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Fluid and electrolyte and acid base balance

Fluids and Electrolytes

Body is 60% fluids

ICF=40%       

ECF=20% (Intravascular=5%; Interstitial=15%)

Solvent – the medium (usually water) that contains some particles.

Solutes – particles that are dissolved in solvent :salts, sugars, amino acids.

Electrolytes

•Chemical compounds in solution that have the ability to conduct an electrical current

Break into charged particles called ions

•Positively charged CATIONS

•Negatively charges : ANIONS

FUNCTIONS OF ELECTROLYTES

•Promote neuromuscular irritability

•Maintain body fluid volume and osmolality

•Distribute body water between fluid compartments

Function of Body Water

ECF

•Maintains blood volume

•Transport system to and from the cell

ICF

•Internal aqueous medium for cellular chemical function

MOVEMENTS OF FLUIDS BETWEEN COMPARTMENTS

•Diffusion

•Osmosis

•Active Transport

•Hydrostatic Pressure

•Colloid Osmotic Pressure

•Filtration

Types of solution

Crystalloids: Intravenous Fluids

1.Isotonic (equal osmolality with plasma)

   0.9% NaCL,Ringer’s Solution,Lactated Ringer’s, D5H20

2.Hypotonic (lower osmolality than plasma)

0.45% NaCL

3.Hypertonic (higher osmolality than plasma)

D5.9% NSS, D5.45% NSS, D10 H20,D5LR

Colloidal Solution

Aminosol 5%

Dextran 40

              INTRAVENOUS THERAPY

Purpose:

1.Maintenance of fluid & electrolyte balance

2.Replacement of fluid & electrolyte loss

3.Provision of nutrients

4.Provision of a route for medications

Average Fluid Intake

1.         Drink = 1,500ml/day.

2.         Food = 800 ml/day.

3.            Oxidation = 300 ml/day.

Average Fluid Loss

1.         Urine = 1,500 ml/day.

2.         Lung = 400 ml/day.

3.         Skin = 600 ml/day.

4.         Feces = 100ml/day.

Fluid Volume Deficit

An imbalance in fluid volume in which there is loss of fluid from the body not compensated for by an adequate intake of water.

•Excess Water Loss = FLUID VOLUME DEFICIT

Example: Simple Dehydration : water and electrolytes are lost in the same proportion

. Assessment

•Dry mucous   membranes

•Concentrated urine, ↓urine output

•Thready,↑PR,↑RR

•Orthostatic hypotension

•↓ BP

•Flat neck veins

•↓ CVP

•Diminished  peripheral pulse

•Dry skin

 Implementation

• fluid replacement

• weigh client daily

• monitor intake and output

• monitor urine specific gravity

Fluid Volume Excess

•           fluid intake or fluid retention exceeds the body’s fluid needs.

•           Also called overhydration or fluid overload

•           Excess Water Intake/Retention = FLUID VOLUME EXCESS

           

Example : Overhydration

1. Assessment

•Lethargy

•Confusion

•Muscle cramps

•Diarrhea

•Delirium

•Weakness

•Seizure

•Rapid PR

•↑Urinary output

•Nausea and vomiting

Nursing Interventions:

•Monitor vital signs, daily weight, and hemodynamic status.

•Monitor I & O.

•Monitor electrolyte levels & body system status.

•Prevent further fluid overload then restore normal fluid balance.

•Administer prescribed diuretics.

•  Report warning signs of hypervolemia.

SODIUM

Normal Value : 135-145 mEq/L

Common Food Sources : table salt, soy sauce, cured meats, dairy products (milk, cheese, butter), ketchup, canned food, snack food (chips, crackers). Note: instant oatmeal has salt.

Hyponatremia

 sodium level below 135 mEq/L

Causes:

1.            Increased sodium excretion.

2.            Inadequate sodium intake.

3.Dilution of serum sodium 

Assessment

•Nausea & vomiting

•Lethargy

•Confusion

•Muscle cramps

•Diarrhea

•Delirium

•Weakness

•Seizure

•Rapid PR

•↑Urinary output

Implementation

•Assess neurological status.

