The Physiology of Cardiopulmonary Resuscitation (CPR) - ECG & ECHO

The physiology of
20/4/23, 07:46 The physiology of cardiopulmonary resuscitation (CPR) – ECG & ECHO
cardiopulmonary resuscitation
(CPR)
Chapter contents Hide
The compression phase
Coronary perfusion pressure (CPP)
The decompression phase
The ventilation phase
References
The forces that drive coronary and cerebral perfusion, and ventilation of
the lungs during cardiopulmonary resuscitation (CPR) differ substantially
from normal circumstances. The purpose of CPR is to create large
variations in intrathoracic pressure by compressing, decompressing and
ventilating. These maneuvers result in arterial blood flowing through the
pulmonary, coronary and cerebral circulation, as well as allowing for gas
exchange in the lungs. A large number of experimental and observational
studies have been conducted to optimize the effectiveness of CPR. Yet,
there are fundamental gaps in knowledge, with some of the most critical
components of current guidelines being based on observational data
(e.g compression rate and depth). With current strategies, compressions
and ventilations can generate a cardiac output equivalent to 15-25% of
normal output (Duggal et al). This, in conjunction with defibrillation, is
sufficient to resuscitate 10-15% of out-of-hospital cardiac arrests (OHCA)
and 30-40% of in-hospital cardiac arrests (IHCA; Jerkeman et al).
Current guidelines recommend a compression depth of 5–6 cm at a rate of
100–120 compressions per minute (Figure 1). These recommendations are
based on observational data (Stiell et al, Idris et al). Randomized clinical
trials are lacking.
Figure 1. Left panel: The association between compression depth and

survival to hospital discharge (Stiell et al). Right panel: The association
between compression rate and survival to hospital discharge (Idris et al).
Defibrillation is the most important intervention if the rhythm is shockable
(ventricular fibrillation [VF], pulseless ventricular tachycardia [VT]). The VF
waveform is initially coarse (i.e fibrillatory waves have large amplitudes)
but as the duration of VF is prolonged, the amplitude gradually diminishes
and fine VF (small fibrillatory amplitudes) ultimately degenerate into
asystole. The gradual progression from coarse VF to fine VF and finally
asystole is the result of diminishing ATP concentration in the myocardium.
ATP depletion results in cellular dysfunction and renders the defibrillation
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ineffective. The likelihood of successful defibrillation is high in coarse VF
(the early phase), but diminishes rapidly as the waveform becomes finer
(Figures 2, 3 and 4).
Figure 2. ATP concentration in the myocardium during induced ventricular

fibrillation (VF).
Figure 3. Association between time to CPR and likelihood of successful

defibrillation.
Figure 4. Progression from coarse ventricular fibrillation (VF) to fine VF.

