Medical-Surgical Nursing LECTURE

NCM 4164 | BATCH 2023

COLLEGE OF NURSING – ATENEO DE DAVAO UNIVERSITY
LECTURER/S: NCM PROFS |
REFERENCES: PPT, Handouts, Internet | Acute Biologic Crisis
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Acute Biologic Crisis

- Condition that may result to patient mortality if left unattended within a brief period of time.
- Condition that warrants immediate attention for the reversal of the disease process and prevention of
further morbidity and mortality.

CARDIOVASCULAR SYSTEM

CORONARY ARTERY DISEASE (CAD)

- Most prevalent type of cardiovascular disease in adults.
- The most common cause of CAD is atherosclerosis, an abnormal accumulation of lipid, or fatty
substances, and fibrous tissue in the lining of arterial blood vessel walls.
- These fatty substances block and narrow the coronary vessels in a way that reduces blood flow to the
myocardium.
Types Of CAD
I. ATHEROSCLEROSIS
Definition Signs and Symptoms
- Most common cause of cardiovascular disability - Chest pain (angina)
that leads to death. - Dyspnea / shortness of breath (SOB)
- Causes narrowing of the artery. - Peripheral edema, weight gain, abdominal
- Incomplete occlusion of the coronary arteries distention
leads to ischemia. - Palpitations
- Complete occlusion of the coronary arteries leads - Indigestion
to Myocardial Infarction. - Nausea
- Numbness

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 - The heart will pump harder to meet the O2
demand leading to Heart Failure.

Nursing Responsibilities
- Controlling cholesterol abnormalities
- Diet and lifestyle change
- Weight reduction and exercise
- Lipid lowering agents

- Smoking cessation
- Management of HPN
- Antihypertensive
- Exercise

- Management of DM
- Hypoglycemic agents

Risk Factors Pathophysiology

Nonmodifiable Modifiable Begin as fatty streaks of lipids that are deposited in
- Increasing age - Hyperlipidemia the intima of the arterial wall (lesions)
- Gender - Cigarette smoking ↓
- Race - Hypertension Triggered by an inflammatory response (injury to the
- Family history of - Diabetes Mellitus vascular endothelium)
CAD - Obesity ↓
- Physical inactivity Attraction of inflammatory cells such as monocytes
(macrophages)
Metabolic Syndrome ↓
- Insulin resistance Macrophages ingest lipids and attaches to the arterial
- Central obesity wall
- Dyslipidemia ↓
- Blood pressure Macrophages release biochemical substances that
persistently greater attract platelets and initiate clotting
than 130/85 mmHg ↓
- Proinflammatory state Smooth muscle cells w/ in the vessel wall proliferate
- Prothrombic state and form a fibrous cap over a core filled with lipid
and inflammatory infiltrate
↓
These plaques protrude and narrow the lumen,
obstructing blood flow

II. ANGINA PECTORIS

Definition Signs and Symptoms

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 - Angina Pectoris is a clinical syndrome usually
characterized by episodes or paroxysms of pain
or pressure in the anterior chest.
- The cause is insufficient coronary blood flow,
resulting in a decreased oxygen supply when
there is increased myocardial demand for oxygen
in response to physical exertion or emotional
stress.
- In other words, the demand for oxygen exceeds
the supply.
- Chest pain radiating to the neck, jaw, shoulders,
and upper arms (usually the left).
- Mild indigestion.
- Choking or heavy sensation in the upper chest.
- Shortness of breath
- Weakness or numbness in the upper extremities
- Other symptoms: pallor, diaphoresis, dizziness,
and N/V

Assessment & Diagnostic Findings (Angina Pectoris)

- Patient’s history (Related to the clinical
manifestations of ischemia)
- 12L-ECG
- C-Reactive Protein (CRP)
- Cardiac Biomarkers

Medical Management Nursing Responsibilities

Pharmacologic Therapy - Treating the Angina
- Nitroglycerin - Instruct patient to stop all activities, lie down
- Beta-Adrenergic Blocking Agents in bed, and place in semi-Fowler’s position
(Metropolol,Atenolol) - Note location and severity of chest pain
- Calcium Channel Blocking Agents - Perform ECG as ordered
(Amlodipine,Diltiazem) - Oxygen administration
- Antiplatelet and Anticoagulant Medications
- Beta Blockers
Oxygen Therapy - Assess pulse rate and blood pressure before
- Instruct patient to stop all activities, lie down in administration; withhold if bradycardia and
bed, and place in semi-Fowler’s position hypotension is noted.
- Note location and severity of chest pain - Administer with food; it may cause GI upset.
- Perform ECG as ordered - Do not administer with asthma; it may cause
- Oxygen administration bronchoconstriction.
- Give with caution to patients w/ DM
(hypoglycemia).
- Antidote for beta blocker poisoning: Glucagon.

- Nitrates (Nitroglycerine)
- Maximum of 3 doses at 5 minutes interval.
- Offer sips of H2O before giving sublingually.
- Rotate skin sites for nitroglycerine patch.

- Aspirin / Anti-Platelets
- Watch out for bleeding
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 - Avoid straining at stool to avoid rectal
bleeding
- Should be given with food
- Observe for toxicity --- Tinnitus (ringing of
ears)
- May cause bronchoconstriction; observe for
wheezing
Pathophysiology
Spasm/obstruction of coronary arteries
↓
Myocardial ischemia
↓
Reduced O2 supply to myocardium
↓
Chest pain---Angina pectoris

ACUTE CORONARY SYNDROME (ACS)

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 Definition Signs and Symptoms
- An emergent situation characterized by an acute - Sudden chest pain not relieved by rest
onset of myocardial ischemia that results in - Shortness of breath (SOB)
myocardial death if definitive measures do not - Indigestion
occur promptly. - Nausea
- The spectrum of ACS includes unstable angina, - Anxiety Cool, pale, moist skin
Non -ST Elevation Myocardial Infarction - Tachycardia
(NSTEMI), and ST Elevation Myocardial Infarction - Tachypnea
(STEMI). Assessment & Diagnostic Findings
- Patient History
- 12-lead ECG
- Echocardiogram (2D-Echo)
- Cardiac biomarkers
• Troponin I & Troponin T, Creatine Kinase MB
(CK-MB), Myoglobin
Nursing Responsibilities
- Controlling cholesterol abnormalities
- Diet and lifestyle change
- Weight reduction and exercise
- Lipid lowering agents

- Smoking cessation
- Management of HPN
- Antihypertensive
- Exercise

- Management of DM
- Hypoglycemic agents
Electrocardiogram (ECG) Pathophysiology
- Should be obtained 10 minutes from the time a Formation of plaque/fatty deposits (Atherosclerosis)
patient reports chest pain. ↓
- Expected ecg changes are t-wave inversion, st- Rupture of atherosclerotic plaque
segment elevation, and development of an • Reduced blood flow in the coronary artery
abnormal q wave. ↓

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 Clot aggregation that forms into a thrombus on top of
the coronary lesion (partial artery occlusion)
↓
Chest pain --- Unstable Angina
Cardiac Biomarkers
Troponin I / Troponin T
- A protein found in the myocardium, regulates the myocardial contractile process.
- There are three isomers of troponin: C, I, and T. Troponins I and T are specific for cardiac muscle.
- An increase in the level of troponin in the serum can be detected within a few hours during acute MI.
- Remains elevated for a long period, often as long as 3 weeks (Recent myocardial damage can be detected).

Creatinine Kinase
- There are three creatine kinase (CK) isoenzymes: CK-MM (skeletal muscle), CK-MB (heart muscle), and CK-
BB (brain tissue).
- CK-MB is the cardiac-specific isoenzyme.
- Found mainly in cardiac cells and therefore increases only when there has been damage to these cells.

Myoglobin
- A heme protein that helps transport oxygen.
- Like CK-MB enzyme, myoglobin is found in cardiac and skeletal muscle.
Myoglobin level starts to increase within 1 to 3 hours and peaks within 12 hours after the onset of symptoms.

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 ACUTE MYOCARDIAL INFARCTION
- Occurs when one of the heart's coronary arteries is blocked suddenly or has extremely slow
blood flow.
- Portion of the cardiac muscle dies.
- Therefore, contractility decreases.
- Impaired ventricular wall motion further decreases cardiac output.

