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

↓Cardiac output ↑LVEDP

↓ Stroke volume Pulmonary Congestion
↓Systemic
perfusion ↓Hypotension Hypoxemia

↓Coronary perfusion pressure Ischemia

Progressive
Myocardial
↓Compensatory Death
vasoconstriction
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 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.
 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 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)
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 β2-
adrenergic agonist
– Treatment: descent from altitude, bedrest,
oxygen, inhaled nitric oxide, nifedipine may
also be effective.