Hemorrhaging: Pulmonary hemorrhage (P-Hem) – TheTreatments

Home of Kyle J. Norton for The Better of Living & Living Health   Hemorrhaging is also known as bleeding or abnormal bleeding as a result of blood loss due to internal.external leaking from blood vessels or through the skin.

 I. Classifications of Hemorrhaging
According to the classification from the American College of Surgeons’ Advanced Trauma Life Support (ATLS), Hemorrhaging is divided into 4 classes, depending to the volumes of blood loss and other factors

Classification of hemorrhage

	Class
Parameter	I	II	III	IV
Blood loss (ml)	<750	750–1500	1500–2000	>2000
Blood loss (%)	<15%	15–30%	30–40%	>40%
Pulse rate (beats/min)	<100	>100	>120	>140
Blood pressure	Normal	Decreased	Decreased	Decreased
Respiratory rate (breaths/min)	14–20	20–30	30–40	>35
Urine output (ml/hour)	>30	20–30	5–15	Negligible
CNS symptoms	Normal	Anxious	Confused	Lethargic

Modified from Committee on Trauma. CNS = central nervous system(1a).

II.  Types of hemorrhaging E.4. Treatments 
Treatments depend on the diagnosis of each patient, if the underlined cause is due to medication, then medicine has to be stopped. 

1. Immediate treatment
According to the Intensive Care Nursery House Staff Manual immediate treatment of P-Hem should include tracheal suction, oxygen and positive pressure ventilation. To assist in decreasing P-Hem, mean airway pressure should be increased, either by a relatively high PEEP (i.e., 6 to 10 cmH2O) or by high frequency ventilation(15). In the infants, reserachers at suggested that current management of PH in VLBW infants includes ventilatory support using high positive end expiratory pressure, transfusion of blood and blood products to support the circulation and correct any hemostatic or coagulation defects and evaluation and treatment for patent ductus arteriousus (PDA). These strategies are often ineffective in preventing a poor outcome. rFVIIa is effective in controlling life-threatening hemorrhage in patients with hemophilia A and B with inhibitors, and innonhemophiliacs with a variety of inherited or acquired hemostatic defects including platelet disorders, liver disease and von Willebrand’s disease.(15a)

 2. Embolization – Interventional treatment of pulmonary arteriovenous malformations
Acording to the study of Dr. Andersen PE and Dr. Kjeldsen AD. at the Odense University Hospital ”Pulmonary arteriovenous malformations (PAVM) are congenital vascular communications in the lungs.  The generally accepted treatment strategy of first choice is embolization of the afferent arteries to the arteriovenous malformations. It is a minimally invasive procedure and at the same time a lungpreserving treatment with a very high technical success, high effectiveness and low morbidity and mortality. Embolization prevents cerebral stroke and abscess as well as pulmonary haemorrhage and further raises the functional level. Embolization is a well-established method of treating PAVM, with a significant effect on oxygenation of the blood. Screening for PAVM in patients at risk is recommended, especially in patients with HHT(16).

3. Corticosteroids 
There is a report of a patient suffered from acute glomerulonephritis with modest renal impairmentand life-threatening pulmonary hemorrhage. The pulmonary hemorrhage caused severe hypoxia thatnecessitated artificial ventilation. As a last resort, 1 g/day of methylprednisolone was administered intravenously. Rapid cessation of pulmonary hemorrhage ensued with clearing of the lungs fields. the suggestion of large doses of glucocorticosteroids should be administered to patients with life-threatening pulmonary hemorrhage before considering bilateral nephrectomy, especially if the renal function is still adequate. Bilateral nephrectomy is an irreversible approach and, as with massive doses of steroids, has yet to be proved to be a consistently effective mode of therapy(17).

Sources
(1a) http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1065003/table/T1/   
(15) http://www.ucsfbenioffchildrens.org/pdf/manuals/29_PulmHemorrhage.pdf
(15a) http://www.nature.com/jp/journal/v22/n8/full/7210787a.html
(16) http://www.ncbi.nlm.nih.gov/pubmed/21160695 
(17) http://annals.org/article.aspx?articleid=689575 

