CAD, ACS, MI, Hypertensive Crisis, Pulmonary Embolism, ARDS, Esophageal Varices, Liver Cirrhosis, Hepatic Encephalopathy

Critical

• Crucial – Crisis – Emergency – Serious

Critical Care Nursing

• care of the seriously-ill clients from point of injury/illness until discharge from intensive care

• Deals with human responses to life-threatening problems

• Comprehensive, specialized, and individualized nursing services which are rendered to patients with life-threatening conditions

Role of a Critical Care Nurse:

• Care for clients who are very ill

• Provide one-to-one care

• Responsible of making life and death decision

• At risk of injury and illness

• COMMUNICATION SKILL is of optimum importance

Goal of a Critical Care Nurse:

• Survival of the critically-ill patients and

• Restoring QUALITY of LIFE

• Helping families of critically-ill patients in coping with stress

Coronary artery disease (CAD)

• is a chronic condition characterized by plaque buildup in the coronary arteries

Acute coronary syndrome (ACS) definition

• is a sudden, severe reduction in blood flow to the heart, potentially leading to a heart attack or unstable angina, and is a manifestation of CAD

ACUTE CORONARY SYNDROME (ACS)

• includes a constellation of syndromes:

  • Chest pain

  • Unstable angina

  • Non ST elevation MI ( Non-STEMI )

  • ST elevation ( STEMI )

• Mortality rates and the risk associated with ACS is greatest during the first 30 days after presentation

  • early diagnosis and treatment is imperative

Pathophysiology of Acute Coronary Syndrome

• Late signs and symptoms of:

  • Stable angina

  • Unstable angina

Atherothrombosis

• Coronary artery with atherosclerotic plaque. The core of the atherosclerotic plaque contains inflammatory cells and lipids, which sustain chronic inflammation in the arterial wall.

• The atherosclerotic plaque is vulnerable (unstable). A rupture or erosion can damage its fibrous cap, releasing highly thrombogenic material. This activates platelets and coagulation factors.

• The activation of platelets and coagulation factors leads to the formation of a thrombus (atherothrombosis). The myocardium supplied by this artery becomes ischemic. If blood flow is not restored within 30 minutes, necrosis occurs.

Triad of I’s in ACS

• Ischemia

• Injury

• Infarct

• IT ALL REPRESENT OXYGEN SUPPLY PROBLEM

Ischemia

• reversible

Injury

• acute injury of both ischemia and infarct

Infarction

• irreversible cell death

ACS History of Presenting Illness:

• The most important diagnostic information is the patient’s “ story “

  • current symptoms

  • time of onset

  • pain assessment

  • past medical history / medications

ACS “Typical” Signs and Symptoms of MI

Chest discomfort:

• Crushing, pressure, tightness

• sustained

• Partially or unrelieved by rest

• Partially or unrelieved by NTG

• Pain radiates to Left arm shoulder and

ACS Associated Signs and Symptoms of MI

• Chest discomfort

• Denial

• Syncope / weakness

• Cool/pale/diaphoretic

• Dyspnea

• N/V

• Sense of impending doom

Unstable Angina/Non ST-Segment Elevation MI

• Diagnosis:

  • pain severity & presenting symptoms

  • ECG findings

  • serum cardiac markers

• When chest pain has been unremitting for >20mins

  • possibility of ST-Segment Elevation MI

Non-ST Elevation Myocardial Infarction (Non-STEMI)

• Differs from unstable angina mostly due to severity of ischemia

• Non-STEMI causes enough myocardial damage to release detectable cardiac markers indicating myocardial injury

  • Troponin I

  • Troponin T

  • Creatinine kinase (CK-MB)

• ECG changes may occur

  • No sustained ST segment elevation

• Can limit the area of infarction through medical and nursing interventions

ST Elevation Myocardial Infarction (STEMI)

• Loss of cardiac myocytes as a result of prolonged ischemia

• Myocardial ischemia does not cause immediate cell death

• It takes at least 4 to 6 hours for complete necrosis

• This is dependent upon the presence of collateral blood flow into the ischemic zone or coronary artery occlusion

ST-Segment Elevation MI (Heart Attack) Diagnosis:

• based on presenting S/Sx

• serum markers

• ECG

  • changes may not be present immediately after symptoms except dysrhythmias;

  • PVCs (Premature Ventricular Contractions) are common after MI

ST-Segment Elevation MI (Heart Attack) is Characterized by?

