Diagnostic Examinations Non-invasive Electrocardiogram (ECG) 1. Noninvasive ECG a graphic record of the electrical activity of the heart 2.

. Portable recorder (Holter monitor) provides continuous recording of ECG for up to 24 hrs. Three electrodes are attached to the patient's chest and connected to a small portable EKG recorder by lead wires. Non-invasive: Types of Holter Monitor 1. Continuous recording - the EKG is recorded continuously during the entire testing period.

2. Event monitor, or loop recording - the EKG is recorded only when the patient starts the recording, when symptoms are felt.

Holter Monitor Non-invasive-Hemodynamic Monitoring

Vital signs HR, BP, and RR Arterial oxygen saturation Transthoracic echocardiography

Invasive-Hemodynamic monitoring

Information obtained through hemodynamic monitoring: Cardiovascular performance (right and left ventricular function) Changes in hemodynamic status and organ perfusion Pharmacologic and nonpharmacologic therapy Prognosis

Invasive-Hemodynamic monitoring Indications: Any deficit or loss of cardiac function: such as AMI, CHF, Cardiomyopathy All types of shock; cardiogenic, neurogenic, or anaphylactic Decreased urine output from dehydration, hemorrhage, G.I. bleed, burns, or surgery

Invasive-Hemodynamic Monitoring

Advantages: Eliminates potential for error due to measurement technique Assessment is not inhibited in low-flow states Recommended for all ICU patients with cardiovascular instability In 50% of shock patients non-invasive methods underestimate BP by > 30 mmHg Invasive-Hemodynamic Monitoring

Swan Ganz Catheter/ Pulmonary Artery Catheter Components of Swan-Ganz Normally has four ports Proximal port [Blue] used to measure central venous pressure/RAP and port for measurement of cardiac output Distal port [Yellow] used to measure pulmonary artery pressure Balloon port [Red] used to determine pulmonary wedge pressure;1.5 special syringe is connected Infusion port [White] used for fluid infusion

Components of the Monitoring System Bedside monitor amplifier is located inside. The amplifier increases the size of signal

Transducer changes the mechanical energy or pressures of pulse into electrical energy; should be level with the phlebostatic axis you can estimate this by intersecting lines from the 4th ICS, mid axillary line

Recorder PCWP PCWP-Pulmonary Capillary Wedge Pressure

It is important to measure PCWP to diagnose the severity of left ventricular failure and to quantify the degree of mitral valve stenosis

Above 20 mmHg - PULMONARY EDEMA By measuring PCWP, the physician can titrate the dose of diuretic drugs and other drugs that are used to reduce pulmonary venous and capillary pressure, and thereby reduce the pulmonary edema.

PCWP Complete set -up

Nursing care to patients with Swan Ganz Catheter

1. a sterile dry dressing should be applied to site and changed every 24 hours; inspect site daily and report signs of infection 2. if catheter is inserted via an extremity, immobilize extremity to prevent catheter dislodgment or trauma 3.Observe catheter site for leakage. Nursing care to patients with Swan Ganz Catheter

5. Continuously monitor PA systolic and diastolic pressures and report significant variations 6. Irrigate line before each reading of PCWP

7. Maintain client in same position for each reading 8. Record PA systolic and diastolic readings at least every hour and PCWP as ordered. CENTRAL VENOUS PRESSURE Blood from the systemic veins flows into the right atrium. The pressure in the right atrium is the CVP. Purposes: 1. Reveals RA pressure, 2. to determine the venous return and intravascular volume of the right atrium 3. Provides an IV route for drawing blood samples, administering fluids or medication, and possibly inserting a pacing catheter

CVP CVP Normal range is 4-10 cmH20; elevation indicates hypervolemia, decreased level indicates hypovolemia

CVP Cardiac Catheterization

Cardiac Catheterization

Invasive ABG Perform Allens test to determine collateral circulation Disorders

Alterations in Cardiovascular Functions TOPICS- CARDIAC DYSFUNCTIONS

CAD Angina Cardiac Failure AMI

Incidence Worldwide: 1 in every 5 deaths are caused by Heart Attack worldwide

Philippines: #1 Killer 12 Million Filipinos are diagnosed with CAD Every 7 minutes, a Filipino dies of Heart Attack

