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Acute heart failure, cardiogenic schock

Causes of AHF
Myopathy (myocarditis, postpartum CMP)
Non-cardiac origin (sepsis, anaemia,tamponade, pulmonary embolism,
shunt, thyreotoxicosis)
Acutely decompensated CHF due to other causes (COPD, drug
abuse, volume-overload, renal failure, infection)
Valvular (endocarditis, aortic dissection)
Acut decompensated CHF:left and right heart congestion, pulmonary
edema, hypotension
Pulmonary edema: orthopnea, tachypnea, low O2 saturation
Hypertensive attack: increased afterload, congestion
Isolated right heart failure: elevated jugular venous pressure, clear
pulmonary sounds, hepatomegalia, anasarca
ACS: during ischemia contractility worsens +/arrhythmic events may
occur (e.g. bradycardia, VT/VF)
Cardiogenic shock: forward failure (low blood pressure, tissue
hypoperfusion), backward failure (congestion), impaired contractility

Stages of Heart Failure (NYHA)

NYHA class I.:Symptoms present only at levels of exertion that would
limit normal individuals.
NYHA class II.:Symptoms present on ordinary exertion.
NYHA class III.:Symptoms present on less-then-ordinary exertion.
NYHA class IV.:Symptoms present at rest.
Stages of Heart Failure (AHA/ACC)
Stage A: At high risk for heart failure butwithout structural heart disease or
symptoms(hypertension, diabetes, obesity, metabolic syndroma,
cardiotoxic drugs)
Stage B: Structural heart disease but without symptoms of heart failure
(previous MI, LV remodeling including LVH and low EF, asymptomatic valv.
Stage C: Structural heart disease with prior or current symptoms of heart
Stage D: Refractory heart failure requiring specialized interventions.

Symptoms, signs



Predominantly Related to Volume Overload

Dyspnea (exertional,
Rales, pleural effusion
paroxysmal nocturnal dyspnea,
orthopnea, or at rest); cough;
Foot and leg discomfort

Peripheral edema (legs, sacral)

Abdominal discomfort/bloating; Ascites/increased abdominal girth; right

early satiety or anorexia
upper quadrant pain or discomfort;
hepatomegaly/splenomegaly; scleral
Increased weight
Elevated jugular venous pressure,
abdominojugular reflux
Increasing S3, accentuated P2
Predominantly Related to Hypoperfusion

Cool extremities

Altered mental status, daytime Pallor, dusky skin discoloration,



drowsiness, confusion, or
difficulty concentrating


Dizziness, presyncope, or

Pulse pressure (narrow)/proportional pulse

pressure (low)
Pulsus alternans

Other Signs and Symptoms of Acute Heart Failure


Orthostatic hypotension (hypovolemia)

Sleep disturbances



Systolic and diastolic cardiac murmurs

genic Shock

Cardiogenic shock
Cardiogenic shock is the most severe clinical expression of left ventricular
Causes in ACS patients: severe myocardial infarction, more vessels, LAD!,
late infarction, mechanical complications such as rupture of the ventricular
septum, a papillary muscle, or free wall with tamponade; right ventricular
infarction; or marked reduction of preload caused by conditions such as
Cardiogenic shock is characterized by marked and persistent (>30
minutes) hypotension with systolic arterial pressure less than 80 mm Hg
and a marked reduction of cardiac index (generally <1.8 liters/min/m 2) in
the face of elevated left ventricular filling pressure (pulmonary capillary
wedge pressure >18 mm Hg).

Right Ventricular Infarction

Right ventricular infarction can have a range of clinical presentations from
mild right ventricular dysfunction through cardiogenic shock. Right-heart
filling pressures (central venous, right atrial, and right ventricular enddiastolic pressures) are elevated, whereas left ventricular filling pressure is
normal or only slightly raised; right ventricular systolic and pulse pressures
are decreased, and cardiac output is often markedly depressed.
The ECG can provide the first clue that right ventricular involvement is
present in the patient with inferior STEMI. Most patients with right
ventricular infarction have ST segment elevation in lead V4R (right
precordial lead in V4 position).

