Fcm - Cv Shock

Front 1

Shock

Back 1

State that exists when the circulation is no longer able to adequately deliver substrates to the tissues that are needed to support metabolism (circulatory), or the tissues are no longer able to metabolize energy containing substrates and oxygen (metabolic). The common denominator is the failure of the normal processes that sustain life.

Front 2

Preload

Back 2

Reflects how well the heart is filled with blood. It can be estimated by ventricular (LV or RV) end diastolic volume which in turn is reflected by the end diastolic pressure within the chamber.

Front 3

Ejection fraction

Back 3

The percentage of blood in the chamber that is actually ejected with each beat. Normal values for this parameter are approximately 55 to 75% for the left ventricle.

Front 4

Afterload

Back 4

Afterload can be approximated by the wall stress of the ventricle during systole. It is proportional to the intracavitary pressure and chamber diameter, and inversely proportional to wall thickness. Afterload is to a large extent determined by the resistance to the ejection of blood from the ventricle. It is usually estimated by the aortic pressure.

Front 5

Contractility

Back 5

Reflects the intrinsic ability of the muscle fibers to develop force, or its inotropic state.

Front 6

Normal value for mean arterial pressure

Back 6

70-105 mmHg

Front 7

Normal value for left atrial pressure

Back 7

4-12 mmHg

Front 8

Normal value for right atrial pressure

Back 8

0-8 mmHg

Front 9

What is the primary perturbation in hypovolumetric shock?

Back 9

Hypovolumetric shock involves the sudden loss of blood volume.

Front 10

What is the primary perturbation in septic shock?

Back 10

A drop in systemic vascular resistance due to inappropriate vasodilation.

Front 11

What is the primary perturbation in cardiogenic shock?

Back 11

A decrease in CO due to an intrinsic abnormality in the heart or surrounding structures.

Front 12

How are cardiac output (CO), pulmonary capillary wedge pressure (PCWP), and systemic vascular resistance (SVR) affected in hypovolemic shock?

Back 12

CO is decreased
PCWP is decreased*
SVR is variable

Front 13

How are cardiac output (CO), pulmonary capillary wedge pressure (PCWP), and systemic vascular resistance (SVR) affected in septic shock?

Back 13

CO is increased at first, then decreases later
PCWP decreases
SVR decreases*

Front 14

How are cardiac output (CO), pulmonary capillary wedge pressure (PCWP), and systemic vascular resistance (SVR) affected in cardiogenic shock?

Back 14

CO is decreased*
PCWP is increased
SVR is increased

Front 15

What serves as a marker of widespread failure of tissue perfusion?

Back 15

Lactic acidosis

Front 16

Most pressors lose their physiologic effectiveness in the presence of what?

Back 16

Severe acidosis

Front 17

What are the two most common cardiac causes of cardiogenic shock?

Back 17

Acute massive ischemia or infarction, or fulminant cardiomyopathy

Front 18

Cardiogenic shock treatment

Back 18

Therapy obviously depends on the cause. If a pulmonary embolism, thrombolytic therapy or surgical/suction embolectomy may be lifesaving. In the case of tamponade, drainage of the pericardial space, pericardiocentesis, often with placement of an indwelling catheter is indicated. Occasionally creation of a surgical "pericardial window" is necessary.

Other methods of circulatory support are often needed. This includes infusion of inotropic and pressor agents such as dobutamine, milrinone, dopamine, or epinephrine. When this approach is ineffective, the use of mechanical support such as with an intra-artic balloon pump or ventricular assist device is needed.

Front 19

Hypovolemic shock treatment

Back 19

Fluid, fluid, fluid, fluid!!!

In the case of bleeding, the ideal volume replacement involves the transfusion of blood, preferably crossmatched. While waiting for this, rapid infusion of crystalloid or a colloidal solution is necessary.

*A standard triple lumen catheter is NOT adequate in this setting, because each lumen is too small to allow adequate volumetric flow.*

SIRS and acidosis arise only during fluid resusciation in hypovolemic shock, so anticipating and treating these is critical.

Front 20

Septic shock treatment

Back 20

Get cultures and rapid administering of antiboitics. Fluid resuscitation is also a critical first step in the management of septic shock. If hemodynamic targets are not being achieved with fluid alone, a pressor agent is usually infused (Norepinephrine is most common).

In general, in the inpatient setting, if a patient becomes hypotensive with no clear-cut cause, sepsis should always be prominent in the differential diagnosis, along with pulmonary embolus.

Front 21

What are the features of systemic inflammatory response syndrome (SIRS)?

Back 21

Two or more of the following:
Temperature > 38C or < 36C

Heart rate > 90 beats/min

Respiratory rate > 20 breaths/min or PaCO2 < 32 mmHg

WBC count > 12,000/mm^3, <4000/mm^3, or >10% band neutrophilia

Front 22

Sepsis syndrome

Back 22

SIRS that has a proven or suspected microbial etiology.

Front 23

Severe sepsis

Back 23

Sepsis associated with organ dysfunction or hypotension; organ dysfunction may include presence of lactic acidosis, oliguria, or altered mental status.

Front 24

Septic shock

Back 24

SIRS with hypotension despite adequate fluid resusitation; septic shock should still be diagnosed if vasopressor therapy has normalized blood pressure.