ISCHEMIA VS. INFARCTION

1. Ischemia – not enough oxygen (oxygen supply to demand imbalance); without tissue death
2. Infarction – tissue death due to ischemia

Basic Pathophysiology
Blocked Coronary Artery
↓
Impeded Blood Flow
↓
Damaged Tissue
Types Of MI
I. STEMI
Definition Signs and Symptoms
- An ST-elevation myocardial infarction (STEMI) is - Chest pain (angina)
a type of heart attack that is more serious and - Dyspnea / shortness of breath (SOB)
has a greater risk of serious complications and - Pressure or tightness in the chest
death. It gets its name from how it mainly affects - Pain in the chest that radiates in the back, jaw,
the heart's lower chambers and changes how and other areas of the upper body.
electrical current travels through them. - Tachycardia
- Sweating
- Nausea and Vomiting
- Cough
- Dizziness

CLASSIFICATION OF SEVERITY: KILLIPS

Class I Class II Class III Class IV

No Findings of Pulmonary Cardiogenic

evidence mild to Edema Shock -
of heart moderate Systolic BP <
failure heart 90 mm Hg
failure and signs of
- S3 gallop hypoperfusion
- Rales < such as
half-way oliguria,
up lung cyanosis, and
fields - sweating
Elevated
jugular
venous
pressure
Medical Management Nursing Responsibilities

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Goal - Relieving Pain and Other Signs & Symptoms of
- To minimize myocardial damage Ischemia
- To preserve myocardial function - Improving Respiratory Function
- To prevent complications - Promoting Adequate Tissue Perfusion Reducing
Anxiety
Reperfusing the area of damage - Monitoring and Managing Potential
- Emergency use of thrombolytic medications Complications
- Percutaneous Coronary Intervention Pharmacologic Therapy
- Analgesics (Morphine)
Minimizing myocardial damage is accomplished by: - Angiotensin-converting enzyme (ACE) inhibitors
- Reducing myocardial oxygen demand - Thrombolytics (Alteplase or t-PA)
- Increasing oxygen supply with medications - Blood Thinners (Aspirin/Clopidogrel)
- Oxygen administration - Nitrates
- Bed rest - Beta Blockers (to reduce cardiac workload)
TREATMENT GUIDELINES FOR ACUTE MI
Use rapid transit to the hospital.
↓
Obtain 12-lead electrocardiogram (ECG) to be read
within 10 minutes.
↓
Obtain laboratory blood specimens of cardiac
biomarkers, including troponin.
↓
Obtain other diagnostics to clarify the diagnosis.

Begin routine medical interventions

- Supplemental oxygen
- Nitroglycerin
- Morphine
- Aspirin 162 to 325 mg
- Beta-blocker
- Angiotensin-converting enzyme inhibitor within
24 hours
- Anticoagulation with heparin and platelet
inhibitors
Evaluate for indications for reperfusion therapy:
- Percutaneous coronary intervention
- Thrombolytic therapy

Continue therapy as indicated:

- Intravenous heparin, low-molecular-weight
heparin, bivalirudin, or fondaparinux
- Clopidogrel (Plavix)
- Glycoprotein IIb/IIIa inhibitor
- Bed rest for a minimum of 12 to 24 hours

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 HEART FAILURE
- Inability of the heart to pump sufficient blood
to meet the needs of the tissues for oxygen
and nutrients.
- Recognized as a clinical syndrome
characterized by signs & symptoms of fluid
overload or of inadequate tissue perfusion.
- In HF, there is a problem with contraction of
the heart (systolic dysfunction) or filling of the
heart (diastolic dysfunction) that may or may
not cause pulmonary or systemic congestion.

Types Of HF
Systolic Heart Failure Diastolic Heart Failure
- More common type - Less common type
- Alteration in ventricular contraction - Alteration in ventricular filling
- Characterized by a weakened heart muscle - Characterized by a stiff and non-
compliant heart muscle

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 Assessment of Heart Failure Nursing Responsibilities

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 - Assessment of left ventricular functioning - Promoting activity tolerance
- Determined via the echocardiogram (2D-Echo) - Managing fluid volume
- An assessment of the ejection fraction (EF) is - Controlling anxiety
performed to assist in determining the type of HF. - Monitoring and managing potential
- EF is calculated by subtracting the amount of blood complications
present in the left ventricle at the end of systole from Medical Management
the amount present at the end of diastole and Goal
calculating the percentage of blood that is ejected. - To relieve patient symptoms
- A normal EF is 55% to 65% of the ventricular volume. - To improve functional status and quality of
life
- To extend survival

- Supplemental oxygen
- Providing comprehensive education and
counseling to the patient and family.
- Lifestyle recommendations include:
- Restriction of dietary sodium
- Avoidance of excessive fluid intake,
alcohol, and smoking
- Weight reduction when indicated
- Regular exercise

Surgical Management
- Coronary artery revascularization with PCI
- Coronary artery bypass (CABG) surgery
- Heart Valve repair/replacement Ventricular
- Assist Device Heart Transplant

Etiology
- Atherosclerosis
- Coronary artery disease
- Cardiomyopathy
- Hypertension
- Valvular disorders
- Diabetes mellitus
Pathophysiology
Myocardial Dysfunction
• AMI
• HPN
• Valvular disease
↓
(I) Decrease in cardiac output; (2) Decrease in
systemic pressure; (3) Decreased perfusion to
kidneys
↓
Activation of baroreceptors
• Left ventricle
• Aortic arch
• Carotid sinus
↓
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 Stimulation of vasomotor regulatory centers in
medulla
↓
Activation of sympathetic nervous system -
vasoconstriction
↓
Ventricular remodeling
• Hypertrophy and dilation of
ventricle
• Large cells
• Impaired contractility

CARDIOMYOPATHY
1. Dilated – ventricular wall is dilated and becomes thin and weak.
2. Hypertrophic – Heart muscle grows thicker than usual, leaving less room for blood filling.
3. Restrictive – heart muscle become rigid and unable to stretch.

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 Clinical Manifestations (Left-Sided HF) Clinical Manifestations (Right-Sided HF)
- Dyspnea - Jugular vein distention
- Cough - Dependent edema
- Crackles - Hepatomegaly
- Low O2 saturation levels - Ascites
- S3 heart sound - Anorexia
- Orthopnea - Nausea
- Paroxysmal nocturnal dyspnea - Weakness
- Oliguria - Weight gain
- Altered digestion
- Dizziness
- Lightheadedness
- Confusion
- Restlessness
- Anxiety
- Tachycardia
- Fatigue
Assessment & Diagnostic Findings Medical Management
2D Echo Goal
• CXR - To relieve patient symptoms
• ECG - To improve functional status and quality of
↓ life
Pro BNP - To extend survival
↓
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 Serum electrolytes Management
↓ - Supplemental oxygen
Blood urea nitrogen (BUN) - Providing comprehensive education and
↓ counseling to the patient and family.
Creatinine - Lifestyle recommendation include:
↓ • Restriction of dietary sodium
Thyroid-stimulating hormone • Avoidance of excessive fluid intake,
↓ alcohol, and smoking
Complete blood cell count • Weight reduction when indicated
↓ • Regular exercise
Routine Urinalysis
Pharmacologic Therapy Surgical Management
1. ACE inhibitors (captopril, enalapril, perindopril) - Coronary artery revascularization with PCI
2. Angiotensin II Receptor Blockers (Valsartan) - Coronary artery bypass (CABG) surgery
3. Betablockers (carvedilol, metoprolol) - Heart valve repair/replacement
4. Diuretics (furosemide, metolazone) - Ventricular assist device
5. Digitalis (digoxin) - Heart transplant
6. Calcium Channel Blockers (amlodipine,
felodipine)
Nursing Responsibilities
- Promoting activity tolerance
- Managing fluid volume
- Controlling anxiety
- Monitoring and managing potential complications

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 Medical-Surgical Nursing LECTURE
NCM 4164 | BATCH 2023
COLLEGE OF NURSING – ATENEO DE DAVAO UNIVERSITY
LECTURER/S: NCM PROFS |
REFERENCES: PPT, Handouts, Internet | Arrhythmias
|
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Arrythmias
- Any disturbance in the heart rate, rhythm, site of origin, or conduction of cardiac electrical impulse.
- Disorder of the formation or conduction (or both) of the electrical impulse within the heart.
- Can be single aberrant (isolated) or prolonged (sustained).
- Diagnosed by analyzing the electrocardiographic (ECG) waveform

HISDEBS
• H – Hypoxia – If the heart id deprived of oxygen
• I – Ischemia and infarction – Damaged heart muscle
• S – Sympathetic Stimulation – Enhanced sympathetic actions (hyperthyroidism, heart failure,
nervousness, and exercise)
• D – Drugs – many drugs can induce arrythmia including anti-arrhythmic drugs 9amiodarone),
bronchodilators salbutamol inhalation), digoxin, metoprolol, ivabradine.
• E – Electrolyte Disturbances – mostly K+, Ca+, and Mg+ imbalance (Kidney failure, Insulin Drip,
Dehydration)
• B – Bradycardia – very slow heart rate that can lead to arrythmia (Sick Sinus Syndrome)
• S – Stretch – Enlarged heart (CHF and Valvular Disease)

How to Diagnose Arrythmias?