•Monitor electrolyte results and I & O accurately

•Administer IV fluids

•Increase oral sodium intake.

•Maintain seizure precautions.

•If hypovolemia: IV saline fluids; If hypervolemia: diuretics.

•If taking Lithium, monitor lithium levels because hyponatremia can cause decrease in lithium excretion and result in toxicity.

B. Hypernatremia  - sodium level exceeding 145 mEq/L

Causes:

1.            Decreased sodium excretion – corticosteroids, renal failure, Cushings Synd.

2.            Increased sodium intake – excess ingestion or IV fluids with sodium.

3.            Decreased water intake – NPO, Low fluid intake.

4.            Increased water loss – fever, diaphoresis.

Symptoms

           decreased contractility and output of heart

-            hypervolemia : pulmonary edema

-            spontaneous muscle twitching later weakness.

-           ** Altered mental/ cerebral functioning is the most common manifestation.

-            Increased urine specific gravity, decreased urine output.

Implementation

•Gradual replacement of water (in excess of sodium)

•ADH replacement, vasopressin administration (for patients with diabetes insipidus)

•Medications:

•Diuretics

•Diet therapy

•↓ Na+

           

POTASSIUM

Normal value = 3.5 – 5.1 mEq/L

Common food sources: avocado, raisins, pork, beef, cantaloupe, spinach, bananas, fish, oranges, strawberries, mushrooms, carrots, potatoes, tomatoes.

** Potassium is the major cation of the intracellular fluid. Small changes in extracellular potassium concentrations are very significant.

A. Hypokalemia

 - level below 3.5 mEq/L

Causes

1.            Potassium Loss – use of meds such as diuretics, Conns Synd (increase in aldosterone), vomiting, diarrhea.

2.            Inadequate intake

3.            Intracellular shift – alkalosis, hyperinsulinism, TPN feedings.

4.         Dilution of serum potassium – water intoxication, IV fluids with low K.

Assessment

•          Thready, weak pulse

•          Cardiac arrhythmias, ECG : ST depression

•          Shallow respiration

•          Anxiety, lethargy, confusion

•          Muscle weakness

•          Decreased GI motility, nausea, vomiting. 

•          Decreased urine specific gravity, increased output.

Implementation

•monitor ECG

•Oral or IV potassium

•Fluids to increase urinary output

•IV fluids

B. Hyperkalemia

- level exceeding 5.1 mEq/L

Causes

1.         Excess intake – overingestion of foods or meds, rapid infusion.

2.            Decreased excretion – potassium-sparing diurectics, renal failure.

3.            Extracellular shift – tissue damage, acidosis, vigorouse drawing of blood destroying RBC’s

Assessment

•           irregular heart rate, dysrhythmias; slow, weak pulse, decreased BP

•           ECG : tall T waves, widened QRS complexes, prolonged PR interval.

•           Skeletal muscle weakness, may lead to respiratory failure.

•           Early: muscle twitching, cramps, paresthesias.

•           Late: profound muscle weakness, paralysis.

•           Increased GI motility, diarrhea.

Implementation

•          monitor VS, affected systems, place on cardiac monitor.

•          Discontinue IV potassium or oral potassium supplements.

•          Restrict K in diet.

•          K excreting diuretics.

•          IV  glucose with insulin to move excess K into cells.

CALCIUM

Normal levels : 8.6 to 10.0 mg/dl

Plays an important role in excitable tissues : heart, muscle, nerves.

Common food sources : yogurt, milk, rhubarb, collard greens, cheese, tofu, spinach, broccoli, green beans, carrots

A. Hypocalcemia

- level below 8.6 mg/dl

Causes

1.            Inadequate absorption – low oral intake, lactose intolerance, malabsorption syndromes such as Crohns disease, celiac sprue, low intake of vit. D, ESRD.

2.            Increased excretion – renal failure, diarrhea, wound drainage.

3.            Conditions that decrese serum levels – alkalosis, medications, acute pancreatitis, **hyperphosphatemia, disease or removal of parathyroid glands.