CORONARY ARTERY DISEASE (CAD)

A. General Information refers to a variety of pathology that cause narrowing or obstruction of the coronary arteries, resulting in decreased blood supply to the myocardium affects the arteries that provide blood, oxygen, & nutrients to the myocardium

Causes: Atherosclerosis- fatty/ plaque Arteriosclerosis- hardening of deposition arterial lumen

Stages of Development If demand exceed supply = 02 deficit!!!!!!!! Myocardial Injury Myocardial Ischemia when insufficient oxygen is supplied to meet the requirements of the myocardium transient/reversible state Myocardial Necrosis when severe ischemia is prolonged & irreversible damage to tissue will result Necrosis - tissue death Normal vessels can dilate 5-6x normal Stenotic diseased vessels cannot

Risk Factors- Modifiable

Diet- fats, cholesterol

Exercise

Sedentary lifestyle

Stress

Cigarette Smoking

Diabetes Mellitus

Obesity Contraceptive Pills

Type A personality: competitiveness, impatience, aggressiveness, time urgency

Uncontrolled Hypertension

Risk Factors- Non-Modifiable

Age- above 40 years old

Gender- male

Race- whites

Heredity

Clinical Manifestations

CAD Surgical Management

Goal: Restore Blood Supply 1.Percutaneous transluminal coronary angioplasty (PTCA) -balloon angioplasty flattens plaque against arterial walls

2.Coronary atherectomy - surgical removal of an atheroma (abnormal mass of fat or lipids) in a major artery

3.Coronary artery stents a rod or threadlike device for supporting tubular structures during surgical anastomosis (connection between 2 vessels )

PTCA Candidates for PTCA: Those with lesions that occlude at least 70% of the lumen of a major coronary artery

Those whose conditions do not respond to medical treatment and who meet criteria for CABG Coronary Artery Disease

Angina

chest pain from myocardial ischemia caused by inadequate myocardial blood and 0xygen supply

s 4Es-Precipitating Factors EXCESSIVE physical EXERTION EXPOSURE to cold ENVIRONMENT EXTREME EMOTIONAL response EXCESSIVE intake of saturated food (EAT

Angina Health History 1. Assess drug use amphetamines, cocaine which cause excessive sympathetic stimulation & cardiac work 2. Pt may describe S/s other than pain. Ex-burning, aching, pressure, smothering or indigestion

Angina Pain Assessment What precipitated pain how do you describe pain use scale 1-10 to rate what relieves pain

 How long does pain last, how often does it occur Do you carry NTG? Last taken, #tabs, relief any other heart meds do you take Limit ADLs? Angina-S/s Angina ANGINA PECTORIS-MEDICAL MGMT Drug therapy: nitrates, beta adrenergic blocking agents, and/or calcium blocking agents, lipid reducing drugs if cholesterol is elevated

Cardiac Failure Cardiac Output CO = Stroke volume X heart rate =70 ml X 60 beats/min =4,200 ml/min.

Volume of blood ejected per minute Each ventricle ejects approximately 70mL of blood/ beat Averages between 4-8L/min

cardiac output (CO)- the amount of blood pumped in 1 minute. stroke volume (SV),which is the amount of blood pumped out of the ventricle with each contraction. Preload-stretching of the cardiac myocytes prior to contraction Afterload- "load" that the heart must eject blood against

Heart Failure

inability of the heart to maintain adequate circulation to meet the metabolic needs of the body due to impaired pumping ability

Etiology It can be caused by : Inappropriate work load (volume or pressure Restricted filling Myocyte loss overload)

Conditions that Precipitate and Exacerbate Heart Failure

Types of Heart Failure Based on left ventricular functioning Systolic heart failure- an alteration in ventricular contraction Diastolic heart failure - an alteration in ventricular filling

Types of Heart Failure Forward failure -diminished cardiac output, an inadequate output of the affected ventricle causes decreased perfusion to vital organs

Backward failure- damming back of blood in the venous system ,blood backs up behind the left ventricle causing increased pressure in the atrium

