This document provides an overview of cardiogenic shock (CS) from an internal medicine perspective. It aims to provide a clinical "toolbox" for diagnosing, differentiating, and managing shock, with an emphasis on cardiovascular etiologies. Part I discusses the initial evaluation of a hypotensive patient in shock, including assessing cardiac rhythm and rate, conducting a physical exam, and raising blood pressure by administering fluids. Part II notes that further consideration is needed when treating CS, such as feeling free to drift off. The document discusses evaluating objective data, differentiating shock types, selecting appropriate pressors/inotropes, and controversies regarding first-line vasoactive agents.

1. Cardiogenic Shock (CS): an
Internal Medicine Perspective
Michael G. Katz, M.D.
Fellow in Cardiovascular Disease
University of Rochester
September 21, 2011

2. “What does it take to save a man who’s heart
has been COMPLETELY DESTROYED?”
2

3. Goal
To provide a clinical “toolbox”
to diagnosis, differentiate, and
manage shock with an
emphasis on cardiovascular
etiologies.
3

4. Part I – Initial Evaluation of the Patient in
Shock
•Pay close attention
Part II – Further Consideration When
Treating Cardiogenic Shock
•Feel free to drift off
4

5. Ventricle with ↓ systolic function
Ventricular Pressure
Ventricle with ↓
Stroke Compliance
Volume
End Diastolic Volume
5

6. Case
Friday night, 1:25am.
Call from Joel Moore:
“Hi, thanks for the call back. Is this the MICU Resident? This is Joel in
the trauma bay. Yeah, I have a 45 year old woman down here who
was found down. Don’t know how long. Anyway, she was unconscious
and intubated in the field. Looks like she’s hypotensive here. We
started her on 5 of dopamine. Could you come down and take a look at
her? No, noone is with her. No, the labs aren’t back yet. EKG? [rustle
of papers] the machine says there’s ST changes and inferolateral
ischemia should be considered. ”
20 mins later, you also find the CCU team evaluating the patient at the
bedside.
6

7. Elevator thoughts:
What is the cause of this patient’s hypotension?
• Cardiogenic
• Hypovolemic
• Septic
• Anaphylactic
• Neurogenic
Is this hypotensive patient in shock?
What objective physical exam and laboratory data do I need
to sort this out?
7

8. Hypotension becomes shock when there is
inadequate tissue perfusion:
• Systolic Blood pressure < 90mmHg, or
• 40mmHg drop in blood pressure from baseline, or
• MAP less than 60mmHg
The diagnosis of shock is easy to make.
Your task as the Internist is to identify the cause of
hypotension and correct it before death spiral of
tissue necrosis, multiorgan system failure, and
death ensues.
(Maybe it’s too late… and the spiral has started.)
8

9. Primary survey - At the beside for
hypotension:
1. Determine if cardiac rhythm and
rate are OK.
2. Conduct “Foot of the bed” exam.
3. Raise BP.
Always remembering: CO = HR x SV
9

10. 1. Determine if cardiac rhythm and rate are
OK.
Of course, some rhythms cannot support life.
Poor CO because:
• HR low (profound bradycardia), or
• SV low (rapid tachycardia and reduced diastolic filling time)
Profound bradycardia: Atropine 0.5 mg IV x 2  Dobutamine drip (world
will not end if given peripherally, fluids wide open)  TCP  call EP
Fellow for TVP (please ask ED staff or 7-16 for “Pacer Box”. It would be
helpful to prep and drape the right neck.
Unstable SVT/AF/Flutter/VT/VF – DCCV (consider IV midazolam if not
sedated).
10

11. 2. Conduct “Foot of the bed” exam.
This should take no more than 60 seconds:
• VS
• Mental status: “Hey, tell me you name. Do you know what hospital we’re
in.”
• Feel pulse (faster than finding a cuff)
• Radial = SBP 80, Femoral = SBP 60, Carotid/Supraclavicular = SBP of
30.
• JVP
• Listen for rales
• Place hand on toes/feet
• Skin temp and color
• Cap refill (normal less than 2 sec) – shout out to med-peds.
• Foley output helpful (shock < 20 cc/hr) but don’t delay exam for this
11

12. (An important digression - Why are we doing
this stuff?)
Historically, PAC is gold standard for hemodynamic monitoring and
differentiating etiologies for shock.
To differentiate types of shock and guide treatment most important
parameters are:
CO and PCWP
By exam:
• Rales, JVP, vascular fullness on CXR (if you have it) = “congestion” =
elevated PCWP
• Cool skin (not to be confused with clamminess) = low CO
12

