YL6: 03.

15 Clinical Approach to Patient in Shock

09/16/2019 Basic Pathologies 1
02:30-03:30PM Jude Erric L. Cinco, MD, FPCP, FPCC
CLINICAL MEDICINE

TABLE OF CONTENTS Perfusion Pressure

• Perfusion pressure = Driving pressure – Resisting pressure
I. INTRODUCTION ............................................................................... 1 → e.g. Brain: Cerebral perfusion pressure = Mean arterial
A. BASIC DEFINITION OF SHOCK.............................................. 1 pressure – Intracranial pressure (Cerebral PP = MAP – ICP)
B. OHM’S LAW ............................................................................ 1 ▪ In severe head injury, ICP may rise and the brain gets
II. REVIEW OF NORMAL PHYSIOLOGY ............................................. 1 herniated which stops blood flow to the brain leading to
A. TISSUE PERFUSION .............................................................. 1
subsequent death
III. SHOCK ........................................................................................... 2
A. CHARACTERISTICS ............................................................... 2 o Driving pressure: Mean Arterial Pressure (MAP)
B. PATHOPHYSIOLOGY ............................................................. 2 o Resisting pressure: Intracranial Pressure (ICP)
C. PHYSIOLOGIC CHARACTERISTICS OF SHOCK ................... 3 → e.g. Heart: Coronary perfusion pressure = Diastolic pressure
D. TYPES OF SHOCKS ............................................................... 3 – Left ventricular end diastolic pressure (Coronary PP = DP -
E. CLINICAL MANIFESTATIONS................................................. 6 LVEDP)
F. GENERAL TREATMENT FOR SHOCK ................................... 6 ▪ In massive heart attacks, DP drops with the ventricle no
IV. HEMODYNAMICS .......................................................................... 7 longer ejecting its contents, which increases LVEDP that
A. PULMONARY ARTERY CATHETER (SWAN-GANZ) .............. 7 leads to subsequent death as the difference between
V. EXTRACORPOREAL MEMBRANE OXYGENATION (ECMO) ......... 9 LVEDP and DP reaches zero
QUICK REVIEW................................................................................... 9 o Driving pressure: Diastolic pressure (DP)
SUMMARY OF TERMS ............................................................... 9 o Resisting pressure: Left ventricular end diastolic
REVIEW QUESTIONS ............................................................... 10
pressure (LVEDP)
APPENDIX ......................................................................................... 10
Oxygen Delivery
I. INTRODUCTION
A. BASIC DEFINITION OF SHOCK
• Clinical syndrome that results from inadequate tissue perfusion
• Clinical expression of circulatory failure
• Results in inadequate cellular oxygen utilization
• State in which there is inadequate blood flow to the tissues to
meet demand