The echocardiogram shows abnormal wall motion of the right ventricle, as

well as right ventricular dilation and depression of right ventricular
ejection fraction
Because of their ability to reduce preload, medications routinely prescribed
for left ventricular infarction may produce profound hypotension in
patients with right ventricular infarction. In patients with hypotension
caused by right ventricular MI, hemodynamics can be improved by a
combination of expanding plasma volume to augment right ventricular
preload and cardiac output and, when left ventricular failure is present,
arterial vasodilators. The initial therapy for hypotension in patients with
right ventricular infarction should almost always be volume expansion.
Right ventricular infarction is common among patients with inferior left
ventricular infarction. Therefore otherwise unexplained systemic arterial
hypotension or diminished cardiac output, or marked hypotension in
response to small doses of nitroglycerin in patients with inferior infarction,
should lead to the prompt consideration of this diagnosis.

Mechanical Causes of Heart Failure

The most dramatic complications of STEMI are those that involve tearing
or rupture of acutely infarcted tissue. The clinical characteristics of these
lesions vary considerably and depend on the site of rupture, which may
involve the papillary muscles, interventricular septum, or free wall
of either ventricle.
The following are some features that characterize this serious complication
1. Occurs more frequently in elderly patients and possibly more
frequently in women than in men with infarction.
2. Appears to be more common in hypertensive than in normotensive
3. Occurs more frequently in the left than in the right ventricle and
seldom occurs in the atria.
4. Usually involves the anterior or lateral walls of the ventricle in the
area of the terminal distribution of the left anterior descending
coronary artery.
5. Is usually associated with a relatively large transmural infarction
involving at least 20 percent of the left ventricle.
6. Occurs between 1 day and 3 weeks, but most commonly 1 to 4 days,
after infarction.
7. Is usually preceded by infarct expansionthat is, thinning and a
disproportionate dilation within the softened necrotic zone
8. Most commonly results from a distinct tear in the myocardial wall or a
dissecting hematoma that perforates a necrotic area of myocardium.

9. Usually occurs near the junction of the infarct and the normal muscle.
10. Occurs less frequently in the center of the infarct, but when rupture
occurs here, it is usually during the second rather than the first week
after the infarct.
11. Rarely occurs in a greatly thickened ventricle or in an$area of
extensive collateral vessels.
12. Most often occurs in patients without previous infarction.
13. There is no evidence that the intensity of anticoagulation influences
the occurrence of rupture.
14. Occurs more commonly in patients who received reperfusion therapy
with a fibrinolytic versus PCI.
Rupture of the free wall of the left ventricle usually leads to
hemopericardium and death from cardiac tamponade.

Diagnostic options
ECG: ischemia (ST-elevation, Q-wave), arrhythmia, conduction
disturbances (eg. LBBB)
Chest X-ray: pulmonary congestion, pleural, pericardial fluids,
Lab tests: electrolyte levels, renal&liver function, blood cell count,
Blood gas analysis: pH, pO2, PCO2, BE, Lactate
Echocardiography: evaluation of systolic and diastolic function,
dysynchronia, valvular disease, mechanical complications
Hemodynamic Classifications of Patients with Acute Myocardial
Infarction (Killip)
A. Based on Clinical

B. Based on Invasive Monitoring

Cla Definition

Subs Definition

Rales and S3 absent

Normal hemodynamics
PCWP < 18, CI > 2.2


Crackles, S3 gallop, elevated

jugular venous pressure


Frank pulmonary edema


Pulmonary congestion
PCWP > 18, CI > 2.2
Peripheral hypoperfusion
PCWP < 18, CI < 2.2




Pulmonary congestion and

A. Based on Clinical

B. Based on Invasive Monitoring

Cla Definition

Subs Definition
peripheral hypoperfusion
PCWP > 18, CI < 2.2

Monitoring techniques
Non-invasive: obligatory at AHF patient (resp. rate, ECG, O2
Invasive: obligatory at unstable AHF patients (Noninvasive AND arterial
central venous line invasive pressures)
PAC (Swan Ganz) right heart catheterisation: unstable AHF and no
to conventional treatment
Pulmonary capillary wedge pressure characterizes the enddiastolic filling
pressures (exept mitral stenosis, aorta regurgitation, pulmonary vein