13. Target State
Consider Sepsis vs. Consider “cardiogenic”
Hypovolemia • inotropes
• diuresis
(bleeding or over
diuresis)
• volume resuscitation
• if resistant, consider pressors
13

14. Final part of beside exam – Does pt need to be
intubated?
obtundation (ensure airway protection)
severe hypoxemia (cyanotic appearing)
inappropriately high pCO2 (do they “have that look” / appear tired?)
(Just do it. They were probably going to be intubated anyway.)
14

15. 3. Raise BP
GIVE FLUID! – Regardless of suspected shock type.
• Diagnostic AND therapeutic
• 250 cc boluses
• “wide open to gravity”  note that this is faster than “999.” Insist
on this.
• Noone ever drowned in a can of Coke
• If they do, they probably needed intubation anyway.
= 12 fl oz = 355 cc
15

16. Consider calcium chloride
• Will increase contractility and raise BP no matter the cause of
hypotension.
• 1amp = 10 mg: can be given in ¼ amps, ½ amps, or full amps based
on severity of hypotension.
• First line tx for hyperkalemia = should be given empirically with wide
complex bradycardia, especially if pt is unstable enough to merrit
MICU/CCU consult.
• Don’t be dissuaded by national shortage.
16

17. Secondary survey – Determine the etiology for
Shock
Make sure you have ordered or reviewed the following:
• EKG: evidence of MI or ischemia
• HCT: rule out hypovolvemic shock from GIB (caution: could be normal)
• ABG: hypoxia and acidosis will need to be corrected at some point
Good exam:
• VS
• JVP (CHF/volume depletion)
• Stridor/wheeze (anaphylaxis/CHF), crackles/effusion (CHF)
• Lateral PMI, gallop (CHF) New murmur (sepsis/CHF/endocarditis)
• HSM (CHF)
• Edema (CHF)
• Melena or hematochezia (GIB)
• Look for tampon if pt is obtunded (sepsis)
• Urticaria (anaphylaxis)
17

18. PAC based approach…
Type CO SVR CVP or Mixed
PAOP Venous
Cardiogenic
Hypovolemic
Distributive
18

19. Bedside approach
19

20. Conditions other than CHF p/w hypotension
and elevated JVP:
Tamponade
Massive PE
SVC syndrome
Tension PTX
20

21. Return to the case
HR 105, sinus tach
BP 80/60 on 5 of dopa
JVP 12 cm H2O
No rales
2+ pitting edema to knees, cool skin
WBC 10.2 HCT 40 Plts 250 SCr 2.1 AST 200 ALT 160 INR 1.3
TropT 0.13 CK 260 CKMB 14
pCXR demonstrates cardiomegally, right sided effusion
EKG: sinus tach, RBBB, diffuse NSSTchanges
Ben McClintic agrees to
ED sends pt for CTA, no evidence of PE bring pt to CCU for medicine
of the highest order
21

22. What about echo?
Not part of the algorithm for acute management.
Would it change management? Does it clarify diagnosis?
Clear evidence that septic shock results in profound (but reversible) depression in LV
function.
• Ann Intern Med 1984;100:483–490
• Crit Care Med 2009; 37:441–447
One study found a 60% incidence of global LV hypokinesis in septic patients
• Crit Care Med 2008; 36:1701–1706
On the flip side, there are plenty of people with low LVEF that aren’t in cardiogenic
shock.
Of course, things are different if your working diagnosis is acute valvular dysfunction or
mechanical complication of MI 22

23. 23

24. Decide etiology
Select appropriate pressor/inotrope
24

25. Receptors utilized by drugs
β Adrenergic Dopaminergic
α Adrenergic
β1
α Ionotropy (strength) Neurologic
Chronotropy (rate)
1
α2
β2
α1 Vasoconstriction
α2 Inhibits vasocontriction
Vasodilation Vasodilation

26. Blood Pressure
Phenylephrine
Time
Purely α1 adrenergic
∀↑ SVR and MAP
Heart Rate
• Can induce reflex
bradycardia Time
• Usually no change in CO
• Most often used for septic
Cardiac Output
shock
Time

27. Blood Pressure
Time
Norepinephrine
Stimulates α1 and β1 receptors
Heart Rate
• Results in ↑ SVR
• May ↑ HR (although ↑ afterload may
abrogate effect on CO)
Time
• Most often used for septic shock
Cardiac Output
Time