Positive End-Expiratory Pressure

1. Indications
   1. Pulmonary condition with widespread alveolar collapse
   2. Adult Respiratory Distress Syndrome (ARDS)
      1. PEEP increases lung compliance
      2. PEEP decreases intrapulmonary shunting
      3. Increases PO2 and allows lower FIO2 below 60%
      4. May increase dead space ventilation
         1. Overdistends normal lung
   3. Pulmonary Edema
      1. PEEP allows decrease in FIO2 below 60%
      2. PEEP may increase extravascular lung water
2. Disproved uses of PEEP
   1. Localized Lung Disease (e.g. lobar Pneumonia)
      1. PEEP may worsen Hypoxemia
         1. Overdistends normal lung
         2. Directs blood flow to diseased lung
      2. PEEP not recommended
         1. Unless selectively applied to diseased lung
   2. Prophylactic PEEP
      1. PEEP does not reduce ARDS Incidence
   3. Routine PEEP
      1. PEEP does not appear indiscriminately beneficial
   4. Mediastinal Bleeding
      1. PEEP does not protect against mediastinal bleeding
3. Physiology
   1. PEEP maintains small end-expiratory pressure
      1. Helps to prevent alveolar collapse
      2. Promotes alveolar-capillary gas exchange
   2. Increases lung function parameters
      1. Increases Functional Residual Capacity (FRC)
   3. Increases cardiac output with low airway pressures
      1. May result in increased Oxygen Delivery
4. Dosing
   1. Usual PEEP setting: 5 to 10 cm H2O
5. Complications
   1. Decreased cardiac output
      1. Associated with higher airway pressures
      2. Associated with decreased ventricular filling
   2. Barotrauma
   3. Fluid Retention
   4. Intracranial Hypertension
6. References
1. Marino (1991) ICU Book, Lea & Febiger, p. 375-9

sources from ：http://www.fpnotebook.com/lung/procedure/PstvEndExprtryPrsr.htm

Comparison of Inhaled Iloprost and Nitric Oxide in Patients With Pulmonary Hypertension During Weaning From Cardiopulmonary Bypass in Cardiac Surgery: A Prospective Randomized Trial

·       Michael Winterhalter, MD, Andre Simon, MD, Stefan Fischer, MD, MSc, Niels Rahe-Meyer, MD, Nicoletta Chamtzidou, Hartmut Hecker, PhD, Janusz Zuk, MD, Siegfried Piepenbrock, MD, PhD,, Martin Strüber, MD, PhD

Journal of Cardiothoracic and Vascular Anesthesia
Volume 22, Issue 3 , Pages 406-413, June 2008

Objective: 
The objective of this study was to compare the efficacy of inhaled iloprost and nitric oxide (iNO) in reducing pulmonary hypertension (PHT) during cardiac surgery immediately after weaning from cardiopulmonary bypass (CPB).
Design: 
A prospective randomized study.
Setting: 
A single-center university hospital.
Participants:
 Forty-six patients with PHT (mean pulmonary artery pressure (mPAP) ≥26 mmHg preoperatively at rest, after anesthesia induction, and at the end of CPB) scheduled to undergo cardiac surgery were enrolled.
Interventions: 
Patients were randomly allocated to receive iloprost (group A, n = 23) or iNO (group B, n = 23) during weaning from CPB.
Measurements and Main Results:
 Heart rate, mean arterial pressure, central venous pressure, pulmonary artery pressure (PAP), pulmonary capillary wedge pressure, and left atrial pressure were recorded continuously. Iloprost and iNO were administered immediately after the end of CPB before heparin reversal. Both substances caused significant reductions in mean PAP (mPAP) and pulmonary vascular resistance (PVR) and significant increases in cardiac output 30 minutes after administration (p < 0.0001). However, in a direct comparison, iloprost caused significantly greater reductions in PVR (p = 0.013) and mPAP (p = 0.0006) and a significantly greater increase in cardiac output (p = 0.002) compared with iNO.
Conclusions:
 PHT after weaning from CPB was significantly reduced by the selective pulmonary vasodilators iNO and iloprost. However, in a direct comparison of the 2 substances, iloprost was found to be significantly more effective.

A comparison of the acute hemodynamic effects of inhaled nitric oxide and aerosolized iloprost in primary pulmonary hypertension FREE

Marius M. Hoeper, MD; Horst Olschewski, MD; Hossein A. Ghofrani, MD; Heinrike Wilkens, MD; Joerg Winkler, MD; Mathias M. Borst, MD; Jost Niedermeyer, MD; Helmut Fabel, MD; Werner Seeger, MD

J Am Coll Cardiol. 2000;35(1):176-182. 

ABSTRACT

BACKGROUND

Inhalation of the stable prostacyclin analogue iloprost has recently been described as a novel therapeutic strategy for PPH and may offer an alternative to continuous intravenous infusion of prostacyclin or inhalation of NO.