Restoration of oxygenation and tissue perfusion
Iv. access
Monitoring invasive if needed
Positioning of the patient: sitting or half-sitting (45)
Symptom guided acute therapy
Etiology evaluation and casual therapy
Evaluation and control of fluid (volume) state of the patient (Stop of
infusion in case of left heart failure)
Stable decompensated CHF: vasodilators, loopdiuretics,
hypoperfusion:positive inotropes
Pulmonary edema: morphin, loopdiuretics, hypertension: vasodilators,
hypoperfusion: inotropes
Cardiogenic shock: fluid challenge, inotropes, vasopressors, intubation,
mechanicalventilation, IABP
Isolated right heart failure: fluids, inotropes, rapid evaluation of
etiology (pulmonary Embolism? AMI?)
Acute coronary syndrome: revascularisation (PCI,CABG)
O2 -target O2 Sat: 95% (COPD:90%) -aim: decrease of pulmonary
Morphin-aim: anxietas, dyspnea, chest pain relief
-dosage: initiating 2-4mg iv. , maitenance 2 mg in 5-15 mins
-AE: antiemetic drug needed (eg. 1mg metoclopramid)

-monitoring is a must (resp. And heart rate, NIBP)

Loop diuretics (furosemid)-effect reduced in acidosis, hyponatraemia
-CAVE: hypokalaemia!
-potentiating effect of ACEi/ARBs, hypotension!
Vasodilators if SBP > 90Hgmm - Nitroglicerine, isosorbide-dinitrate,
Decreases hypertension (afterload)
CAVE: significant aortic valvular stenosis! (i.v. hypotensio)
Beta-receptor blockers, ACEi, ARB are CONTRAINDICATED in AHF!
Ca-channel blockers are CONTRAINDICATED in AHF!
Inotropes / Dopamin:
2-5 micg/kg/min: DA-R: renal perfusion, diuresis increase
5-10micg/kg/min: adjuvant B1-R.: + Inotrop, contractility increases
10+ micg/kg/min: adjuvant Alfa-1-R: vasoconstiction, SBP increases
Note: risk for arrhythmias
Inotropes/ Dobutamin: dose dependent B1-R effect: +inotropic,
Monitoring needed, risk for arrhythmia!
Phosphodiesterase inhibitors (PDEi)-milrinon, enoximone
i.c. cAMP increase: +Inotropic, peripheral vasodilation
Vasopressin antagonists(tolvaptan, conivaptan-not in
Hungary)renal aqua channels outloading inhibition>>water
reabsorption inhib. Acute symptom relief,but 1 year mortality is not
decreased (EVEREST trial)
Levosimendan - Ca-sensitiser (Troponin C), inodilator!
Cardiac contractility (stroke volume ) CO , Systemic and pulmonary
Hemodinamic response in severals days
Monitoring is necessary (hypotension, arrythmia)
Vasopressor/ Norepinephrine: Not first choice of treatment!
1., cardiogenic shock (when ineffective combination of inotrop agents and
fluid challenge to restore 90Hgmm SBP)
2., sepsis and AHF

Temporary mechanical circulatory support or acute

bridge therapy even until heart transplantation

IABP (intraaortic balloon pump)

IABP is one type of mechanical hemodynamic support, and it has emerged
as the single most widely used circulatory assist device.
Cardiogenic shock (left ventricular failure or mechanical complications of
an acute myocardial infarction: VSD, ruptured mitral chordae tendineae)
Intractable angina
Low cardiac output after cardiopulmonary bypass
Adjunctive therapy in high risk or complicated angioplasty
Prophylaxis in patients with severe left main coronary arterial stenosis in
whom surgery is pending
Intractable myocardial ischemia awaiting further therapy
Refractory heart failure as a bridge to further therapy

Intractable ventricular arrhythmias as a bridge to further therapy

TECHNICAL ASPECTS The system is composed of two principal parts:

A flexible catheter with one lumen that allows for either distal
aspiration/flushing or pressure monitoring and a second that permits
the periodic delivery and removal of helium gas to a closed balloon.
A mobile console that contains the system for helium transfer as well
as computer control of the inflation and deflation cycle.

