SHOCK Goal:

➔ Inadequate delivery of oxygen and nutrients to ● To maintain perfusion in the heart and brain
maintain normal tissue and cellular functions (which needs to be perfused in the event of
hypoperfusion, other organs are compromised
HISTORICAL BACKGROUND because the circulation is directed to these
Alfred Blalock (1934) – 4 Categories of Shock organs)
1. Hypovolemic
2. Vasogenic
3. Cardiogenic
4. Neurogenic

Recent Studies – 6 Categories of Shock

1. Hypovolemic
2. Vasogenic
3. Cardiogenic
4. Neurogenic
5. Obstructive shock
6. Traumatic shock

CONCEPTS IN THE MAINTENANCE OF TISSUE

PERFUSION
1. Cardiac Output
➔ Depends on the ability of the heart to
pump.
2. Circulatory Volume Problem in circulation will cause problem in local
➔ Amount of blood present in the microvascular parts of the body → e.g. kidney
vascular vessel (acute/chronic)
3. Systemic Vascular Resistance (SVR) - Needs immediate medical intervention
➔ Responsible for ↑ blood pressure
➔ Influenced by RAAS (↑ BP ) HORMONAL RESPONSE
4. ANS (Autonomic Nervous System) Stress
Response ● Activation of ANS and hypothalamic-pituitary
5. Hormones adrenal axis
➔ Catecholamines (secreted by the ● Neuroendocrine response
adrenal medulla) - Renin-angiotensin
● Epinephrine - Cortisol
● Norepinephrine - Aldosterone
● Dopamine - ADH
➔ RAAS (aldosterone) ★Angiotensin II – most powerful vasoconstrictor
➔ ADH ● Use of ACE inhibitor to prevent conversion of
➔ Influence tissue perfusions Angiotensin I to Angiotensin II → prevents ↑
BP
Good tissue perfusion → blood reaches and sends
nutrients down to the cellular level Affectations of Microcirculation (after hemorrhage)
→ larger arterioles vasocontricts (distal = dilates)
Check the circulation:
● Temperature (may vary if circulation is not
proper)
● Diagnostic exam (Doppler)
● Color and Appearance

Initial insult activates the mediator response of:

1. Neuroendocrine response
2. Inflammatory response
Goal is to maintain perfusion in heart and brain

1
 CELLULAR LEVEL ORGAN LEVEL
Mitochondria
● The powerhouse of the cell
● Most susceptible to the decrease of oxygen
supply
● Inadequate oxygen delivery → ↓ generation of
ATP (energy) → pyruvate → lactic acid →
acidosis
**Cellular effects of shock → problem in the liver

Under hypoxic conditions:

Response to Shock
Activation of immune and inflammatory response →
release of mediator cells both pro- and
anti-inflammatory

Pro-inflammatory:
Liver ● Initiates non-specific immune response
● Antechamber of the heart ● Tries to maintain/restores homeostasis → but
● Tries to detoxify blood if in excess, promotes cellular and organ
● Rich in Kupffer cells – responsible for damage/dysfunction
engulfing microorganisms; that’s why we don’t ● Overproduction of inflammatory response →
easily develop infection/sepsis cellular damage

FORMS OF SHOCK
1. Hemorrhagic or Hypovolemic Shock
● Actual blood loss
2. Cardiogenic shock
● No problem w/ fluid
3. Distributive shock (vasodilatory)
● Vessels are too wide → slow blood
flow/weak pressure
● septic/toxic shock
● Anaphylactic shock
4. Neurogenic shock – the brain cannot
respond to the needs or there is no activation
of ANS to tell blood vessels to constrict
● All forms of shock → vasodilation →
septic shock
5. Traumatic shock
● d/t trauma e.g. vehicular accidents
6. Obstructive shock
● Common: pulmonary embolism

2
 STAGES OF SHOCK
Initial / Compensated / Non-progressive
➔ Vital signs are still normal
➔ Activation of compensatory mechanism
(seconds to minutes; depends on what type of
shock)
➔ SNS: catecholamines → ADH/vasopressin
(can cause arterioles to vasoconstrict) →
water conservation → ↑ vascular volume → ↑
blood pressure → activation of RAAS
GIT
● ↓ perfusion → ↓ peristalsis (motility) →
paralytic ileus → necrosis of intestinal mucosa
→ release of endotoxin → septic shock
Liver
● ↓ perfusion = ↓ metabolic functions of the liver
→ Kupffer cells → bacteria goes to general
circulation → ↑ production of endotoxin →
septic shock

Progressive / Decompensated Irreversible Stage

➔ Compensatory mechanism is ineffective ➔ Extent of shock is very severe → may lead to

➔ Systemic manifestations death

PHYSIOLOGIC RESPONSE TO SHOCK

1. Vasoconstriction
● SNS activation → adrenal gland
(cortex, medulla)
● Cortex – ↑ cortisol, aldosterone
● Medulla – ↑ catecholamines
2. Tachycardia – ↑ HR
3. Tachypnea – ↓ RR
4. Skin
● Color & temperature changes
● Cold, clammy skin
5. Hypotension
● Failure of compensatory mechanism
6. Coagulation abnormality
● Check lab tests
● DIC = hemorrhage
● Thrombocytopenia → presence occurs
in septic shock
7. Hyperglycemia
● Stress – Activation of
hypothalamic-pituitary-adrenal axis →
↑ gluconeogenesis → ↑ glucose
8. Fluid shifting
● Intravascular → intracellular → ↓
Kidney plasma volume = hypovolemia
● ↓ GFR – chronic acute failure & acute renal 9. Activation of RAAS
failure 10. End-organ damage

Brain
● ↓ LOC

Heart
● ↑ MDF → ↓ cardiac output = cardiac arrest

Lungs
● ↓ surfactant → lung collapse → ARDS
● V/Q (ventilation perfusion) mismatch
concentration gradient → hypoxia →
respiratory acidosis → ARF (acute renal
failure)

