Shock Flashcards
what can a Swan-Ganz catheter be used for at the bedside?
measure right heart and pulmonary artery pressure
can evaluate patients in shock, those with suspected pulmonary artery HTN, suspected intracardiac shunt, etc
put in through internal jugular vein, thread into heart - measures pressure as it travels
what are the 5 pressures that Swan-Ganz catheters can measure?
- SVC/ central venous pressure (CVP)
- right atrium
- right ventricle
- pulmonary artery
- PCWP: pulmonary capillary wedge pressure
can also measure CO and mixed venous O2 saturation
what do the a, c, v, x, and y waves represent on the right atrial pressure wave form?
a = atrial contraction
c = tricuspid valve closure
v = passive atrial filling (ventricular contraction)
x = atrial diastole
y = atrial emptying
what would cause an elevation in RV systolic vs diastolic pressure?
increased afterload (pulmonary HTN, pulmonic stenosis) —> increased systolic RV pressure
diastolic dysfunction (RV infarction, restrictive cardiomyopathy) —> increased diastolic RV pressure
what is the major cause of an increase in pulmonary artery pressure?
left heart disease - pressure backs up into pulmonary circulation
(there are other causes as well - lung disease, hypoxemia, COPD, pulmonary artery HTN - but left heart disease is major reason)
what does pulmonary capillary wedge pressure represent?
PCWP is reflection of left atrial pressure, and in absence of mitral valve disease, is indication of LVEDP and LVEDV
if all pressures measured by a Swan-Ganz catheter are low, what does this indicate?
reflects low effective circulating volume, for example due to hemorrhage or sepsis
what is shock characterized by?
insufficient oxygen delivery to tissues
patients can maintain their BP in normal range despite profound tissue hypo-perfusion (shock) through these 2 compensatory mechanisms:
- baroreceptor response: decreased firing of carotid sinus (CN 9, glossopharyngeal) and aortic arch (CN X, vagus) baroreceptors disinhibits SNS signaling in CNS —> increased SNS tone (vasoconstriction)
- renin-angiotensin-aldosterone (RAAS): renal hypoperfusion means less Na+ reaching macula densa —> beta1 stimulation and renin release from JGA (juxta-glomerular apparatus) —> sodium/water reabsorption, vasoconstriction
how does the pH of blood change if tissues are not being adequately perfused with oxygen?
lactic acidosis due to anaerobic metabolism
this will trigger reflex tachypnea (compensatory respiratory alkalosis)
what are the 4 categories of shock?
- cardiogenic (high pressures)
- hypovolemic (low pressures)
- obstructive
- distributive (peripheral issues - anaphylaxis, sepsis)
what is the leading cause of death for patients (already hospitalized) with acute myocardial infarction?
cardiogenic shock - primary pump failure following loss of >40% LV myocardium
occurs 5-7 hours post-MI (STEMI, transmural occlusion), very high mortality
cardiogenic shock can also occur with long-standing LV dysfunction - dilated cardiomyopathy, arrhythmia, valvular heart disease, etc
what occurs in cardiogenic shock?
STEMI/other injury depresses myocardial contractility —> reduced CO and low BP
induces compensatory mechanisms (baroreceptors, RAAS) —> vasoconstriction
which leads to volume overload and worsening coronary insufficiency —> systolic (low EF) heart failure
cell inflammation causes production of iNOS (inducible) —> high NO levels override SNS and vasodilation begins to occur —> lower tissue perfusion, end stage drop in BP
what are some of the clinical findings of cardiogenic shock?
ischemic injury —> low CO/BP —> compensatory vasoconstriction/ fluid retention —> volume overload —> systolic HF
findings:
- hypotension and low CO causes reflex tachycardia, faint pulses, soft heart sounds
- hypoperfusion causes disorientation, cool/clammy/cyanotic extremities (look at mucosa)
- pulmonary congestion causes pulmonary rales and elevated JVP, S3 is heard and PMI is displaced (high LV volume)
how does cardiogenic shock affect the following parameters, and what are the physical findings associated with these changes?
a. filling pressures
b. TPR
c. CO
d. cardiac contractility
a. filling pressures: HIGH (PCWP) —> JVD, rales/wheezing, S3
b. TPR: HIGH —> cool/clammy/cyanotic skin
c. CO: LOW —> decreased MAP
d. cardiac contractility: LOW —> decreased SV
what occurs in hypovolemic shock?
loss of blood cell mass or plasma volume (bowel obstruction, Cholera, burn, trauma, etc) —> decreased preload AND O2 carrying capacity (loss of Hgb)
decreased preload —> increases SNS tone —> peripheral vasoconstriction
decreased Hgb —> systemic anaerobic metabolism —> lactic acidosis —> ROS —> systemic inflammation
loss of blood volume can also deplete clotting factors/platelets —> coagulopathy —> bleeding —> more volume loss —> hypothermia (cannot maintain body temp)
how can hypovolemic shock be recognized?
loss of blood cell mass, plasma volume —> decreased preload AND O2 carrying capacity (loss of Hgb)
clinical findings:
- narrow pulse pressure: early sign
- weak, thready pulse
- tachycardia, tachypnea
- cold/clammy skin
- pale/mottled skin
- altered mental status
how does hypovolemic shock affect the following parameters, and what are the physical findings associated with these changes?