Assessment

•          Decrease heart rate and contractility

•          Hypotension, diminished pulses.

•          Irritable skeletal muscles: twitching, cramps

•          Hyperactive deep tendon reflexes.

•          +Trousseau’s and Chvostek’s sign.

  

Implementation

• monitor VS and systems affected.

•Oral calcium or IV supplements

•Meds that increase calcium : aluminum hydroxide reduces phosphorus causing increase in calcium; vitamin D aids in absorption.

•Quiet environment, seizure precautions.

B. Hypercalcemia

 - level beyond 10 mg/dl.

Causes

1.            Increased absorption – excess oral intake of calcium or vit.D.

2.            Decreased excretion – renal failure, thiazide diuretics.

3.            Increased bone resorption – malignancy, immobility, hyperparathyroid/thyroid

4.            Hemoconcentration – dehydration

Assessment

•     Increased heart rate early but   bradycardia in late stage.

•           Increased BP, bounding pulses

•           Weak respiration, muscle weakness

•           Disorientation, lethargy, coma.

•           Formation of renal calculi

•           Decreased GI motility, anorexia, nausea.

Implementation

-           monitor VS, systems affected, cardiac monitor.

-            Discontinue oral or IV solutions with calcium, vit. D

-           IV normal saline to restore balance

-           Severe: dialysis

 •  

MAGNESIUM

Normal value: 1.6 – 2.6 mg/dl

Common food sources: green leafy vegetables, avocado, white tuna, milk, yogurt, oats

-           As calcium goes, so does magnesium. Hypocalcemia frequently accompanies hypomagnesemia, so signs are similar and interventions also aim to restore normal serum calcium level.

-            Monitor for reduced deep tendon reflexes when administering magnesium since reduced DTR’s suggest hypermagnesemia.

PHOSPHORUS

Normal value: 2.7 – 4.5 mg/dl

Common food sources: fish, pork, beef, chicken, organ meats, nuts.

   A decrease in phosphorus is accompanied by increase in calcium. Inverse relationship. Problems that occur in hyperphosphatemia center on the hypocalcemia that results when serum phosphorus levels increase. 

Acid – is a proton donor (HCL, Sulfuric,phosphoric ,carbonic acids

            A strong acid is the one that highly dissociate and produces a high concentration   

            Of hydrogen ions

Base – a hydrogen ion acceptor.They bind free hydrogen ions,reducing their concentration

Buffer – a substance that reduces the change in free hydrogen ion concentration of a solution on the addition of an acid or base

Acid Base Balance

The body has two main defense mechanisms against too much acid:

(There are other mechanisms but these are the important ones.

1. Respiratory

- if too much H2CO3 is produced by the above reactions, the lungs can remove it in the form of CO2.

- inability to remove CO2 due to hypoventilation causes acidosis.

- removal of too much CO2 by hyperventilation causes alkalosis.

2. Metabolic

- the kidneys can supply (recover) additional buffer base HCO3 to compensate for acidosis.

 - inability of the kidneys to recover HCO3 causes acidosis.

Drawing Arterial Blood Gases

1.         Obtain vital signs.

2.            Determine if arterial line is in place so arterial puncture is not necessary.

3.         Do Allen Test for determining patency of collateral circulation

a.         Apply direct pressure over the clients ulnar and radial arteries simultaneously.

b.         While pressure is applied, ask the client to open and close the hand repeatedly; the hand should blanch.

c.         Release pressure from the ulnar artery while compressing the radial artery and assess the color of the extremity distal to the pressure point.

d.         If pinkness fails to return within 6 seconds, the ulnar artery is insufficient, indicating that the radial artery should not be used for obtaining a blood specimen.