3
 HEMORRHAGIC SHOCK
➔ Most common
➔ Acute blood loss results in reflexive decreased
baroreceptor stimulation → increased
chemoreceptor stimulation of Vasomotor
centers → increased vasoconstriction and
peripheral arterial resistance
➔ Hypotension, tachycardia, confusion,
decreased level of consciousness
Diagnosis
● The clinical signs of shock may be evident
with:
- agitated patient
- cool clammy extremities
- tachycardia, hypotension
- at least 25-30% loss of the blood
volume
● Marked tachycardia, hypotension, confusion
may not be evident until >30% blood loss
● CBC w/ platelet
Treatment
● Secure the airway – d/t loss of blood →
compromised oxygen
● Intravenous volume resuscitation
● ET Tube- invasive
● Blood Transfusion
- Properly typed and crossmatched
- Hemolytic reaction d/t Rh
incompatibility
- 2 RN check
- Expiration of blood is approx. 3
months (120 days)
- Hemolyzed → potassium leaks ⇒
hyperexcitability of the heart
- 2 bags – furosemide (to excrete
unnecessary fluid e.g. potassium)
- Be careful in pt w/ heart and renal
problems → prone to fluid overload,
ARDS
- Crystalloid – IV fluids (PNSS; no D5
containing solution because it attracts
water out of the cell) – easy to deplete
- Colloid – albumin
**The actively bleeding pt cannot be resuscitated until
control of ongoing hemorrhage is achieved
CARDIOGENIC SHOCK
➔ Circulatory pump failure leading to decrease
flow and hypoxia
➔ Problem: Pumping mechanism of the heart
→ hypoxia (blood volume and intravascular
tone are normal)
➔ Common Condition: Pump failure due to MI
Hemodynamic Criteria
● Sustained hypotension (<90mmhg SBP)
● Reduced cardiac index (<2.2 L/min m2)
● Elevated pulmonary artery wedge pressure
(>15 mmHg)
Causes
● Acute Myocardial infarction
○ Pump failure
○ Mechanical complications
○ Right ventricular infarctions
● Other causes
○ Myocarditis
○ End-stage cardiomyopathy
○ Acute aortic insufficiency; acute mitral
regurgitation
○ Obstruction to left ventricular filling
Diagnosis
● In evaluation of possible cardiogenic shock,
other causes of hypotension must be excluded
● Making the diagnosis of cardiogenic shock
involves the identification of cardiac
dysfunction or acute heart failure insusceptible
patient
● Problems in the valve → blood will go back or
mix with oxygenated & non-oxygenated blood
● Origin of Problem: HEART
Treatment
● Maintain adequate oxygenation
● Judicious fluid administration – to avoid
congestion
● Pain is treated with IV morphine sulfate –
avoid in pt w/ increased IOP & ICP
● Antiarrhythmic drugs
● Cardioversion
VASODILATORY SHOCK
➔ Hypotension results from failure of the
vascular smooth muscle to constrict
appropriately, resistant to treatment with
vasopressors
➔ Most common form: septic shock
Other Causes of Vasodilatory Shock
● Hypoxic lactic acidosis
● Carbon monoxide poisoning
● Terminal cardiogenic shock
**Represent the FINAL COMMON PATHWAY for
profound and prolonged shock of any etiology
Diagnosis
● Evidence of infection, fever, tachycardia,
leukocytosis, tachypnea, signs of
4
 hypoperfusion such as confusion, malaise, OBSTRUCTIVE SHOCK
oliguria or hypotension
Causes
Treatment ● Pulmonary embolism or tension pneumothorax
● Adequacy of airway and ventilation ● Resulting in depressed cardiac output, which
● Empiric antibiotics – highest/max dose results from mechanical impediment to
● IV fluids circulation RATHER THAN A PRIMARY
● Arginine vasopressin CARDIAC FAILURE
● Tight glucose management
● Corticosteroids The Diagnosis Of Tension Pneumothorax
● Made on clinical examination, includes
SEPTIC/TOXIC SHOCK respiratory distress, hypotension, diminished
➔ Results from severe and profound conditions BS, shift of mediastinal structures
of generalized vascular collapse secondary to ● Definitive tx of tension pneumothorax is
a systemic infection commonly caused by immediate tube thoracostomy
gram (-) organisms
➔ Endotoxins cause massive vasodilatation CARDIAC TAMPONADE
➔ All types of shock have septic components ➔ Results from the accumulation of blood within
due to lysis of colonic microorganisms and the pericardial sac
destruction of Kupffer cells ➔ Classic findings include dyspnea, cough, chest
pain, tachycardia, Beck's triad (low blood
NEUROGENIC SHOCK pressure, distension of the jugular veins, and
➔ Diminished tissue perfusion as a result of loss muffled heart sounds)
of vasomotor tone to peripheral arterial beds ➔ Immediate pericardial decompression is
usually sec to spinal cord injury needed usually through a left thoracotomy
➔ Affects medulla and SNS
➔ Interference with SNS → disrupts vasomotor TRAUMATIC SHOCK
tone → vasodilatation ➔ Soft tissue injury and long bone fractures that
➔ Seen in head injuries, SCI, drug overdose, use occur in association with blood loss yield an
of general anesthetics upregulation of proinflammatory mediators that
is more complex than simple hemorrhagic
Diagnosis shock.
● Classic description consist of decreased blood
pressure associated with bradycardia, warm Treatment
extremities, motor and sensory deficit, ● Secure airway
radiographic evidence of vertebral column ● Control bleeding
fracture ● IV fluids
● Debridement of nonviable tissue
Treatment ● Stabilization of bony injuries
● Secure airway ● Treatment of soft tissue injuries
● IV fluids
● Administration of vasoconstrictors (Dopamine)
DIFFERENTIAL DIAGNOSTIC OF SHOCK BASED ON
HEMODYNAMIC PARAMETERS
ANAPHYLACTIC SHOCK
➔ There is profound peripheral vascular collapse TYPE CVP CO SVR O2 SAT
induced by severe allergic reaction
Hypovolemic ⇩ ⇩ ⇧ ⇩
➔ Mediated by histamine, kinims, PgE,
Leukotrienes Cardiogenic ⇧ ⇩ ⇧ ⇩
➔ Large quantities of fluid may leak out of
capillaries causing severe hypovolemia Septic ⇧⇩ ⇧ ⇩ ⇧

