Transcript Cardiac Dysfunction - UBC Critical Care Medicine

Naisan Garraway
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45 yr old lady admitted for work up of chest
pain and SOB. ICU called as she is now on 80%
FiO2. When she is assessed she looks
comfortable, with RR of 26 but sats are 93%.
She has L and R chest pain that does not
radiate. She has not voided in 2 hours.
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Her past Hx is significant for primary pulmonary
hypertension (Mild), type 2 DM, ORIF of L femur
# 1 year ago, and smokes 1 PPD, 1-4 marijuana,
and crack (when she can afford it).
On exam, she is obese, diaphoretic, temp 38.5oC,
BP 90/40, HR 120. Chest has decreased A/E RLL,
heart sounds: normal S1 & S2 with grade 3
pansystolic murmur is heard along the lower left
sternal border. Jugular venous distention with a
prominent V wave. RUQ fullness but no
tenderness on abdo exam.
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Labs: WBC 15, Hb 100, plt 250, Na 141, K 5.1,
Creat 189, Trop I 5.1, lactate 5. Liver enzymes
are elevated. ABG: 7.34/25/69/17.
ECG shows sinus tachy, and CXR is clear
except possible RLL infiltrate and an enlarged
heart silhouette and loss of PA window.
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What is the differential dx?
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Respiratory
Cardiac
Sepsis
What is associated with an elevated
Troponin in the critically ill?
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As you bring her down to the Unit her sats
drop to 88% and her pressure drops to 80/40!
You intubate her (grade 2 airway) but her sats
are still 90% on FiO2 1.0 and her BP is 84/37.
Question 3. What physiological effect does
mechanical ventilation and PEEP have on the R
ventricle?
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in patients free of previous cardiorespiratory
disease, mechanical ventilation with a normal
Vt does not have any discernible hemodynamic
consequences
In the presence of a pulmonary or cardiac
disease PPV related adverse hemodynamic
effects may seriously complicate respiratory
support.
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On the one hand, tidal ventilation or PEEP
application changes in transpulmonary
pressure directly affect RV outflow impedance.
On the other hand, tidal ventilation or PEEP
increase in pleural pressure increases RV
effective elastance, a factor limiting diastolic
filling.
Jellinek H, Influence of positive airway
pressure on the pressure gradient for
venous return in humans. J Appl Physiol
88:926–932
During diastole, when
pleural pressure is
increased, a higher filling
pressure is necessary to
obtain an adequate end
diastolic volume.
Jardin F, et al; Chest 99:162–168
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Question 4. What imaging modalities are there
for the heart and what are their advantages and
disadvantages?
TTE
 TEE
 SPECT and Multigated (MUGA)
 MRI
 MDCT
 coronary angiography
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Real-time 3dimensional
echocardiography
(RT3DE)
hand-carried
ultrasound (HCU)
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Bedside echo show a very dilated R ventricle
and mod-severe TR. Her septum is D shaped
and PA pressures estimate to be 50 mmHg.
Her L ventricle has some decreased function
but is also empty. There is no wall motion
defects noted.
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Yes: it is possible
evidence suggests that despite the differences
between the ventricles in structure and
function, right ventricular dysfunction in septic
shock closely parallels left.
Ventricular function in both sepsis and septic
shock is characterized by ventricular dilation
and decreased L/RVEF. In septic shock
survivors, these changes resolve over 7 to 14
days.
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Multiple cytokines are potentially responsible
for the cardiac dysfunction, possibly through
NO and cGMP pathways.
TNFa
 IL-1b
 IL-2 and IL-6
 IFN-gamma
 Cytokine synergy also may play a major role in
septic myocardial depression
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Survival from septic shock is associated with
acute, reversible left ventricular dilation and
decrease in LVEF.
Nonsurvivors only undergo this process
inconsistently.
Reversible right ventricular dilation and
decrease in EF also are seen, but the prognostic
significance is uncertain
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RV and LV dysfunction in sepsis are not
thought to be caused by coronary
hypoperfusion
But….
RV more at risk of hypoperfusion than left
(coronary perfusion is 50% in systole vs only
20% on left side)
RV very dependent on systolic pressure.