NEED TO KNOW: SHOCK AND HYPOTENSION

• Shock results
→ from inadequate tissue perfusion
→ in inadequate cellular oxygen utilization Figure 1. Oxygen Delivery (Cinco, 2019)
• Hypotension is NOT required to be present to rule in shock; you
can be in shock even if your blood pressure is normal! • Oxygen delivery is a product of two things:
→ Cardiac Output
→ Arterial Oxygen Content
B. OHM’S LAW
• General basis of most cardiovascular disorders and shock Cardiac Output (CO)
• Flow = Pressure / Resistance (F = P / R) • Amount of blood ejected from the ventricle in one (1) minute
→ Flow is directly proportional to pressure and inversely • Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR)
proportional to resistance → Stroke Volume (mL/beat)
• Pressure = Flow x Resistance (P = F x R) ▪ Amount of blood ejected from ventricle in one (1) beat
→ Serves as the basis for the equation for blood pressure ▪ Determinants:
• Blood Pressure = [1] Cardiac Output x [2] Systemic Vascular o Preload: Filling pressure at end of diastole
Resistance (BP = CO x SVR) o Afterload: Resists ejection of contents of the heart
→ [1] Cardiac Output = Stroke Volume x Heart Rate (CO = SV o Contractility: Strength of cardiac muscle
x HR) → Heart Rate (Beats/min)
▪ “Most important equation to remember (Cinco, 2019)”
→ [2] Blood Pressure = (Stroke Volume x Heart Rate) x NICE TO KNOW: NORMAL CARDIAC VALUES
Systemic Vascular Resistance (BP = SV x HR x SVR) • Normal Cardiac Output: 4-8 L/min
• Normal Cardiac Index: 2.5-4 L/min/m^2
NEED TO KNOW: BLOOD PRESSURE COMPONENTS → CI = CO/BSA
• Three (3) things to know when talking about blood pressure: → BSA = Body Surface Area
→ Stroke Volume (SV) • Normal Heart Range: 60-100 BPM
→ Heart Rate (HR) • Normal Stroke Volume 60-100 mL/Beat
→ Systemic Vascular Resistance (SVR)
• Given the central equation CO = SV x HR, treatment for shock
is easily understood as follows: Arterial Oxygen Content
→ Volume problem (i.e. Decreased SV): Infusion of blood • AOC= [(1.38 x Hemoglobin x SaO2) + (PaO2 x 0.0031)]
→ Heart rate problem (i.e. Decreased HR): Medication to → PaO2 = Partial pressure of dissolved oxygen in blood
increase heart rate → SaO2 = Arterial oxygen saturation
→ Vasodilated state (i.e. Decreased SVR): Vasoconstrictors • Major determinants:
→ Hemoglobin
▪ “If you do not have good oxygen, no matter how good
II. REVIEW OF NORMAL PHYSIOLOGY your heart rate is, there’s nothing to carry it, so you need
A. TISSUE PERFUSION good hemoglobin levels (Cinco, 2019)”
• Tissue perfusion is dependent on two (2) things: → Saturation
→ Perfusion pressure
→ Oxygen delivery

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 NEED TO KNOW: COMPONENTS OF OXYGEN DELIVERY
• Four (4) components of oxygen delivery that can be manipulated
in dealing with shock
→ Cardiac Output
▪ Stroke Volume
▪ Heart Rate
→ Arterial Oxygen Content
▪ Hemoglobin
▪ Arterial Oxygen Saturation

NEED TO KNOW: NEGLIGIBLE PRESSURE (PaO2)

• There is little to no contribution at all from the partial pressure of Figure 3. Central Line (i.e Internal Jugular Vein Access) (Cinco, 2019)
oxygen, so it is considered to be negligible.
NEED TO KNOW: LACTATE AND SCVO2 LEVELS
• Normal: ↓ lactate, ↑ ScVO2
Measures of Perfusion
• Shock: ↑ lactate, ↓ ScVO2
• Resistive pressures cannot be measured without doing invasive
procedures
→ e.g. In cerebral perfusion pressure, you can readily measure III. SHOCK
MAP, but cannot measure ICP without an intracranial probe
A. CHARACTERISTICS
• Non-invasive methods of measuring perfusion include lactate
and ScVO2 • Cellular dysfunction
• Damage-associated molecular patterns (DAMPs or “danger
Lactate signals”) and inflammatory mediators
• Molecule used for energy • Multiple organ failure (MOF)
• By-product of anaerobic metabolism • Death
• Increases when there is hypoperfusion during shock
→ Morbidity: 2x of normal levels B. PATHOPHYSIOLOGY
→ Mortality: 4x of normal levels
• If patient is suspected for shock:
→ Measure baseline lactate level
▪ Expected to be high
→ Provide treatment depending on type of shock
→ Measure lactate level again after 6 hours
▪ Expected to drop
→ Inadequate resuscitation occurred if there is still maintained
or increasing level of lactate
▪ Adjust treatment plan for shock accordingly