Traumatic ⇧ ⇧⇩ ⇧⇩ ⇩
Treatment
● Epinephrine Neurogenic ⇩ ⇩ ⇩ ⇩

5
Signs and Symptoms COLLABORATIVE MANAGEMENT
EARLY STAGE 1. Assess the primary cause of shock in case of
● Increase NS activity → Stress response 3rd space shifting to prevent further volume
● Increase HR (rapid but weak), increase loss
shallow respiration (Respiratory Alkalosis), ● Promote fluid balance and CO
increase BP (decrease pulse pressure) ● Replacement of fluid losses
● Diaphoresis, cool clammy skin (warm, flushed - Colloids (albumin),
skin in septic shock) Crystalloids (IV fluids), Blood
● Thirst, dry mucous membranes products
● Decrease urine output 2. Assess hemodynamic status and all major
● N/V, weakness body systems
● Restlessness, increase alertness ● I/O, CVP, VS
3. Maintain airway and provide cardiac and
LATE STAGE pulmonary support
● Apathetic, unresponsive, confusion, decreased ● Oxygen, MV, DBCE, Suction
LOC 4. Assisting with Renal support
● Eyes sunken with vacant expression ● Hourly UO monitoring; BUN/Crea,
● Dilated pupils Fluid replacement
● Mottled skin appearance (Neurogenic/ 5. Assisting with Gl support
Vasogenic) ● Decompression (NGT)
● Hypotension → cyanosis 6. Promoting safety
● Decrease temperature ● Soft restraints if restless
● Oliguria, Anuria → Hyperkalemia ● Strict asepsis
● Decreased bowel sounds → abdominal - Prevent complications of
distention → paralytic ileus immobility
● Metabolic/ Respiratory acidosis - Protect from chills which
● DIC cause sludging of blood in
circulation
ASSESSMENT PARAMETERS 7. Institute management for specific causes
8. Provide supportive care as indicated
1. Hemodynamic monitoring
● VS, PAP/PCWP, CVP, ECG, Cardiac PHARMACOLOGIC THERAPY
output 1. Vasoconstrictors
2. Respiratory Monitoring ➢ Epinephrine, Dopamine/Dobutamine,
● Breath Sounds, ABG Levophed
3. Fluid Electrolyte Monitoring 2. Vasodilators
● Serum electrolytes, ABG, I/O, ➢ Nitrates, Ca Channel Blockers,
BUN/Creatinine, Urine specific gravity Hydralazine
4. CNS Monitoring 3. NaHCO3 → Acidosis
● LOC 4. Antibiotics → sepsis
5. Hematologic Monitoring 5. Heparin/ LMWH → DIC
● CBC with PC, Clotting Factors 6. Steroids → edema; decrease inflammatory
effect
FIRST AID AND PREVENTIVE MANAGEMENT IN 7. Glucagon, D50% W → increase glucose
SHOCK 8. H2 Blockers/ Proton pump Inhibitors
1. Proper Position 9. Naloxone → blocks endorphin-mediated hpn
● Keep patient lying down flat (safest 10. Analgesics
position) 11. Antidysrhythmics
● Modified T-Berg ➢ Lidocaine, Amiodarone, Procainamide,
● Place patient on his back with head AtSO4, Isoproterenol
and shoulder raised (if with DOB)
● Keep patient on his side opposite his ENDPOINTS IN RESUSCITATION
injury (Recovery Position) ● The goal in the treatment of shock is the
2. Proper Body Heat restoration of adequate organ perfusion
● Maintain body temperature (must not and tissue oxygenation
be shivering or perspiring)

6
● Resuscitation is complete when oxygen debt is
repaid, tissue acidosis is corrected and
aerobic metabolism is restored
● Systemic/global
○ Lactate, base deficit, cardiac output
● Tissue-specific
○ Gastric tonometry, tissue pH, O2 level
● Cellular level
○ Membrane potential
○ ATP

➔ Several recent review papers and

meta-analysis has confirmed that either fluid,
crystalloid or colloid, can be used to
resuscitate the trauma patient adequately.
➔ According to Dr. G. Tom Shires, only infusion
of both shed blood plus LR solution
replenished the BC mass, plasma volume, and
ECF space and had long-term survivorship of
about 70%, compared to blood alone (20%),
blood plus plasma (30%).
➔ The clinical dilemma faced in a patient with
shock is that the etiology may not be apparent,
thus treatment of the patient is empiric, while
the underlying etiology is investigated.

7
 CARDIOVASCULAR DISEASE Lactic Dehydrogenase (LDH1)
● One of the most accurate/sensitive indicator of
NON-MODIFIABLE RISK FACTORS MI damage
● Age ● Normal: LDH2 > LDH1
● Sex ● MI: LDH1 > LDH 2 (flip ratio)
● Race ● Normal: 100-225 mu/ml
● Genetics ● Initial/onset: 12 hours after MI
● Peak: 48 hours
MODIFIABLE RISK FACTORS ● Return to normal: 10-14 days

● Stress Troponin I/T

● Nicotine – vasoconstriction, ↓HDL (good ● Both are contractive enzyme
cholesterol) ● Troponin I – more common; confirmatory test
● Diet – ↑Na, fats, carbs for MI
● Exercise – ↑tPA (anticoagulant) ● ↑ levels = damage to heart contractility
- 15-30 mins a day (young) ● Normal: varies
- 45 mins a week (elderly) ● Initial: 3-4 hours
● DM ● Peak: 4-24 hours
● Obesity ● Return to normal: 1-3 weeks
● Hyperlipidemia
● Oral contraceptives Myoglobin (low-molecular weight)
● Not usually used for MI
DIAGNOSTICS ● Heme protein – damage in muscles = ↑
1. Stress test myoglobin levels (false positive)
➢ To identify ischemic heart disease ● Useful for myocardial necrosis
➢ Like ECG ● Rapidly increase within 1-2 hours
2. Cardiac catheterization ● Not cardiac-specific
➢ Swan-Ganz catheter ● Renal damage = ↑ myoglobin level
➢ CVP ● Once result doubles in value = (+) MI
➢ (stenting, balloon catheterization) ● Initial: 1-2 hours
3. ECG ● Peak: 4 hours
➢ Electrical impulses ● Return to normal: within 24 hours
4. CVP
5. PAP, PCWP ELECTROLYTE EXAM
➢ PCWP: 4-12 mmHg ➢ Na: 135-148 meq/L – ↑Na (hypernatremia) =
↑fluid (most likely to occur in unconscious pt)
ENZYME STUDIES ➢ K: 3.5-5 meq/L – ↑↓K = cardiac problem
Aspartate Aminotransferase (AST) (dysrhythmia)
● ↑ AST = tissue necrosis ➢ Mg: 1.3-2.1 meq/L – ↓Mg = cardiac
● Normal: 7-40 mu/ml dysrhythmias
● Initial elevation: 4-6 hours after MI ➢ Ca: 4.5-5.3 meq/L – ↓Ca = tetany; Ca is very
● Peak rate: 24-36 hours after MI necessary for blood clotting and
● Return to normal: 4-7 days neuromuscular activity

Creatinine Phosphokinase (CK-MB) / CPK-MB LIPID/CHOLESTEROL PROFILE

● CPK-MM – ↑ when there’s an insult in muscles ● HDL (good cholesterol)
● CPK-BB – ↑ in stroke or problem in brain - Normal: 30-85 mg/dL
● CPK-MB – most cardiac-specific enzyme - ↓ HDL = predispose pt to CVD
- Accurate indicator of MI ● LDL (bad cholesterol)
● Normal values: - Normal: 50-140 mg/dL
- Male: 50-325 mu/ml - ↑ LDL = predispose pt to CVD
- Female: 50-251 mu/ml - Plaque formation → atherosclerotic
● Initial: 3-6 hours after MI disease
● Peak: 12-16 hours ● Triglyceride
● Return to normal: after 3-4 days - Normal: 10-150 mg/dL
- ↑ level = > risk for heart disease (MI)