4.         Draw into heparinized syringe.

5.         Must be sterile.

6.         Discard if in contact with room air.

7.         Keep on ice, transport to lab immediately.

8.         Apply pressure to puncture site for 5 to 10 minutes.

9.         On the lab form always record the clients temperature and any oxygen being received.

Analyzing Arterial Blood Gases

Normal Values

pH: 7.35-7.45

PCO2: 35-45 mmHg

HCO3: 22-27 mEq/L

PO2: 80-100 mmHg

step 1 - examine pH

if low, indicates acidosis --
if high, indicates alkalosis --
if normal, check to see if borderline (may be compensation)

step 2 - examine CO2

if high, indicates respiratory acidosis (with low pH)
if low, indicates respiratory alkalosis (with high pH)
if normal, check for compensatory problem

step 3 - examine HCO3

üif high, indicates metabolic alkalosis (with high pH)
if low, indicates metabolic acidosis (with low pH)
if normal, check for compensatory condition

step 4 - check PO2 levels

üif low, indicates an interference with ventilation process (should evaluate the patient)
if normal, indicates patient is getting enough oxygen

step 5 - check signs/symptoms of patient

üThis analysis is for the patient whose respiratory status is fairly stable clinically, but acid/base balance is questionable. Following is a step-by-step account of how to analyze ABG if the prime concern is oxygenation.

pH 7.51, pCO2 40, HCO3- 31:

            a.            Normal

            b.            Uncompensated metabolic alkalosis

            c.            compensated respiratory acidosis

            d.            Uncompensated respiratory alkalosis

pH 7.33, pCO2 29, HCO3- 16:

            a.            Uncompensated respiratory alkalosis

            b.            Uncompensated metabolic acidosis

            c.            Compensated respiratory acidosis

            d.            Uncompensated metabolic acidosis

           

pH 7.40, pCO2 40, HCO3- 24:

            a.            Normal

            b.            Uncompensated metabolic acidosis

            c.            Compensated respiratory acidosis

            d.            Compensated metabolic acidosis

pH 7.12, pCO2 60, HCO3- 29:

            a.            Uncompensated metabolic acidosis

            b.            Uncompensated respiratory acidosis

            c.            Compensated respiratory acidosis

            d.            Compensated metabolic acidosis

pH 7.48, pCO2 30, HCO3- 23:

            a.            Uncompensated metabolic alkalosis

            b.            Uncompensated respiratory alkalosis

            c.            Compensated respiratory alkalosis

            d.            Compensated metabolic alkalosis

pH 7.62, pCO2 47, HCO3- 30:     

            a.            Uncompensated metabolic alkalosis

            b.            Uncompensated respiratory alkalosis

            c. compensated respiratory alkalosis

            d. compensated metabolic alkalosis

Cardiology

Click here for cardiac auscultation video


Diagnostic tests

A. CARDIAC ENZYMES

CK-MB (creatine kinase, )

An elevation occurs within 4 to 6 hours and peaks 18 to 24 hours following an acute ischemic attack
Total CK- 26-174 units/L
Lactic dehydrogenase (LDH)
Elevates 24 hours following myocardial infarction and peak in 48 to 72 hours
Normal value : 140-280 units/l

Troponin

Troponin I : 0 - 0.1 ng/ml
Troponin T : 0 - 0.2.ng ng/ml
Gold Standard in the diagnosis of MI

Myoglobin

Level rises within 1 hour after cell death peaks in 4 to 6 hours and returns to normal within 24 to 36 hours
Normal values
Male -10-95 ng/ml
Female - 10-65 ng/ml

SGOT (Serum glutamic-oxaloacetic transaminase
Normal values : 5-40 units

Complete blood count

The red blood cell (RBC) count
The white blood cell (WBC)
Erythrocyte Sedimentation rate

Serum lipids
Cholesterol < 200mg/dl
LDL <130 mg/dl
HDL -30 to 70mg/dl

Blood Coagulation test
PTT ( 60-70 seconds )
PT ( 11 -12 seconds )
Clotting time – 9 minutes

Blood urea nitrogen (BUN )- test is a measure of the amount of nitrogen in the blood that comes from urea.