28. Heart Rate
Epinephrine
Stimulates β1 mostly, but also α1 and Time
β2
Cardiac Output
∀ ↑ Heart Rate
∀ ↑ CO
∀ ↑ SVR
∀ ↑SBP from α1 vasoconstriction in mesentary
and skin Time
∀ ↓DBP from β2 mediated vasodilation in
skeletal muscle
Blood presssure
• At high doses, α1 exceeds β2 effect,
therefore MAP increases
• Used for anaphylaxis, septic shock,
cardiogenic shock (severe)
Time

29. Heart Rate
Dopamine
Low doses: Dopaminergic receptor Time
agonist 
Cardiac Output
vasodilation of mesentery and renal
arterioles
Medium doses: Direct stimulation of
β1 receptors  Time
↑ HR, contractility and ultimately CO
High doses: Direct and indirect
Blood Pressure
stimulation of α1(NE release) 
vasoconstriction
Time

30. Heart Rate
Dobutamine
Mostly β1, minimal α1 and B2 Time
∀↑ Heart rate and Contractility
Cardiac Output
increase CO
∀↓ MAP
∀ ↑ Cardiac output  vasodilation
• At higher doses, β2 overcomes α1 Time
additional vasodilation
• Used in heart failure with an adequate
Blood pressure
or elevated MAP
Time

31. Milrinone
Heart Rate
Phosphodiesterase 3 inhibitor. Potentiates cAMP activity. In turn
activates cardiac calcium channels.
Time
Positive inotrope
• increased calcium influx from sarcoplasmic reticulum (SR) during
phase 2 of the cardiac action potential.
Cardiac Output
Lusitropic effect
• Inreased reflux of calcium into the SR following the plateau
phase increases relaxation speed
Vasodilatation
Time
• cAMP normally inhibits myosin light chain kinase, the enzyme
that is responsible for phosphorylating smooth muscle myosin
and causing contraction
Blood pressure
Again, Ideal agent for heart failure with an
adequate or elevated MAP.
Time

32. Controversy Warning: Vasoactive agent of
choice?
37

33. “When blood pressure is low, dopamine is the agent of first
choice. If the patient is markedly hypotensive, intravenous
norepinephrine, which is a more potent vasoconstrictor with less
potential for tachycardia, should be administered until systolic
arterial pressure rises to at least 80 mm Hg, at which time a
change to dopamine may be attempted, initiated at 2.5 to 5
mcg/kg/min and titrated as needed to 5 to 15 mcg/kg/min. Once
arterial pressure is brought to at least 90 mm Hg, intravenous
dobutamine may be given simultaneously in an attempt to reduce
the rate of the dopamine infusion.”
38

34. However…
Observational studies found that dopamine may be associated with rates of
death that are higher than those associated with the administration of
norepinephrine.
Sepsis Occurrence in Acutely Ill Patients (SOAP) study
• Observational trial of 1058 patients who were in shock, showed that
administration of dopamine was an independent risk factor for death in the
intensive care unit (ICU). Crit Care Med 2006;34:589-97
Overall, there was/is a dearth of RCT data regarding vasopressors for shock.
• In a meta-analysis, only three randomized studies, with a totalof just 62
patients, were identified that compared the effects of dopamine and
norepinephrine in patients with septic shock. Cochrane Database Syst Rev
2004;3:CD003709
39

35. • In this comparative-effectiveness trial, there was no significant
difference in the overall survival rate between patients with shock
who were treated with dopamine and those who were treated with
norepinephrine
• However, dopamine was associated with more cardiac
arrhythmias and with a higher mortality rate among patients with
cardiogenic shock
40

36. • RCT in 8 centers in Austria, Spain and Belgium.
• trial included 1679 patients, of whom 858 were assigned to dopamine
and 821 to norepinephrine for first line tx of shock.
• Intervention was dopamine or noradrenaline to 20ug/kg/min or
0.19ug/kg/min respectively, at which point additional inotropic /
vasopressor was allowed (cross over).
• Of note, requirement for “adequacy” of fluid resuscitation was minimal
• 500 -1000mls clear fluids in, no goal directed therapy)
• thus patients may well have been under filled when the intervention
began.
• study was powered to have an 80% chance of detecting a 15 %
mortality difference at 28 days – pretty good.
41

37. No significant difference 52 vs 48% OR 1.17 (0.97-1.42)
Kaplan-Meier Curves for 28-Day Survival in the Intention-to-Treat Population

38. Dopamine Norepi
43

39. 44

40. The Cardiology/CCU perspective
• LV pump failure is
usually primary
derangement
• BUT other parts of
circulatory system
contribute because of
inadequate
compensation or defects
• Many parts of the
cascade are completely
or partially reversible 
which may explain good
outcomes in CS
survivors.
45

