ñiyhp´kop

1. UNIVERSIDAD TECNICA DE MACHALA
ACADEMIC UNIT OF CHEMICAL
SCIENCES AND HEALTH
MEDICINE SCHOOL
ENGLISH
CARDIOGENIC
SHOCK
STUDENTS
William Cruz
Kevin Herrera
TEACHER:
Mgs. Barreto Huilcapi Lina Maribel
CLASS:
EIGHTH SEMESTER ‘’A’’
Machala, El Oro
2018

2. CARDIOGENIC SHOCK
DEFINITION
Shock or shock is defined as the clinical and hemodynamic situation
corresponding to a state of general decrease and tissue perfusion.
ETIOLOGY
The etiology of shock is multiple, can be grouped into four types such as
decreased circulating volume (hypovolemic shock), cardiac, including loss of
contractile function of the myocardium (cardiogenic shock), obstruction to blood
flow as in pulmonary embolism and finally vasomotor dysfunction due to loss of
vascular tone (neurogenic shock).
 Alterations of myocardial contractility: The loss of muscle mass is the
main cause of cardiogenic shock in MI. Other diseases with primary

3. alteration of myocardial contractility, such as myocarditis, may also be
accompanied by shock due to myocardial contractility deficit.
 Alterations of cardiac mechanics: There are several factors that can
contribute to the development of cardiogenic shock or be the main cause
of it, even in the absence of significant alterations in myocardial
contractility such as rupture of the interventricular septum, acute valvular
insufficiency, cardiac tamponade, pulmonary embolism, right ventricular
infarction and prosthetic obstruction.
CONTRIBUTING FACTORS
 Hypovolemia: May be secondary to vomiting, profuse diaphoresis,
excessive or inappropriate use of diuretics, hyperventilation, fever, etc.
 Arrhythmias: Tachycardia or bradycardia of any origin.
 Drugs: As sedatives and vasodilators.
 Pain: Pain and stress during the first hours of MI evolution can be an
important contributing factor.
Pathophysiology and SIGNS OR SYMPTONS
Cardiogenic shock is the extreme manifestation of heart failure, in which
compensation mechanisms have resolved insufficient to maintain adequate blood
supply to the vital minimum needs of tissue nutrition.
COMPENSATION MECHANISMS

4.  Cardiac compensation mechanisms.- They include dilation and
ventricular hypertrophy, where the latter is irrelevant in acute forms of
heart failure such as shock
 Peripheral compensation mechanisms.- They have an immediate action
against the decrease in blood pressure or minute volume and include:
redistribution of blood flow, increase of oxygen extraction at the tissue
level, and increase in anaerobic metabolism.
 Hormone activation.- It mainly includes the increase of the sympathetic
tone and adrenergic discharge, the activation of the renin-angiotensin-
aldosterone system, less relevant in acute heart failure.
EVOLUTIONARY DEGREES OF SHOCK
 Phase of compensated hypotension: In the initial stages of peripheral
hypoperfusion, compensatory mechanisms such as tachycardia and
increased systemic vascular resistance.
 Decompensated hypotension phase: When the etiological cause is
maintained, the compensatory mechanisms may be insufficient or even
harmful.
 Irreversible phase: There is a maximum decrease in minute volume,
blood pressure and tissue perfusion with prolonged ischemia that produces
irreversible cellular damage in different organs.
ORGANIC CONDITION
 Kidney: Hypotension and compensatory vasoconstriction decrease renal
flow and, therefore, glomerular filtration. Prolonged hypoperfusion causes
tubular necrosis with impaired renal function

5.  Heart: Hypotension and increased left ventricular end-diastolic pressure
cause myocardial hypoperfusion, which aggravates ischemia, which
contributes to perpetuate the shock
 Lung: The increase in pulmonary capillary pressure secondary to heart
failure produces pulmonary congestion and lung edema, which makes gas
exchange difficult and contributes to general hypoxia. It also decreases the
production of surfactant, which favors the formation of atelectasis and
functional short circuits.
 Liver: There will be an elevation of liver enzymes and occasionally an
increase in bilirubins. In the advanced stages, coagulation alterations occur
due to the lack of hepatic production of factors related to it and these
alterations in an advanced form can produce hemorrhages and
intravascular thrombosis.
 Inflammatory state: There is an elevation of inflammatory markers such
as body temperature, leukocytosis, increased C-reactive protein, nitric
oxide, interleukins and TNF.
EVOLUTIONARY DEGREES OF SHOCK
 Phase of compensated hypotension: In the initial stages of peripheral
hypoperfusion, compensatory mechanisms such as tachycardia and
increased systemic vascular resistance.
 Decompensated hypotension phase: When the etiological cause is
maintained, the compensatory mechanisms may be insufficient or even
harmful.
 Irreversible phase: There is a maximum decrease in minute volume,
blood pressure and tissue perfusion with prolonged ischemia that produces
irreversible cellular damage in different organs.
DIAGNOSIS

6. Shock is a clinical syndrome, and in practice for diagnosis requires the presence
of criteria such as systolic blood pressure less than 90mmHg or, in hypertensive
patients, a reduction of 30% with respect to the previous basal level, maintained
for more than half an hour; signs of tissue hypoperfusion, diuresis less than 20 mL
/ h.
Complementary examinations.- Laboratory data, electrocardiogram, chest x-ray,
echocardiogram and hemodynamic monitoring.
MORTALITY
The greatest difficulty in the prognostic assessment and in the therapeutic
approach of cardiogenic shock lies in the lack of a uniform diagnostic criterion,
although cardiogenic shock is defined as a severe form of peripheral
hypoperfusion secondary to decreased myocardial contractility, From the clinical
point of view it is a relatively ambiguous entity, characterized by the presence of
arterial hypotension, oliguria and signs of tissue hypoperfusion.
PROGNOSTIC FACTORS
 Gravity of hemodynamic deterioration
 Shock evolution time
 Presence of tissue lesions in different organs
 Advanced age
 Impossibility to correct contributing factors
 The cause that causes the shock
Cardiogenic shock itself has a mortality higher than 60% through the use of
appropriate treatment. Cardiogenic shock secondary to right ventricular infarction

7. has something more favorable. Other forms of shock, secondary to ruptures of the
interventricular septum, a papillary muscle or the ventricular wall, are associated
with variable mortality according to the possibilities of surgical treatment.
TREATMENT
The treatment of cardiogenic shock is complex and must be individualized in all
cases. Despite the poor prognosis should not be considered an intractable
situation, since the surviving patients are due to the establishment of appropriate
treatment and often the simple correction of triggers improves or makes disappear
the shock situation. The patient must be admitted to a coronary or intensive care
unit. The treatment is directed to the causes of the shock, triggering factors and
also contributing factors to the state of the shock and finally the respective
corrections of the hemodynamic alterations.

8. BIBLIOGRAPHIC REFERENCE:
• J. López-Sendón "Cardiogenic Shock" In: Farreras Valenti- C. Rozman. Internal
Medicine XVIII. Elsevier Edition Spain (Barcelona) 2016 p. 424-430