CPR re-induces coarse VF by means of increasing coronary blood flow.
In circumstances with non-shockable rhythm or with prolonged periods of
VF (fine VF resistant to defibrillations), the purpose of CPR is to induce
myocardial electrical activity by generating adequate coronary perfusion
pressure (CPP). Myocardial activity is necessary to salvage the brain, and
is therefore of prime importance. This is achieved by performing effective
chest compressions and decompressions that result in perfusion of
cardiac, cerebral and pulmonary tissue.
Chest compressions produce perfusion of vital organs by increasing the
pressure in the atria, ventricles and large vessels. This results in blood
being propelled forward (assuming that valvular function is normal).
Unfortunately, the compressions also increases pressure in the thoracic
veins (paravertebral veins, epidural veins) that drain the brain. Increased
pressure in these veins is propagated to the brain and counteracts
cerebral arterial blood flow (cerebral blood flow is determined by the
gradient [difference] between cerebral arterial and venous pressure). This
is one of the major challenges in improving resuscitation outcomes.
Various experiments (e.g head tilting, passive leg raising, etc) have been
tried to improve cerebral perfusion during CPR (Debaty et al, Youcef et al).
Figure 5. Pressure curves during CPR with head positioned at 0°, head-up
+30°, and head-down -30° (Lurie et al, Debaty et al).
The compression phase
Chest compressions reduce thoracic volume and increase thoracic
pressure. This leads to compression of all structures, including the atria,
ventricles, airways, and large vessels. The heart is squeezed between the
sternum and the vertebral column, and blood is forced in anterograde
direction. Provided that the valvular apparatus is functioning normally,
blood is only ejected in anterograde direction, such that the pressure is
not transduced to the large veins (which would counteract arterial blood
flow).
Coronary perfusion pressure (CPP)
Coronary perfusion is fundamental for restoring and maintaining cardiac
electrical activity. Studies demonstrate that a coronary perfusion pressure
(CPP) of 15 mmHg is required in order to induce electrical activity in the
myocardium (Paradis et al). The coronary perfusion pressure (CPP) can be
calculated as follows:
CPP = Paorta – RAP
Paorta is the intra-aortic pressure (where the coronary arteries
originate)
RAP is right atrial pressure (where venous coronary blood is emptied)
However, CPP is approximately 0 mmHg (i.e there is no coronary blood
flow) during the compression phase, which is explained by the fact that
the pressure is equally elevated in the aorta and the right atrium. Coronary
blood flow occurs during the decompression phase ("CPR diastole").
Thoracic volume expands rapidly during the decompression. Right atrial,
right ventricular and left ventricular pressure drops abruptly, but the
closing of the aortic valve allows the intra-aortic pressure to remain high.
The resulting pressure difference between right atrial pressure (RAP) and
intra-aortic pressure (Paorta) is the CPP. The decrease in right atrial
pressure and ventricular pressure is also important because it allows for
passive flow of blood to the atria and ventricles (Halperin et al).
Figure 6. Coronary perfusion pressure (CPP) during CPR.

CPP is very sensitive to interruptions in the compressions. Brief
interruptions (seconds) abolishes the CPP completely and it takes
around15 compressions to re-establish the CPP after an interruption
(Steet et al, Berg et al). This is reflected in animal studies demonstrating
that survival decreased by 7% for every 5 seconds of pause before
defibrillation (Cheskes et al).
Because coronary perfusion occurs during the decompression phase,
effective decompression is essential to generate high CPP and maximize
passive reflow to the heart (Niemann et al).
The compressions also lead to increased pressure in the veins in the
thorax (paravertebral veins, epidural veins) and the spinal fluid.
Unfortunately, this increase in pressure is propagated to the brain and
leads to an increase in venous cerebral pressure, and subsequently
increased intracranial pressure (ICP). High ICP counteracts the cerebral
perfusion pressure (CerPP). Thus, compressions lead to increased
intracranial pressure (ICP), which reduces cerebral perfusion (CerPP). Yet,
it is essential to generate a high CPP as it is required to induce cardiac
activity.
During the compression phase, passive expiration occurs as the lung
tissue is compressed. This enables minimal gas exchange. The
effectiveness of this gas exchange diminishes gradually unless positive
pressure ventilation (PPV) is provided. This is explained by the fact that
PPV expands the pulmonary tissue – including bronchioles, arteries and
veins – and thus lowers resistance in these compartments.
Compression
↑ Intrathoracic pressure Passive expiration
Transduction of pressure to brain

↑ Right atrial pressure (RAP) ↑ Intraaortic pressure via paravertebral veins, epidural
veins and spinal fluid
↑ Pulmonary circulation Coronary and cerebral perfusion ↑ Intracranial pressure (ICP)
↓ CerPP
Figure 7. Effects during the compression phase of CPR. CerPP = cerebral

perfusion pressure.
The decompression phase
During decompression, a passive recoil (expansion) of the thorax occurs.
This leads to a rapid decrease in intrathoracic pressure. The resulting
vacuum in the lungs draws air into the alveoli. The right and left ventricles
are passively filled with blood (mainly because low right-sided pressure
causes venous return to the right atrium and ventricle). Decompression
also reduces ICP (through the reduction of pressure in the intrathoracic
veins draining the head) and thereby facilitates cerebral perfusion during
the next compression phase.
Decompression
Passive chest wall recoil
↓ Intrathoracic pressure ↓ Intracranial pressure (ICP)
Left ventricular filling Venous return to right ventricle Passive inspiration ↑ CerPP next compression
Figure 8. The decompression phase of CPR.

