypoalbuminemia,

hyponatremia, and hypocloremia– Furosemide – venodilator that can reduce preload

rapidly• Diuretic of choice (≤0.5mg/kg)



• Nitrates – Nitroglycerin (NTG) and isosorbide dinitrate– Venodilators with coronary vasodilating properties– Rapid onset– Sublingual NTG (0.4mg x 3 every 5 mins)

• 1st line therapy for acute cardiogenic pulmonary edema

– IV nitroprusside – if pulmonary edema persist when without hypotension

• Potent venous and arterial vasodilator• Useful but not recommended in states of reduced

coronary artery perfusion

• Nitrates – Nitroglycerin (NTG) and isosorbide dinitrate– Venodilators with coronary vasodilating properties– Rapid onset– Sublingual NTG (0.4mg x 3 every 5 mins)

• 1st line therapy for acute cardiogenic pulmonary edema

– IV nitroprusside – if pulmonary edema persist when without hypotension

• Potent venous and arterial vasodilator• Useful but not recommended in states of reduced

coronary artery perfusion



• Morphine– Transient venodilator that reduces preload while

relieving dyspnea and anxiety– 2 to 4 mg– Diminish stress, cathecolamine levels,

tachycardia, and ventricular afterload in patients with pulmonary edema and systemic hypertension

• ACE inhibitors– Reduce both afterload and preload– Recommended in HPN patients– Reduce short and long term mortality

• Morphine– Transient venodilator that reduces preload while

relieving dyspnea and anxiety– 2 to 4 mg– Diminish stress, cathecolamine levels,

tachycardia, and ventricular afterload in patients with pulmonary edema and systemic hypertension

• ACE inhibitors– Reduce both afterload and preload– Recommended in HPN patients– Reduce short and long term mortality



• Other preload reducing agents– IV recombinant brain natriuretic peptide

(nesiritide)• Potent vasodilator with diuretic properties• Reserved for refractory patients• Not recommended in the setting of ischemia or

MI

• Physical Methods– Sitting position with the legs dangling along

the side of the bed• Reduces venous return

• Other preload reducing agents– IV recombinant brain natriuretic peptide

(nesiritide)• Potent vasodilator with diuretic properties• Reserved for refractory patients• Not recommended in the setting of ischemia or

MI

• Physical Methods– Sitting position with the legs dangling along

the side of the bed• Reduces venous return



• Inotrophic and Inodilator Drugs– Dopamine and Dobutamine– Bipyridine phosphodiesterase-3 inhibitors –

Milrinone• Stimulate mypcardial contractility while

promoting peripheral and pulmonary vasodilation

• Digitalis Glycoside– Rarely used– For rapid AF or flutter and LV dysfunction

• Inotrophic and Inodilator Drugs– Dopamine and Dobutamine– Bipyridine phosphodiesterase-3 inhibitors –

Milrinone• Stimulate mypcardial contractility while

promoting peripheral and pulmonary vasodilation

• Digitalis Glycoside– Rarely used– For rapid AF or flutter and LV dysfunction



• IABP or LV assist devices– Useful in bridging therapy to cardiac

transplantation in patients with refractory pulmonary edema secondary to myocarditis or cardiomyopathy

• Cardioversion– For atrial fibrillation

• Stimulation of Alveolar Fluid Clearance– In patients with acute lung injury IV β-adrenergic

agonist treatment decreases extravascular lung water

• IABP or LV assist devices– Useful in bridging therapy to cardiac

transplantation in patients with refractory pulmonary edema secondary to myocarditis or cardiomyopathy

• Cardioversion– For atrial fibrillation

• Stimulation of Alveolar Fluid Clearance– In patients with acute lung injury IV β-adrenergic

agonist treatment decreases extravascular lung water

Special ConsiderationsSpecial Considerations

• ACS– Acute STEMI complicated by pulmonary

edema • Hospital mortality 20%-40%• Primary PCI is preferable• Fribrinolytic agent should be administered• Early coronoray angiography• PCI/CABG• IABP – if hypotension develops

• ACS– Acute STEMI complicated by pulmonary

edema • Hospital mortality 20%-40%• Primary PCI is preferable• Fribrinolytic agent should be administered• Early coronoray angiography• PCI/CABG• IABP – if hypotension develops

Special ConsiderationsSpecial Considerations

• Reexpansion Pulmonary Edema– Develops afeter removal of air and fluid

that has been in the pleural space for some time

• High-altitude pulmonary edema– Prevented by use of dexamethasone,

calcium channel-blocking drugs, long acting inhaled β2-adrenergic agonist

– Treatment: descent from altitude, bedrest, oxygen, inhaled nitric oxide, nifedipine may also be effective.

• Reexpansion Pulmonary Edema– Develops afeter removal of air and fluid

that has been in the pleural space for some time

• High-altitude pulmonary edema– Prevented by use of dexamethasone,

calcium channel-blocking drugs, long acting inhaled β2-adrenergic agonist

– Treatment: descent from altitude, bedrest, oxygen, inhaled nitric oxide, nifedipine may also be effective.

Documents

Cardiogenic Shock and Pulmonary Edema