ScVO2
• Indicates central venous saturation of oxygen
→ Arterial side carries 100% oxygenated blood
→ Tissue proceeds to consume transported oxygen
▪ Normal oxygen consumption is 30-45%
→ Venous side carries 55-70% of unconsumed oxygen
• Decreases as tissues consume more oxygen in shock
→ In a state of shock, tissues will “eat” more therefore, whatever
is remaining in the venous system gets lower
• Obtained by getting blood from a central line (i.e. Internal Jugular Figure 4. Shock-Induced Vicious Cycle (Cinco, 2019)
Vein Access)
• All arrows pointing towards each other making it a vicious cycle
• e.g. Patient that was stabbed and bleeding was brought to the ER
→ First event would be hypovolemia due to the loss of blood
→ Hypovolemia will trigger a series of events that include:
▪ Low cardiac output
▪ Hypoperfusion
▪ Hypoxia
▪ Dysregulation of sympathetic & neuroendocrine system
▪ Microvascular stasis & thrombosis
▪ Fibrinolysis
▪ Cell damage
▪ Immune activation
▪ Pro-inflammatory phenotype/inflammatory mediators
▪ Multiple organ dysfunction syndrome
→ All of these promote capillary leak and further contribute to
maintaining hypovolemic state

“As a doctor, it is therefore your goal to avoid septic shock at all

costs, or if unavoidable, to act fast to save the patient. (Cinco,
2019)”

Figure 2. Central Venous Oxygen Content (Cinco, 2019)

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 Figure 6. Hemodynamic characteristics of the major types of shock
(CVP = right atrial pressure, PCWP = left atrial pressure)

Hypovolemic Shock
Figure 5. Host Immunoinflammatory Response to Shock (Cinco, 2019)

NOTE: HOST IMMUNOINFLAMMATORY RESPONSE TO SHOCK

This topic was in Doc Cinco’s slides but was skipped and not
discussed.

C. PHYSIOLOGIC CHARACTERISTICS OF SHOCK

Table 1. Physiologic characteristics of the various forms of shock.
(Harrisons, 19th ed., p. 1748)
CVP Systemic
Cardiac Venous O2
Type and Vascular
Output Saturation
PCWP Resistance
Hypovolemic ↓ ↓ ↑ ↓
Cardiogenic ↑ ↓ ↑ ↓
Septic
Hyperdynamic ↓↑ ↑ ↓ ↑
Hypodynamic ↓↑ ↓ ↑ ↓↑

Traumatic ↓ ↓↑ ↑↓ ↓
Neurogenic ↓ ↓ ↓ ↓
Hypoadrenal ↓ ↓ =↓ ↓

• Know how to differentiate the types, note the top three in the table:
→ Hypovolemic shock is loss of fluid and presents as low CVP
and low cardiac output
→ This affects the sympathetic nervous system and increases
vasoconstriction & increases vascular resistance
→ Cardiogenic shock (i.e. myocardial infarction)
▪ CVP and PCWP are high because whatever blood
enters the heart can’t eject because the heart has
stopped pumping
▪ Cardiac output is low because blood does not escape the
heart
→ Septic shock main characteristics:
▪ Drop in SVR
▪ Body will have a compensatory increase in cardiac
output

D. TYPES OF SHOCKS
• Why do we need to know what type of shock it is?
→ We need to classify them so that we know what our primary
treatment will be
→ It is not unusual that the shock is a mixed mechanism
• Initial assessment of shock states:
→ Algorithm starts with the most common presentation –
Arterial Hypotension
▪ However according to Doc, hypotension can be minimal
or absent
• NOTE: Doc said a lot the questions will come from this part!
Figure 7. Hypovolemic Shock (Vincent and de Becker, 2013)
• Characteristics: Low right atrial pressure and left atrial pressure,
low cardiac output, high systemic vascular pressure
→ Caused by loss of plasma or blood volume
→ Brought out by major hemorrhage 

→ Severe diarrhea or dehydration 

• Low preload leads to low cardiac output
• Sympathetic activation leads to high systemic vascular
resistance (i.e. “vasoconstricted everywhere”)

• SV is low in a hypovolemic shock

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 Advanced Trauma Life Support (ATLS ®) Chart

Figure 9b. Cardiogenic Shock (Vincent and de Becker, 2013)