8
 - Increases if has high consumption of 2. Described as heaviness or tightness of the
rice chest, “indigestion”, crushing
★ Nursing Responsibility: 3. Radiates down one or both arms, left shoulder,
➔ NPO: 10-12 hours (fasting) jaw, neck, and back
4. Precipitated by activity or exertion
OTHER TESTS 5. Relieved by rest and nitroglycerine
➢ BUN – determines renal function
- Normal: 10-20 mg/dL PRECIPITATING EVENTS OF ANGINA PECTORIS
- ↓ CO → ↓ renal tissue perfusion → ↓ ● Exertion. Vigorous exercise done sporadically.
GRF = ↑ BUN ● Emotions. Excitement, sexual activity.
➢ CBC ● Eating a heavy meal.
- Clotting time, Bleeding time ● Environment. Exposure to cold.
- PT, APTT
➢ ESR MANAGEMENT OF ANGINA PECTORIS
- ↑ ESR = inflammation Medications
➢ Urinalysis Vasodilators
- Assess renal function/systemic ➢ ↓ vasospasm = ↑ oxygen supply
disease ➢ Nitrates (Nitroglycerine, Amyl Nitrate,
- (+) albumin/protein = kidney problem Isosorbide)
- Myoglobinuria = (+) myoglobin in urine ➢ Effect: direct relaxation on vascular smooth
= support diagnosis of MI muscles = generalized vasodilation →↓
➢ Holter monitoring peripheral vascular resistance → ↓ systolic
- Attached to the pt for 24 hours to know pressure → ↓ preload & afterload ⇒ more
the status of the heart (portable ECG) efficient distribution of myocardial blood flow
➢ ECG ➢ Routes:
- Ultrasound ● SL / IV
- 2D-echo (standard) – to visualize the - SL: give water before
structure of the heart administration to prevent
dryness (dryness decreases
ANGINA PECTORIS absorption)
➔ Myocardial ischemia (may lead to necrosis) ● Transdermal
➔ Myocardial oxygen demand > myocardial - 30-60 mins
oxygen supply - Duration: 24 hours
- Removed during night or
TYPES sleep time for nitrate-free
1. Classic (Stable) intervals (holiday period)
● r/t stress or exertion ➢ Change positions slowly – to prevent
● Relieved by rest or nitroglycerin orthostatic hypotension
2. Unstable (Pre-Infarct) ➢ Stored in a dark, airtight container, away from
● Progressing severity direct sunlight exposure (photosensitive)
● Not relieved by rest or meds - Replenish meds within 6 months
● Impending MI = “medical emergency” - Do not buy stock for more than 2
● Proceed to the hospital immediately months
3. Variant (Vasospastic, Prinzmetal)
● Occurs even at rest Beta-adrenergic Blocking Agents
● r/t vasospasm ➢ “-olol” groups
● Relieved by rest and nitroglycerin ➢ ↓ HR, BP = ↓ myocardial contractility
- 3 tabs consume in 5 minutes ➢ Not effective for Variant angina
interval ➢ Cardio-selective: Metoprolol
- Not relieved = go to the ➢ Noncardio-selective: Propranolol
hospital - Contraindicated if pt is w/ pulmonary
condition, asthma
SIGNS AND SYMPTOMS - Causes bronchoconstriction
1. Transient, paroxysmal substernal or precordial - ↓ glycogenolysis – DM type II
pain ➢ SE: N/V, depression, impotence (male)

9
Calcium-channel Blockers
➢ Inhibits ion transport to myocardial cells
➢ (-) inotropic effect = ↓ cardiac workload
➢ Vasodilatory effect = reduces coronary spasm
➢ Effective to Variant type of angina
➢ Verapamil (Isoptin, Calan)
➢ Nifedipine (Procardia, Adalat, Calcibloc)
➢ Diltiazem (Cardizem)
➢ Nx responsibility:
- Assess HR, BP prior to administration
- Monitor for good hepatic/renal
functions
- Give 1 hour before meal or 2 hours
after meal
- No food – because food delays
absorption
Platelet Aggregation Inhibitors
➢ ↓ thrombus formation
➢ ASA (aspirin)
➢ Dipyridamole (Persantin)
➢ Ticlopidine (Ticlid)
➢ Nx responsibility:
- Given w/ food (in the morning after
breakfast) – may cause gastric ulcer
- Monitor stool – check for presence of
melena (upper GI bleeding)
- Avoid dark-colored foods
Anticoagulants
➢ Heparin Na (Heparin Leo), LMWH (Enoxaparin
Na, Clexane)
● Inactivates thrombin (clotting factor) →
no conversion of fibrinogen to fibrin
(clot formation) ⇒ ↓ platelet
aggregation
➢ Warfarin Sodium (Coumadin)
● Inhibits hepatic synthesis of Vitamin K
➢ Dicumarol
➢ Nursing responsibility:
● Assess for s/sx of bleeding
● Avoid straining of stool
● Do NOT give aspirin together w/
warfarin
● Aspirin toxicity = tinnitus
● Heparin antidote – Protamine Sulfate
● Monitor CT, APTT
● Do NOT give for more than 2 weeks
Treatment
● Percutaneous Transluminal Coronary
Angioplasty (PTCA)
- Single lumen – single vessel
- CABG/bypass – multiple
Nursing Interventions
● Diet
- Low Na, fat, and cholesterol; high fiber
- Avoid saturated fats (animal fats)
- White meat e.g. chicken w/o skin and
fish are low in cholesterol
● Read labels
● Activity
- No restrictions are placed in activity
within the pt’s limitations (only for
single-lumen)
SURGICAL MANAGEMENT OF ANGINA PECTORIS
Coronary Artery Bypass Graft (CABG)
➔ To reduce angina and improve pt activity
➔ For severe narrowing of one or more branches
➔ Main purpose: myocardial revascularization
➔ Saphenous vein, internal mammary artery
Nursing Interventions: Preoperative
1. Explain the anatomy of the heart, function of
coronary arteries, and effects of CAD
2. Explain events of the day of surgery
3. Orient to the critical and coronary care units
and introduce staff
4. Explain the equipment to be used (monitors,
hemodynamic procedures, ventilators, ET, etc)
5. Demonstrate activity and exercise
6. Reassure availability of pain medications
Nursing Interventions: Post-operative
1. Maintain patent airway
2. Promote lung re-expansion
3. Monitor cardiac status
4. Maintain fluid and electrolyte balance
5. Maintain adequate cerebral circulation
6. Provide pain relief
7. Prevent abdominal distension
8. Monitor for and prevent the following
complications:
● Thrombophlebitis/pulmonary embolism
● Cardiac tamponade
● Arrhythmias
● CHF
9. Provide client teaching and discharge planning
concerning
● Limitation w/ progressive increase in
activities
Nursing Management in CABG
1. Promoting comfort
● Relieve pain → Nitroglycerine (drug of
choice)
2. Promoting tissue perfusion
● Instruct the client to avoid overfatigue
10
 ● Stop activity immediately in the - “Gas pains around the heart”, nausea
presence of chest pain, dyspnea, and vomiting
lightheadedness, or faintness which ● R/T pain, vasovagal reflexes, denial of pain
indicates low tissue perfusion.
3. Promoting activity and rest ACUTE PULMONARY EDEMA
4. Encourage slower activity or shorter periods of ➔ Sense of suffocation, dyspnea, orthopnea
activity w/ more rest periods. Avoid ➔ Lung auscultation – gurgling/bubbling
overexertion respiration
5. Plan for a regular activity program ➔ If there is no circulation coming from the heart,
6. Take nitroglycerine before exercise there will be a pooling of blood in pulmonary
7. Increase the extent of exercise gradually area → myocardial infarction
8. Promoting relief of anxiety and feeling of ➔ Ambu bag hooked in oxygen w/ humidifier
well-being ➔ Chest compressions
➔ ECG Changes
MYOCARDIAL INFARCTION ● MI – elevation of ST segment,
➔ The formation of localized necrotic areas inversion of T wave, and
within the myocardium. MI usually follows enlargement of Q wave (pathologic
sudden coronary occlusion and the abrupt Q wave)
cessation of blood and oxygen flow to the ● Q wave develops from the area of
heart muscle. infarction
➔ The prolonged ischemia lasting more than 35 ● Elevated ST segment results from the
to 45 minutes produces irreversible cellular area of injury
damage and necrosis of the myocardium. ● Inverted T wave originates from the
zone of ischemia
CAUSES ● Elevation of ST segment heralds a
1. CAD / CAHD pattern of injury and usually occurs as
2. Coronary thrombosis/embolism an initial change in MI
3. Shock **ECG – faster results than cardiac enzymes; old MI
4. Direct trauma are seen because infarcted areas heal but is replaced
with scar tissues
SIGNS AND SYMPTOMS
MANAGEMENT OF MYOCARDIAL INFARCTION
● Pain Medications
- Morphine sulfate (contraindicated if
pt has increased ICP, IOP) Analgesics
- Crushing, severe, prolonged, ● For relief of pain. This is a priority. Pain may
unrelieved by rest or nitroglycerine; cause shock.
often radiating to one or both arms, ● Morphine Sulfate, Lidocaine or Nitroglycerine
the neck, and the back administered intravenously
● Anxiety and apprehension - Assess neurologic status changes
● Feeling of “doom”, restlessness which may indicate GI bleeding or
● Shock cardiac tamponade
- Systolic pressure below 80 mmHg, ● Beta-adrenergic blocking agents
gray, facial color, lethargy, cold ● Diazepam – seizure, respiratory depressant;
diaphoresis, peripheral cyanosis, given when pt is intubated
tachycardia/bradycardia, weak pulse - Decreased LOC = decreased
● R/T severe pain, a severe reduction in cardiac perfusion to the brain
output, and inadequate tissue perfusion
● Oliguria CAB for MI/cardiac problems
- Urine flow of less than 30 ml/hr ★ Compressions
● Fever ★ Airway
- Slight elevation of temperature occurs ★ Breathing
within 24 hrs and extends 3 to 7 days
accompanied by leukocytosis and
elevated ESR
● R/T tissue destruction, ↑ ESR
● “Indigestion”