41. Peripheral Vasculature, Neurohormones,
and Inflammation
• Ongoing ischemia triggers release of catecholamines, which constrict
peripheral arterioles to maintain perfusion of vital organs.
• Vasopressin and angiotensin II levels increase in the setting of MI and
shock
• improvement in coronary and peripheral perfusion at the cost of
increased afterload, which may further impair myocardial function
• salt and water retention; this may improve perfusion but exacerbates
pulmonary edema.
So, SVR goes up?
48

42. Not necessarily…
• In SHOCK trial: median SVR during CS in the normal range
despite vasopressor therapy.
• SVR may even be low!
• sepsis was suspected in 18% of the SHOCK trial cohort.
(Arch Intern Med 2005;165)
• 74% of whom developed positive bacterial cultures
• low SVR preceded the clinical diagnosis of infection and
culture positivity by days
49

43. Were those people in SHOCK
misdiagnosed with CS which was really
sepsis?
OR
Does CS beget SIRS, which facilitates
the development of sepsis?
50

44. SIRS is more common with increasing duration of shock (Int J Cardiol.
1999;72:3)
• SIRS results in impaired perfusion of the intestinal tract, which enables
transmigration of bacteria and sepsis
Cytokine levels (IL-6 and TNF-a) rise more dramatically over the 24 to 72
hours after MI (Eur Heart J. 2005;26:1964)
Other circulating factors (complement, procalcitonin, neopterin, C-
reactive protein, and others) have been reported to contribute to SIRS
in CS.
Despite a promising randomized phase 2 study, a trial of complement
(C5) inhibition in patients with MI found that pexelizumab did not reduce
the development of shock or mortality (Circulation. 2003;108:1184,
JAMA. 2007;297:43)
51

45. General Measures
• Aithrombotic therapy with aspirin and heparin.
• Clopidogrel
• may be deferred until after emergency angiography, because on the
basis of angiographic findings, coronary artery bypass grafting
(CABG) may be performed immediately.
• indicated in all patients who undergo PCI, and on the basis of
extrapolation of data from MI patients who were not in shock
• Negative inotropes and vasodilators (including nitroglycerin) should be
avoided.
• Arterial oxygenation and near-normal pH should be maintained to
minimize ischemia.
• Intensive insulin management with “tight” BG control. (Circulation.
2004;110:588–636)
52

46. Watch word = “optimization”
CO = HR X SV
CO = HR X (EDV – ESV)
HR Preload Distensibility Afterload Contractility
Lower transpulmomonary capillary pressures
Good filling pressures
Afterload reduction Coronary Flow
53

47. Hemodynamic Monitoring and Management
PA (Swan-Ganz) catheters can be helpful to
• confirm the diagnosis of CS
• ensure that filling pressures are adequate
• and to guide changes in therapy
There has been a decline in PA catheter use relating to controversy
sparked by a prospective observational study that suggested that PA
catheters were associated with poor outcome (JAMA. 1996;276:889).
No such association has been shown in
CS. (Am J Med. 2005;118:482)
54

48. CVP does not necessarily reflect PCWP (or LA
pressure by extension)
May be due to:
• Compliance
• Contractility
• Afterload
Sprung et al. Direct measurements and
derived calculations using the pulmonary
artery catheter. In: The pulmonary
artery catheter: methodology and clinical
applications. 1983:105-140.
55

49. Mechanical
Support
Revascularization
56

50. Mechanical Support – IABP
• Mainstay of mechanical therapy for CS. IABP
• Improves coronary and peripheral perfusion via diastolic balloon inflation
and augments LV performance via systolic balloon deflation with an acute
decrease in afterload.
• Not every patient has a hemodynamic response to IABP; response predicts
better outcome. (Circulation. 2003;108(suppl I):I-672)
• IABP support should be instituted as quickly as possible, even before any
transfer for revascularization if a skilled operator is available and insertion
can be performed quickly.
• In the large National Registry of Myocardial Infarction, IABP use was
independently associated with survival at centers with higher rates of IABP
use, whether PCI, fibrinolytic therapy, or no reperfusion had been used.
(Circulation. 2003;108:951–957). However, no RCT have been completed
to date.
57

51. Revascularization
58

52. Aimed to test the superiority of a strategy of early committed
revascularization (ERV) over that of initial medical stabilization (IMS)
1492 screened shock
pts
1190 pts placed in
SHOCK registry
To detect a 20%
mortality difference
between groups,
study sought to
enroll 328 pts
Ultimately 302 pts
enrolled
• 152 ERV
• 150 IMS
The primary end point of the study, 30-day all-cause mortality.
59