1. 12 Lead ECG – the most typical
2. Holter Monitoring – if the patient has signs of suspected arrythmias but difficulty/unlikely to be
captured.
3. Telemetry – continuous monitoring when the patient is admitted.

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 SINUS NODE ARRYTHMIAS / DYSRRYTHMIAS
- Sinus arrhythmia is a variation of normal sinus rhythm that characteristically presents with an irregular
rate in which the change in the R-R interval is greater than 0.12 seconds.
Types Of Sinus Node Arrythmias / Dysrhythmias
I. SINUS TACHYCARDIA
- Occurs when the sinus node creates an impulse at a faster-than-normal rate.
1. Ventricular and atrial rate: Greater than 100 in the adult, but usually less than 120.
2. Ventricular and atrial rhythm: Regular
3. QRS shape and duration: Usually normal but may be regularly abnormal.
4. P wave: Normal and consistent shape; always in front of the QRS, but may be buried in the preceding
T wave
5. PR interval: Consistent interval between 0.12 and 0.20 seconds
6. P:QRS ratio: 1:1

II. SINUS BRADYCARDIA

- Occurs when the sinus node creates an impulse at a slower-than-normal rate.

1. Ventricular and atrial rate: Less than 60 in adults.

2. Ventricular and atrial rhythm: Regular
3. QRS shape and duration: Usually normal but may be regularly abnormal.
4. P wave: Normal and consistent shape; always in front of the QRS
5. PR interval: Consistent interval between 0.12 and 0.20 seconds

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 6. P:QRS ratio: 1:1

III. SINUS ARRYTHMIA

- It involves cyclic changes in the heart rate during breathing.
- Occurs when the sinus node create an impulse at an irregular rhythm.
- The rate usually increases with inspiration and decreases with expiration.

1. Ventricular and atrial rate: 60 to 100 in the adult.

2. Ventricular and atrial rhythm: Irregular
3. QRS shape and duration: Usually normal but may be regularly abnormal.
4. P wave: Normal and consistent shape; always in front of the QRS
5. PR interval: Consistent interval between 0.12 and 0.20 seconds
6. P:QRS ratio: 1:1

IV. SINUS ARREST

- AKA “sinus pause”
- A medical condition wherein the sinoatrial node of the heart transiently ceases to generate the electrical
impulses that normally stimulate the myocardial tissues to contract and thus the heart to beat.

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 SINUS ARREST WITH JUNCTIONAL ESCAPED BEAT
- AV node takes over; presence of sinus pause.

JUNCTIONAL ESCAPE BEATS

- AV node takes over. HR is between 40-60 bpm.

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 SUPRAVENTRICULAR ARRYTHMIAS (ATRIUM)
- A supraventricular arrhythmia is an irregular heart rate that begins above the ventricles, which are the
two lower chambers of the heart. Most, but not all, supraventricular arrhythmias begin in the atria, the
top chambers of the heart. They may cause the heart to beat too fast, too slow, or irregularly.
Types Of Supraventricular Arrythmias
I. PREMATURE ATRIAL CONTRACTION (PAC)
- An atrial premature beat that comes too early; that is, it intrudes itself before the next anticipated sinus
wave.
- Originates from the atrium; caused by an impulse from an “ectopic” site.
- Caused by cardiac excitability (caffeine, alcohol, nicotine, stretched atrial myocardium, anxiety,
hypokalemia, atrial ischemia, injury or infarction).
1. Ventricular and atrial rate: Depends on the underlying rhythm (eg, sinus tachycardia).
2. Ventricular and atrial rhythm: Irregular due to early P waves, creating a P-P interval that is shorter than
the others.
3. QRS shape and duration: The QRS that follows the early P wave is usually normal, but it may be
abnormal (aberrantly conducted PAC).
4. P wave: An early and different P wave may be seen or may be hidden in the T wave; other P waves in
the strip are consistent.
5. PR interval: The early P wave has a shorter-than-normal PR interval, but still between 0.12 and 0.20
seconds.
6. P:QRS ratio: 1:1

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 II. PREMATURE JUNCTIONAL COMPLEX (PJC)
- No visible P wave, but sometimes a retrograde P wave may be seen.
- It is an aberrant impulse that originates in the atrioventricular node (junctional tissue) and occurs early or
prematurely before the next expected P wave.
- Caused by cardiac excitability; Originates from the AV node area (or junction)

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 III. SUPRAVENTRICULAR TACHYCARDIA (SVT)
- A rhythm that originates in the conduction system above the ventricles.

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 - Its onset is sudden, usually initiated by a premature supraventricular contraction (atrial or junctional), and
its termination is just as abrupt.
- An abnormally fast heartbeat (ranging from 160-200bpm) originating above the ventricles (the atria and
the AV node/junction).

Causes of SVT
- Heart failure/Heart Disease
- Thyroid disease
- Chronic lung disease
- Smoking
- Excessive alcohol intake
- Excessive caffeine intake
- Drug use, such as cocaine and methamphetamines
- Certain medications, including asthma medications and over-the-counter cold and allergy drugs
- Surgery (Open-heart surgery)

Clinical Manifestations of SVT

- A fluttering in your chest
- Palpitations
- Shortness of breath (SOB)
- Lightheadedness or dizziness
- Profuse sweating
- A pounding sensation in the neck
- Syncope
-

IV. ATRIAL FLUTTER

- Occurs because of a conduction defect in the atrium and causes a rapid, regular atrial rate, usually between
250 and 400 times per minute.
- Caused by an electrical impulse that travels around in a localized, self-perpetuating loop that is commonly
located in the right atrium.
- Atrial Flutter denotes a “sawtooth” presentation in the electrocardiogram (ECG).

1. Ventricular and atrial rate: Atrial rate ranges between 250 and 400; ventricular rate usually ranges
between 75 and 150.
2. Ventricular and atrial rhythm: The atrial rhythm is regular; the ventricular rhythm is usually regular but
may be irregular because of a change in the AV conduction QRS shape and duration: Usually normal,
but may be abnormal or may be absent.
3. P wave: Absent normal P-wave; Saw-toothed shape; these waves are referred to as F waves.
4. PR interval: Multiple F waves may make it difficult to determine the PR interval.
5. P:QRS ratio: 2:1, 3:1, or 4:1

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 Causes of Atrial Flutter
- Pulmonary embolus, pulmonary disease, post-operative, pericarditis.
- Ischemic heart disease, idiopathic (“lone AF”), intravenous central line (in right atrium).
- Rheumatic valvular disease (specifically mitral stenosis or mitral regurgitation).
- Anemia, alcohol (“holiday heart”), advanced age, autonomic tone (vagally-mediated atrial fibrillation).
- Thyroid disease (hyperthyroidism).
- Elevated blood pressure (hypertension), electrocution.
- Sleep apnea, sepsis, surgery

Clinical Manifestations of Atrial Flutters

- Fast heart rate
- Palpitations
- Shortness of breath (SOB)
- Tightness in the chest
- Dizziness or lightheadedness
- Fatigability
V. ATRIAL FIBRILLATION
- Irregularly Irregular heartbeat.
- An uncoordinated atrial electrical activation that causes a rapid, disorganized, and uncoordinated
twitching of atrial musculature.
- This causes the atria to twitch, quiver, and is felt as an irregular heartbeat or pulse.

