Page 516 - Cardiac Nursing

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492 P A R T III / Assessment of Heart Disease
have pacemakers that use “minute ventilation” to guide the firing and PAOP, LVEDP, and the degree of pulmonary fluid and conges-
rate. In this case, the ICG signal interferes with the pacemaker tion. In the Medtronic Impedance Diagnostics in Heart Failure Pa-
signal and potentially cause a rapid increase in firing rate. 410 tients trial (MidHeFT), which evaluated intrathoracic impedance
ICG monitoring also has been performed in the emergency de- using the OptiVol device (Medtronic, Minneapolis, Minnesota) in
F
F
partment to describe cardiopulmonary and tissue perfusion patterns patients with NYHA Class III/IV HF, intrathoracic impedance de-
in survivors and nonsurvivors of trauma or septic shock, which may creased on average 15 days before the onset of symptoms, 419 and
aid in the earlier identification and treatment of patients with oc- results from the Fluid Accumulation Status Trial (FAST) suggest
cult hypoperfusion or cardiovascular impairment. 411–413 For exam- that decreasing impedance can predict health care use (e.g., hos-
ple, in acute trauma patients, CI by ICG and thermodilution pitalization for HF, modification of diuretic therapy). 421 A thresh-
2
agreed ( 0.07 0.47 L/min/m ) and noninvasive CI (along with old trigger of 60 is also a sensitive but not specific indicator of
other MAP and other oxygenation and perfusion indices) was clinical deterioration independent of clinical signs and symp-
higher in survivors versus nonsurvivors. 414 In addition, indices ob- toms. 422 However, the important clinical question that has not yet
tained with noninvasive monitoring of cardiac, pulmonary, and been answered is whether use of these devices improves the tailor-
perfusion indices (CI, SpO 2 , and transcutaneous O 2 /FiO 2 ) were ing of therapy, decreases hospitalizations, and improves quality of
predictors of morbidity and mortality. 414,415 life for these individuals.
Other factors that may decrease intrathoracic impedance in-
Implantable Hemodynamic Monitors clude pneumonia, pleural effusions, and revision of the pocket for
implantation of the device (must wait 34 days before beginning to
Although the hemodynamic profile of ADHF is often thought to re- use the device). An increase in intrathoracic impedance may also
flect low CO, preliminary analysis of data from 107,362 patients in occur with dehydration or decreased intravascular volume, pneu-
the Acute Decompensate Heart Failure Registry (ADHERE) suggest mothorax, and increased air trapping (e.g., chronic obstructive
that a typical hemodynamic profile is increased PAOP and vascular pulmonary disease or positive pressure ventilation).
resistance with a CO within normal range. Forty-six percent of
the patients had mild or no impairment in systolic function and Implantable Continuous Pressure
50% presented with an SBP 140 mm Hg. In these patients the Monitoring
primary cause of admission was volume overload. 416 In the Orga-
nized Program to Initiate Lifesaving Treatment in Hospitalized Pa- Research is ongoing using an IHM that provides a continuous es-
tients with Heart Failure (OPTIMIZE-HF) study, which had more timation of the PAEDP from a lead placed permanently in the RV
than 34,000 patients in the registry, 47% of the patients had pre- outflow track. 423 The Chronicle Offers Management to Patients
served LV function and 48% had an SBP 140 mm Hg, and in a with Advanced Signs and Symptoms of Heart Failure (COM-
study of 3,580 patients in the EuroHeart Failure Survey II (EHFS PASS-HF) study, which compared the effect of HF management
II), 34% of the patients had preserved systolic function (EF using standard therapy versus standard therapy plus IHM data,
45%). 417 In all these studies, less than 2% of patients presented with failed to find any difference in HF-related events, although the
an SBP 90 mm Hg or cardiogenic shock. IHM group had a significantly longer time to the first HF-related
Two subtypes of acute HF have been suggested: (1) acute de- hospitalization. 424 The HeartPod, which is a device that is im-
compensated cardiac failure, characterized by deterioration of car- planted into the left atrial septum and provides continuous mon-
diac performance over days to weeks leading to decompensation; itoring of left atrial pressures, is also under investigation. 425,426
and (2) acute vascular failure, characterized by acute hypertension Similar to continuous intrathoracic impedance monitoring, it re-
and increased vascular stiffness. 418 Dividing acute HF into these mains to be demonstrated if use of IHM technology improves
subtypes suggests the need for different types of monitoring and outcomes for individuals with HF. 427
therapies. Although use of a PA catheter in patients with HF was
not found to improve outcomes in patients who presented with
severe HF (average left ventricular ejection fraction 19%), 158 im- OXYGEN SUPPLY AND DEMAND
plantable hemodynamic monitors (IHMs) may allow for earlier de-
tection of hemodynamic deterioration (ADHF) before the onset In critically ill patients, the monitoring and evaluation of spe-
of symptoms and the initiation of preventative measures. 419,420 cific indicators of tissue hypoxia are warranted, because the stan-
These early preventive measures may be important as there are dard indices of hemodynamic stability (i.e., BP, HR, and urine
negative effects from hemodynamic congestion (e.g., increased LV output [UOP]) may be normal in the presence of continued
wall stress with increased myocardial remodeling and hypertrophy, tissue hypoxia (e.g., occult hypoperfusion or cryptic shock). For
increased angiotensin II release, subendocardial ischemia) that oc- example, 36 critically ill patients who despite being resuscitated
cur before the onset of signs and symptoms (clinical congestion— to a HR of 50 to 120 bpm and a MAP of 70 to 110 mm Hg con-
dyspnea, jugular vein distention, peripheral edema, pulmonary tinued to have signs of tissue hypoxia (lactate 2 mmol/L and a
crackles/rales). 159 central venous oxygen saturation [ ] 65%). Although in-
terventions were undertaken to improve tissue oxygenation for
Intrathoracic Impedance Monitoring these patients (as indicated by a decrease in lactate and an in-
crease in ), there were no changes in the BP or HR. 428
Intrathoracic impedance monitoring is based on a software that is Similar results were observed in patients with cardiogenic
integrated into a cardiovascular resynchronization therapy pace- shock 429 and trauma victims. 430 Use of standard endpoints (e.g.,
maker and/or implantable cardioverter–defibrillators. Intrathoracic MAP 60 mm Hg) may also be insufficient in ensuring ade-
impedance is measured between the RV lead and the device casing. quate tissue perfusion. For example, in patients with septic shock
There is an inverse relationship between intrathoracic impedance whose MAP was increased with norepinephrine from 65 to 85 mm