METHODS

During right heart catheterization, 35 patients with PPH sequentially inhaled 40 ppm of NO and 14 to 17 μg of iloprost, and the effects on hemodynamics and blood gases were monitored.

RESULTS

Both NO and iloprost caused significant increases in cardiac output, mixed-venous oxygen saturation and stroke volume as well as significant decreases in pulmonary artery pressure and pulmonary vascular resistance, whereas only inhaled iloprost significantly increased the arterial Po₂ (p = 0.01). Compared with inhaled NO, aerosolized iloprost was more effective in reducing pulmonary artery pressure (−8.3 ± 7.5 mm Hg vs. −4.3 ± 8.8 mm Hg; p = 0.0001) and the pulmonary vascular resistance (−447 ± 340 dynes·s·cm⁻⁵ vs. −183 ± 305 dyne·s·cm⁻⁵; p < 0.0001). Furthermore, aerosolized iloprost caused a significantly greater increase of the cardiac output compared with NO (+0.7 ± 0.6 liter/min vs. +0.3 ± 0.4 liter/min; p = 0.0002) and had a more pronounced effect on the mixed-venous oxygen saturation (p = 0.003).

CONCLUSIONS

During acute drug testing, aerosolized iloprost was more potent than inhaled NO as a pulmonary vasodilator in PPH at the doses used in this study.

比較 iNO與噴霧吸入ILOPROST治療CABG術後肺高壓小孩的效果

Comparison of inhaled nitric oxide with aerosolized iloprost for treatment of pulmonary hypertension in children after cardiopulmonary bypass surgery

Loukanov T, Bucsenez D, Springer W, Sebening C, Rauch H, Roesch E, Karck M, Gorenflo M.

Clinical Research in Cardiology

July 2011, Volume 100, Issue 7, pp 595-602

Abstract

Objectives

Pilot study to compare the effect of inhaled nitric oxide (iNO) and aerosolized iloprost in preventing perioperative pulmonary hypertensive crises (PHTCs).

Background

Guidelines recommend the use of iNO to treat PHTCs, but treatment with iNO is not an ideal vasodilator. Aerosolized iloprost may be a possible alternative to iNO in this setting.

Methods

Investigator-initiated, open-label, randomized clinical trial in 15 infants (age range 77–257 days) with left-to-right shunt (11 out of 15 with additional trisomy 21), and pulmonary hypertension (i.e. mean pulmonary artery pressure [PAP] >25 mmHg) after weaning from cardiopulmonary bypass. Patients were randomized to treatment with iNO at 10 ppm or aerosolized iloprost at 0.5 µg/kg (every 2 h). The observation period was 72 h after weaning from cardiopulmonary bypass. The primary endpoint was the occurrence of PHTCs; the secondary endpoints were mean PAP, duration of mechanical ventilation, safety of administration, and in-hospital mortality.

Results

Seven patients received iNO and eight patients received iloprost. During the observation period, 13 of the 15 patients had at least one major or minor PHTC. There was no difference between the groups with regard to the frequency of PHTCs, mean PAP and duration of mechanical ventilation (p > 0.05).

Conclusions

In this pilot study, aerosolized iloprost had a favorable safety profile. Larger trials are needed to compare its efficacy to iNO for the treatment of perioperative pulmonary hypertension. However, neither treatment alone abolished the occurrence of PHTCs.

Base Excess 的臨床意義

ABG (Arterial Blood Gas)

http://www.brooksidepress.org/Products/OperationalMedicine/DATA/operationalmed/Lab/ABG_ArterialBloodGas.htm

pH is a measurement of the acidity of the blood, reflecting the number of hydrogen ions present. 

Lower numbers mean more acidity; higher number mean more alkalinity.

pH is Elevated (more alkaline, higher pH) with:

·        Hyperventilation

·        Anxiety, pain

·        Anemia

·        Shock

·        Some degrees of Pulmonary disease

·        Some degrees of Congestive heart failure

·        Myocardial infarction

·        Hypokalemia (decreased potassium)

·        Gastric suctioning or vomiting

·        Antacid administration

·        Aspirin intoxication

·        Lasix

·        Steroid

pH is Decreased (more acid, lower pH) with:

• Strenuous physical exercise
• Obesity
• Starvation
• Diarrhea
• Ventilatory failure
• More severe degrees of Pulmonary Disease
• More severe degrees of Congestive Heart Failure
• Pulmonary edema
• Cardiac arrest
• Renal failure
• Lactic acidosis
• Ketoacidosis in diabetes

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pCO2 (Partial Pressure of Carbon Dioxide) reflects the the amount of carbon dioxide gas dissolved in the blood. 

