Monday 30 April 2018

CORONARY ATHEROSCLEROSIS

Coronary Artery Disease is also known as Ischemic Heart Disease

Stages of Development of Coronary Artery Disease

  Arterial  Injury - Atherosclerosis

  Myocardial Ischemia – Angina Pectoris

  Myocardial Necrosis – Myocardial Infarction

CORONARY ATHEROSCLEROSIS

        Coronary Atherosclerosis is an abnormal accumulation of lipid or fatty substances and fibrous tissue in the vessel wall.

        These substances create blockages or narrow the vessel in a way that reduces blood flow to the myocardium.

        Atherosclerosis is a progressive and potentially life-threatening process

ATHEROSCLEROSIS

ARTERIOSCLEROSIS

- Narrowing of Artery

- Lipid or Fat Deposits (Plaques)

- Tunica Intima

- Hardening of Artery, Thicken

- Calcium And Protein Deposits

- Tunica Media

 PATHOPHYSIOLOGY

        Atherosclerosis begins as fatty streaks, lipids that are deposited in the intima of the arterial wall

        T lymphocytes and monocytes (that become macrophages) infiltrate the area to ingest the lipids and then die; this causes smooth muscle cells within the vessel to proliferate and form a fibrous cap over the dead fatty core.

        These deposits, called Atheromas or plaques, protrude into the lumen of the vessel, narrowing it and obstructing blood flow

        If the fibrous cap of the plaque is thick and the lipid pool remains relatively stable, it can resist the stress from blood flow and vessel movement.

        If the cap is thin, the lipid core may grow, causing it to rupture and hemorrhage into the plaque, allowing a thrombus to develop.

        The thrombus may obstruct blood flow, leading to sudden cardiac death or an acute myocardial infarction (MI), which is the death of heart tissue.

        Angles of the coronary arteries. The many angles and curves of the coronary arteries contribute to the vessels' susceptibility to atheromatous plaques.

RISK FACTORS

Non-modifiable

        Family history of CAD (first-degree relative with cardiovascular disease at 55 years of age or younger for men and at 65 years of age or younger for women)

        Increasing age (more than 45 years for men; more than 55 years for women)

        Gender (men develop CAD at an earlier age than women)

        Race – black (higher incidence in African Americans)

Modifiable Risk Factors

        Hyperlipidemia

        Cigarette smoking, tobacco use

        Hypertension

        Diabetes mellitus

        Metabolic syndrome

        Obesity

        Physical inactivity

CLINICAL MANIFESTATIONS

        Symptoms and Complications according to:

  Location and degree of narrowing of the arterial lumen

  Thrombus formation

  Obstruction of blood flow to the myocardium

        Clinical Manifestations are -

  May be asymptomatic( in those older, women, have diabetes , a history of heart failure)

  Acute onset of chest pain

  Typical symptoms: Dyspnea, Tachycardia, Palpitations, Diaphoresis

PREVENTION OF CORONARY ARTERY DISEASE

Four modifiable risk factors— Cholesterol Abnormalities, Tobacco Use, Hypertension, and Diabetes Mellitus have been cited as major risk factors for CAD and its complications. So the CAD is prevented by the controlling these factors.

CONTROLLING CHOLESTEROL ABNORMALITIES

        The desired goal is to maintain low LDL values and high HDL values.

        The desired level of LDL depends on the patient -

  Less than 160 mg/dL for patients with one or no risk factors

  Less than 130 mg/dL for patients with two or more risk factors

  Less than 100 mg/dL for patients with CAD or a CAD risk equivalent

        A fasting lipid profile should

  LDL cholesterol less than 100 mg/dL (less than 70 mg/dL for very high-risk patients)

  Total cholesterol less than 200 mg/dL

  HDL cholesterol greater than 60 mg/dL

  Triglyceride less than 150 mg/dL

        Serum cholesterol and LDL levels can be controlled by –

  Dietary Modification –- Balance intake of  Total calories and expenditure to maintain desirable weight

  Total fat  - 25%–35% of total calories

  Saturated fat - <7% of total calories

  Polyunsaturated fat- Up to 10% of total calories

  Monounsaturated fat - Up to 20% of total calories

  Carbohydrate- 50%–60% of total calories

  Protein Approximately - 15% of total calories

  Dietary fiber - 20–30 g/day

  Cholesterol - < 200 mg/day

  Physical Activity - The goal is a total of 30 minutes of moderate exercise (such as walking) daily. Physical activity and weight reduction increases HDL levels and reduces triglyceride levels, decreasing the incidence of coronary events and reducing overall mortality risk.