Figure 8. Advanced Trauma Life Support (ATLS ®) Chart. Notice that
hemoglobin is not present in this chart (McGee et al., 2010) • Characteristics: low cardiac output
• Caused by pump failure
• This chart illustrates certain physiologic changes in patients • SV is low in a cardiogenic shock due to poor contractility
transitioning from hypovolemia to severe hypovolemia 
 • Can be caused by myocardial infarction (MI)
• NOTE: hemoglobin is NOT part of the parameters → Cardiac tamponade
→ Hemoglobin is measured in terms of proportion (g/dL) 
 ▪ Prevents the heart from properly filling
→ Even if patient is bleeding excessively, the proportion would ▪ Occurs when fluid accumulates in the pericardial sac
still 
be the same so hemoglobin may still be normal at this (outside the heart)
point → Low cardiac output from pump failure (blood cannot exit the
→ It will only adjust after resuscitation and volume expansion heart)

→ High preload due to inability to eject blood
Treatment
of Hypovolemic Shock → Sympathetic activation leads to high systemic vascular
• Treatment of hypovolemic shock is dependent on three factors: resistance 

→ Intravenous fluids 

ECG of Patient with ST Elevation MI
→ Blood and blood products 

→ Hemorrhage control 


Cardiogenic Shock

Figure 10. ECG presents Tombstoning (Cinco, 2019)

• Tombstoning

→ Tombstone like patterns in the ECG seen in MI patients 

• Patient is in cardiogenic shock
→ Coronary perfusion to left ventricle (LV) is dependent on
diastolic blood pressure
Figure 9a. Cardiogenic Shock (Vincent and de Becker, 2013) → LV function is dependent on coronary perfusion
→ Tachycardia decreases duration of diastole
• Death
→ Low BP
→ Low perfusion to coronary arteries
→ High HR

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 Treatment of Cardiogenic Shock Distributive Shock
• Restore perfusion 

• Treatment of ischemia 

• Perform pericardiocentesis for cardiac tamponade 
(basically
draining it out)
→ Pericardiocentesis is the aspiration of fluid from the pericardial
space that surrounds the heart
• Give inotropes (e.g. Norepinephrine, Dobutamine, Dopamine,
Milrinone)
→ Inotropes are drugs that increase the contractility of the heart
• Utilize mechanical devices like an intra-aortic balloon pump 


Obstructive Shock

NOTE
Doc said he won’t ask about obstructive shock in the exam, only the
other three: hypovolemic, cardiogenic, and distributive.

Figure 12. Distributive Shock (Vincent and de Becker, 2013)

• Characteristics: low systemic vascular resistance (i.e.

vasodilated state)
→ Generalized vasodilation
→ SVR is low due to vasodilation
 The most common cause of distributive shock is sepsis (Harrisons,
20th ed)
→ Thus, septic shock is a kind of distributive shock.
→ Sepsis has recently been redefined as the dysregulated host
response to infection resulting in life-threatening organ
dysfunction.

Septic Shock
• More than 30 million sepsis cases worldwide and 6 million deaths
from sepsis (WHO)
• Focus of infection plus systemic inflammatory response syndrome
• There are two types: hyperdynamic or hypodynamic shock
→ Hyperdynamic: vasodilation – low systemic vascular
resistance, high cardiac output, variable preload
→ Hypodynamic: low cardiac output, high systemic vascular
resistance, variable preload
Figure 11. Obstructive Shock (Vincent and de Becker, 2013)
Treatment of Septic Shock
• Can be caused by pericardial tamponade • Control source

• Cardiac output is low → Drain abscess
→ Operate on appendicitis
• Give antibiotics 

• Give intravenous fluids 

• Use vasopressors (Norepinephrine, Vasopressin) 

