Cardio. Shock 09-x (1) Flashcards
What belongs to distributive shock?
SEPTIC
ANAPHYLAXIC
NEUROGENIC
Neurogenic shock. Primary disturbance?
Nerve injury –> no SNS response
Sepsis. Primary disturbance?
peripheral vasodilation
Sepsis. Result of venous dilation?
decr preload –> decr. CVP and PCWP
Sepsis. Result of arterial dilation?
decr. afterload (decr. SVR) –> decr. BP.
Sepsis. Mechanism that leads to decr. CVP and PCWP? 2
- peripheral venous dilation (due to proinflammatory mediators) –> pooling of blood in dilated veins
- increased vascular (capilary) permeability (third-spacing).
Sepsis early stage features?
EARLY STAGE (hyperdynamic stage):
decr. SVR, decr. BP, incr. CO and HR. (warm)
Sepsis early stage mechanism that incr. CO?
Hypotension + inflammation from sepsis –>
A compensatory increase in sympathetic drive increases
I. cardiac contractility and II. HR
resulting in increased cardiac output (CO)/cardiac index (CO per body surface area) despite reduced left ventricular preload).
ALSO:
1. the large decrease in SVR and 2. a baroreceptor reflex–mediated increase in heart rate (ie, tachycardia) –> incr. CO.
sepsis. whats the point of incr. CO?
CO increased to maintain tissue perfusion.
sepsis. what venous oxygen?
Incr. MvO2
The high rate of blood flow through the systemic capillaries prevents complete extraction of oxygen by the tissues=incomplete extraction of oxygen, resulting in high mixed venous oxygen saturation –> May develop lactic acidosis from tissue hypoperfusion.
sepsis. late stage features?
LATE STAGE (hypodynamic):
incr. SVR, decr. CO –> grave deterioration (cold)
!!!As shock progresses, tissue ischemia and accumulation of cytotoxic mediators eventually cause a reduction in CO –> with end-organ dysfunction./In shock end-organ damage = due to inadequate oxygen delivery to the organs and tissues of the body.
septic shock temperature?
SEPTIC SHOCK – hyper and hypothermia. Septic shock can present with either hyper- or hypothermia; hypothermic presentation may be due to cytokine-induced dysregulation of temperature control in the hypothalamus and is associated with poorer outcomes.
neurogenic shock. mechanism?
No SNS response –> NO SNS mediated incr. in HR and cardiac contractility –> decr. CO.
neurogenic shock. features?
decr. SVR, bradycardia, low cardiac index (output), low PCWP
neurogenic shock. what oxygen (MvO2)?
decr. MvO2 = improved peripheral oxygen extraction due to lower flow
CVP distributive - septic?
decreased
PCWP distributive - septic?
decreased
Cardiac index (LV output), distributive - septic?
increased (early phase)
decreased in late stage when deterioration happens
SVR distributive - septic?
decreased
SvO2 distributive - septic?
increased (fast flow –> incomplete extraction of O2 in tissues)
CVP distributive - neurogenic?
decreased
PCWP distributive - neurogenic?
decreased
Cardiac index (LV output), distributive - neurogenic?
decreased (no SNS response, reflex)
SVR, distributive - neurogenic?
decreased (no SNS response, reflex)
SvO2, distributive - neurogenic?
decreased (slow flow –> maintained extraction of O2 in tissues)
Cardiogenic shock. primary disturbance?
Left ventricle failure
PCWP cardiogenic shock?
increased
CVP cardiogenic shock?
increased
Also incr. pressure in right atrium
Cardiac index (LV output) cardiogenic shock?
DECREASED (main feature)
SVR cardiogenic shock?
increased (compensatory increase due to low CO)
SvO2 cardiogenic shock?
decreased
Hypovolemic shock main disturbance
decreased blood volume
CVP Hypovolemic shock?
decreased
PCWP Hypovolemic shock?
decreased
CO Hypovolemic shock?
decreased
SVR Hypovolemic shock?
Increased (compensatory incr.)
SvO2 Hypovolemic shock?
decreased
in hypovolemic what is activated as compensation?
SNS and RAAS
hypovolemic. How CO is maintained?
Stimulation of the heart (SNS) results in increased contractility and heart rate, helping to maintain cardiac output.
hypovolemic. kidney role?
Increased renal sodium and water retention help to prevent further volume loss.
Per raas sistema
hypovolemic resuscitation with i/v fluids. what is result? 2
Intravenous fluids increase the intravascular and left ventricular end-diastolic volumes. The increase in preload stretches the myocardium and increases the end-diastolic sarcomere length, leading to an increase in SV and CO by the Frank-Starling mechanism.
if hypovolemia due to diarrhea. what electrolyte disturbance?
loss of bicarbonate in the stool, further contributing to metabolic acidosis and a compensatory increase in ventilation.
obstructive shock primary disturbance?
impeded cardiopulmonary blood flow (PE, PTX, tamponade)
CVP in obstructive shock?
increased
PCWP in obstructive shock?
decreased
CO in obstructive shock?
decreased
SVR in obstructive shock?
increased (compensation)
SvO2 in obstructive shock?
decreased
PCWP specifically in tamponade (obstructive shock)?
preload of left heart is decreased, BUT duo to external compression PCWP is paradoxically increased