53. Inclusion and Exclusion
Cardiogenic shock: clinical criteria
• Systolic blood pressure <90 mm Hg for 30 minutes before
inotropes/vasopressors, or vasopressors or IABP are required to maintain
systolic blood pressure ≥90 mm Hg
• Evidence of decreased organ perfusion
• Heart rate ≥60 beats per minute (including paced rhythms)
Cardiogenic shock: hemodynamic criteria
• PCWP ≥15 mm Hg
• Cardiac index ≤2.2 L/min/m2
Only patients with CS arising from predominant left ventricular (LV) failure following MI
with ST elevation or new left bundle branch block were included. PAC not necessary if
AMI and congestion on CXR.
60

54. Exclusion criteria:
• ventricular septal rupture
• cardiac tamponade
• severe valvular disease
• isolated right ventricular CS
• known dilated cardiomyopathy
• shock from other causes (e.g., sepsis, hypovolemia)
• prior severe systemic illness
• refusal by the patient's physician, and failure to provide informed
consent
61

55. Findings of SHOCK and 1 year FU
Reperfusion
• 13% absolute increase in 1-year survival in patients assigned to early
Revascularization.
• NNT < 8 to save 1 life
62

56. Timing and success of PCI
• Increasing long-term mortality as time to revascularization increased from 0
to 8 hours
• However, there is a survival benefit as long as 48 hours after MI and 18
hours after shock onset
• 77% procedural success with percutaneous intervention in this setting is
consistent with that of earlier reports and lower than that reported with
primary angioplasty in the setting of all ST elevation MIs
• This is presumably due to a combination of diffuse multivessel disease,
large thrombus burden, and coronary hypoperfusion.
• No reflow phenomenon may occur more often in CS
• Successful percutaneous intervention in this setting is clearly associated
with a superior outcome and procedural failure is associated with increased
30-day mortality (38% vs.79%; p=0.003)
63

57. PCI or CABG?
• 37% of revascularization pts underwent CABG at a median of 2.7
hours after randomization.
• Despite a higher prevalence of triple-vessel or left main disease and
diabetes mellitus in patients who underwent CABG compared with PCI,
survival and quality of life were similar.
The rate of emergency CABG in CS is much lower in the community
(10%) (JAMA. 2005;294:448–454)
Only 15.2% of CABG got a LIMA.
64

58. Role of IABP
• overall utilization of IABP in IMS was 86%, considerably higher than
previous studies
• (Some speculate that IABP improves thrombolytic efficacy see NRMI
and TACTICS. TACTICS was terminated prematurely because of
insufficient patient recruitment, but the results suggest a 9% absolute
reduction of mortality at 6 months (p=0.23) with the combination of
thrombolysis and IABP.)
65

59. Subgroup analysis, risk stratification, and take
away points from SHOCK
Mortality from CS is high (~50%), but not as bad has historical figures of 80 to 90%
Important considerations:
• Age,
• peripheral hypoperfusion,
• anoxic brain damage,
• LVEF, and
• LV stroke work
Female sex does not appear to be an independent predictor of poor outcome.
Revascularization provides benefit at every level of risk. The initial misperception that
elderly patients do not benefit from PCI arose from the interaction between treatment
effect and age in the SHOCK trial. Lack of benefit for the elderly in the SHOCK trial was
likely due to imbalances in baseline ejection fraction between groups.
66

60. Health Care Policy and “Soft Rationing”
Most models, especially those derived from SHOCK demonstrate that
benefit is derived across the risk spectrum.
It may not be feasible (or ethical) to perform PCI or CABG when the
associated mortality rate is 80%.
ACC/AHA guidelines recommend (Circulation. 2004;110:588–636)
• early revascularization in CS for those 75 years of age (class I), and
• for suitable candidates 75 years of age (class IIa).
Real-world revascularization rates range from 27% to 54% (JAMA.
2005;294:448–454)
67

61. Why are real world numbers so low? Does
getting “dinged” matter? – YES.
In 2006, the New
York Department of
Health began to
exclude cases of
cardiogenic shock
from public reports
(367 cases 2004-
2006).
68

62. A group exists for whom additional treatment is futile:
• irreversible multiple end-organ failure , or
• anoxic brain damage has occurred
Revascularization approach must be individualized.
Most important consideration, especially for the elderly, is functional
status before the index event.
69

63. 70