Even worse in RCA disease
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1. Volume overload
2. Direct compression of the RV
pericardial effusion,
 pericardial fibrosis,
 tumor,
 massive pleural effusion
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3. Lower extremity edema due to
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extrinsic compression of venous or lymphatics, renal
failure, alterations in the renin-angiotensin system,
or drug therapy
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You try to float a PA catheter but are unable
even with fluoroscopy and anesthesia assisting
(true story). Your resident gets the central line
in and asks if you want to bolus the patient
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RV may have some compensatory reserve so
volume loading may improve RV output.
excessive volume loading may paradoxically
worsen RV contractile function through RV
dilation
impediment to LV filling through the
interventricular septum or through pericardial
restriction
 Leads to low CO and RV hypoperfusion
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Vasopressors and Inotropes.
Dobutamine
 Norepinephrine
 Milrinone
 Levosimendan (sensitizes myofilaments to calcium)
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Post hoc analysis showed that treatment with
levosimendan was associated with a greater
reduction in those hepatic markers of rightventr
Padley, J et al; Journal of Cardiac Failure, Volume 13, Issue 6, Pages S142-S142
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Minimize hypoxia/hypercarbia
Diuretics
Anticoagulants
Atrial Septostomy
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very high associated morbidity and mortality in
critically ill patients with severe right ventricular
failure
not be performed when mean right atrial pressures is
>20 mm Hg, significant hypoxemia, and a PVR index
>4400 dynes sec/cm 5/m2
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Treatment is started and there is some
improvement on echo of her R ventricular
function and PA pressures.
That night her Hb dropped to 80 and she was
transfused 2 U by the resident on call. She
dropped her sats 2 hours later and her CXR
looked like bilateral “white out”.
She does not progress well over the next few
days and it is apparent her L ventricular
function is worse now. Your resident suggests
contacting CV surgery about implanting an
“assist devise”.
Question 10. What are the different categories
and mechanisms of assist devises for the heart?
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Pulsatile?
Energy
source
Partial vs
Total
ECG?
Complicatio
ns
IntraAortic
Balloon
Pump
Pulsatile
External
Driveline
(Pneumatic)
-Partial
-left only
Yes
-Leg
-Augmented
ischemia (ad diastolic
10%)
-MAP
-infection
Impella
No, but heart External
can eject
driveline
Partial
-L : percut
-R or Bi:
open
Yes
-Leg Ischemia
Partial to
total
L, R or
BiVAD
Yes
-Infection
-Vej x rate =
-Emboli
CO
-Thrombosis
Type
Devices
VAD: 1st
-Thoratec
Generation -BVS 5000
-AB 5000
-Novacor
Pulsatile
-Pneumatic
-Pneumatic
-Pneumatic
-Mechanical
Monitoring
RPM α CO
-Infection
-misplacement
/electric
LVAD :
Axial flow
Pumps
-Heartmate II Non
External
Pulsatile, but Driveline
-Micromed
heart could
DeBakey
eject
Partial to
total
Yes
-Thrombosis RPM α CO
-Infection
-Thrombosis
of Ao Valve
ECMO
Heparin
coated
canulae and
oxygenators
Biomedicus
pump
(Centrifugal)
Partial to
total,
central or
peripheral
Yes
-leg
ischemia
(leg
perfusion)
RPM α CO
(until heart
unfilled)
-External
Total
No
-infection
- Bleeding
CO = Vej x
Rate
Non
Pulsatile,
Heart can
eject
Total
-CardioWest Pulsatile
Implantable -Abiocor
Heart
driveline
-transcutaneous
transmission
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Thoratec: Anticoag, intra or paracorporeal
Thoratec Heartmate: No anticoag, long
term
(Used at SPH)
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Novacor: anticoag, Big, long term
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BVS 5000: Good for transport, 10 days max
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AB5000: Anticoag, long term
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If cardiac arrest:
May be in asystole and have a pulse
 If have a pulse: no CPR
 If no pulse: CPR may generate a pulse
(and/or more problems…)
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Heartmate II
(Used at SPH)
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Micromed DeBakey
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If cardiac arrest:
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May have asystole and no pulse but have a normal
cardiac output
If monitor indicates adequate flow, give pressors for
desired mean art pressure (invasive measurment
only)
If asystole and no flow: CPR may generate flow
Make sure no flow before CPR (may cause damage)
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CardioWest
Used in Canada
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Abiocor
-14 cases worldwide: all dead
-Abiocor II in construction
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Asystole: Normal
Pulseless: use hand pump at bedside, if does
not work - find etiology fast
No CPR (useless, rigid plastic box)
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She finally responds to treatment enough to be
extubated and is sent to the ward. She will be
assessed by the transplant team while in
hospital.
Bonus question : What is the long-term
survival of heart lung transplant patients for
Pulmonary HTN and heart failure?