1. Ventricular and atrial rate: Atrial rate is 300 to 600; ventricular rate is usually 120 to 200 in untreated
atrial fibrillation.
2. Ventricular and atrial rhythm: Highly irregular.
3. QRS shape and duration: Usually normal, but may be abnormal.
4. P wave: No discernible P waves; irregular undulating waves that vary in amplitude and shape are seen
and are referred to as fibrillatory or f waves.
5. PR interval: Cannot be measured.
6. P:QRS ratio: Many:1

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Causes of A-Fib
- High blood pressure
- Heart attack
- Coronary artery disease
- Abnormal heart valves
- Congenital heart defects
- An overactive thyroid gland or other metabolic imbalance
- Exposure to stimulants, such as medications, caffeine, tobacco or alcohol
- Sick sinus syndrome — improper functioning of the heart's natural pacemaker
- Lung diseases
- Previous heart surgery
- Stress due to surgery, pneumonia or other illnesses
- Sleep apnea

Clinical Manifestations of A-Fib

- Palpitations, which are sensations of a racing, uncomfortable, irregular heartbeat or a flip-flopping in your
chest.
- Weakness
- Reduced ability to exercise
- Fatigue
- Lightheadedness
- Dizziness
- Shortness of breath
- Chest pain

Treatment of A-Flut and A-Fib

2 Approaches:
1. Rate control
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 2. rhythm control

Treatment – Rate Control Treatment – Ryhthm Control

- beta blockers (Metopolol, Carvedilol, Atenolol) A rhythm control strategy is employed when rate
- Nondihydropyridine Calcium Channel Blockers control is not successful in completely eliminating
(Diltiazem, Verapamil) symptoms from atrial flutter.
- Digoxin
a. Cardioversion
b. Anti-arrhythmic drug therapy
c. Ablation

Synchronized Cardioversion
- Synchronized cardioversion is a procedure that
a transthoracic electrical current is applied to
the anterior chest to terminate a life-
threatening or unstable tachycardic arrhythmia.
- It is performed on patients that still have a pulse
but are hemodynamically unstable.
Nursing Interventions (Independent) Nursing Interventions (Dependent)
- Encourage a heart-healthy diet (low salt, low fat - Administer antiarrhythmic and anticoagulant
diet) medications as ordered
- Encourage to increase physical activity and - Synchronized cardioversion
frequent exercise - ECG monitoring
- Advise to avoid smoking
- Advise to keep a healthy weight (according to
normal BMI)
- Encourage to limit or avoid excessive alcohol
intake
- Advise importance of reduction of stress
- Encourage to have adequate rest periods
- Instruct to avoid over-the-counter medications,
as some cold and cough medications contain
stimulants that may trigger a rapid heartbeat
- Discourage intake of stimulant drugs such as
cocaine and methamphetamines

VENTRICULAR DYSRHYTHMIAS
- Ventricular arrhythmias are abnormal heart rhythms that make the lower chambers of your heart twitch
instead of pump. This can limit or stop your heart from supplying blood to your body. While some of these
arrhythmias are harmless and don't cause symptoms, some can have serious — or even deadly — effects
on your body.

Types Of Ventricular Dysrhythmias

I. Premature Ventricular Contraction (PVC)

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 - An impulse that starts in a ventricle and is conducted through the ventricles before the next normal sinus
impulse.
- PVC’s are extra, abnormal heartbeats that begin in the ventricles and disrupt your regular heart rhythm,
sometimes causing you to feel a skipped beat or palpitations.
- Can be isolated or intermittent/alternately with normal sinus beats
1. Ventricular and atrial rate: Depends on the underlying rhythm (eg, sinus rhythm).
2. Ventricular and atrial rhythm: Irregular due to early QRS, creating one PR interval that is shorter than
the others. PP interval may be regular.
3. QRS shape and duration: Duration is 0.12 seconds or longer; shape is bizarre and abnormal.
4. P wave: Visibility of P wave depends on the timing of the PVC; may be absent (hidden in the QRS orT
wave) or in front of the QRS.
5. PR interval: If the P wave is in front of the QRS, the PR interval is less than 0.12 seconds.
6. P:QRS ratio: 0:1; 1:1

II. VENTRICULAR TACHYCARDIA (V-TACH)

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 - Defined as three or more PVCs in a row, occurring at a rate exceeding 100 bpm.
- A regular, very fast rhythm that arises from the ventricles.
- V-tach can be polymorphic.
- Sustained V-tach signifies cardiac arrest and needs immediate treatment.

1. Ventricular and atrial rate: Ventricular rate is 100 to 200 bpm; atrial rate depends on the underlying
rhythm (eg, sinus rhythm).
2. Ventricular and atrial rhythm: Usually regular; atrial rhythm may also be regular.
3. QRS shape and duration: Duration is 0.12 seconds or more; bizarre, abnormal shape; wide and even
QRS (like tombstones).
4. P wave: No P-wave or very difficult to detect, so atrial rate and rhythm may be indeterminable.
5. PR interval: None or very irregular, if P waves are seen.
6. P:QRS ratio: Difficult to determine, but if P waves are apparent, there are usually more QRS complexes
thanP waves.

Causes of V-Tach
- Heart disease / Heart failure
- Caffeine intake
- Excessive alcohol intake
- Nicotine intake
- AMI
- Hypoxia
- Electrolyte Imbalance

Clinical Manifestations of V-Tach

- Chest pain
- Dizziness
- Desaturation
- Fainting (syncope)
- Shortness of breath
- Lethargy
- Palpitations
- Elevated heart rate cardiac arrest

Treatments of V-Tach
- Synchronized Cardioversion (if with pulse)
- Anti-arrhythmic Drug Therapy
- Ablation

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 III. VENTRICULAR FIBRILLATION (V-FIB)
- Occurs when the heart beats with rapid, erratic electrical impulses. This causes pumping chambers in your
heart (the ventricles) to quiver uselessly.
- Characterized by the absence of an audible heartbeat, a palpable pulse, and respirations.
- 1 of only 2 Shockable rhythms
- Because there is no coordinated cardiac activity, cardiac arrest and death are imminent if the dysrhythmia
is not corrected.
- Characterized by irregular random waveforms of varying amplitude, with no identifiable P wave, QRS
complex or T wave.

1. Ventricular rate: Greater than 300 per minute

2. Ventricular rhythm: Extremely irregular, without a specific pattern
3. QRS shape and duration: Irregular, undulating waves without recognizable QRS complexes
4. P wave: No P wave seen

Causes of V-Fib Treatment of V-Fib

- Heart Disease / Heart Failure - Cardiopulmonary Resuscitation
- - Defibrillation
- Caffeine intake - Epinephrine
- Excessive alcohol intake - Amiodarone
- Nicotine Intake
- AMI
- Hypoxia
- Electrolyte Imbalance

Clinical Manifestations of SVT

- Chest pain
- Rapid heartbeat (tachycardia)
- Dizziness
- Nausea
- Shortness of breath
- Loss of consciousness

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 - Pulselessness
Medical-Surgical Nursing LECTURE
NCM 4164 | BATCH 2023
COLLEGE OF NURSING – ATENEO DE DAVAO UNIVERSITY
LECTURER/S: NCM PROFS |
REFERENCES: PPT, Handouts, Internet | Heart Blocks
|
____________________________________________________________________________________

Heart Blocks
- A heart block is a conduction disorder characterized by an abnormal heart rhythm manifested by an
interference with electrical signals that usually move from the atria to the ventricles.
- In heart block, the electrical signals that tell the heart to contract are partially or totally blocked
between the atria and the ventricles

Causes of Heart Blocks

- Medications (eg, digitalis, calcium channel blockers,
beta-blockers)
- Lyme disease
- Myocardial ischemia and infarction
- Valvular disorders
- Cardiomyopathy
- Endocarditis
- Myocarditis

Types of Heart Blocks

- First Degree Heart Block (first degree AV block)
- Second Degree Heart Block (second degree AV block)
- Third Degree Heart Block (third degree AV block)

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Types Of Heart Blocks
I. FIRST DEGREE HEART BLOCK
“FAR AWAY P”

- Occurs when all the atrial impulses are conducted through the AV node into the ventricles at a rate slower
than normal.
- There is a prolonged PR interval
- PR interval is greater than 0.20 seconds (Normal: 0.12 and 0.20 Seconds)
- PR interval measurement is constant
- Regular Rhythm
- Regular heart rate or slower

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 II. SECOND DEGREE HEART BLOCK
- Characterized by a disturbance, delay or interruption of electrical impulse through the AV node to the
ventricles.
- The electrical signals between your atria and ventricles can intermittently fail to conduct.
- 2 Types:
• Mobitz I (Wenckebach)
• Mobitz II

Mobitz I (Wenckebach)

“LONGER THEN DROP”

- Occurs when there is a repeating pattern in which all but one of a series of atrial impulses are conducted
through the AV node into the ventricles.
- There is progressive prolongation of PR interval until it reaches a moment of dropped beat (dropped QRS)
• PR interval is longest before a dropped beat
• PR interval is shortest after a dropped beat

- Constant PP interval
- Irregular rhythm
- Normal or slightly slow heart rate

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Mobitz II

“DROP RANDOMLY”

- Occurs when only some of the atrial impulses are conducted through the AV node into the ventricles.
- There are intermittent non-conducted P waves without progressive prolongation of the PR interval.