  Medication Therapy - If diet & Physical Activity  alone cannot normalize serum cholesterol levels, medications can have a synergistic effect with the prescribed diet and control cholesterol levels.

PROMOTING CESSATION OF TOBACCO USE

        Effects of smoking

  The inhalation of smoke increases the blood carbon monoxide level, causing hemoglobin to combine with CO than with O2.  A decreased amount of available oxygen may decrease the heart's ability to pump.

  The nicotinic acid in tobacco triggers the release of catecholamine's, which raise the heart rate and BP.

  Nicotinic acid can also cause the coronary arteries Vasoconstriction.

  Use of tobacco increases platelet adhesion, leading to a increase the probability of thrombus formation

        To Stop Smoking –

  Reduce the risk of CAD up to 30-50% within the 1st  year, and

  The risk continues to decline as long as they refrain from smoking.

MANAGING HYPERTENSION

        Hypertension – BP repeatedly exceed 140/90 mm Hg.

        Long-standing elevated BP may result in increased stiffness of the vessel walls, leading to vessel injury and a resulting inflammatory response within the intima.

        Hypertension can also increase the work of the left ventricle, which must pump harder to eject blood into the arteries. Over time, the increased workload causes the heart to enlarge and thicken (ie, hypertrophy), a condition that may eventually lead to cardiac failure.

CONTROLLING DIABETES MELLITUS

        For 65% to 75% of patients with diabetes, cardiovascular disease is listed as the cause of death.

        Hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered red blood cell function, which can lead to thrombus formation

TREATMENT

        PTCA - Percutaneous Transluminal Coronary Angioplasty

  Objectives of PTCA

  Revascularize myocardium

  To prevent angina

  Increase survival rate

        CABG - Coronary Arterial Bypass And Graft Surgery


Tuesday 24 April 2018

SETTINGS, MODES & ALARMS OF MECHANICAL VENTILATOR

Ventilator Settings

Ventilator settings are ordered by the physician and are individualized for each patient. Ventilators are designed to monitor many components of the patient’s respiratory status. Various alarms and parameters can be set to warn healthcare providers that the patient is having difficulty with the settings.

Respiratory Rate (RR)

The respiratory rate is the number of breaths the ventilator delivers to the patient each minute. The rate chosen depends on the tidal volume, the type of pulmonary pathology, and the patient’s target PaCO2. The respiratory rate parameters are set above and below this number and the alarm will then sound if the patient’s actual rate is outside of the desired range.

(The following are guidelines.) For patients with obstructive lung disease, the rate should be set at 6-8 breaths/minute to avoid the development of auto-PEEP and hyperventilation, or “blowing off CO2”. Patients with restrictive lung disease usually tolerate a range of 12-20 breaths/minute. Patients with normal pulmonary mechanics can tolerate a rate of 8-12 breaths/minute. The patient should be monitored on the initial rate setting and adjustments made as necessary.

Tidal Volume (VT)

The tidal volume is the volume of gas the ventilator delivers to the patient with each breath. The tidal volume parameters are set above and below the desired number, and the alarm will sound if the patient’s actual tidal volume is outside of the desired range. This is especially helpful if the patient is breathing spontaneously between ventilator-delivered breaths, since the patient’s own tidal volume can be compared with the tidal volume delivered by the ventilator.

The usual setting is 5-15 cc/kg, based on compliance, resistance, and type of pathology. Patients with normal lungs can tolerate a tidal volume of 12-15 cc/kg, whereas patients with restrictive lung disease may need a tidal volume of 5-8 cc/kg.

Fractional Inspired Oxygen (FiO2)

The fractional inspired oxygen is the amount of oxygen delivered to the patient. It can range from 21% (room air) to 100%. It’s recommended that the FiO2 be set at 1.0 (100%) upon the initiation of mechanical ventilation to allow the patient to get used to the ventilator without experiencing hypoxia. However, 100% oxygen should not be used continuously for long periods of time because of the risk of oxygen toxicity. Oxygen toxicity causes structural changes at the alveolar-capillary membrane, pulmonary edema, atelectasis, and decreased PaO2. Once the patient is stabilized, the FiO2 can be weaned down based on pulse oximetry and arterial blood gas values. The FiO2 should only be as high as is necessary to keep the PaO2 in the desired range.

Most ventilators have a temporary 100% oxygen setting that delivers 100% oxygen for only a few breaths. This should always be used prior to and after suctioning; during bronchoscopy, chest physiotherapy, or other stressful procedures; and during patient transport.

