Transcript EKG Basics - Hastaneciyiz's Blog

Shock
Outline
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Definition of Shock
Signs and Symptoms of Shock
Categorization of Shock
The PA Catheter
Replacement Fluids
Vasopressors and Inotropes
Example Cases
What is Shock?
Shock is a physiologic state characterized
by a systemic impairment in oxygen delivery
as a result of reduced tissue perfusion,
almost universally mediated by low blood
pressure.
What is Shock?
The general physiologic mechanisms of how
shock leads to irreversible cell damage and
death include:
– Cell membrane ion pump dysfunction
– Intracellular edema
– Leakage of intracellular contents into the
extracellular space
– Inadequate regulation of intracellular pH
Signs/Symptoms of Shock
Cardiovascular – Hypotension
Nervous – Agitation  Delirium  Coma
Pulmonary – Tachypnea; hypoxia
Epidermal – Cool, clammy skin; peripheral
cyanosis
Kidneys – Oliguria; increased BUN/Cr ratio
GI – Ileus, hemorrhage; hepatic
dysfunction
Hematologic – Coagulopathy  DIC
Diffuse Cellular Injury – Lactic acidosis
Physiologic Description of Shock
Pressure Gradient = Flow x Resistance
(i.e. Ohm’s Law  V=IR)
Perfusion Pressure = MAP – CVP
Perfusion Pressure = CO x SVR
Perfusion Pressure = HR x SV x SVR
SV is dependent upon preload, afterload,
and myocardial contractility
Categories of Shock
Hypovolemic
Decreased Preload (from an
extracardiopulmonary process)
Distributive
Decreased SVR
Cardiogenic
Decreased Contractility
Obstructive
Decreased Preload (from an
intracardiopulmonary process)
Etiologies of Shock
Hypovolemic
– Loss of blood volume
– Loss of plasma volume
Distributive
–
–
–
–
SIRS / Sepsis
Anaphylaxis
Myxedema Coma
Neurogenic Shock
Cardiogenic
– MI
– Heart failure
– Myocarditis
– Arrhythmias
– Paplillary muscle rupture
– Acute AI
Obstructive
– Massive PE
– Tension pneumothorax
– Cardiac tamponade
The Pulmonary Artery (PA) Catheter
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The PA Catheter
The PA catheter allows measurement of 3 types of data:
1. Central venous, pulmonary artery, and pulmonary
capillary occlusion (or “wedge”) pressures
2. Cardiac output and vascular resistence
3. Sampling of mixed venous blood
Situations in which PA catheters are most helpful:
1. Guiding the management of severe CHF
2. Estimating fluid status in non-cardiogenic pulmonary
edema
3. Diagnosing pulmonary hypertension
4. Diagnosing right heart infarction
The PA Catheter
As the catheter is “floated” from either the
internal jugular or subclavian veins, and
advanced from the RA to the RV, and from
the RV to the PA, a number of specific
pressure waveforms should be observed.
The PA Catheter
Right Atrium
The PA Catheter
Right Ventricle
The PA Catheter
Pulmonary Artery
The PA Catheter
Pulmonary Capillary Wedge Pressure (PCWP)
Replacement Fluids
IV replacement fluids can be divided into two
categories based on whether they do or do
not have a tendency to stay intravascular:
Crystalloid – Normal saline, lactated Ringer’s,
D5W
Colloid – Fresh frozen plasma, albumin
Replacement Fluids
Although there are theoretical reasons to
favor colloids over crystalloids for volume
resuscitation in patients with shock, no
data to date has shown any significant
outcome difference.
Therefore, crystalloid is almost always the
preferred choice, given its decreased cost
and decreased risk.
Vasopressors and Inotropes
Vasopressors – Act to increase SVR, and
subsequently increase BP.
Inotropes – Act to increase CO. BP may
either be increased or decreased.
Together, vasopressors and inotropes are colloquially
known as “pressors”.
Vasopressors and Inotropes
A given drug may have an effect on multiple
receptors, and which receptors it interacts with
may be dose dependent.
Hypovolemia must be corrected prior to the
institution of vasopressor therapy. Therefore,
pressors are generally not helpful in
hypovolemic shock.
A given agent may affect systemic blood
pressure through both direct actions, as well as
indirect reflex actions.
Vasopressors and Inotropes
Drug
Alpha1
Beta-1
Beta-2
Dopa.