- There are recurrent appearances of non-conducted P waves that is not followed by a QRS complex.
- PR interval and PP interval is constant.
- QRS is usually abnormal but may be normal.

III. THIRD DEGREE HEART BLOCK

“BEAT INDEPENDENTLY”

- Complete heart block

- Occurs when no atrial impulse is conducted through the AV node into the ventricles.

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 - Dissociation between P wave and QRS complex
- P wave may overlap on T wave or QRS complex
- PR interval is no constant
- Rate usually less than 40 bpm
- QRS shape and duration are usually abnorma

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General Nursing Responsibilities
1. Cardiac Monitoring – for close observation
2. Oxygen Therapy – to manage desaturated patients
3. IV Access – to support blood pressure with fluids
4. Atropine Standby – to treat bradycardia
5. Bed Rest – to decrease cardiac workload

Nursing Responsibilities – FIRST DEGREE HEART BLOCK

- Usually ASYMPTOMATIC and not indicated for treatment
- Close monitoring of hemodynamic status
- D/C meds that cause bradycardia (beta blockers, calcium channel blockers, digoxin)

Nursing Responsibilities – SECOND- & THIRD-DEGREE HEART BLOCKS

- Usually associated with severe bradycardia which can be treated by atropine
- Associated conditions should be treated correctly such as:

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 • Myocardial infarction
• Electrolyte imbalance
• Digitalis toxicity
- A permanent pacemaker may be necessary if the block persists.
- If the patient does not respond to atropine, has advanced AV block, or has had an acute MI, temporary
transcutaneous pacing may be started.
- If the patient has no pulse, treatment is the same as for ventricular asystole.

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 Medical-Surgical Nursing LECTURE
NCM 4164 | BATCH 2023
COLLEGE OF NURSING – ATENEO DE DAVAO UNIVERSITY
LECTURER/S: NCM PROFS |
REFERENCES: PPT, Handouts, Internet | Respiratory Conditions in Acute Biologic
| Crisis

____________________________________________________________________________________

Respiratory System
1. Acute Respiratory Failure
2. Acute Severe Asthma (Formerly called Status Asthmaticus)
3. Anaphylactic Shock
4. Acute Respiratory Distress Syndrome (ARDS)
5. Chronic Obstructive Pulmonary Disease (COPD)

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 RESPIRATORY SYSTEM ACUTE BIOLOGIC CRISIS
Types Of Respiratory Conditions
I. ACUTE RESPIRATORY FAILURE
Definition Signs and Symptoms

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 - Sudden and life-threatening deterioration of the Early Signs
gas exchange function of the lung. - Dyspnea
- Indicates failure of the lungs to provide adequate - Air hunger
oxygenation or ventilation for the blood. - Restlessness
- A decrease in arterial oxygen tension (PaO2) to - Fatigue
less than 50 mmHg (hypoxia) and an increase in - Headache
arterial carbon dioxide tension (PaCO2) to - Tachycardia
greater than 50 mmHg (hypercapnia), with an - Increased blood pressure BP
arterial pH of less than 7.35.
As Hypoxemia progresses:
- Confusion
- Lethargy
- Tachypnea
- Central cyanosis
Assessment & Diagnostic Findings
- Chest X-ray (CXR)
- Chest CT Scan
- Arterial Blood Gas (ABG)
Nursing Responsibilities
- Monitor patient’s respiratory status include the
vital signs.
- Monitor level of response and oxygen
saturation.
- Arterial blood gas (ABG)
Medical Management
- Bronchodilators (Salbutamol inhalation)
- Steroids (hydrocortisone)
- Antibiotics (treat underlying infection)
- Non-invasive positive pressure ventilation (CPAP
or BiPAP)
- Oxygen Therapy
- Intubation and mechanical ventilation
CONTINUOUS POSOTIVE AIRWAY PRESSURE (CPAP)

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______________________________________________________________________________ 48
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 Types of Respiratory Failure Pathophysiology
Type 1 (Hypoxemic)
- Failure to exchange oxygen in the lungs. IMPAIRED VENTILATION & PERFUSION MECHANISM
IN THE LUNG
Type 1 (Hypercapnic) Impaired Neuromuscular Musculoskeletal Pulmonary
- Failure to exchange or remove carbon dioxide in CNS dysfunction dysfunction dysfunction
function
the lungs.

Type 3 (Perioperative) ↓
- Subtype of type 1 that results from lung or Oxygenation failure
alveolar atelectasis.
- General anesthesia can cause collapse of Airway Obstruction
dependent lung alveoli. ↓
Head injury
In the post-op period, especially after major ↓
thoracic or abdominal surgery, inadequate Pneumonia
ventilation and respiratory failure may occur ↓
because of the effects of anesthetic, analgesic, and Asthma
sedative agents, which may depress respiration or ↓
enhance the effects of opioids and lead to COPD
hypoventilation. ↓
↓ Severe obesity
A ventilation–perfusion (V/Q) mismatch is the ↓
usual cause of acute respiratory failure after Stroke
major abdominal, cardiac, or thoracic surgery. ↓
High V/Q ratio – more Low V/Q ratio – less Pulmonary Embolism
ventilation, less ventilation, more
perfusion (Deadspace) perfusion (Shunt)

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 II. ACUTE SEVERE ASTHMA
Definition Signs and Symptoms
- Formerly known as status asthmaticus, is defined - Difficulty breathing
as severe asthma unresponsive to repeated - Heavy sweating
courses of beta-agonist therapy such as inhaled - Coughing, wheezing
Albuterol, Levalbuterol, or Subcutaneous - Fatigue and weakness
Epinephrine. - Abdominal, back, or neck muscle pain
- Panic or confusion
Causes - Blue-tinted lips or skin
- Upper respiratory tract infections - Loss of consciousness
- Insufficient use of inhaled or oral corticosteroids.
- Allergen Exposure (Pets, drugs, dust, pollen, etc.) Assessment & Diagnostic Findings
- Irritant Inhalation (tobacco smoke, paint, etc.), - Chest X-ray (CXR) rule out pneumonia
- Exercise or Physical Exhaustion - ECG to rule out heart condition
- Arterial Blood Gas (ABG)
Medical Management Nursing Responsibilities
- Oxygen therapy; Monitor oxygen saturation
Treatment - Administer bronchodilators (Salbutamol)
- Parenteral corticosteroids - Administer pressurised metered dose inhaler as
- Nebulization (Ipratropium Bromide) ordered
- Epinephrine - Corticosteroid therapy (Hydrocortisone,
- Breathing and Oxygenation Assistance Terbutaline)
- Monitor vital signs including the O2 saturation
Pathophysiology
Spasm/obstruction of coronary arteries
↓
Myocardial ischemia
↓
Reduced O2 supply to myocardium
↓
Chest pain---Angina pectoris

III. ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS)

Definition Signs and Symptoms
- Severe from of acute lung injury - Rapid onset of dyspnea
Chracterized by: - Arterial hypoxemia
- A sudden and progressive pulmonary edema - Bilateral infiltrates that quickly worsen
- Increasing bilateral infiltrates on chest x-ray - Alveolitis w/ persistent, severe hypoxemia
- Hypoxemia unresponsive to oxygen - Increased alveolar dead space
supplementation regardless of the amount of - Decreased pulmonary compliance
PEEP Etiology
- - Aspiration
- Absence of an elevated left atrial pressure. - Drug ingestion and overdose
- Mortality rate of 25-58%. - Hematologic disorders