ECHOCARDIOGRAPHY
A non invasive procedure based on the principles of ultrasound
It evaluates structural and functional changes in the heart

Electrocardiogram
Records electrical activity of cardiac cells

CARDIAC CATHETERIZATION
To measure oxygen concentration , saturation ,tension and pressure in various chamber of the heart
Implementation
Asses for allergy
NPO 6- 8 hours before the procedure
Check peripheral and apical pulse q 15 min for 2-4 hours.
Check puncture site for bleeding
Keep extremity extended 4-6 hours

HYPERTENSION
Systolic arterial pressure of 120–139 mmHg and a diastolic arterial pressure of 80–89 mmHg is considered prehypertension.
Factors that affect arterial blood pressure:

• Peripheral resistance
• Cardiac output
• Blood viscosity
• Age – BP often increases with age
• Weight – it directly proportional to blood pressure
• Exercise – increased blood pressure in exercise is a physiologic response. It should return to normal in 5 mins after rest.
• Autonomic Nervous System influence – adrenergic stimulation increases BP and vagal stimulation decreases blood pressure

Types of hypertension:
A) Essential hypertension: the cause idiopathic; accounts for 90 – 95% of all cases.
The following are considered risk factors of primary hypertension:

• Obesity
• Family history
• Inactivity
• Smoking
• Excessive alcohol intake
• Stress

B) Secondary hypertension: an elevated blood pressure that results from a known ailment or disorder. E.g. Hyperaldosteronism, atherosclerosis or kidney disease

Assessment

• Asymptomatic
• Headache
• Fatigue
• Dizziness
• Facial flushing
• Blurred vission

Implementation

• Non pharmacological techniques are used first
• Life style modifications
• Avoid excessive sodium intake
• Moderate exercise
• Reduce alcohol consumption
• Weight reduction
• Diet low in saturated fats
• Stop smoking

B) Antihypertensive agents

• Diuretics
• Beta-blockers
• Ace inhibitors
• Angiotensin receptor blockers
• Calcium channel blockers
• Symphatolytic drugs

CORONARY ARTERY DISEASE
An atherosclerotic disease process that narrows the lumen of the coronary arteries, resulting in ischemia to a myocardium and other cardiac tissues; can progress to injury or death (cardiac arrest).

Multiple risk factors are linked to atherosclerosis:
Non-modifiable risk factors: age, sex, race, family history of CAD.
Modifiable risk factors: cigarette smoking, high blood pressure, elevated cholesterol levels and LDL levels, elevated blood homocystine, obesity, inactivity and stress.
Contributory disease – diabetes mellitus

Signs & Symptoms:

• Substernal, crushing, squeezing pain that can develop slowly or quickly.
• May radiate to the shoulders, arms, jaw, neck, back.
• Usually lasts less than 5 minutes; however, can last up to 15 to 20 minutes.
• Relieved by rest or NTG

Patterns of angina

• Stable angina – relieved with rest and/with nitrates.
• Unstable angina – poorly relieved with rest or oral nitrates.
• Prinzmetal’s agina – resting angina associated with ST-segment elevation caused by focal coronary artery spasm.
• Microvascular angina – caused by constriction of myocardial capillaries.
• Crescendo angina – effort-induced pain that occurs more and more often.

Medications

• Nitroglycerin
• Beta-blockers
• ACE inhibitors
• Statins e.g atorvastatin
• Aspirin

Surgical procedures

• PTCA
• Atherectomy
• Coronary artery bypass
• Vascular stents

Implementation

• Provide relief from pain
• Instruct regarding diet
• Behavior modification

Myocardial infarction
Prolonged ischemia, injury and death of an area of the myocardium caused by occlusion of one or more of the coronary artery.
Etiology:

• Coronary thrombosis – most common cause
• Arterial Spasm
• Embolism
• Cocaine toxicity

Assessment:

• Chest pain unrelieved by nitrates or rest; crushing substernal pain that may radiate to jaw, neck, back or left arm with feeling of impending doom.
• Feeling of “indigestion”.
• Diaphoresis.
• Nausea, vomiting, dyspnea.
• Bradycardia and hypotension – in patient with inferior MI.