• Give inotropes (Dobutamine, Dopamine

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 E. CLINICAL MANIFESTATIONS NEED TO KNOW: MOTTLING SCORE
• Shock manifests from head to toe as seen in the following table: • The mottling score starts from 0 to 5:
→ 0 – No mottling
Table 2. Clinical Manifestations of Shock → 1 – Coin sized mottling area on the knee.
System Clinical Manifestations → 2 – To the superior area of the knee cap.
• Anxiety → 3 – Mottling up to the middle thigh
Central Nervous
• Restlessness → 4 – Mottling up to the fold of the groin
System
• Stupor and coma → 5– Severe mottling that extends beyond the the groin.
• Hypotension • At score 4 or 5, the patient only has 10% chance of survival
Cardiovascular • Cold clammy skin • If mottling is extensive, patient will not be able to survive
System • Peripheral vasoconstriction
• Variable hemodynamic profile
Respiratory • Tachypnea
System • Desaturation
• Malabsorption
Gastrointestinal
• Increase in liver enzymes (“shock
System
liver”)
Genitourinary • Oliguria
System • Electrolyte abnormalities
• Hypothermia
ID System
• Fever if it’s the warm phase of sepsis
Hematopoietic • Anemia
System • Coagulopathy
• Hypo/hyperglycemia
Endocrine System
• Hyper/hypercortisolism

• Shock is therefore a multi-organ disease as all the organ systems

need oxygen and will thus be affected if there is loss of oxygen Figure 14. Mottling Score (Cinco, 2019)
• A typical image of a shock patient:
→ Increased heart rate due to compensation of blood loss F. GENERAL TREATMENT FOR SHOCK
→ Decreased oxygen saturation • Only rapid restoration of oxygen delivery can reverse the
→ Decreased blood pressure progression of the shock state 

→ Increased respiratory rate • The fundamental approach to management is:
→ Patient with mottling → To recognize overt and impending shock in a timely
▪ Mottling is due to the body naturally prioritizing the major fashion
organs compared to the skin → To intervene emergently to restore perfusion 

• Treatment is directed towards the underlying cause 

• Supportive treatment is provided for all organ systems 

• Supplemental oxygen and mechanical ventilation maybe needed
to increase oxygen delivery and decrease work of breathing 

• Pain control and sedation may be needed to lower oxygen demand
• REMEMBER: Hypotension is NOT required to be present to rule in
shock

Table 3. Key Principles in the Treatment of Shock (Harrisons, 20th ed,

p. 2041)
# Principle
1 Recognize shock early
2 Assess for type of shock present
3 Initiate therapy simultaneous with the evaluation into the etiology
of shock
4 Restoration of oxygen delivery is the aim of therapy
5 Identify etiologies of shock which require additional lifesaving
interventions

Four Phases in the Treatment of Shock

Figure 13. Clinical Manifestations of Shock in the ICU

[Seatbelt car accident, Mottling (L-R)] (Cinco, 2018)

Figure 15. Four Phases in the Treatment of Shock (Vincent and de

Backer, 2013).

1. Salvage Phase
 The goal of therapy is to achieve a minimum blood pressure
and cardiac output compatible with immediate survival.

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  Minimal monitoring is needed; in most cases, invasive
monitoring can be restricted to arterial and central venous
catheters.
 Lifesaving procedures (e.g., surgery for trauma, pericardial
drainage, revascularization for acute myocardial infarction,
and antibiotics for sepsis) are needed to treat the underlying
cause.
2. Optimization Phase

 The goal is to increase cellular oxygen availability, and there
is a narrow window of opportunity for interventions targeting
hemodynamic status.
 Adequate hemodynamic resuscitation reduces inflammation,
mitochondrial dysfunction, and caspase activation.
 Measurements of SvO2 and lactate levels may help guide
therapy, and monitoring of cardiac output should be
considered.
3. Stabilization Phase
 The goal is to prevent organ dysfunction, even after
hemodynamic stability has been achieved.
 Oxygen supply to the tissues is no longer the key problem,
and organ support becomes more relevant.
4. De-escalation Phase
 The goal is to wean the patient from vasoactive agents and
promote spontaneous polyuria or provoke fluid elimination
through the use of diuretics or ultrafiltration to achieve a
negative fluid balance.

Figure 17. Approach to the patient in shock. EGDT, early goal directed
therapy; JVP, Jugular venous pulse. (Harrisons, 19th ed, p. 1731).