Types of Heart Failure Low output failure- not enough CO is available to meet the demands of the body High output failure -occurs when a condition causes the heart to work harder to meet the demands of the body Types of Heart Failure Left sided

Right sided

Biventricular

CLASSIFICATIONS- New York Heart Association (NYHA)Classification of Heart Failure

CONGESTIVE HEART FAILURE Diagnostic tests: RVF - chest x-ray: reveals cardiac hypertrophy -echocardiography: indicates size of cardiac chambers CVP, ALT(SGPT), PO2 Diagnostic tests: LVF ECG, chest x-ray (cardiomegaly, pleural effusion), echocardiography, cardiac catheterization, dec. PO2, inc. PCO2 - B-type natriuretic peptide

CONGESTIVE HEART FAILURE Medical Management: 1. determination and elimination/control of underlying cause 2. Drug therapy: - Diuretics: Furosemide, Spironolactone - Dilators: ACE inhibitors, nitrates - Digitalis: digoxin 3. Diet: low salt, low cholesterol If medical therapies unsuccessful, mechanical assist devices (intra-aortic balloon pump), cardiac transplantation or mechanical hearts may be employed.

Diuretic Therapy The most effective symptomatic relief Mild symptoms Block Na reabsorbtion in loop of henle and distal convoluted tubules Thiazides are ineffective with GFR < 30 --/min

Side Effects Pre-renal azotemia Skin rashes Neutropenia Thrombocytopenia Hyperglycemia Uric Acid Hepatic dysfunction

Diuretics (cont.) More severe heart failure loop diuretics Lasix (20 320 mg QD), Furosemide Bumex (Bumetanide 1-8mg) Torsemide (20-200mg) Mechanism of action: Inhibit chloride reabsortion in ascending limb of loop of Henle results in natriuresis, kaliuresis and metabolic alkalosis Adverse reaction: pre-renal azotemia Hypokalemia Skin rash ototoxicity

K+ Sparing Agents Triamterene & amiloride acts on distal tubules to K secretion Spironolactone (Aldosterone inhibitor) recent evidence suggests that it may improve survival in CHF patients due to the effect on reninangiotensin-aldosterone system with subsequent effect on myocardial remodeling and fibrosis Inhibitors of renin-angiotensin- aldosterone system

Renin-angiotensin-aldosterone system is activation early in the course of heart failure and plays an important role in the progression of the syndrome Angiotensin converting enzyme inhibitors Angiotensin receptors blockers Spironolactone Angiotensin Converting Enzyme Inhibitors

They block the R-A-A system by inhibiting the conversion of angiotensin I to angiotensin II vasodilation and Na retention Ace Inhibitors were found to improve survival in CHF patients Delay onset & progression of HF in pts with asymptomatic LV dysfunction cardiac remodeling

Side effects of ACE inhibitors Angioedema Hypotension Renal insuffiency Rash cough Angiotensin II receptor blockers

Has comparable effect to ACE I

Can be used in certain conditions when ACE I are contraindicated (angioneurotic edema, cough) Digitalis Mechanism of Action +ve inotropic effect by intracellular Ca & enhancing actin-myosin cross bride formation (binds to the Na-K ATPase inhibits Na pump intracellular Na Na-Ca exchange Vagotonic effect Arrhythmogenic effect Effects of Cardiac Glycosides Increased force of myocardial contraction (+ INOTROPIC EFFECT)

Increased renal perfusion (DIURETIC EFFECT) Slowed heart rate (- CHRONOTROPIC EFFECT) Decreased conduction velocity through the AV node ( -DROMOTROPIC EFFECT). Nursing Responsibilities Recognize signs and symptoms of digoxin toxicity Cardiac Sinoatrial arrest or block Third-degree AV block (complete) Ventricular arrhythmias Bradycardia Gastrointestinal Abdominal pain Anorexia Diarrhea Nausea Vomiting

Nursing Responsibilities Recognize signs and symptoms of digoxin toxicity Neurologic Blue-yellow color blindness Blurred vision

Colored dots in vision Confusion Depression Disorientation Flickering lights Headache Insomnia White halos on dark objects Nursing Management-CHF Nursing Management 6. Monitor heart rate and presence of dysrhythmias by cardiac monitor.