Screening & Diagnosis:

• Patient history and physical examination.
• ECG (12 lead).
• ST segment elevation (key diagnostic indicator of MI), T wave inversion (indicates ischemia), abnormal Q wave.
• ST depression – presence of ischemia.
• Lab work:
• ↑ CK – MB = peaks within 24 hrs of MI.
• ↑ Troponin I & T = elevates within hours and remains. elevated even for 3 weeks. Reliable and critical marker of MI.
• Echocardiogram – evaluates ventricular function and determines the ejection fraction.

Therapeutics:
1. Give Oxygen via nasal cannula x 24 hours (especially if with heart failure or Oxygen saturation <90% )
Nitrostat 0.4 mg SL up to 3 doses stat q 5 min and PRN for chest pains then start
Isosorbide Dinitrate (Isoket) Drip x 24-48 hours until chest pain then subsides
Transderm patch 5-10 mg OD to anterior chest wall
Isosorbide mononitrate (imdur) 60 mg OD
Isosorbide dinitrate (Isordil) 10-20 mg TID

Pain relief : Morphine ( IV)
AspirinBID


Thrombolytic drugs

• Streptokinase
• Alteplase
• Reteplase
• Urokinase

Beta-blockers

• Metropolol 50 mg ½ -1 tab q 8-12 hrs
• Esmolol 10-20 mg IV
• ACE-inhibitors:
• Captopril 25 mg ¼ tab q 12 hr x days
• 
  
• Atorvastatin 20 mg tab OD or Simvastatin 20 mg tab OD HS
• Diazepam 2-5 mg tab BID (especially for anxious patients)
• Duphalac 20-30 ml HS defer for LBM. Instruct patients not to strain

Complications of MI

Early:
Arrhythmia: dizziness, palpitations, syncope

Congestive heart failure: dyspnea, orthopnea, rales, wheezes (cardiac asthma), cardiogenic shock.

Pericarditis: Occurs 1-3 days after MI, pleuritic pain, non-responsive to nitrates, self limited.



Days to Weeks:
Myocardial rupture: tamponade, shock, death, typically occurs with small infarcts.

Papillary Muscle rupture: hyperacute onset pulmonary edema, loud systolic murmur (mitral regurgitation)


Implementation
bed rest for 24-48 hours (semi-fowlers position)
avoid straining, since this increases blood pressure (stool softeners if needed)
monitor ECG, ABGs and blood pressure.
monitor for complication: congestive heart failure, arrhythmias

DYSRHYTHMIAS

• Abnormality in the electrical activity of the heart leading to a disturbance of the normal heart rate and rhythm.
• Etiology: Any factors that may interrupt the normal electrical conduction, from the intrinsic and extrinsic conducting systems, that regulates the myocardial function (inotropy and chronotropy).
• Such as:
• Ischemia, MI or atrioventricular blocks
• electrolyte imbalances
• acidosis and/or alkalosis
• hypotension
• shock
• emotional stress
• drugs (e.g. amphetamines, beta blockers), caffeine and alcohol

Management of dysrhythmia
Vagal Maneuvers
Carotid sinus massage
Valsalva maneuver

Cardioversion - Synchronous counter shocks give at a specific time in the cardiac cycle ( R-wave)
Click here to see video of cardioversion

Nursing Intervention
Informed consent
Administer sedation as prescribed
Hold digoxin 48 hours pre procedure
Stop O2 ( during)
Keep airway open (open)
Monitor V/S
Monitor cardiac rhythm

Defibrillation
Asynchronous countershock used to terminate pulseless VT or VF
Three rapid consecutive shock beginning at 200 j

Pacemaker
Settings

• Synchronous or demand
• Asynchronous or fixed rate

Monitor

• Failure to capture
• Failure to sense

Nursing intervention
1) Monitor Vital signs and notify AP

Implementation 

• Avoid heavy lifting
• Avoid difficult arm maneuvers, stretching or bending
• Report hiccups, palpitation or dizziness immediately
• Caution with electromagnetic devices: transformers, cautery, electric razors, anti-theft devices.
• Carry ID card.
• Wear loose fitting clothes
• Avoid contact sport