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 - Patients with ARDS usually require mechanical - Prolonged inhalation of high concentrations of
ventilator with a higher-than-normal airway oxygen, smoke, or corrosive substances
pressure. - Localized infection
- 2 major factors associated with the development - Metabolic disorders
of ARDS: - Shock (any cause)
• Direct injury: cigarette smoking - Trauma
• Indirect insult: shock, trauma - Major surgery
- Major cause of death in ARDS: non-pulmonary - Fat or air embolism
multiple-system organ failure, often with sepsis - Systemic sepsis
Pathophysiology
Positive End Expiratory Pressure (PEEP) Injury to alveolar-capillary membrane
- PEEP is a pressure applied by the ventilator at the ↓
end of each breath to ensure that the alveoli are Damage type II alveolar cell
not so prone to collapse. ↓
- The goal of PEEP in patients with ARDS is to Decreased alveolar compliance and recoil
maximize and maintain alveolar recruitment, ↓
thereby improving oxygenation and limiting Decreased lung compliance
oxygen toxicity. ↓
Impaired gas exchange
↓
ARDS
Assessment & Diagnostics Findings
- No specific test to identify ARDS
- Diagnosis is based on the physical exam, chest X-
ray and oxygen levels.
- Imaging
• Chest X-ray
• Chest CT Scan
- ABG
- CBC
- 2D Echo
- Plasma brain natriuretic peptide (BNP) levels
- Transthoracic echocardiography
- Pulmonary artery catheterization

Medical Management
- Supplemental oxygen
- Endotracheal Intubation
Uses of PEEP - Mechanical ventilation (with PEEP)
- Improves arterial oxygenation by alleviating - Arterial blood gas analysis
pulmonary shunting. - Pulse oximetry
- Helps the respiratory muscles to decrease the - Bedside pulmonary function testing
work of breathing. - Pharmacologic therapy (Treat symptoms)
- Decreases the rate of infiltrated and atelectatic
tissues. Complications
- Increases functional residual capacity. - Blood clots (DVT)
- Collapsed lung
- Infections
- Scarring (pulmonary fibrosis)
- Breathing problems

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 - Depression

Nursing Interventions (5 P’s)

Perfusion / Positioning / Protective Lung Ventilation / Protocol Weaning / Preventing Complications

1. PERFUSION
GOAL OF CARE for ARDS patients is to maximize perfusion in the pulmonary capillary system by increasing
oxygen transport between the alveoli and pulmonary capillaries.

- Increase fluid volume without overloading the patient

- Oxygen therapy
- Administer Inotropes/Vasodilators as ordered
- Strict monitoring of vital signs including central venous pressure (CVP) and left atrial pressure

2. POSITIONING
- Proper positioning of the patient aids in drainage of lung secretions.
- Promotes mobility to improve blood perfusion.
- Turning to sides every 1-2 hours

3. PROTECTIVE LUNG VENTILATION

- Assist in intubation and mechanical ventilation
- Suction secretions per ET and per mouth
- Monitor tidal volume (VT) and positive end expiratory pressure (PEEP) of the ventilator
- Prevention of Ventilator-Induced Lung Injury (VILI)
- BiPAP / CPAP

4. PROTOCOL WEANING
- Carry out weaning orders as ordered by the Pulmonologist
- Monitor and assess patient’s response to weaning
- Weaning precautions (WOF: respiratory distress, untoward vitals signs)

5. PREVENTING COMPLICATIONS
- Deep Vein Thrombosis (DVT): Passive ROM exercises, Frequent position changes, Anticoagulant
prophylaxis, Anti-embolic stockings
- Pressure Ulcers: Frequent position changes, Promoting adequate nutrition, Frequent skin assessment and
proper skin care, Implementing pressure-relieving devices (air mattress)
- Poor Nutrition: Monitor nutritional status, Administer parenteral nutrition as ordered
- Ventilator Acquired Pneumonia (VAP): Compliance to Infection Control Protocols, Oral/Mouth care

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 Medical-Surgical Nursing LECTURE
NCM 4164 | BATCH 2023
COLLEGE OF NURSING – ATENEO DE DAVAO UNIVERSITY
LECTURER/S: NCM PROFS |
REFERENCES: PPT, Handouts, Internet | Chronic Kidney Disease and End-Stage Renal
| Disease (Acute Biologic Crisis)

____________________________________________________________________________________

Functions of the Kidney

- Urine formation
- Regulation of electrolytes
- Control of water balance
- Excretion of waste products
- Regulation of acid–base balance
- Control of blood pressure
- Renal clearance
- Regulation of red blood cell production
- Synthesis of vitamin D to active form
- Secretion of prostaglandins
- Regulates calcium and phosphorus balance

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 Urine
Formation
- Glomerular filtration
- Tubular reabsorption
- Tubular secretion

I. Chronic Kidney Disease (CKD)

Definition Stages of Chronic Kidney Disease
- Describes kidney damage or a decrease Stages are based on the glomerular filtration
in the glomerular filtration rate (GFR) rate (GFR) the normal GFR is
for 3 or more months. 125mL/min/1.73m2.
- Kidneys are unable to filter wastes and Stage 1
excess fluids from the blood and fails to - GFR ≥ 90mL/min/1.73m2
excrete these wastes via the urine. - Kidney damage with normal or
- If left untreated, leads to end stage increased GFR
renal disease (ESRD). Stage 2
- GFR = 60-89 mL/min/1.73m2
- Mild decrease in GFR
Stage 3
- GFR = 30-59 mL/min/1.73m2
- Moderate decrease in GFR
Stage 4
- GFR = 15-29mL/min/1.73m2
- Severe decrease in GFR
Stage 5
- GFR < 15mL/min/1.73m2
- Kidney failure (end-stage renal disease
[ESRD])

Risk Factors Clinical Manifestations

- Diabetes (Primary cause) - Increased creatinine level
- Cardiovascular disease - Anemia
- Hypertension - Metabolic acidosis
- Obesity - Hyperphosphatemia
- Glomerulonephritis - Hypocalcemia
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 - Pyelonephritis - Edema
- Polycystic kidney disease - Uncontrolled hypertension
- Hereditary or congenital disorders
- Renal cancers Other Clinical Manifestations
- Nausea
- Vomiting
- Loss of appetite
- Fatigue and weakness
- Sleep problems
- Changes in how much you urinate
- Decreased mental sharpness
- Muscle twitches and cramps
- Swelling of feet and ankles
- Persistent itching
- Chest pain, if fluid builds up around the
lining of the heart
- Shortness of breath, if fluid builds up in the
lung.
Complications of CKD Diagnostic
Impaired sodium balance: Blood test
- Sodium retention - Serum electrolytes, BUN, creatinine, CBC,
- Volume overload GFR, serum albumin

Decreased potassium excretion Urine test

- Hyperkalemia - Urinalysis (including urinary sediment
examination)
Impaired acid excretion - Urine Albumin
- Metabolic acidosis - Quantitative urine protein

Calcium/phosphate balance Ultrasonography

- Hyperphosphatemia
- Hypocalcemia Renal Biopsy

Erythropoiesis
- Anemia

Urine Albumin Treatment

- A urine albumin results below 30 is normal. 1. Treatment of underlying cause:

- A urine albumin results above 30 may DM, HPN,CVD, hyperlipidemia
mean kidney disease.
1. Blood pressure control:
What is urine albumin? Lifestyle change & Exercise

- Albunin is a protein found in the blood. A 2. Diabetes management:

healthy kidney does not let albumin pass Control of glucose intake
into the urine. A damaged kidney lets some
albumin pass into the urine. The less 3. Diet modification
albumin in your urine, the better. Low salt, low fat, diabetic diet

4. Pharmacological treatment
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 - Diuretics: for sodium and fluid retention
(hypernatremia)
- Sodium Bicarbonate (metabolic acidosis)
- Phosphate binders and calcimimetics
(hperphosphatemia & hypocalcemia)
- Iron supplement for anemia

5. Dialysis
6. Kidney transplantation
7. Supportive care

Nursing Management

- Limit OFI
- Proper IVF regulation
- Strict monitoring of VS and I&O
- Monitor for sudden changes in sensorium
- Encourage low salt, low fat diet
- Reinforcement dialysis and transplant
options
- Improve quality of life
II. End Stage Renal Disease
Definition Clinical Manifestations
- When a patient has sustained enough Because virtually every body system is affected
kidney damage to require renal in ESRD, patients exhibit a number of signs and
replacement therapy on a permanent symptoms:
basis. - Neurologic
- The patient has moved into the fifth or final - Integumentary
stage of CKD. - Cardiovascular
- Also referred to as chronic renal failure - Pulmonary
(CRF). - Gastrointestinal
- Hematologic
- Reproductive
- Musculoskeletal