11
Treatment Promoting Comfort
Goals: ● Relieve pain
1. Prevention of further tissue injury and ● Morphine sulfate ⇒ decreases sympathetic
limitation of infarct size stimulation → increases myocardial
- Ischemic cascade – Ca irritates cell oxygenation → prevents shock from severe
→ lysosome is activated → *sasabog* pain
→ area of infarction increases
2. Maximize myocardial tissue perfusion and Providing Rest
reduce myocardial tissue demands. ● The client is usually placed on bed rest without
3. Supplemental oxygen by nasal cannula. This commode privileges for 24 to 48 hours.
increases myocardial oxygen supply; and ● Without commode privileges – cardiac rehab
relieves pain. ● Provide bedside commode/bedpan; indwelling
- 2 LPM oxygen administration foley catheter or diaper
4. Cardiac monitoring to detect the occurrence of
dysrhythmias. Promoting Activity
- Hooked-in cardiac monitor (3-leads) ● Gradual increase in activity is encouraged
5. Percutaneous Transluminal Coronary after the first 24 to 48 hours.
Angioplasty may be done to reopen an
occluded artery. Promoting nutrition and elimination
6. Diet: low-cholesterol, low-salt diet is ● Provide small, frequent feedings
prescribed ● Address DM
7. Activity: Bed rest is usually prescribed for 24 to ● Low sodium, cholesterol – no condiments,
48 hours to decrease oxygen demand. ketchup, soy sauce
Progressive ambulation is implemented as ● Avoid stimulant food – coffee
soon as possible, unless complications ● Avoid very hot or cold food
- CBR s BPR (complete bed rest w/o ● Avoid gas-forming food → stimulates
bathroom privileges) vasovagal reflexes → decreased cardiac rate
(less than 60)
Nursing Management ● No straining (to prevent Valsalva maneuver)
- Stool softener – Colace (sodium
Promoting Oxygen and Tissue Perfusion decussate)
● Instruct pt to avoid overfatigue; stop the - increase OFI if not contraindicated
activity immediately in presence of chest pain, - high fiber diet; decrease high protein &
dyspnea, lightheadedness or faintness. fat diet
● Oxygen therapy by cannula for the first 24-48
hours or longer if pain, hypotension, dyspnea, Promoting relief of anxiety and feeling of
or dysrhythmias persist. well-being
● Monitor VS changes, initiative of ● Explain procedure to pt to alleviate anxiety
complications.
● Position the pt in semi-Fowler’s to allow Teaching and Counseling
greater diaphragm expansion, thereby lung ● Self-management education guide
expansion and better carbon dioxide-oxygen ● Discharge after MI
exchange. ● Diet – weight gain reduction; bland diet
● Avoid weightlifting – pressure on the buttocks
Promoting Adequate Cardiac Output
Monitor the following parameters: Teaching guide on resumption of sexual activity
● Dysrhythmias on ECG tracings ● Assume less fatiguing position
● O2 sat, VS, urine output ● 4-6 weeks after discharge
- Good urine output = good cardiac ● No anal sex
output
● Effects of daily activities on cardiac status Complications of MI
● Rate and rhythm of pulse
● Hemodynamically stable – pt should still be ➢ Dysrhythmias
monitored continuously ➢ Cardiogenic shock
➢ Thromboembolism
Administer Pharmacotherapy as prescribed ➢ Pericarditis
➢ Rupture of myocardium
➢ Ventricular aneurysm
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 ➢ Congestive heart failure MANAGEMENT
Medications
CONGESTIVE HEART FAILURE Digitalis Therapy
➔ It is a state of congestion produced by ● Lanoxin (Digoxin) – very narrow therapeutic
myocardial dysfunction. index
➔ Heart failure is the inability of the heart to ● (+) inotropic – increases the force of the
pump the amount of oxygenated blood heartbeat
necessary to affect venous return and to meet ● (-) chronotropic – decreases the heart rate
the metabolic requirements of the body. ● Assess cardiac rate prior to administration
➔ post-MI; cardiomegaly ● Monitor potassium – hypokalemia potentiates
- Ability of ventricles to empty – lessen digitalis toxicity (good cardiac output = good
- Residual volume increases = muscle urine output)
enlarges - be very careful if w/ furosemide ⇒
hypokalemia
CAUSES - low potassium, cardiac rate ⇒ stop
➢ Direct damage of the heart digitalis
● Mitral myocarditis, ventricular ● Assess for s/sx of digitalis toxicity:
aneurysm - Bradycardia
➢ Ventricular overload - Anorexia
➢ Increased preload - N/V
● Mitral or aortic regurgitation, atrial or - diarrhea
ventricular septal defects, or rapid - alterations in visual perception
infusion of large volumes of IV fluids ● SE: gynecomastia, decrease libido, impotence
(KVO) – in male
➢ Increased afterload
● Aortic or pulmonary valve stenosis, Diuretic Therapy
systemic hypertension, pulmonary ● To decrease cardiac workload → decrease
hypertension. circulating volume → reduce preload
➢ Constriction of the ventricles ● Assess for s/sx for hypokalemia when
● cardiac tamponade, pericarditis, administering Thiazide and loop diuretics
restrictive cardiomyopathies. ● The diuretics used in the treatment of CHF are
as follows:
CLASSIFICATION - Thiazides (hydrochlorothiazide)
LEFT-SIDED CHF - Loop diuretics (furosemide)
Causes: - Potassium-sparing
➔ MI – left anterior descending coronary artery - WOF: hyperkalemia (increase
(LADA) cardiac rate)
➔ HPN
➔ Aortic stenosis Vasodilators
➔ Mitral stenosis ● Given to decrease afterload
● The most commonly used drugs as follows:
RIGHT-SIDED CHF - Nitroprusside (Nipride)
Causes: - Hydralazine (Apresoline)
➔ LSCHF - Nifedipine – a calcium-channel blocker
➔ Pulmonary embolism with vasodilator effect
➔ RVF - Captopril (Capoten) – also has a
➔ Congenital septal defects vasodilator effect
❖ Nicardipine – as vasodilator to decreased
Signs and Symptoms blood pressure → decrease resistance to
ventricular emptying
❖ RSCHF – systemic congestion; generalized
edema Other drugs:
❖ LSCHF – pulmonary; s/sx of atrial Sympathomimetics
insufficiency; rales upon auscultation ● Dopamine
● Dobutamine