HEART FAILURE (Congestive Heart Failure/CHF)
A condition in which the heart can not pump enough blood throughout the body.
Types of CHF depend on which part of the heart fails.
Assessment:
signs of left or right heart failure

TREATMENT

• Combined alpha- and beta-blockers (labetalol)
• ACE inhibitors
• Vasodilators
• Inotropic drugs
• Diuretics
• Implementation:
• High Fowlers position
• Reduce physical activity
• Monitor central vein pressure
• Monitor body weight
• Auscultate lungs for crackles (fluid accumulation)
• Watch for deep vein thrombosis (high risk due to vascular congestion

Client Education:
Diet:

• restrict salt and fluid
• avoid food high in sodium
• avoid potassium loss (unless potassium sparing diuretics are used).

RHEUMATIC HEART DISEASE (RHD)
The most serious complication of rheumatic fever. Varying degrees of pancarditis with associated valve insufficiency, heart failure and even death can result from this grave condition.

Pathogen: group A beta-hemolytic streptococci
Acute Rheumatic Fever Rheumatic Heart Disease
occurs 1-4 weeks after tonsillitis occurs many years after rheumatic fever
(streptococcal infection) - involves: mitral valve - aortic valve
affects children 5-15 years manifests in adults

Assessment
Major Signs & Symptoms:

• Pancarditis – the most serious and 2nd most common complication of RF (50%).
• In advanced cases of pancarditis, the ff may be present:
• Dyspnea
• Mild-to-moderate chest discomfort
• Pleuritic chest pain
• Edema
• Cough and orthopnea
• Heart murmurs and pericardial friction rub
• Sydemham’s chorea or “Saint Vitus Dance” – 20-30% of patient with RF.
• Erythema marginatum
• Migratory polyarthritis – 70% in patient with RF
• Subcutaneous nodules/Aschoff bodies

Minor signs

• Malaise and Fever
• Arthralgia
• Prolonged PR interval on ECG
• Elevated ESR
• Presence of C-reactive protein
• Leukocytosis

Treatment:

• Management is directed toward:
• Eliminating the group A streptococcal pharyngitis.
• Oral penicillin
• IM benzathine penicillin G
• Erythromycin/1st generation cephalosporin .
• Ssuppressing inflammation
• Salicylates and steroids

Supportive treatment for congestive heart failure

• ACE inhibitors
• Loop diuretics
• Digoxin
• Supplemental oxygen
• Bed rest
• Sodium and fluid restriction

Antistreptococcal prophylaxis should be maintained continuously after the initial episode of ARF to prevent recurrences

SHOCK
It occurs when the systems/organs in the body severely lack blood, fluids and/or oxygen. Cells undergo metabolic process and then organs eventually fail.
Stages of shock

Initial stage

• ↓cardiac output and systemic perfusion
• Cellular function disrupted
• ↑ Anaerobic metabolism
• No clinical symptoms yet

Compensatory stage

Baroreceptors in aorta activate sympathetic NS: ↑ HR, blood shunted to the vital organs, mydriasis

• ↑ angiotensin, aldosterone and vasopressin secretions in an attempt to restore blood volume and pressure
• ↑ RR due to hypoxemia → will result to respiratory alkalosis

Progressive stage

• If no medical intervention, compensatory mechanisms of the body would seem futile.
• Severe hypoperfusion would occur
• Massive cell death
• Vital organs begin to fail
• Loss of conciousness

Refractory stage

• Shock irreversible; multiple organ failure is evident
• Cardiac failure
• Renal failure
• Respiratory failure
• Then eventually, DEATH

Treatment:

• Determine first the cause of shock and then correct the underlying cause.
• Implementation
• Supine position, legs elevated
• Airway management
• IV fluids
• Monitor ABG
• Monitor I and O

Cardiac Tamponade
accumulation of fluid in pericardial space

Assessment:

• dyspnea
• cyanosis
• Hypotension
• increased CVP  distended neck veins
• pulsus paradoxus

Implementation
Pericardiocentesis   click here to see video of pericardiocentesis