Indirectly, the pCO2 reflects the exchange of this gas through the lungs to the outside air. Two factors each have a significant impact on the pCO2. The first is how rapidly and deeply the individual is breathing:

• Someone who is hyperventilating will "blow off" more CO2, leading to lower pCO2 levels
• Someone who is holding their breath will retain CO2, leading to increased pCO2 levels

The second is the lungs capacity for freely exchanging CO2 across the alveolar membrane:

• With pulmonary edema, there is an extra layer of fluid in the alveoli that interferes with the lungs' ability to get rid of CO2. This leads to a rise in pCO2.
• With an acute asthmatic attack, even though the alveoli are functioning normally, there may be enough upper and middle airway obstruction to block alveolar ventilation, leading to CO2 retention.

Increased pCO2 is caused by:

• Pulmonary edema
• Obstructive lung disease

Decreased pCO2 is caused by:

• Hyperventilation
• Hypoxia
• Anxiety
• Pregnancy
• Pulmonary Embolism (This leads to hyperventilation, a more important consideration than the embolized/infarcted areas of the lung that do not function properly. In cases of massive pulmonary embolism, the infarcted or non-functioning areas of the lung assume greater significance and the pCO2 may increase.)

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PO2 (Partial Pressure of Oxygen) reflects the amount of oxygen gas dissolved in the blood. It primarily measures the effectiveness of the lungs in pulling oxygen into the blood stream from the atmosphere.

Elevated pO2 levels are associated with:

• Increased oxygen levels in the inhaled air
• Polycythemia

Decreased PO2 levels are associated with:

• Decreased oxygen levels in the inhaled air
• Anemia
• Heart decompensation
• Chronic obstructive pulmonary disease
• Restrictive pulmonary disease
• Hypoventilation

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CO2 Content is a measurement of all the CO2 in the blood. 

Most of this is in the form of bicarbonate (HCO3), controlled by the kidney. A small amount (5%) of the CO2 is dissolved in the blood, and in the form of soluble carbonic acid (H2CO3).

For this reason, changes in CO2 content generally reflect such metabolic issues as renal function and unusual losses (diarrhea). Respiratory disease can ultimately effect CO2 content, but only slightly and only if prolonged.

Elevated CO2 levels are seen in:

• Severe vomiting
• Use of mercurial diuretics
• COPD
• Aldosteronism

Decreased CO2 levels are seen in:

• Renal failure or dysfunction
• Severe diarrhea
• Starvation
• Diabetic Acidosis
• Chlorthiazide diuretic use

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Base Excess or Base Deficit

Whenever there is an accumulation of metabolically-produced acids, the body attempts to neutralize those acids to maintain a constant acid-base balance. 

This neutralizing is achieved by using up various "buffering" compounds in the blood stream, to bind the acids, disallowing them from contributing to more acidity.

About half of these buffering compounds come from HCO3, and the other half from plasma and red blood cell proteins and phosphates.

The words "base deficit" and "base excess" are equivalent and are generally used interchangeably. The only difference is that base deficit is expressed as a positive number and base excess is expressed as a negative number.

A "Base Deficit" of 10 means that 10 mEqu/L of buffer has been used up to neutralize metabolic acids (like lactic acid). Another way to say the same thing would be the "Base Excess is minus 10."

More Negative Values of Base Excess may Indicate:

• Lactic Acidosis
• Ketoacidosis
• Ingestion of acids
• Cardiopulmonary collapse
• Shock

More Positive Values of Base Excess may Indicate:

• Loss of buffer base
• Hemorrhage
• Diarrhea
• Ingestion of alkali
  
  
  Source from： http://en.wikipedia.org/wiki/Base_excess
  
  

  Comparison of the base excess with the reference range assists in determining whether an acid/base disturbance is caused by a respiratory, metabolic, or mixed metabolic/respiratory problem. While carbon dioxide defines the respiratory component of acid-base balance, base excess defines the metabolic component. Accordingly, measurement of base excess is defined under a standardized pressure of carbon dioxide, by titrating back to a standardized blood pH of 7.40.

  The predominant base contributing to base excess is bicarbonate. Thus, a deviation of serum bicarbonate from the reference range is ordinarily mirrored by a deviation in base excess. However, base excess is a more comprehensive measurement, encompassing all metabolic contributions.