• Know how to diagnose patient

→ For cold clammy patient → low cardiac output → heart is
unable to pump or is “full” → cardiogenic shock

→ For warm patient → with high cardiac output → septic →
hyperdynamic shock

IV. HEMODYNAMICS
A. PULMONARY ARTERY CATHETER (SWAN-GANZ)

VIDEO
• The videos demonstrating the placement of the Swan-Ganz
catheter can be viewed using these links:

tinyurl.com/pulmartcath
tinyurl.com/sgplacement

• It is used to measure the pressure of all four chambers of the heart

• Three (3) components
→ Catheter
→ Balloon
→ Syringe
▪ Used to inflate the balloon

Figure 16. An algorithm for the resuscitation of patient in shock.

*Monitor SvO2, SVRI, and RVEDVI as additional markers of correction
for perfusion and hypovolemia. Consider age-adjusted CI. CI, cardiac
index in (L/min) per m2 ; CVP, central venous pressure; ECHO,
echocardiogram; Hct, hematocrit; HR, heart rate; PAC, pulmonary
artery catheter; PCWP, pulmonary capillary wedge pressure in mmHg;
RVEDVI, right ventricular end-diastolic volume index; SBP, systolic
blood pressure; SVO2, saturation of hemoglobin with O2 in venous
blood; SVRI, systemic vascular resistance index; VS, vital signs; W/U,
workup (Harrisons, 19th ed, p. 1749).

Figure 18. Swanz-Ganz Catheter and pathway. 3. Balloon

Not Shown: Syringe (Cinco, 2019)

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 Insertion of the Pulmonary Artery Catheter
• Swan-Ganz catheter is inserted into a vein (e.g. Internal jugular,
subclavian, or femoral veins)
• Catheter and balloon are sent through the right side of the heart
• When balloon can go no further, that means it is wedged to the end
of pulmonary artery and can now measure pulmonary capillary
wedge pressure (PCWP)
→ PCWP basically measures the left atrial pressure

Figure 21. Equations of pressures of the other chambers of the heart

[Shown here is PADP (pulmonary artery diastolic pressure) which is
Figure 19. Pathway of the Catheter in the Heart from Inferior Vena
Cava (Cinco, 2019)
When the balloon is inflated and it can go no further, you are
looking at the LA pressure (aka wedge pressure).
Measurement
• By inserting a Swan-Ganz catheter on right side of the heart, one
can measure the pressure of all four (4) chambers of the heart
→ Right atrium (RA), right ventricle (RV), and pulmonary
artery (PA) pressures are all measured directly
→ Left atrial (LA) pressure is indirectly measured using the
pulmonary capillary wedge pressure (PCWP)
▪ During diastole, the mitral valve opens and LA pressure
is equal to LV end-diastolic pressure (LVEDP)
▪ When the heart contracts, the aortic valve opens and LV
systolic pressure is the same as systolic/aortic
pressure
close to the value of PCWP] (Cinco, 2018)
By inserting a catheter in the right side of the heart, you can
measure [the pressure] all four chambers of the heart.
[But] how can you measure [the pressure of] all four chambers from
the right side? (In reference to Figure 19)
From the right side, you can measure RA directly, RV too you can
measure directly, PA you can measure directly. Ito namang wedge
[pressure] is the LA pressure.
So how do you measure the LV pressure? When the [mitral] valve
is open between the LA and the LV, they’re like one chamber.
So if you know the LA pressure in diastole, that’s the LV EDP
(end-diastolic pressure). And when the heart contracts, bubukas
naman ‘yung aortic valve, so whatever your systolic pressure is,
that’s the LV systolic pressure.