Implementation

• Ausculate heart and lung sounds after   
• Obtain chest x-ray post procedure. Assess pneumothorax or hemothorax.
• Continue observing the pericardiocentesis site for bleeding.
• Report any bleeding or hematoma to the site.    
• Report any arrhythmia, edema, or purulent discharge or foul smell at the site. 
• The nurse will change dressing daily as needed.Minimizes infection.
• Report any changes on patient’s condition

Aneurysms
weakened arterial wall local distention  risk of rupture

Types of aneurysm:

• Saccular: outpouching of one wall in a circumscribed area
• 
  
• Fusiform: involves complete circumference of artery
• 
  
• Dissecting: accumulation of blood separating the layers of the arterial wall
• Berry

Signs & Symptoms:

• It is usually asymptomatic and hard to detect. Some patient may experience:
• Pulsating mass in the mid and upper abdomen
• Bruit over the mass
• Pain in the midabdominal area or lower back
• Tenderness or pain in the abdomen or chest – may represent rupture of the aneurysm
• Dyspnea and distended neck veins

Medications
Antihypertensive medication: to lower the other all blood pressure thus lowering the pressure in the area of aneurysm
Statins (e.g simvastatin) - cholesterol lowering medication that will help maintain the health of the blood vessel.

Post –op care
Routine nursing care
Instruct client not to lift objects heavier than 15 – 20 pounds for 6 weeks
Avoid driving untill aproved by physicain

Peripheral Vascular Disorders
THROMBOANGIITIS OBLITERANS (Buerger’s disease)
Characterized by a combination of inflammation and clots in the SMALL blood vessels, which impairs blood flow. Begins distally (hands and feet) and progresses proximally

Assessment

• Intermittent claudication
• Weak or absent pulse in the limb
• Cold legs or feet
• Loss of hair in the legs and/or feet
• Paleness or cyanosis

Treatment:
Pharmacological interventions:
Vasodilators – to manage claudication
Pentoxifylline (Trental®) – ↑ RBC deformability, ↓ plasma viscosity and ↓ fibrinogen concentration = ↓ leg pain
Cilostazol (Pletal®) – induces vasodilation and inhibits platelet aggregation and proliferation on the smooth muscle
Clopidogrel (Plavix®) and aspirin – help prevent the formation of thromboemboli.

• Exercise (Physical Therapy) – increases collateral circulation and improves peripheral utilization of oxygen = decreases intermittent claudication
• Percutaneous endovascular therapy
• Percutaneous transluminal angioplasty
• Stenting
• Thrombolytic therapy
• Surgical:
• Bypass grafting
• Resection with graft replacement and thromboendarterectomy

Implementation

• Instruct client to stop smoking
• Monitor peripheral pulse
• Instruct to avoid injury
• Administer vasodilators as prescribed

Raynaud’s Disease
vasospasm of arteries in hand
Raynaud’s phenomenon
occurs secondary to many different causes

Raynaud’s phenomenon
occurs secondary to many different causes

• Scleroderma
• SLE
• Rheumatoid arthritis
• Sjogren’s syndrome
• Disease of the arteries (e.g Buerger’s)
• Carpal Tunnel Syndrome

Assessment:

• cold, numb hands
• atrophy of nails
• Numbness and color changes
• Burning sensation
• ulceration and gangrene of finger tips
• Allen’s test reveals circulatory problems

Diagnosis

• Clinical examination
• Cold-simulation test – the doctor exposes the fingers to cold air/water to elicit the signs and symptoms

Medications:

• Analgesics, vasodilators
• Implementation
• Instruct client to avoid smoking
• Advise client to avoid exposure to cold
• Instruct client to avoid injury to fingers and hand

Venous thrombosis/thrombophebitis/DVT

• Thrombophebitis
• Phlebothrombosis
• Phlebitis
• Deep vein thrombosis

Assessment

• Edema
• Swelling
• Pain, redness

Medication

• Heparin
• Oral anticoagulants
• Thrombolytics

Implementation

• Recommend bed rest
• Elevate the extremity
• Do not massage the extremity
• Apply warm moist heat
• Analgesic for pain