  Definition

  Base excess is defined as the amount of strong acid that must be added to each liter of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO₂ of 40 mmHg (5.3 kPa).^[2] A base deficit (i.e., a negative base excess) can be correspondingly defined in terms of the amount of strong base that must be added.

  A further distinction can be made between actual and standard base excess: actual base excess is that present in the blood, while standard base excess is the value when thehemoglobin is at 5 g/dl. The latter gives a better view of the base excess of the entire extracellular fluid.^[3]

  The term and concept of base excess were first introduced by Poul Astrup and Ole Siggaard-Andersen in 1958.

  Estimation

  Base excess can be estimated from the serum bicarbonate concentration ([HCO₃^-]) and pH by the equation:^[4]

  

  with units of mEq/L. The same can be alternatively expressed as

  

  
  

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Oxygen Saturation (SO2) measures the percent of hemoglobin which is fully combined with oxygen. 

While this measurement can be obtained from an arterial or venous blood sample, it's major attractive feature is that it can be obtained non-invasively and continuously through the use of a "pulseoximeter."

Normally, oxygen saturation on room air is in excess of 95%. With deep or rapid breathing, this can be increased to 98-99%. While breathing oxygen-enriched air (40% - 100%), the oxygen saturation can be pushed to 100%.

Oxygen Saturation will fall if:

• Inspired oxygen levels are diminished, such as at increased altitudes.
• Upper or middle airway obstruction exists (such as during an acute asthmatic attack)
• Significant alveolar lung disease exists, interfering with the free flow of oxygen across the alveolar membrane.

Oxygen Saturation will rise if:

• Deep or rapid breathing occurs
• Inspired oxygen levels are increased, such as breathing from a 100% oxygen source

Protocolized versus non-protocolized weaning for reducing the duration of mechanical ventilation in critically ill adult patients (Review)

The Cochrane Library 2011, Issue 7

Blackwood B, Alderdice F, Burns KEA, Cardwell CR, Lavery G, O’Halloran P

Grand round reporter：林美妙

Date：101.12.5

Background

Reducingweaning time is desirable inminimizing potential complications frommechanical ventilation. Standardizedweaning protocols are purported to reduce time spent onmechanical ventilation.However, evidence supporting their use in clinical practice is inconsistent.

Objectives

To assess the effects of protocolized weaning from mechanical ventilation on the total duration of mechanical ventilation for critically ill adults; ascertain differences between protocolized and non-protocolized weaning in terms of mortality, adverse events, quality of life, weaning duration, intensive care unit (ICU) and hospital length of stay (LOS); and explore variation in outcomes by type of ICU, type of protocol and approach to delivering the protocol.

Search methods

We searched the Cochrane Central Register of Controlled Trials (The Cochrane Library Issue 1, 2010), MEDLINE (1950 to 2010),EMBASE (1988 to 2010), CINAHL (1937 to 2010), LILACS (1982 to 2010), ISI Web of Science and ISI Conference Proceedings (1970 to 2010), Cambridge Scientific Abstracts (inception to 2010) and reference lists of articles.We did not apply language restrictions.

Selection criteria

We included randomized and quasi-randomized controlled trials of protocolized weaning versus non-protocolized weaning from mechanical ventilation in critically ill adults.

Data collection and analysis

Three authors independently assessed trial quality and extracted data. A priori subgroup and sensitivity analyses were performed. We contacted study authors for additional information.

Main results

Eleven trials that included 1971 patients met the inclusion criteria. The total duration of mechanical ventilation geometric mean in the protocolized weaning group was on average reduced by 25% compared with the usual care group (N = 10 trials, 95% CI 9% to 39%, P = 0.006); weaning duration was reduced by 78% (N = 6 trials, 95% CI 31% to 93%, P = 0.009); and ICU LOS by 10% (N = 8 trials, 95% CI 2% to 19%, P = 0.02). There was significant heterogeneity among studies for total duration of mechanical ventilation (I2 = 76%, P < 0.01) and weaning duration (I2 = 97%, P < 0.01), which could not be explained by subgroup analyses based on type of unit or type of approach.

Authors’ conclusions

There is some evidence of a reduction in the duration of mechanical ventilation, weaning duration and ICU LOS with use of standardized protocols, but there is significant heterogeneity among studies and an insufficient number of studies to investigate the source of this heterogeneity. Although some study authors suggest that organizational context may influence outcomes, these factors were not considered in all included studies and therefore could not be evaluated.