Signs and Symptoms Assessment and Diagnostic Findings

Integumentary Glomerular Filtration Rate

- Gray -bronze skin color As the GFR decreases (due to
- Dry, flaky skin nonfunctioningglomeruli), the creatinine
- Pruitus clearance decreases, while the serum creatinine
- Ecchymosis and BUN levels increase.
- Purpura
- Thin, brittle nails Sodium and Water Retention
- Coarse, thinning hair - Sodium and water are retained, increasing
the risk for edema, heart failure, and
Neurologic hypertension.
- Weakness and fatigue - Hypertension may also result
- Confusion fromactivation of the renin–angiotensin–
- Inability to concentrate aldosterone axis and the concomitant
- Disorientation increased aldosterone secretion.
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 - Tremors
- Seizures Acidosis
- Asterixis - Decreased acid secretion results from the
- Restlessness of legs inability of the kidney tubules to excrete
- Burning of soles of feet ammonia (NH3–) and to reabsorb sodium
- Behaviour changes bicarbonate (HCO3–).
- There is also decreased excretion of
Cardiovascular phosphates and other organic acids.
- Hypertension
- Pitting edema (feet, hands, sacrum)
- Periobital edema
- Pericardial neck veins Anemia
- Pericarditis - There is inadequate erythropoietin
- Pericardial tamponade production, the shortened lifespan of RBCs,
- Hyperkalemia nutritional deficiencies, and the patient’s
- Hyperlipidemia tendency to bleed, particularly from the GI
tract.
Pulmonary - Erythropoietin production decreases and
- Crackles profound anemia results, producing
- Thick, tenacious sputum fatigue, angina, and shortness of breath.
- Depressed cough reflex
- Pleuritic pain Calcium and Phosphorus imbalance
- Shortness of breath - The decreased serum calcium level causes
- Tachypnea increased secretion of parathormone from
- Kussmaul-type respirations the parathyroid glands.
- Uremic pneumontis - Body does not respond normally to the
increased secretion of parathormone; as a
Musculoskeletal result, calcium leaves the bone, often
- Muscle cramps producing bone changes and bone disease
- Loss of muscle streght as well as calcification of major blood
- Renal osteodystrophy vessels in the body.
- Bone pain - The active metabolite of vitamin D (1,25-
- Bone fractures dihydroxycholecalciferol) normally
- Foot drop manufactured by the kidney decreases as
renal failure progresses.
Gastrointestinal
- Ammonia odor to breath (“uremic fetor”) Complications
- Metallic taste
- Mouth ulcerations and bleeding - Hyperkalemia
- Anorexia,nausea, and vomiting - Pericarditis, pericardial effusion, and
- Hiccups pericardial tamponade
- Constipation or diarrhea - Hypertension
- Bleeding from gastrointestical tract - Anemia
- Bone disease and metastatic and
Hematologic vascularcalcifications
- Anemia
- Thrombocytopenia Medical Management

Reproductive 1. Pharmacologic Therapy

- Amenorrhea - Calcium and Phosphorus Binders

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 - Testicular atrophy - Antihypertensive and Cardiovascular
- Infertility Agents
- Decreased libido - Antiseizure Agents
- Erythropoietin

2. Nutritional Therapy
3. Dialysis

Nursing Management

- Assessing fluid status

- Implementing a dietary program
- Provide explanations and information
- Identifyingpotential sources of imbalance
- Promoting positive feelings
- Emotional support

Medical-Surgical Nursing LECTURE

NCM 4164 | BATCH 2023
COLLEGE OF NURSING – ATENEO DE DAVAO UNIVERSITY
LECTURER/S: NCM PROFS |
REFERENCES: PPT, Handouts, Internet | Neurologic Conditions in Acute Biologic
| Crisis

____________________________________________________________________________________

Nervous System
- Consists of 2 major parts: the central nervous system (CNS), which includes the brain and the spinal cord;
and the peripheral nervous system, which includes the cranial nerves, spinal nerves, and the autonomic
nervous system.

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- The function of the nervous system is to control motor, sensory, autonomic, cognitive, and behavioral
activities.
- The basic functional unit of the brain is the NEURON (composed of dendrites, a cell body, and an axon).

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 NEUROLOGIC CONDITIONS ACUTE BIOLOGIC CRISIS
Types Of Neurologic Conditions
I. CEREBROVASCULAR ACCIDENT – CVA (STROKE)
- “Stroke” or “Brain Attack”
- Affects 780,000 people each year
- 600,00 are new cases
- 180,000 are recurrent cases
- 2 types:
- Ischemic Stroke (85%)
- Hemorrhagic Stroke (15%)

I.A. ISCHEMIC STROKE

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 - Sudden loss of function resulting from disruption of the blood supply to a part of the brain.
- 1996 - approval of thrombolytic therapy greatly improved survival and recovery rate of patients.
- Divided into 5 different subtypes depending on the etiology.
- When symptoms of a stroke last only a short time (less than an hour), it called a transient ischemic attack
(TIA) or ministroke.
- The middle cerebral artery (MCA) is the most common artery involved in stroke.

1. Transient Ischemic Attack (TIA)

- AKA “mini stroke”
- A temporary decrease in blood supply to a part of the brain, which may last as little as five minutes.
- TIA occurs when a clot or debris blocks blood flow to part of your nervous system — but there is no
permanent tissue damage and no lasting symptoms.
- Having a TIA puts you at greater risk of having a full-blown stroke, causing permanent damage later.

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 Clinical Manifestations Diagnostics
Cranial CT scan
1. Cincinnati Stroke Scale - Initial diagnosis
- Fscial Droop - Done emergently to guide treatment
- Arm Drift
- Speech Impairment 12-lead ECG
- Determine any cardiac dysrhythmias

Carotid Ultrasound
- Determines presence of plaque or clot

CT Angiography
MRI/MRA
Transcranial Doppler
SPECT scan
Assessment

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 2. Manifestations vary greatly depending on:
- Lcoation of lesion
- Seize of the area
- Amount of collateral blood flow

3. Motor Loss
Motor disturbance in one side of the body
may indicate damage to the opposite.
- Hemiplegia/Hemiparesis
- Flaccid Paralysis
- DTR Hyporeflexia
- Spasticity (48)

4. Communciation Loss
Stroke is the most common cause of
aphasia. Prevention
- Dysrthria Best approach in managing stroke is Primary Prevention
- Dysphasia/Aphasia
- Apraxia Modifiable Risk Factors
- Hypertension (Major risk factor)
5. Perceptual Disturbance - Atrial Fibrillation
Loss of abilit to interpret sensation. - Hyperlipidemia
- Diabetes Mellitus
- Smoking and excessive alcohol Intake
- Asymptomatic Carotid Stenosis
- Obesity
- Periodontal disease

Non-Modifiable Risk Factors

- Advanced age (55 up)
- Gender (Men)
- Race (African-American)

- Smoking Cessation
- Maintaining a healthy weight
- Healthy diet (DASH)
- Modest Alcohol Consumption
- Daily Exercise
- Health teaching for vulnerable population

Medical Management
Aims to promtoe Secodnary Prevention
6. Sensory Loss
Ranges from mild to severe sensory
Atrial Fibrillation (AF)
disturbance.
- Anticoagulants
- Agnosia
- Warfarin (Coumadin)
- Loss of prioception
- Aspirin
7. Cognitive Impairment
Transient Ischemic Attack (TIA)
Impaired learning capacity, memory or other
- Platelet-inhibitors
higher cortical functions.
- Aspirin
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 - Short/long-term memory - Clopidogrel (Plavix)
- Decreased attention span
- Poor abstract reasoning Hyperlipidemia
- Altered judgement - 3-hydroxyl-2-methyl-glutaryl-coenzyme A
(Antihyperlipidemic)
8. Psychological Effects - Simvastatin (Zocor)
Presence pg psychological and emotional
disturbances Hypertension
- Depression - Angiotensin-Converting-Enzyme (ACE) Inhibitors
- Emotional lability and Thiazides
- Hostility - Captopril (Capoten)/ Enalapril (Vasotec)
- Frustration - HCTZ