a. filling pressures
b. TPR
c. CO
d. cardiac compliance
a. filling pressures: LOW —> flat neck veins, clear lungs
b. TPR: HIGH —> cool/clammy/pale skin
c. CO: LOW —> decreased MAP, SV
d. cardiac compliance: may decrease as shock worsens
how would preload, PCWP, and TPR compare in cardiogenic vs hypovolemic shock?
cardiogenic shock: HIGH preload, HIGH PCWP, HIGH TPR
hypovolemic shock: LOW preload, LOW PCWP, HIGH TPR
PCWP = pulmonary capillary wedge pressure, representative of LA pressure
what causes obstructive shock?
problem: heart can’t fill properly (decrease preload), therefore can’t produce adequate SV
can be caused by pericardial at tamponade (squeezing of heart), tension pneumothorax (air getting trapped in chest wall squishes heart), or massive pulmonary embolus
explain why pulsus paradoxus occurs in cardiac tamponade
inspiration lowers intrathoracic pressure (bronchioles, alveoli expand with air)
this sucks in blood from the right side of heart, therefore right side fills (with incoming blood) more quickly
on the left side, decreased intrathoracic pressure lowers the pressure gradient driving blood into the heart, so the left side doesn’t fill as much
together, the RV expands more than the LV
when there is cardiac tamponade, this causes RV to push the IV septum over, impeding filling of the LV further —> big drop in BP
what are the classic clinical features of pericardial tamponade and tension pneumothorax, respectively, both of which are common causes of obstructive shock?
cardiac tamponade: hypotension + muffled heart sounds + JVD (Beck’s triad)
tension pneumothorax: absent breath sounds + JVD + tracheal deviation
how does obstructive shock affect the following parameters, and what are the physical findings associated with these changes?
a. filling pressures
b. PVR (peripheral vascular resistance)
c. CO
a. filling pressures: HIGH —> JVD
b. PVR: HIGH —> cool/clammy/pale skin
c. CO: LOW —> decreased MAP, SV
what type of shock is caused by septic shock, neurogenic shock, and anaphylactic shock? what is the common factor among these?
all types of distributive shock: profound decrease in peripheral vascular resistance
septic shock: decrease in PVR despite increased vasopressors
neurogenic shock: spinal cord injury causes decreased SNS tone
anaphylactic shock: histamine, leukotriene C4, prostaglandin D2 all cause profound vasodilation
how does septic shock cause distributive shock?
[distributive shock: profound decrease in peripheral vascular resistance]
bacterial endotoxins cause endothelial cell injury:
—> iNOS induces profound vasodilation
—> loss of cell-cell contacts leads to increased permeability
—> microvascular thrombosis (DIC) causes tissue ischemia
this all leads to hypovolemia, edema, multiorgan failure
what is the mechanism of distributive shock?
marked decrease in total peripheral resistance (sepsis, anaphylaxis, etc)
—> increased CO (low afterload) but low filling pressures
—> decreased peripheral oxygen utilization (fluid leaking out all over the place)
how do patients with distributive shock present?
marked decrease in total peripheral resistance (sepsis, anaphylaxis, etc) —> increased CO but low tissue perfusion
clinical features:
- fever
- bounding pulses
- warm skin (no vasoconstriction)
- tachycardia/tachypnea
- elevated WBC count
- disorientation
how is distributive shock as caused by septic treated?
marked decrease in total peripheral resistance (sepsis, anaphylaxis, etc) —> increased CO but low tissue perfusion
first give fluid (trying to raise BP), then given norepinephrine (vasoconstriction)
how does distributive shock caused by sepsis affect the following parameters, and what are the physical findings associated with these changes?
a. filling pressures
b. TPR
c. CO
a. filling pressures: LOW —> flat neck veins, clear lungs, sinus tachycardia
b. TPR: LOW —> warm skin, bounding pulses
c. CO: HIGH —> decreased MAP (determined by diastolic BP)
how do the following forms of shock affect mixed venous oxygen saturation (MVO2 or SvO2)?
a. cardiogenic
b. hypovolemic
c. tension PTX (obstructive)
d. septic (distributive)
MOV2/SvO2 = oxygen content of the blood that returns to the heart after meeting tissue needs
a. cardiogenic: LOW mvo2
b. hypovolemic: LOW mvo2
c. tension PTX (obstructive): LOW mvo2
d. septic (distributive): HIGH mvo2 - profound decrease in TPR, lots of fluids leaking out and low tissue perfusion
in which of the following types of shock will preload be increased?
a. cardiogenic
b. hypovolemic
c. tension PTX (obstructive)
d. septic (distributive)
a. cardiogenic - volume overload puts HIGH pressure on heart
in which of the following types of shock will CO be increased?
a. cardiogenic
b. hypovolemic
c. tension PTX (obstructive)
d. septic (distributive)
d. septic shock (type of distributive shock) - profound decrease in TPR causes decrease in afterload, leading to increase in CO
there’s not a lot of volume in the heart, but because afterload is so little it can generate strong contractions that cause high CO