Interventions that amplify the recoil (expansion of the thorax) will result in
improved preload (ventricular filling) and subsequently larger stroke
volumes during the compression phase. CPP will also increase. There is
ongoing development of devices that improve recoil through various
means. Active decompression through suction devices (e.g the suction
cup on LUCAS) are already in use (Figure 9).
Figure 9. LUCAS CPR device enables active decompression using a

suction cup.
Leaning on the chest during decompression can be fatal. Animal studies
show that a recoil of 75% (compared to 100%) reduces CPP by
approximately 30% and CerPP by 50% (Yannopoulos et al). Observational
studies show that leaning occurs in over 90% of cases (Fried et al).
The ventilation phase
Ventilation during CPR is performed with positive pressure ventilation
(PVV), forcing air into the lungs. This differs significantly from normal
respiration, during which the chest wall is expanded using respiratory
muscles. The latter creates a negative intrathoracic pressure, with the
resulting vacuum drawing air into the alveoli so that gas exchange can take
place. The respiratory muscles are paralyzed during cardiac arrest, so that
PPV is the only possibility to achieve ventilation.
There is evidence that ventilation is less important than compression.
Survival is virtually impossible without compressions (CPP must reach 15
mmHg to induce cardiac electrical activity). Ventilation is less critical
during the first 4–5 minutes. Several studies have tested compression-
only CPR, which entails deferring ventilations during the initial phase. In a
large Swedish randomized study, there was no difference in survival when
bystanders performed compression-only CPR compared to standard CPR
for out-of-hospital cardiac arrest (Svensson et al). Similar results were
reported in a large observational study (Jerkeman et al). As mentioned
above, compressions result in some, albeit minimal, ventilation
(McDannold et al). Yet, positive pressure ventilation is recommended as
soon as possible because the effectiveness of the compressions
diminishes after a few minutes of compressions. This is explained by the
fact that the pulmonary vessels and bronchioles collapse gradually during
the compression phase (Dunnham-Snary et al). To expand the pulmonary
vessels and bronchioles, positive pressure ventilation must be performed
(Markstaller et al).
Hyperventilation must always be avoided during cardiopulmonary
resuscitation. It prevents the pressure drop in the thorax, which
counteracts the passive filling. Hyperventilation also leads to increased
right atrial pressure during diastole, which reduces CPP. In an animal
study, CPP decreased by 28% during hyperventilation (Aufderheide et al).
Hyperventilation is also unnecessary because cardiac output is low during
CPR, which means that small tidal volumes are sufficient to eliminate
CO2 and oxygenate the blood.
Positive Pressure
Ventilation
Inflation of lungs ↑ ICP
Opening of pulmonary Alveoli compresses

vasculature ↑ Intrathoracic pressure veins ↓ CerPP
Reduced pulmonary Reduced Increased

Oxygen delivery vascular resistance venous return RV afterload ↑ LV preload
Respiration and Reduced RV preload

pulmonary circulation and increased afterload ↑ Stroke volume
Figure 10. Effects of positive pressure ventilation (PPV) during CPR.