The catheter is inserted in most cases through a common femoral artery

and advanced under fluoroscopic guidance such that the distal end is
positioned in the proximal descending aorta, usually about one centimeter
distal to the origin of the left subclavian artery. Alternative insertion sites,
such as the right subclavian artery, have been reported.
Pumping is initiated and controlled by the console using input from both
the aortic pressure and the electrocardiogram. Inflation occurs
immediately after aortic valve closure and deflation just before aortic
valve opening.
HEMODYNAMIC EFFECTS Inflation and deflation of the balloon has
two major consequences:
Blood is displaced to the proximal aorta by inflation during diastole.
Aortic volume (and thus afterload) is reduced during systole through a
vacuum effect created by rapid balloon deflation.
Expected changes in the hemodynamic profile in the majority of patients
with cardiogenic shock include:

A decrease in systolic pressure

An increase in aortic diastolic pressure, which may raise coronary
blood flow
An increase in mean arterial pressure especially in patients with
shock due to an acute mechanical abnormality such as mitral
regurgitation (MR) or ventricular septal defect (VSD).
A reduction of the heart rate
A decrease in the mean pulmonary capillary wedge pressure
An elevation in the cardiac output, especially in patients with MR,
VSD, or a large territory of medically refractory ischemia that is
improved by the addition of counterpulsation
The reductions in afterload and wall stress lead to a fall in
myocardial oxygen consumption, which is one of the goals of
treatment of patients with myocardial ischemia.


Significant (more than mild) aortic regurgitation since the degree of

aortic regurgitation will be increased by counterpulsation
Uncontrolled bleeding disorder

Severe peripheral artery disease that cannot be pretreated with

Clinically significant abdominal aortic aneurysm or aortic dissection
Uncontrolled sepsis

Vascular Vascular complications remain the major risk. The most
common major complications include:

Limb (and visceral) ischemia

Vascular laceration necessitating surgical repair
Major hemorrhage

Other Other complications include:

Cholesterol embolization
Cerebrovascular accident is a rare complication of IABP, since the
balloon is normally positioned distal to the left subclavian artery.
Cerebral ischemia only occurs when the IABP has been placed too
proximally or has accidentally migrated proximally, or the central
balloon lumen has been flushed vigorously and dislodged a
Balloon rupture
Additional complications: fall in platelet count, hemolysis, seromas,
groin infection, and peripheral neuropathy

ROUTINE CARE OF A PATIENT WITH IABP The following routine care

measures likely decrease complication rates:

A chest x-ray should be obtained after initial insertion and daily to

document the position of the catheter tip, which should be at the
level of bifurcation of left and right main bronchi.
Documentation of the distal pulses should occur before, after, and
three times every day.
The pressure wave form should be evaluated by a practitioner
knowledgeable with the use of the system twice daily.
Daily measurement of the hematocrit, platelet count, and creatinine.

The graph of aortic pressure throughout the cardiac cycle displays a small dip ( the
"incisure" or "dicrotic notch") which coincides with the aortic valve closure.

impella Recover
extracorporal membrane oxigenisation (ECMO)
continuous aortic-flow-augmentation Cancion-system
left-, right-or. biventricular assist device (VAD)
Temporary pacemaker therapy
Mechanical ventilation recovery of gas exchange, decrease work
of breathing
invasive mechanical ventilation

noninvasive respiratory support (CPAP, BiPAP)

PEEP 5-10 Hgmm (against edema)
Positive pressure ventilation (pre and afterload decrese)
Overtake breathing work
Sedation: analgesia, hipnotic effect, amnesia
Renal replacement therapy: IHD / CVVH(DF)
Liver replacementtherapy: MARS not routinely used in Hungary