Effect on SVR
Effect on
HR
Effect on
contractility
Typical Dose
+++
0
0
0
↑↑
↔/↑
↔
20-200 μg/min
0
0
0
0
↑↑
↔
↔
0.01-0.04 U/min
Norepinephrine
+++
++
0
0
↑↑
↑
↑
0.5-20 μg/min
Epinephrine
+++
+++
++
0
↓ (low dose)
↔ / ↑ (high dose)
↑
↑
2-10 μg/min
Dopamine 0.5 – 2
5 – 10
10 – 20
(μg/kg/min)
0
+
++
+
++
++
0
0
0
++
++
++
↔
↑
↑↑
↑
↑
↔
↑
↑
↔
1-20 μg/kg/min
Dobutamine
0/+
+++
++
0
↓
↑
↔/↑
2.5-20 μg/kg/min
Isoproternol
0
+++
+++
0
↓
↑
1-10 μg/min
Milrinone (acts as
a phosphodiesterase inhibitor)
0
0
0
0
↓
Phenylephrine
Vasopressin
(mechanism of
action poorly
understood)
↑
↔
↑↑
Load: 50 μg/kg
over 10 min
Maintenance:
0.375 – 0.75
μg/kg/min
Vasopressors and Inotropes
(Generalized Summary)
Phenylepherine
Norepinepherine
Epinepherine
Dopamine
Dobutamine
Milrinone
↑ SVR
No effect on contractility
↓ SVR
↑ Contractility
Case 1
A 35 year old construction worker is brought
in to the ER following a 20-30 foot fall off a
ladder. His past medical history is unknown.
On exam, his vitals are: HR=120, BP=82/45,
and RR=8. He is on a backboard and in a
cervical collar. He withdraws from painful
stimuli, but is otherwise non-responsive.
Upon a quick superficial examination, he
has an obvious fracture of his right femur
and numerous mild lacerations.
Case 2
A 68 year old woman is brought to the ER by
ambulance after developing severe shortness of
breath 30 minutes ago. Although her symptoms
were initially only respiratory in nature, upon
arriving in the ER she is now complaining of
lightheadedness and nausea. Vitals are as
follows: HR=95, BP=84/36, RR=32, O2 sat=89%
on 2L, temperature=36.5. Exam is otherwise
significant for loud bilateral crackles, an S3. She is
mildly agitated, but otherwise has a grossly intact
neurologic exam.
Case 3
A 76 year old nursing home patient is
brought to the ER by ambulance after
becoming progressively incoherent over the
preceding 24 hours. His past medical
history is unavailable. On exam, his vitals
are: HR=127, BP=78/45, RR=24, O2 sat=
97% on RA, temp=34.7. He is acutely illappearing, cachectic, and non-responsive.
His neurologic exam is non-focal. Aside
from the vital sign abnormalities, his cardiac
and respiratory exams are unremarkable.
Case 4
As the on-call intern, you are called on a cross-cover patient on
another service for low blood pressure and shortness of breath.
All you initially know about the patient is that they are a 64 year
old man who was admitted for an uncomplicated NSTEMI 4
days ago, who was supposed to be discharged to home
tomorrow. The patient had been feeling fine all day until 10
minutes ago when he very acutely developed shortness of
breath. He is now complaining of lightheadedness and is
developing a visibly waning level of consciousness.
Vitals now:
HR=130, BP 82/64, RR=28, O2 sat=94% on 2L.
Vitals 5hrs ago: HR=84, BP 134/70, RR=20, O2 sat=99% on 2L.
Case 5
You are on-call in the ICU, and are paged in the middle of the
night regarding a patient 3 days post-op from a CABG that had
been complicated by a intraoperative cardiac arrest from
ventricular fibrillation. He continues to be on pressors and is
intubated, due to concerns regarding hemodynamic instability
in the immediate post-op period, which continues to be
incompletely explained. His nurse has noted that his blood
pressure has been trending downward over the past 6 hours,
requiring progressively higher doses of dopamine to maintain
mean arterial pressures (MAP) of 60mmHg. His exam is
notable for a 2/6 systolic murmur over the right upper sternal
border, and coarse crackles at the left lung base. As you have
never examined him before, you have no idea if these findings
are old or new. His CXR from the previous morning was
notable only for mild pulmonary edema, that you remember the
team did not seem particularly worried about.
Case 5
(continued)
Time
HR
MAP
CO
SVR
Dopa
Dobut
Epi
(L/min) (dynes/sec (μg/kg/min) (μg/kg/ (μg/min)
/cm5)
min)
12pm
90
72
3.5
1460
5
4
2
8pm
105
68
3.8
1260
5
4
2
10pm
113
64
4.2
1100
6
4
2
12am
118
58
4,9
865
8
4
2
2am
123
56
6.1
670
12
4
2