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Activity
➔ Cardiac rehab – increase oxygen supply than
oxygen demand
Diet
➔ No sodium – to prevent fluid excess
NURSING MANAGEMENT
1. Providing oxygenation
● 2 to 6 lpm via nasal cannula; semi-Fowler’s
position
● Promoting rest and activity
● Bed rest or limited activity may be necessary
during the acute phase
● Provide an overbed table close to the pt to
allow resting the head and arms
● Administer Diazepam (Valium) 2 to 10 mg for
3 to 4 times a day as ordered to allay
apprehension.
● Gradual ambulation is encouraged to prevent
the risk of venous thrombosis and embolism
due to prolonged immobility.
● Activities should progress through dangling,
sitting up in a chair, and then walking at
increased distances under close supervision.
● Assess for signs of activity tolerance such as
dyspnea, fatigue, and increased pulse rate
that do not stabilize readily.
2. Decreasing anxiety
● Increase restlessness → perceived by the pt
as increased heart failure
3. Facilitating fluid balance
● ↓ Na, give diuretics and digitalis
● Monitor I and O, weight and VS
● Weight gain within a short period of time →
water gain
● Dry phlebotomy – rotating tourniquet to limit
blood to return immediately in the blood since
it's congested – rotated every 15 minutes or
once nails darken (no more than 30 mins
should be occluded in one extremity)
- Tourniquet at the thigh (above the
knee) to allow the heart to rest
4. Providing skincare
● Edematous skin is poorly nourished and
susceptible to pressure sores
● Change position every 2 hours
● Assess bony prominences (sacral area)
● Use protective devices to prevent pressure
sores
● Devices – donut, no wrinkles in bedding
5. Promoting nutrition
● Provide bland, low-calorie, low-residue with
vitamin supplements during the acute phase
● Frequent small feedings minimize exertion and
reduce gastrointestinal blood requirements.
● There may be no need to severely restrict the
sodium intake of a client who receives diuretic.
6. Promoting elimination
● Advice to avoid straining at defecation which
involves Valsalva’s maneuver – increases
cardiac workload
● Administer laxative
● Encourage use of bedside commode.
7. Facilitating learning
● Teach client and family about the disorder and
self-care
● Monitor s/sx of recurring CHF e.g. weight gain,
loss of appetite, dyspnea, orthopnea, edema
of the legs, persistent cough, and report these
to the physician.
● Avoid fatigue, balance rest with activity
● Observe prescribed sodium restrictions
● Eat small, frequent meals rather than 3 large
meals a day
● Take prescribed medication on a regular basis,
e.g. digitalis, diuretics, vasodilators. Monitor:
- Digitalis – cardiac rate
- Diuretics – blood pressure
● Observe regular follow-up care as directed
PULMONARY EDEMA R/T MI
● Place in high-Fowler’s position
● Morphine sulfate 10 to 15 ms IV as ordered
- To allay anxiety, reduce preload &
afterload
● Oxygen therapy
● Aminophylline – IV
- Given when there’s bronchospasm
- Decreases congestion
- Increase urine output
● Rapid digitalization
● Diuretic therapy
● Vasodilators
● Dopamine or Dobutamine
● Monitor serum potassium
HYPERTENSION
➔ Abnormal elevation of BP over 140/90
➔ Crisis: >180/100 – IV
➔ HPN: 140/90 – oral/SL
CAUSES
1. Arteriosclerosis – increases pressure
2. Hypercoagulability – narrowing = increase
pressure
3. Fluid overload
4. Stress – SNS stimulation; all increase except
GIT/GUT
5. High Na diet, low K intake
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 6. Obesity – compresses portal vein = HPN PREVENTING NON-COMPLIANCE
7. Smoking – constriction of vascular smooth 1. Inform pt that absence of symptoms does not
muscles indicate control of BP – monitoring
8. Genetics 2. Advise pt against any abrupt withdrawal of
medication – to prevent rebound hypertension
SIGNS AND SYMPTOMS ● Gradual withdrawal; tapering dose
1. Headache – most characteristic sign 3. Device ways of remembering of taking
2. Epistaxis medications – alarms
3. Dizziness
4. Tinnitus CARDIAC ARREST
5. Unsteadiness ➔ General Info: sudden, unexpected cessation of
6. Blurred vision breathing and adequate circulation of blood by
7. Nocturia the heart
➔ Main concern: to return hemodynamic
MANAGEMENT circulation
● Low sodium, fats in diet ➔ CAB
● Ideal body weight
● Exercise MEDICAL MANAGEMENT
● Smoking cessation 1. Cardiopulmonary resuscitation (CPR)
● Alcohol moderation 2. Drug therapy:
● Effective coping a) Lidocaine, Procainamide, Verapamil –
for dysrhythmias
ANTI-HPN DRUGS b) Dopamine, Isoproterenol,
1. Diuretics Norepinephrine
2. Beta-blockers c) Epinephrine – to enhance myocardial
3. Ca-channel blockers automaticity → so that heart beats
4. ACE inhibitors again
5. Aldosterone Receptor Blockers d) Atropine sulfate – to control vagal
6. Vasodilators stimulation; increase cardiac rate;
7. Centrally Acting Alpha Blockers diminish secretion over the airway
● Clonidine e) Sodium bicarbonate – given during the
8. Alpha1 Adrenergic Blockers first few moments to address mix
● Terazosin acidosis
f) Calcium chloride – Ca ion helps the
MANAGEMENT FOR ANTI-HPN DRUGS heart beat more effectively by
➢ Side effect → orthostatic hypotension enhancing myocardium contractile
➢ Sit or lie down force
➢ Take regular 3. Defibrillation
➢ Gradual position change
➢ Avoid warm baths ASSESSMENT FINDINGS
➢ Avoid prolonged sitting ● Unresponsiveness, cessation of respiration,
➢ Avoid alcoholic beverages pallor cyanosis, absence of HR/BP/pulses,
➢ Avoid tyramine-containing foods dilation of pupils, ventricular fibrillation
● Tyramine – increases BP ● Asystole – absence of HR
● Beer, wine, liver, aged cheese, ● Ventricular fibrillation – 20 bpm; blood
chocolate, soy sauce circulates only in the ventricle
● Ventricular tachycardia ⇒ ventricular fibrillation
NURSING MANAGEMENT - Needs defibrillation
1. Low salt, low-fat diet - VTach – cardioversion
2. Stress therapy - 25-35 mins – irreversible damage (?)
3. Avoid stimulants – coffee, alcohol
4. Weight reduction and exercise – increase tPA NURSING INTERVENTIONS
limits risk for stroke 1. Begin pericardial pump and if successful,
administer lidocaine (d/t presence of
arrhythmias)
2. If unsuccessful, defibrillation → CPR
15
 3. Assist w/ administration of and monitor effects ➔ Collapsed alveoli ⇒ inadequate oxygen
of emergency drugs exchange
➔ Pt is given oxygen trough mechanical
ACUTE RESPIRATORY DISTRESS SYNDROME ventilator
Characterized by: ➔ Inhale → can’t exhale = so lungs can remain
1. Sudden and progressive pulmonary edema open
2. Increase bilateral infiltrates on lungs (CXR) – ➔ Administer Morphine, Ativan, Diprivan,
white parts in x-ray Pavulon, muscle relaxant – to reduce
3. Hypoxemia refractory of oxygen resistance to PEEP
supplementation ➔ May cause decrease cardiac output
4. Reduced lung compliance ➔ Monitor PAP, CVP
★ Occurring in the absence of CHF ➔ Pt should not be resistant to PEEP
➔ Nx responsibility: always monitor pt based on
ETIOLOGY the improvement and reaction to PEEP
● Shock – fluid shifting ➔ Avoid loss of power/electricity supply of the
● Aspiration machine
● Inhalation of toxic agents
● Near-drowning PHARMACOLOGIC THERAPY
● Trauma ● Milrinone (Primacor) – pulmonary specific
● Infection – COVID-19 vasodilator
● DIC ● Steroids – has surfactant property
● Fat emboli ● Antibiotics – prophylaxis; to prevent sepsis
● Oxygen toxicity ● WOF:
- Hypovolemia – fluid leaks d/t PEEP
ASSESSMENT therapy
● RR - Hypotension
● Dyspnea – air hunger
● Intercostal retractions NURSING MANAGEMENT
● Central cyanosis, clubbing of fingers 1. Supportive
● Dry cough ➢ Rest
● Fine crackles ➢ Monitor physiologic parameters –
● Fever (low-grade) – may be accompanied by respiratory modalities e.g. does the pt
infection use accessory muscles when
● Alteration in LOC breathing?
● ↓ FRC (functional residual capacity) – volume 2. Ventilatory care
of air that remained into the lungs after certain ➢ PEEP therapy
normal respirations → decreased oxygen ➢ Monitor PAP, CVP, VS
received 3. Emotional support
➢ To relieve anxiety
MANAGEMENT ➢ Orient pt to not resist PEEP → can
● Oxygen therapy: 8-10 LPM nasal cannula, breathe but w/ difficulty until breathing
non-rebreather mask is synchronized w/ the machine
● Position: semi to high Fowler’s ➢ Orient to enhance cooperation of pt
● CPT ➢ Difficulty of breathing d/t ARDS +
● Increase fluid intake balanced w/ diuretics anxiety = precipitated DOB