9. Other Clinical Manifestations Gold Treatment: Thrombolytic Therapy

- Confusion or mental changes Recombinant t-PA (Tissue Plasminogen Activator)
- Visual disturbances - Genetically engineered from endogenous t-PA
- Shuffled gait, loss or balance and coordination - Must be initiated within 3 hours of attack
- Dizziness
- Sudden severe headache

Dosage and Administration of t-PA

- 0.9mg/kg
- Max dose: 90 mg
- 10% is given via IV bolus over 1 minute
- 90% is transfused IV for 1 hour via infusion pump

Nursing Responsibilities:
- Monitor pt closely on ASU/ICU
- Continuous Cardiac monitoring
- VS and NVS Monitoring
- Q 15 minutes for 1st 2 hours
- Q 30 minutes for next 6 hours
- Q hourly until 24 hours post mgt
- Maintain BP
- SBP < 180 mm Hg
- DBP < 105 mm Hg

Side Effects of t-PA

- Intracranial bleeding (6.4%)
- Factors:
o 70 yo and up
o NIHSS score > 20
o Serum Glucose >300mg/dL

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 o Edema/mass effect in CT-scan
- Nursing Resp:
o Closely monitor for bleeding
o Delay cannulation and catheter insertion for 24
hours

Goal of Treatment: Maintain Cerebral Hemodynamic

- Anticoagulants
- IV Heparin Osmotic Diuretics – Mannitol
- PaCO2 of 30-35 mmHg
- High Back Rest
- Endotracheal Intubation
- Maintain BP at 220/120mmHg and gradual
decrease

Managing Potential Complications: Ensuring Adequate

Oxygenation
- Pulmonary Care
o Maintaining patent airway
o Adequate gas exchange

Surgical Prevention
Carotid Endarterectomy
- Removal of atherosclerotic plaque or thrombus
formation from the carotid artery
- Indicated for pts with TIA symptoms found to be
caused by moderate to severe carotid stenosis

Carotid Stenting
- Less invasive procedure
- Indicated for pts at high risk for surgery

Nursing Diagnosis
-
Impaired Physical Mobility RT hemiparesis, loss of
balance and coordination, spasticity and brain
injury
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 - Impaired Swallowing
- Acute Pain (Shoulder) RT hemiplegia and disuse
Impaired verbal communication
- Disturbed thought process
- Disturbed Sensory Perception
- Sexual Dysfunction
Nursing Management
Improving Mobility and Preventing Joint Deformities
- Correct positioning to prevent contracture
- Preventing Shoulder Adduction
- Positioning hands and fingers
- Changing positions
- Establishing an exercise program

Enhancing Self Care

- Maintain independence with adequate assistance

Managing Sensory-Perceptual Deficits

- Position self in the side where visual field is intact
- Provide visual stimuli on good side

Assisting with Nutrition

- Entral tube feeding initially
- Gradual progressive diet
- Speech therapist to address swallowing and
chewing

Attaining Bowel and Bladder Control

- Catheterization initially
- Establish voiding and bowel patterns
- High fiber diet

Improving Communication Process

- Speech therapist referral to establish and describe
deficits
- DO NOT finish the patient’s sentence for him/her

I.B. HEMORRHAGIC STROKE

- A type of stroke that is primarily caused by Intracranial or subarachnoid bleeding.
- Caused by bleeding into: – Brain tissue – Ventricles – Subarachnoid space

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Primary Intracerebral Hemorrhage (80%)
- Uncontrolled Hypertension
- Cerebral Amyloid Angiopathy

Secondary Intracerebral Hemorrhage

AVMs

Intracranial Aneurysms
Intracranial Neoplasms
Medications

Subarachnoid Hemorrhage
Ruptured intracranial aneurysm

Diagnostics Clinical Manifestations

Cranial CT Scan/MRI - Symptoms are similar to ischemic stroke but more
- Determines type of stroke, location and size of severe
hematoma - Severe headache
- Notes presence of ventricular bluff and - Vomiting
hydrocephalus - Early sudden change in LOC
- Focal Seizures Loss of consciousness
Cerebral Angiography - Nuchal and spine rigidity
- Confirms diagnosis of intracranial aneurysm - Visual Disturbances
and AVMs
- Shows location, size of the lesion Little neurologic deficits
- Provide information about affected vessels Aneurysm or AVM leaks blood leading to clot formation
that seals the site of bleeding.
Lumbar Puncture
- Done in the absence of increased ICP, negative Severe Cerebral Damage
CT Scan Lumbar Puncture Severe bleeding that caused rapid coma and death
- Confirmation of subarachnoid haemorrhage

Toxicology Screens
- Performed for patients younger than 40 years
old Toxicology Screens
- Determines use of ilicit drugs

Prevention Pathophysiology
Primary Prevention Greatly depends on the cause and type of
- Managing hypertension cerebrovascular disorder present
- Ameliorating non-modifiable risk factors
Hemorrhage
Non-Modifiable Risk Factors Blood leaks into the surrounding tissues
- Increased age Decreased blood supply to brain cells
- Male gender Irritation of blood vessels
↓
Modifiable Risk Factors Disrupted Brain Metabolism
- Excessive alcohol intake Bleeding compresses brain tissues
- Illicit drug use Ischemia occurs in other neurons
Complications ↓

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Cerebral Hypoxia
- Extends area of injury
- Provide adequate oxygenation and hgb and
hct levels
Decreased Blood Flow
- Dependent on blood pressure and cardiac
output
- Hydrate adequately to reduce blood
viscosity and improve cerebral blood flow
- Maintain normal blood pressure ensure
perfusion while preventing further injury
Vasospasm
- Serious complication of subarachnoid
bleeding
- Leading cause of morbidity and mortality
- *Monitor for vasospasm
- **Calcium channel blocker
- *** Triple H therapy
o Hypervolemia (plasma volume
expanders)
o Induced Arterial hypertension
o Hemodilution
Increased Intracranial Pressure
- Almost always follows subarachnoid
haemorrhage
- Closely monitor increasing ICP
- Administer Mannitol carefully
Hypertension
- Increases severity of bleeding
- Systolic BP increases size of hematoma
- Manage BP depending on ICP
- Closely monitor BP while one anti-
hypertensive medications
Medical Management
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Vasospasm
Secondary ischemia (stroke)
↓
Increased ICP
Blood leaks in the brain tissue
Blood crowds the CSF circulation
Intracerebral Hemorrhage
- Most common in pts with hypertension and
cerebral atherosclerosis
- Other causes: Arterial Pathology, brain tumors
and drugs
- Bleeding occurs in the cerebral lobes, basal
ganglia, thalamus, brain stem and cerebellum
- Bleeding may also rupture the wall of lateral
ventricles causing intraventricular hemorrhage
Intracranial (Cerebral) Aneurysm
- May be d/t atherosclerosis, congenital defect
of the vessel wall, hypertensive vascular
disease, head trauma or advancing age
- Usually occurs in the bifurcations of the circle
of Willis
- Arteries affected: ICA, ACA, ACoA, PCoA, PCA,
MCA
Arteriovenous Malformations
- Embryonal development abnormality that leads
to a tangle of arteries and veins that lack a
capillary bed
- Leads to dilation of arteries and veins and
eventually ruptures
Subarachnoid Hemorrhage
- Occurs as a result of an AVM, intracranial
aneurysm, trauma or hypertension
- Most common: leaking aneurysm in the area of
the circle of Willis
Nursing Diagnoses
68
Hydrocephalus - Ineffective cerebral tissue perfusion RT
- Obstruction of CSF causes dilation of the bleeding. Vasospasms
ventricles - Disturbed sensory perception RT medically
- Watch out for sudden onset of stupor or imposed restrictions
coma - Decreased Physical Mobility RT neuromuscular
- Mgt: Ventriculostomy, Ventriculopertoneal impairment
shunt - Risk for aspiration RT diminished gag reflex
- Risk for injury RT one-sided paralysis
Seizures
- Seizure precaution must be initiated at all Nursing Interventions
times - Optimizing Cerebral Tissue Perfusion
- DOC: Phenytoin (Dilantin) o Implementing aneurysm precaution: non-
stimulating, stress free environment

- Preventing complications of immobility

o Turn to sides
o Passive ROM
o Use of antiembolic stockings

- Nutritional support
o Enteral/parenteral support

Surgical Management

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Surgical Clipping (Aneurysm)

Endovascular Embolization (Coiling)

Surgical AVM removal

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