Inspiratory: Expiratory (I: E) Ratio

The I: E ratio is usually set at 1:2 or 1:1.5 to approximate the normal physiology of inspiration and expiration. Occasionally, a longer inspiratory than expiratory time is desired to allow more time to oxygenate the patient’s lungs. This is called inverse ratio ventilation, and will be discussed later.

Pressure Limit

The pressure limit regulates the amount of pressure the volume-cycled ventilator can generate to deliver the preset tidal volume. Because high pressures can cause lung injury, it’s recommended that the plateau pressure not exceed 35 cm H2O. If this limit is reached, the ventilator stops delivering the breath and alarms. This may be an indication that the patient’s airway is obstructed with mucus, in which case, the high pressure is usually resolved with suctioning. It can also be caused by the patient coughing, biting on the ETT, breathing against the ventilator, or by a kink in the ventilator tubing.

Flow rate

The flow rate is the speed with which the tidal volume is delivered. The usual setting is 40-100 liters per minute.

Sensitivity/Trigger

The sensitivity determines the amount of effort required by the patient to initiate inspiration. It can be set to be triggered by pressure or flow. Flow triggering is a better setting for patients who can breathe spontaneously because it reduces the work of breathing.

Sigh

The ventilator can be programmed to deliver an occasional sigh with a larger tidal volume. The use of frequent sighs was popular during the 1970s because it was thought that it prevented collapse of the alveoli (atelectasis), which can result from the patient constantly inspiring the same volume of gas. However, recently there has been concern that the increased pressure produced in the alveoli may heighten the risk of the alveoli rupturing and causing pneumothorax.

Ventilator Settings summary that nurses deal with the most

S.No.

SETTING

FUNCTION

USUAL PARAMETERS

  1.  

Respiratory Rate (RR)

Number of breaths delivered by the ventilator per minute

Usually 4-20 breaths per minute

  1.  

Tidal Volume (VT)

Volume of gas delivered during each ventilator breath

Usually 5-15 cc/kg

  1.  

Fractional Inspired Oxygen (FiO2)

Amount of oxygen delivered by ventilator to patient

21% to 100%; usually set to keep

PaO2 > 60 mmHg or SaO2 > 90%

  1.  

Inspiratory:Expiratory (I:E) Ratio

Length of inspiration compared to length of expiration

Usually 1:2 or 1:1.5 unless inverse ratio ventilation is required

  1.  

Pressure Limit

Maximum amount of pressure the ventilator can use to deliver breath

10-20 cm H2O above peak inspiratory pressure; maximum is 35 cm H2O

Modes of mechanical ventilation

Modes of mechanical ventilation are described by the relationships between the various types of breaths and by the variables that can occur during the inspiratory phase of ventilation. Each mode of ventilation is distinguished by how it initiates a breath (trigger), how it sustains a breath (limit), and how it terminates a breath (cycle); these are referred to as phase variables.

The best mode of mechanical ventilation is the one that provides maximum therapeutic benefit with the fewest side effects. Mode selection and individual ventilator settings are geared towards the patient’s diagnosis and history as well as integrated data from laboratory, radiology and physical examination.

Basic modes of ventilation

1.      Continuous Mandatory Ventilation (CMV)

2.      Assist Control (A/C) Ventilation

3.      Intermittent Mandatory Ventilation (IMV)

4.      Positive End Expiratory Pressure (PEEP)

5.      Continuous Positive Airway Pressure (CPAP)

Continuous Mandatory Ventilation (CMV)

·        CMV completely controls the patient’s ventilation. The ventilator provides a mechanical breath on a preset timing. Patient respiratory efforts are ignored.

·        This is generally uncomfortable for children and adults who are conscious and is usually only used in an unconscious patient.

·        In this mode the ventilator delivers a mechanical breath with pre-set volumes at a pre-set rate and a pre-set flow rate.

·        The patient CANNOT generate spontaneous breaths, volumes, or flow rates in this mode.

Fig: Diagram shows display of volume, flow and pressure waveforms as seen in the CMV mode. The shaded areas marked with “E” represent the expiratory phase.

Disadvantage

The major disadvantage of CMV is that it is not synchronized with the efforts of the patient. When the patient is “out of sync” with the ventilator, he attempts to exhale as the ventilator is in the inspiratory phase. As a result, airway pressure builds to abnormally high levels and the remainder of the inspiratory volume is not delivered. This “bucking” causes a high-pressure alarm. Signs and symptoms of ventilator dys-synchrony include:

         Agitation

         Diaphoresis

         Tachycardia

         Tachypnea

         Paradoxical thoraco-abdominal breathing pattern

         Increased PIP (peak inspiratory pressure)

Assist Control (A/C) Ventilation

·        The A/C mode is similar to CMV, but it allows the patient to trigger an assisted breath at any time.