Thermodilution Technique: “Batis Principle”

• Thermistor in the catheter can detect temperature
• Cold saline solution is injected into one (1) port of the catheter
which generates a waveform that can be measured through
another port
→ Waveform represents the cardiac output
▪ NOTE: Types of waveforms will NOT be asked
→ Rate of temperature change is measured which can be used
to determine cardiac output

Figure 20. Pulmonary artery occlusion pressure (or PCWP) is

equal to the LA pressure and LV end-diastolic pressure (LVEDP)
(Cinco, 2019) Figure 22. Examples of Waveforms Generated in Thermodilution
Technique (Cinco, 2019)

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 MEMORY TECHNIQUE: STREAM (OR BATIS) ANALOGY
• Person A and Person B are taking a bath in a stream
• Person A, located farther upstream, wants to prank Person B
• Person A continues prank by pouring a bucket of ice into the
stream so Person B will eventually feel cold
• Time from when Person A dumps the bucket of ice in the water
to when Person B will feel cold is directly proportional to the
strength of the stream
• Summary: Rate (area under the curve) that the ice water travels
is directly proportional to the strength of the stream (CO)

V. EXTRACORPOREAL MEMBRANE OXYGENATION

(ECMO)

ECMO is an artificial heart and lung which you can use to buy time.
It’s like a bridge or a time machine. It’s a bridge kasi you bridge the
patient to the next stage of illness—kapag na-reverse mo ‘yung
shock state, you can remove the ECMO. Or it’s a time machine
because you can buy time before the patient dies.
• Essentially, an artificial heart and lung
• Two types:
→ Veno-Venous (V-V) ECMO
▪ Blood from the patient’s vein is put to the machine where
it recieves oxygen, and is then pumped back to the
venous side (e.g. internal jugular vein)
▪ Indication
o If the patient’s heart is functioning but the lungs
are not (e.g. ARDS)
Figure 23. Veno-Venous ECMO
NEED TO KNOW
Doc Cinco explicitly said in class that a question he may ask about
ECMO is when is V-V ECMO indicated.
Answer: If the patient’s heart is functioning but the lungs are
not
→ Veno-Arterial (V-A) ECMO
▪ Blood from the vein is brought to the oxygenator of the
pump and gets returned to the arterial side (e.g. femoral
artery)
▪ Here, the patient’s heart is not needed for ECMO to wok
▪ Indication
o Patient is in cardiogenic shock
Figure 24. Veno-Arterial ECMO
QUICK REVIEW
SUMMARY OF TERMS
• Shock results:
→ from inadequate tissue perfusion
→ in inadequate cellular oxygen utilization
• Ohm’s Law: general basis of most cardiovascular disorders and
shock
→ Pressure = Flow x Resistance (P = F x R)
→ Blood Pressure = Cardiac Output x Systemic Vascular
Resistance (BP = CO x SVR)
→ Cardiac Output = Stroke Volume x Heart Rate (CO = SV x
HR)
→ Blood Pressure = Stroke Volume x Heart Rate x Systemic
Vascular Resistance (BP = SV x HR x SVR)
• Treatments for shock:
→ Infusion of blood
→ Medication to increase heart rate
→ Vasoconstrictors
• Tissue perfusion dependent on:
→ Perfusion pressure: equal to driving pressure minus
resisting pressure
→ Oxygen Delivery is a product of:
▪ Cardiac Output: amount of blood ejected from the
ventricle in one (1) minute (Stroke Volume x Heart Rate)
▪ Arterial Oxygen Content: determined by Hemoglobin
and O2 Saturation
• Measures of perfusion during shock
→ Lactate: by-product of anaerobic metabolism which increases
when there is hypoperfusion
▪ Morbidity: 2x of normal levels
▪ Mortality: 4x of normal levels
→ ScVO2: indicate saturation central venous O2 which is
normally at 55-70% and decreases as tissues consume more
oxygen in shock
• Characteristics of shock
→ Cellular dysfunction
→ Damage-associated molecular patterns (DAMPs or “danger
signals”) and inflammatory mediators
→ Multiple organ failure (MOF)
→ Death
• Shock-induced vicious cycle: starts with hypovolemia which
ultimately promotes capillary leak
• Types of Shock
→ Hypovolemic shock: caused by loss of plasma or blood
volume wherein SV is low in a hypovolemic shock
→ Cardiogenic shock: caused by pump failure wherein SV is
low due to poor contractility (seen in cardiac tamponade)
→ Obstructive shock: can be caused by pericardial tamponade
wherein the cardiac output is low
→ Distributive shock: generalized vasodilation wherein the
SVR is low (most common cause of distributive shock is
sepsis)
→ Septic shock: focus of infection plus systemic inflammatory
response syndrome