• ischemic death of myocardial tissue associated with atherosclerotic disease of coronary arteries

• Area of infarction is determined by the affected coronary artery & its distribution of blood flow

  • right coronary artery

  • left anterior descending artery

  • left circumflex artery

ACS Goal

• Early Reperfusion Therapy

ACS Reperfusion Therapy Outcomes Dependent Upon

• Time to treatment

• Early and full restoration of blood flow

Reperfusion Therapy

• Fibrinolytic therapy

• PTCA

Management of MI

• Morphine

  • Analgesia via IV

  • vasodilator property also

• Oxygen therapy via nasal prongs

• NTG (unless contraindicated)

  • SL

  • IV may be given to limit infarction size

  • most effective if given within 4hrs of onset

• Anticoagulants & Antiplatelets:

  • Heparin, ASA

• Thrombolytic Therapy

  • best results occur if initiated within 60-90mins of onset

  • Streptokinase & Urokinase –promote conversion of plasminogen to plasmin

• Anti-arrhythmics

  • Lidocaine

  • Atropine

  • Propranolol

• Stool softeners

• ECG monitoring

HYPERTENSIVE CRISIS

• is any clinical condition requiring immediate reduction in BP.

• is an acute and life threatening condition.

• The accelerated hypertension requires emergency treatment because target organ damage (brain, heart, kidneys, retina of the eye) can occur quickly.

• Death can be caused by stroke, kidney failure, or cardiac disease.

HYPERTENSIVE CRISIS ASSESSMENT

• An extremely high BP; usually the diastolic

• pressure is higher than 120 mm Hg

• Headache

• Drowsiness and confusion

• Blurred vision

• Changes in neurological status

• Tachycardia and tachypnea

• Dyspnea

• Cyanosis

• Seizures

HYPERTENSIVE CRISIS NURSING INTERVENTIONS

1. Maintain a patent airway.

2. Administer antihypertensive medications

3. intravenously as prescribed.

4. Monitor vital signs, assessing the BP every 5 minutes.

5. Maintain bed rest, with the HOB elevated at 45 degrees.

6. Assess for hypotension during the administration of antihypertensives; place the client in a supine position if hypotension occurs.

7. Have emergency medications and resuscitation equipment readily available.

8. Monitor IV therapy, assessing for fluid overload.

9. Insert a Foley catheter as prescribed.

10. Monitor intake and urinary output; if oliguria or anuria occurs, notify the HCP.

PULMONARY EMBOLISM

• This is a thrombotic or non-thrombotic embolus that lodges in the pulmonary artery system.

• It can damage part of the lung due to;

  • restricted blood flow

  • hypoxemia

  • affect other organs as well.

  • can be life-threatening

PULMONARY EMBOLISM RISK FACTORS

1. Injury or damage leading to blood clot formation

2. Inactivity for prolonged periods

3. Medical conditions or treatment procedures that cause blood to clot easily e.g. surgery DVT

PULMONARY EMBOLISM CAUSES

• Clinical Manifestations

• Virchow’s triad:

  • venous stasis,

  • coagulation problems,

  • vessel wall injury

• Chest pain

• Tachycardia, tachypnea

• Anxiety, restlessness

• Clammy or bluish skin

PULMONARY EMBOLISM DIAGNOSTICS

• CXR

• ABG analysis

• D-dimer test

  • detects clot fragments from clot lysis

• ECG

• V/Q scan / Pulmonary angiography/ spiral CT scan

PULMONARY EMBOLISM TREATMENT

• Oxygenation

  • = ET and mechanical ventilation

• Heparin therapy

• Surgery

  • = umbrella filter

  • = pulmonary embolectomy

• Prevention of development of DVT

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

• This is a syndrome with

  • inflammation and

  • increased permeability of the alveolocapillary membrane

• occurs as a result of an injury to the lungs.

• fatal when left undiagnosed or treated for 48hrs.

• Increase permeability of alveolo-capillary membrane

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) RISK FACTORS

• Critically ill patients

• Age (60y/o and above)

• Malignancy (cancers)

• Cigarette smoking, COPD

Direct Cause of ARDS

• drowning

Indirect Cause of ARDS

• drug overdose

• burns

• shock

COMMON CAUSES OF ARDS

• Aspiration

• Acute Pancreatitis

• Air Embolism

• Drug Overdose

• Diffuse Lung Disease

• Drowning

• Radiation

• Shock

• Sepsis

• Smoke Inhalation

STAGES OF ARDS

1. Exudative Phase

2. Proliferative

3. Fibrotic

EXUDATIVE PHASE

• 24 h after injury

• damage to the capillary membrane

• leak of fluid and CHON

• pulmonary edema

• damaged surfactants

• HYPOXEMIA = hallmark

• Inc RR, dec CO2

PROLIFERATIVE

• 14 days after

• Grow and reproduce

• Repair structure

• Reabsorption fluid

• Very dense and fibrous tissue

• HYPOXEMIA = worse

FIBROTIC

• 3 weeks after injury

• fibrosis of lung tissue

• major lung damage

• dead space in lungs

• poor prognosis

• Respiratory alkalosis

• NOT all patients enter this

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) CLINICAL MANIFESTATIONS

• Signs and symptoms are often exhibited within 24-48 hours after initial insult to the lungs