·        A/C delivers the pre-set volumes at a pre-set rate and a pre-set flow rate in response to the patient’s own inspiratory effort, but will initiate the breath if the patient does not do so within the set amount of time.

·        The patient CANNOT generate spontaneous volumes, or flow rates in this mode. All delivered breaths, whether mandatory or patient-triggered, will be delivered by the ventilator according to the set parameters. i.e. All breaths in the assist-control mode receive the same FiO2 and tidal volume.

·        Hyperventilation and respiratory alkalosis may result from occurrences that increase the patient’s spontaneous rate such as anxiety or neurological factors. A high sensitivity setting that causes the machine to cycle too frequently can also cause this problem. An increased risk of air trapping with high respiratory rates may also potentially occur with the A/C ventilation.

·        The A/C rate is the minimum number of full ventilator breaths the patient will receive. The actual respiratory rate is equal to the A/C rate plus any patient-triggered breaths per minute.

·        This mode is used for patients who can initiate a breath but who have weakened respiratory muscles.

Intermittent Mandatory Ventilation (IMV) & Synchronous IMV (SIMV)

IMV

·        IMV is the most commonly used modes of ventilation.

·        In this mode the ventilator delivers a preset rate, tidal volume (or inspiratory pressure) and FiO2.

·        The patient may also draw spontaneous breaths in-between mandatory breaths. Unlike A/C, breaths that the patient takes spontaneously do not trigger or cycle the ventilator.

·        Patient-initiated breaths are completely spontaneous, neither assisted nor supported by the ventilator.

SIMV

·        SIMV was developed as a result of the problem of high respiratory rates associated with A/C.

·        SIMV delivers the preset volume or pressure and rate while allowing the patient to breathe spontaneously in between ventilator breaths. Each ventilator breath is delivered in synchrony with the patient’s breaths, yet the patient is allowed to completely control the spontaneous breaths.

·        SIMV allows the patient to generate spontaneous breaths, volumes, and flow rates between the set breaths.

·        SIMV is used as a primary mode of ventilation, as well as a weaning mode. During weaning, the preset rate is gradually reduced, allowing the patient to slowly regain breathing on his or her own.

Advantages

·        Maintains respiratory muscle strength by avoiding muscle atrophy

·        Decreases mean airway pressure

·        Facilitates ventilator discontinuation – “weaning”

·        Decreased chance of hyperventilation,

·        Decreased atrophy of accessory muscles, and

·        Improved distribution of gas throughout the lungs by the action of the diaphragm.

Disadvantages

·        This mode may increase the work of breathing and respiratory muscle fatigue.

·        In IMV mode the mechanical rate and spontaneous rate may asynchronous causing “stacking” and that may cause barotrauma or volutrauma

Spontaneous Modes OR Customized Adjuncts to Ventilator Modes

PEEP (Positive End Expiratory Pressure)

·        According to its purest definition, the term PEEP is defined as positive pressure at the end of exhalation during either spontaneous breathing or mechanical ventilation. However, use of the term commonly implies that the patient is also receiving mandatory breaths from a ventilator.

·        One method of improving the patient’s oxygenation without increasing the FiO2 is the use of PEEP. Basically, PEEP does not allow airway pressure to return to zero at the end of expiration.

·        PEEP is not a mode of ventilation in itself. It is an adjunctive therapy added to other modes. It is intended to improve oxygenation, not to provide ventilation, which is the movement of air into the lungs followed by exhalation

·        PEEP is added to increase functional residual capacity (FRC) and allow for a decrease in the FiO2. PEEP helps to prevent small airway and alveolar collapse, improves alveolar ventilation and may decrease the work of breathing (at low levels). PEEP facilitates oxygen diffusion at lower FiO2 levels, which is safer for the patient.

·        PEEP of 5cm H2O pressure is referred to as “physiologic” PEEP because it is equivalent to the effect of the closed glottis. Therapeutic PEEP usually ranges from 10-30cm H2O in adults.

·        PEEP is an effective therapy for disease processes involving atelectasis; it is a cornerstone of therapy for ARDS.

Disadvantage

·        Decreased cardiac output with or without hypotension occurs because PEEP increases intra-thoracic pressure, which in turn decreases the venous return to the heart (preload).

·        Potential volutrauma and barotrauma,

·        Increased intracranial pressure and

·        Potential loss of tidal volume

Continuous Positive Airway Pressure (CPAP)

·        CPAP is similar to PEEP except that it works only for patients who are breathing spontaneously.