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• Shock manifests from head to toe (multi-organ disease) which 7. What type of ECMO is used when the heart is functioning well, but
leads to deprivation of O2 the lungs are not?
→ Increased heart rate due to compensation of blood loss a) Veno-Arterial ECMO
→ Decreased oxygen saturation b) Veno-Venous ECMO
→ Decreased blood pressure c) Arterial-Veno ECMO
→ Increased respiratory rate d) Artero-Arterial ECMO
→ Patient with mottling 8. What type of shock results from a diarrhea or dehydration?
• Key principles in treatment of shock a) Cardiogenic shock
b) Hypovolemic shock
→ Recognize shock early
c) Obstructive shock
→ Assess for type of shock present
d) Distributive shock
→ Initiate therapy simultaneous with the evaluation into the 9. TRUE OR FALSE. In both hypovolemic shock and cardiogenic
etiology of shock shock, cardiac output is decreased while systemic vascular
→ Restoration of oxygen delivery is the aim of therapy resistance is increased.
→ Identify etiologies of shock which require additional lifesaving 10. In which of the following phases in the treatment of shock is organ
interventions support most prioritized?
• Four Phases of General Treatment a) Salvage
→ Salvage Phase: achieve a minimal BP b) Optimization
→ Optimization Phase: increase cellular oxygen availability c) Stabilization
→ Stabilization Phase: prevent organ dysfunction d) De-escalation
→ De-escalation Phase: wean from vasoactive agents
• Pulmonary Artery Catheter (Swan-Ganz): used to measure the Answers
pressure in all four chambers of the heart 1D, 2B, 3T, 4D, 5A, 6D, 7B, 8B, 9T, 10C
→ Catheter
→ Balloon APPENDIX
→ Syringe
• Pulmonary capillary wedge pressure (PCWP) is used to
measure the left atrial pressure
• Thermodilution Technique: Batis Principle
→ Thermistor in the catheter can detect temperature which is
used to determine cardiac output
• Extracorporeal Membrane Oxygenation: an artificial heart and
lung
→ Veno-Venous (V-V) ECMO: used when the patient’s heart is
functioning but the lungs are not
→ Veno-Arterial (V-A) ECMO: used when the patient is in
cardiogenic shock

REVIEW QUESTIONS
1. Eric, a 28-year old race car driver decided to test the limits of his
new car. Unfortunately, Eric crashed his car and experienced
shock due to multiple injuries. The following manifestations would
be observed in Eric EXCEPT:
a) Mottling
b) Hypotension
c) Tachypnea
d) Polyuria Figure 21. Swan-Ganz- Right Heart Catherization
e) None of the above (Cinco, 2019)
2. What type of shock is characterized the loss of plasma volume with
low CVP, low PCWP, low CO, but high SVR?
a) Cardiogenic shock EVALUATION FORM
b) Hypovolemic shock https://tinyurl.com/AcadsTransFeedback
c) Septic shock
d) Distributive shock
3. TRUE OR FALSE. In a patient experiencing shock, capillary leak
contributes to the cause of hypovolemia.
4. Which of the following is measured with pulmonary capillary wedge
pressure (PCWP)?
a) Right Atrial Pressure
b) Right Ventricular Pressure
c) Left Ventricular Pressure
d) Left Atrial Pressure
e) Cardiac Output
5. What type of shock is characterized by ventricular failure with high
CVP, high PCWP, low CO, but high SVR?
a) Cardiogenic shock
b) Hypovolemic shock
c) Septic shock
d) Distributive shock
6. Which of the following CANNOT be manipulated during oxygen
delivery care for patients in shock?
a) Stroke Volume
b) Hemoglobin
c) Arterial Oxygen Saturation
d) Arterial Oxygen Tension
e) Heart Rate

Basic Pathologies 1: Clinical Approach to Patient in Shock 10 of 10

YL6: 03.15 Errata submission: tinyurl.com/transerratasubmit
Errata tracker: https://tinyurl.com/ErrataTracker