References
Keith G. Lurie, MD, Edward C. Nemergut, MD, Demetris Yannopoulos, MD,
and Michael Sweeney, MD. The Physiology of Cardiopulmonary
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Duggal C, Weil MH, Gazmuri RJ, Tang W, Sun S, O’Connell F, Ali M.
Regional blood flow during closed-chest cardiac resuscitation in rats. J
Appl Physiol 1993;74:147–52.
Matilda Jerkeman, Peter Lundgren, Elmir Omerovic, Anneli Strömsöe,
Gabriel Riva, Jacob Hollenberg, Per Nivedahl, Johan Herlitz, Araz
Rawshani. Association between type of bystander cardiopulmonary
resuscitation and survival in out-of-hospital cardiac arrest: A machine
learning studyResuscitation Plus. 2022 Jun 14;10:100245.
Debaty G, Shin SD, Metzger A, Kim T, Ryu HH, Rees J, McKnite S,
Matsuura T, Lick M, Yannopoulos D, Lurie K. Tilting for perfusion: head-up
position during cardiopulmonary resuscitation improves brain flow in a
porcine model of cardiac arrest. Resuscitation 2015;87:38–43.
Stiell IG, Brown SP, Christenson J, Cheskes S, Nichol G, Powell J, Bigham
B, Morrison LJ, Larsen J, Hess E, Vaillancourt C, Davis DP, Callaway CW;
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Idris AH, Guffey D, Aufderheide TP, Brown S, Morrison LJ, Nichols P, Powell
J, Daya M, Bigham BL, Atkins DL, Berg R, Davis D, Stiell I, Sopko G, Nichol
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rescuers and survival from out-of-hospital cardiac arrest. JAMA.
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Markstaller K, Rudolph A, Karmrodt J, et al. Effect of chest compressions
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McDannold R, Bobrow BJ, Chikani V, Silver A, Spaite DW, Vadeboncoeur T.
Quantification of ventilation volumes produced by compressions during
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Maaret Castrèn, M.D., Ph.D., Hans Pettersson, Ph.D., Lars Engerström,
M.D., Johan Herlitz, M.D., Ph.D., and Mårten Rosenqvist, M.D., Ph.D.
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porcine model of cardiac arrest. Resuscitation 2015;87:38–43
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B, Morrison LJ, Larsen J, Hess E, Vaillancourt C, Davis DP, Callaway CW;
Resuscitation Outcomes Consortium (ROC) Investigators. What is the role
of chest compression depth during out-of-hospital cardiac arrest
resuscitation? Crit Care Med 2012;40:1192–8 8.
Idris AH, Guffey D, Aufderheide TP, Brown S, Morrison LJ, Nichols P, Powell
J, Daya M, Bigham BL, Atkins DL, Berg R, Davis D, Stiell I, Sopko G, Nichol
G; Resuscitation Outcomes Consortium (ROC) Investigators. Relationship
between chest compression rates and outcomes from cardiac arrest.
Circulation 2012;125:3004–12
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Bobrow BJ, Spaite DW, Berg RA, et al. Chest compression-only CPR by lay
rescuers and survival from out-of-hospital cardiac arrest. JAMA – J Am
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Markstaller K, Rudolph A, Karmrodt J, et al. Effect of chest compressions
only during experimental basic life support on alveolar collapse and
recruitment. Resuscitation. 2008;79(1):125-132.
McDannold R, Bobrow BJ, Chikani V, Silver A, Spaite DW, Vadeboncoeur T.
Quantification of ventilation volumes produced by compressions during
emergency department cardiopulmonary resuscitation. Am J Emerg Med.
2018;36(9):1640-1644.
Dunham-Snary KJ, Wu D, Sykes EA, et al. Hypoxic Pulmonary
Vasoconstriction: From Molecular Mechanisms to Medicine. Chest.
2017;151(1):181-192.
Compression-Only CPR or Standard CPR in Out-of-Hospital Cardiac Arrest
List of authors. Leif Svensson, M.D., Ph.D., Katarina Bohm, R.N., Ph.D.,
Maaret Castrèn, M.D., Ph.D., Hans Pettersson, Ph.D., Lars Engerström,
M.D., Johan Herlitz, M.D., Ph.D., and Mårten Rosenqvist, M.D., Ph.D
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The physiology of

Figure 1. Left panel: The association between compression depth and

Figure 2. ATP concentration in the myocardium during induced ventricular

Figure 3. Association between time to CPR and likelihood of successful

Figure 4. Progression from coarse ventricular fibrillation (VF) to fine VF.

Figure 6. Coronary perfusion pressure (CPP) during CPR.

↑ Intrathoracic pressure Passive expiration

Transduction of pressure to brain

↑ Pulmonary circulation Coronary and cerebral perfusion ↑ Intracranial pressure (ICP)

Figure 7. Effects during the compression phase of CPR. CerPP = cerebral

Passive chest wall recoil

↓ Intrathoracic pressure ↓ Intracranial pressure (ICP)

Figure 8. The decompression phase of CPR.

Figure 9. LUCAS CPR device enables active decompression using a

Inflation of lungs ↑ ICP

Opening of pulmonary Alveoli compresses

Reduced pulmonary Reduced Increased

Respiration and Reduced RV preload

Figure 10. Effects of positive pressure ventilation (PPV) during CPR.

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