·        CPAP is PEEP with no set rate on the ventilator. CPAP is primarily used as a mode of non-invasive mechanical ventilation. It is occasionally used in the final stages of ventilator weaning, but has minimal application for the mechanically ventilated patient.

·        Patients on CPAP do not receive positive pressure breaths from the ventilator. All breaths are initiated and ended by the patient; tidal volumes and pressures are variable from breath to breath.

·        CPAP can also be administered using a mask and CPAP machine for patients who do not require mechanical ventilation, but who need respiratory support; for example, patients with sleep apnea.

·        CPAP aids in promotion of oxygenation in the same way PEEP does. It has no influence on ventilation.

Advantage

·        Ventilator can monitor the patient’s breathing and activate an alarm if something undesirable occurs

·        Helpful for improving oxygenation in patients with refractory hypoxemia and a low FRC

·        CPAP setting is adjusted to provide the best oxygenation with the lowest positive pressure and the lowest FiO2

S.No.

MODE

FUNCTION

CLINICAL USE

1.       

Control Ventilation (CV)

Delivers preset volume or pressure regardless of patient’s own inspiratory efforts

Usually used for patients who are apneic

2.       

Assist-Control Ventilation (A/C)

Delivers breath in response to patient effort and if patient fails to do so within preset amount of time

Usually used for spontaneously breathing patients with weakened respiratory muscles

3.       

Synchronous Intermittent Mandatory

Ventilation (SIMV)

Ventilator breaths are synchronized with patient’s respiratory effort

Usually used to wean patients from mechanical ventilation

4.       

Pressure Support Ventilation (PSV)

Preset pressure that augments the patient’s inspiratory effort and decreases the work of breathing

Often used with SIMV during weaning

5.       

Positive End Expiratory Pressure

(PEEP)

Positive pressure applied at the end of expiration

Used with CV, A/C, and SIMV to improve oxygenation by opening collapsed alveoli

6.       

Constant Positive Airway Pressure

(CPAP)

Similar to PEEP but used only with spontaneously breathing patients

Maintains constant positive pressure in airways so resistance is decreased

7.       

Independent Lung Ventilation (ILV)

Ventilates each lung separately; requires two ventilators and sedation/paralysis

Used for patients with unilateral lung disease or different disease process in each lung

8.       

High Frequency Ventilation (HFV)

Delivers small amounts of gas at a rapid rate (60-100 breaths/minute); requires sedation/paralysis

Used for hemodynamic instability, during short-term procedures, or if patient is at risk for pneumothorax

9.       

Positive End Expiratory Pressure

(PEEP)

Positive pressure applied at the end of expiration

Used with CV, A/C, and SIMV to improve oxygenation by opening collapsed alveoli

Alarms and Common Causes

As mentioned earlier, the ventilator is designed to monitor many aspects of the patient’s respiratory status, and there are many different alarms that can be set to warn healthcare providers that the patient isn’t tolerating the mode or settings. The following are common ventilator alarms and their most frequent causes.

High Pressure Limit

Low Pressure

High Respiratory Rate

Low Exhaled Volume

·         Secretions in ETT/airway or condensation in tubing

·         Kink in ventilator tubing

·         Patient biting on ETT

·         Patient coughing, gagging, or trying to talk

·         Increased airway pressure from bronchospasm or pneumothorax

·         Vent tubing not connected

·         Displaced ETT or tracheostomy tube

·         Patient anxiety or pain

·         Secretions in ETT/airway

·         Hypoxia

·         Hypercapnia

·         Vent tubing not connected

·         Leak in cuff or inadequate cuff seal

·         Occurrence of another alarm preventing full delivery of breath

 

 

BIBLIOGRAPHY

Books

1.       Brunner LS, Suddarth DS, Smeltzer SCO. Brunner & Suddarth’s textbook of medical-surgical nursing. Philadelphia: Lippincott Williams & Wilkins; 2008. Page No. 739-754

2.       Nettina SM, Lippincott Williams & Wilkins. Lippincott manual of nursing practice. Philadelphia: Wolters Kluwer Health : Lippincott Williams & Wilkins; 2010. Page No. 255-267

3.       Longo DL, Harrison T. Harrison’s principles of internal medicine. New York, N.Y., [etc.]: McGraw-Hill Medical; 2012. Page No-

4.       Colledge NR, Walker BR, Ralston S, Davidson S. Davidson’s principles and practice of medicine. Edinburgh; New York: Churchill Livingstone/Elsevier; 2010. Page No. 194-198

Web page

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