1. Restlessness

2. Hyperventilation, tachycardia, SOB

3. Hypoxemia

4. Severe: hypotension, cyanosis, decreased UO

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) RISK FACTORS

• Old age

• Smoking

• Drinking

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) DIAGNOSTICS

• After a pulse is found, a blood sample is taken from the artery

• Diagnostics

  • chest x-ray

  • white out lungs

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) TREATMENT & GOALS

• Goal: → improving and maintaining oxygenation and prevent respiratory and metabolic complications

1. Fluid management to maintain tissue perfusion

2. Corticosteroid therapy to decrease permeability of the alveolocapillary

   Goal: → improving and maintaining oxygenation and prevent respiratory and metabolic complications

3. Nutrition – enteral feeding

4. Supplemental oxygen

   • Mechanical Ventilation

     • a form of artificial ventilation that takes over all or part of the work performed by the respiratory muscles and organs

     • Modes, Settings, Alarms

Major Liver Functions

1. Biotransformation

2. Storage

3. Synthesis

Major Liver Functions: Biotransformation

• Ammonia

• Hemoglobin

• Drugs

• Xenobiotics

• Glucose

Major Liver Functions: Storage

• Vitamins

• Glycogen

• Lipids

Major Liver Functions: Synthesis

• Albumin

• Growth factors

• Urea

Liver Normal Function

1. Stores glycogen

2. Synthesizes proteins

3. Synthesizes globulins

4. Synthesizes clotting factors

5. Secretes BILES

6. Converts ammonia to urea

7. Stores Vit and minerals

8. Metabolizes estrogen

Liver Failure is also known as?

• Hepatic Failure

• a condition in which the organ fails to fulfill its functions or is unable to meet the demands placed upon it.

Signs of liver disease

• Jaundice

• Easy bleeding or bruising

• Ascites

• Esophageal varices

Complication:

• bleeding

Others:

• Jaundice (yellow skin and eyes)

• Encephalopathy (confusion)

• Spider angioma

• Lack of body hair

• Muscle wasting

• Widened blood vessels

• Ascites (fluid buildup)

• Red palms

COMPLICATIONS: CIRRHOSIS

1. Portal Hypertension

• persistent increase in pressure in the portal vein that develops as a result of obstruction to flow

2. Ascites

• results from venous congestion of the hepatic capillaries

• Accumulation of fluid in the peritoneal cavity

• leads to plasma leaking directly from the liver surface and portal vein.

3. Bleeding esophageal varices

• Fragile, thin-walled, distended esophageal veins that become irritated and rupture

Esophageal Varices Symptoms

• hematemesis

• melena

• light headedness

• loss of consciousness in severe cases

Treatment: Esophageal Varices

1. Esophageal varices

• Vasopressin

  • first line treatment

2. Use of Balloon Tamponade

• Sengstaken-Blakemore

• Minnesota tubes

3. First-line treatment to decrease bleeding

• volume replacement

  • especially for signs of shock

• IV fluid and / or blood products

• Gastric lavage

• Blood transfusion

  • Limit: Hemoglobin level of 7 g/dL

• Prophylactic Antibiotic

  • IV Ceftriaxone 1 gm daily x 7 days

  • Oral Norfloxacin 400 mg BID x 7 days

• Liver transplant

Treatment: Re-Bleeding - Esophageal Varices

• Beta blocker

  • Non-selective beta-blockers (NSBBs)

  • cornerstone of treatment for prevention of first bleeding and rebleeding of esophageal varices in patients with cirrhosis

    • Propranolol

    • Nadolol

    • Timolol

    • Carvedilol

      • a new NSBB that is increasingly used

      • has a greater portal pressure reducing effect than propranolol

      • safe in patients with compensated and decompensated cirrhosis

• Endoscopic Band Ligation

COMPLICATIONS: CIRRHOSIS

4. Coagulation defects

   • Decreased synthesis of bile fats in the liver prevents the absorption of fat-soluble vitamins.

   • Without vitamin K and clotting factors II, VII, IX, and X, the client is prone to bleeding.

5. Hepatic Encephalopathy

   • End-stage hepatic failure

Hepatic Encephalopathy Pathophysiology

• Brain impairment due to diminished liver function

• Underlying causes:

  • Increased levels of ammonia

  • Diminished cellular energy supplies

  • Change in blood-brain barrier permeability

Cirrhosis Treatment goals:

• Identification of cause

• Correct the cause or

• Slow progression

• Supportive therapy

  • Lactulose

  • Neomycin

Hepatic Encephalopathy - Management:

• Mainly supportive

• Ensure that LOC status is not from other cause

  • Check blood glucose levels

  • Assess for trauma and overdose

  • Take a medical history

  • Monitor asterixis

Hepatic Encephalopathy - Pharmacotherapeutics:

• Lactulose

  • decreases the pH of the bowel

  • decreases production of ammonia by bacteria in the bowel

  • facilitates the excretion of ammonia.

• Neomycin

  • inhibit protein synthesis in bacteria and decrease the production of ammonia.