Cardiogenic Shock And Pulmonary Edema

Cardiogenic Shock and Pulmonary Edema Marysol I. Dalisay, MD

Cardiogenic Shock

Cardiogenic 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%

Cardiogenic Shock • Circulatory Failure: – Caused by primary myocardial failure • Secondary to – – – –

Acute MI – most common Cardiomyopathy Myocarditis Cardiac tamponade

Incidence • 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

Pathophysiology MI Myocardial Dysfunction Systolic Diastolic

↓Systemic perfusion

↓Cardiac output ↓ Stroke volume

↑LVEDP Pulmonary Congestion

↓Hypotension

Hypoxemia

↓Coronary perfusion pressure ↓Compensatory vasoconstriction

Ischemia

Progressive Myocardial Death

Death

Patient 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

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

Clinical 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

Clinical Findings • Precordium – Quiet, weak apical pulse

• • • •

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

Laboratory 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

Electrocardiogram • • • • •

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

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

Echocardiogram • Should be obtained promply • Left to right shunt – VSR • Proximal aortic dissection with AR or tamponade – visualized • Pulmonary embolism

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

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

Acute Myocardial Infarction

General 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

Vasopressors • 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

Vasopressor • 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

Vasopressor • Dobutamine – Synthetic sympathomimetic amine – Positive inotropic – Positive chronotropic activity • Minimal – At low doses (2.5 µg/kg/min)

• Moderate – At higher doses

Aortic 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

Reperfusion-Revascularization • Rapid establishment of blood flow in the infarctrelated 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.

Prognosis • 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 • 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 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

Ventricular 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

Free 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

Acute 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

Pulmonary Edema

Diagnosis • • • • •

Rapid onset of dyspnea at rest Tachypnea Severe hypoxemia Rales and Wheezing – airway compression HPN – release of endogenous cathecholamines

Diagnosis • 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)

Management • Oxygen therapy • Positive-Pressure Ventilation – Improve oxygenation and cardiac function and reduce the need for intubation – Mechanical ventilation with positive endexpiratory 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)

Management – Reduction of Preload • 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

Management – Reduction of Preload • 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

Management – Reduction of Preload • 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

Management – Reduction of Preload • 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

Management – Reduction of Preload • 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 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

Special 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 β2adrenergic agonist – Treatment: descent from altitude, bedrest, oxygen, inhaled nitric oxide, nifedipine may also be effective.