PEEP (Positive End Expiratory Pressure) ASTHMA

➔ USA: 2-3% of the population & still rising
➔ positive pressure maintained by the ventilator ➔ Chronic inflammatory disorder of the airways
at the end of exhalation (instead of a normal ➔ Reversible – an obstructive disease of the
zero pressure) to increase functional residual lower respiratory tract
capacity and open collapsed alveoli; improves ➔ Many cells play a role:
oxygenation with lower FiO2 ● Mast cells
➔ Invasive oxygen – uses pressure to keep the ● Eosinophils
airways and alveoli open to allow for proper ● Neutrophils
oxygen exchange

16
3 AIRWAY RESPONSES ➢ r/t external allergens such as:
1. Spasm of bronchial smooth muscles ● Contactants – dust, soaps
2. Edema ● Inhalants – smoke, spray
3. Accumulation of tenacious secretions ● Ingestants – food, milk, egg, chicken
**Chronic – because as you grow older, you become ● Sudden changes of temperature
more sensitive to triggers
Intrinsic or Non-Atopic Asthma
● Hypersensitivity ➢ Not r/t external allergens; not r/y
● Increase occurrence in males hypersensitivity to protein
● Onset age 12 years ➢ Asthma w/ physiologic cause
● Familial history ➢ Stress
● Cough ➢ Fatigue
● Increase mucus ➢ Lack of sleep
● Shortness of breath – distinct characteristic ➢ Anxiety
● Expiratory wheezes – they can breathe in but **endpoint = airway is hyperactive
they cannot expel the air d/t narrow
passageway → retention of CO2 Mixed Type of Asthma
● Increase CO2 retention ➢ Both types are present
● Prolonged expiration
● Hypoxemia Status Asthmaticus
- Tachycardia ● Severe form of constriction and inflammation
- Increase restlessness despite treatment
- Tachypnea ● May lead to respiratory or cardiac failure
● Retractions
COMMON FACTORS THAT TRIGGERS AN ATTACK
EMERGENCY ➔ Environmental factors – temp, humidity
➔ If symptoms do not respond to usual treatment ➔ Atmospheric pollutants – industrial smoke
in 30 minutes, the client should seek medical ➔ Strong odors – perfume, insecticide
attention ➔ Allergens – dust, pollen, laundry detergent
➔ Status Asthmaticus ➔ Exercise
● Emergency; life-threatening condition ➔ Stress or emotional upset
● Coma → seizure d/t lack of oxygen ➔ Medications – ASA, NSAIDs
into brain
ASSESSMENT
BRONCHIAL ASTHMA ● Spasm, hypersecretion and edema – triad
● Chronic, reversible, obstructive airway disease of asthma
characterized by wheezing. ● Severe dyspnea
● It is caused by smooth muscle spasm w/ ● Wheezing – classic sign
hypertrophy of the bronchial tubes, or swelling ● Anxiety
of the bronchial mucosa, after exposure to ● Fever – low-grade fever (non-specific
various stimuli. immunity)
● Hypersecretion of mucus ● Orthopneic position – use overbed table or
● Most common chronic disease in childhood pillow ⇒ opens lungs and enhance lungs
● Most children experience their first sx by 5 y/o capacity to hold pressure for better gas
● Exercise, nocturnal occurrence, seasonal, hx exchange
of allergy, stress
● Bronchiectasis – super dilatation of bronchial
tubes; active secretion of the cells → COPD
- with phlegm/mucus secretions

TYPES OF BRONCHIAL ASTHMA

Extrinsic or Atopic Asthma
➢ Results from an allergic reaction to inhalants
(fumes, seasonal change)
➢ Onset occurs in childhood – genetically
transmitted
17
PATHOPHYSIOLOGY OF ASTHMA Short-term Goal:
a. Liquefy secretions
b. Easily expectorate and drain secretions
c. Relieve spasms
d. Decrease swelling of airways

NURSING DIAGNOSIS
1. Impaired gas exchange r/t bronchial
obstruction, atelectasis, and hyperinflation
2. Parental anxiety r/t respiratory distress in child

Management:
● Nebulization
● Hydration – to decrease secretion
● Oxygen – O2 sat
● Positioning – orthopneic, upright, high flower
● TSB
● Support – emotional support

MEDICATIONS
Bronchodilators
➔ Xanthines, aminophylline
➔ Theophylline
Adrenergics
➔ Isuprel (isoproterenol)
➔ SE: increase heart rate tachycardia
DIAGNOSIS
Expectorant
● Bronchodilator reversibility exam – administer ➔ Guaifenesin, Robitussin
bronchodilators Mucolytics
➔ s/sx gone; reacts to bronchodilator – ➔ Acetylcysteine, Flumosil
asthma ➔ Mucomyst 600 mg/tab
➔ s/sx remains – COPD Steroids
➔ Given w/ PPI
S – Secretions — whitish, copious ➔ Prednisone
S – Spasm — laryngotracheal bronchospasm Prophylaxis (anti-allergy)
S – Swelling — edema in airway ➔ Na Intal
⇒ Airway obstruction → dyspnea ➔ Cromolyn Na

SIGNS AND SYMPTOMS OF BRONCHIAL ASTHMA NEBULIZER

● Successive episodes of coughing: dry,
hacking, non-productive cough
● Increased respiratory secretions: whitish,
stringy
● Wheezing on expiration
● Prolonged expiration
● Dry lips and mucous membranes
● Dyspnea, tachypnea, tachycardia
● Apprehension and restlessness
NURSING INTERVENTIONS
Long-term Goal:
● Pt will achieve an open airway and adequate
ventilation as manifested by normal VS and
relief of symptoms
● 3x w/ 15 mins interval
● e.g. 8:00 to 8:15: 1st nebulizer
- 8:30: next nebulizer
- PEFR (peak expiratory flow rate) –
done before and after nebulization; a
total of 6 times
- Ask pt to blow → check expiratory flow
rate on the calibration of the nebulizer
- Ask pt to blow again – document
- **must progress; number must
improve as we go along w/ the
nebulizations
● Deep breathing → inhale → exhale → check
PEFR
● After 3x pt still has DOB → pt may develop
status asthmaticus → intubation

18
 ● Obstructed; tube cannot go through
tracheostomy (more invasive)
● Check cardiac rate
METERED DOSE INHALER (MDI)
● Breathe in and breathe out all the way through
the mouth (not nose)
● Press down the inhaler and then breathe IN
slowly through the mouth – keep breathing in
until no longer able
● 3 puffs consecutively; maximum
Leukotriene Modifiers
Mechanism of Action:
➢ Selective and competitive antagonist of
leukotriene → affects the inflammatory
responses involved in asthma and allergic
rhinitis
➢ Newest generation of anti asthma drugs
➢ Leukotriene (LT) – chemical mediator that
can cause inflammatory changes in the lungs;
promote eosinophil migration → goes to
goblet cells → increased mucus production →
swelling → bronchoconstriction
Examples:
➢ Montelukast – for 6 y/o above
➢ Zafirlukast – 12 y/o and up
Indication:
➢ Do not use for treatment of acute episodes of
asthma
➢ Used only for prophylactic and maintenance
drug therapy for pt w/ chronic asthma
➢ Effective in reducing inflammatory symptoms
of asthma triggered by allergic and
environmental stimuli
Mast Cell Stabilizers
Mechanism of Action:
➢ Inhibits sensitized and mast cells
degranulation that occurs after exposure to
specific antigens
➢ Inhibits the release of mediators, histamine,
and SRS-A (the slow-acting substance of
anaphylaxis, a leukotriene) from the mast cell
➢ Indirectly inhibits calcium ions from entering
the mast cell, resulting in prevention of
mediator release
→ ➢ Inhibits intermediate and non-intermediate
bronchoconstrictive reactions induced by the
inhalation of antigens
➢ Cromolyn (Intal) – has no bronchodilatory
property; not used for acute episodes
Indication:
➢ Useful in children and some adults only as
maintenance therapy
➢ Cannot be used in the treatment of an acute
attack
➢ Safest antiasthmatic drugs
➢ Prophylactic treatment of bronchial asthma –
ask pt to take this daily
Administration:
➢ Inhalation
● Can be used w/ beta agonist and
xanthine derivatives
● Should not be discontinued abruptly –
rebound asthma → status asthmaticus
Side Effects:
➢ Cough
➢ Bad taste – give w/ water before and after
inhalation; metallic taste
➢ Bronchospasm
NURSING INTERVENTIONS
1. Administer bronchodilators, steroids, and
oxygen as ordered
2. Antibiotics as prescribed
3. Provide inhalant therapy when indicated
4. Proper bronchial hygiene
5. Minotaur breath sounds, O2 saturation
(95-100%)
6. Health teachings
TEACHINGS & DISCHARGE PLANNING
● Well-ventilated room
● Damp, dusting, avoid rugs, stuffed animals,
natural fibers
● Moderate exercise: swimming
● Deep breathing exercises
● Early treatment for upper respiratory tract
infection
● Avoid extremes of temperature
● Avoid powerful odors
● Seek medical attention to avoid complication
of Status Asthmaticus
19