7. Insert foley catheter as prescribed and monitor

urine output.

8. MIO

9. Avoid unnecessary IV administration of fluids.

10. Monitor weight to determine response to

treatment.

Nursing Management Nursing Management Check for Medical Emergency: Acute Pulmonary Edema: frothy sputum, impending doom, panic, orthopnea, cough w/pink-tinged sputum

TX: add morphine to relieve anxiety, slow respiratory rate, and decrease peripheral vascular resistance plus cardiac glycoside (Digoxin), and loop diuretic(Lasix), bronchodilators, and oxygen for hypoxia Nursing Management Monitor Intake and output Maintain bed rest for the first 24-36 hours Assess respiratory rate and characteristics. This may indicate heart failure. Provide reassurance to the family and client.

CARDIAC SURGERIES CORONARY ARTERY BYPASS SURGERY A. General information: A coronary artery bypass graft is the surgery of choice for clients with severe CAD New supply of blood brought to diseased/occluded coronary artery by bypassing the obstruction with a graft that is attached to the aorta proximally and to the coronary artery distally.

Coronary Artery Bypass Grafting (CABG) Candidates for CABG

Angina cannot be controlled by medical Rx

Unstable angina A positive exercise tolerance test & lesions or blockage that cannot be treated by PTCA A left main coronary artery lesion or blockage of more than 70% Individuals who have complications from unsuccessful PTCAs CORONARY ARTERY BYPASS SURGERY B. Nursing interventions: preoperative 1. Explain anatomy of the heart, function of coronary arteries, effects of CAD 2. Explain events of the day of surgery 3. Orient to the critical and coronary care units and introduce to staff 4. Explain equipments to be used (monitors, hemodynamic procedures, ventilators, ET, etc) 5. Demonstrate activity and exercise 6. Reassure availability of pain medications CORONARY ARTERY BYPASS SURGERY C. Nursing interventions: post-operative 1. Maintain patent airway 2. Promote lung re-expansion-deep breathing & coughing, incentive spirometer 3. monitor cardiac status 4. maintain fluid and electrolyte balance/monitor drainage in chest tubes (report if 100150cc/hr) 5. maintain adequate cerebral circulation 6. provide pain relief-splinting,meds 7. prevent abdominal distension CORONARY ARTERY BYPASS SURGERY 8. Monitor for and prevent the ff. complications: a. Thrombophlebitis / pulmonary embolism b. Cardiac tamponade

c. arrhythmias d. CHF 9. Provide client teaching and discharge planning concerning: a. limitation with progressive increase in activities CORONARY ARTERY BYPASS SURGERY b. sexual intercourse can usually be resumed by 3rd or 4th week post-op c. medical regimen d. meal planning with prescribed modifications e. wound cleansing daily and report for any signs of infection f. Symptoms to be reported: - fever, dyspnea, chest pain with minimal exertion ALTERATION IN RESPIRATORY FUNCTION

VENTILATION & PERFUSION RATIO (V/Q)

PULMONARY/RESPIRATORY FAILURE inability of the lung to meet the metabolic demands of the body. This can be from failure of tissue oxygenation and/or failure of CO2 homeostasis.

Classification Respiratory Failure Symptoms CNS: Headache

Visual Disturbances Anxiety Confusion Memory Loss Weakness Decreased Functional Performance Respiratory Failure Symptoms Pulmonary: Cough Chest pains Sputum production Stridor Dyspnea

Respiratory Failure Symptoms Cardiac: Orthopnea Peripheral edema Chest pain

Other: Fever, Abdominal pain, Anemia, Bleeding Clinical Respiratory compensation

Sympathetic stimulation Tissue hypoxia Hemoglobin desaturation

Clinical Respiratory compensation Tachypnoea RR > 35 Breath /min Accessory muscles Recesssion Nasal flaring Sympathetic stimulation Tissue hypoxia Haemoglobin desaturation

Clinical Respiratory compensation Sympathetic stimulation

sweating Tissue hypoxia Haemoglobin desaturation

Clinical Respiratory compensation

Sympathetic stimulation Tissue hypoxia Altered mental state (late) Haemoglobin desaturation

Clinical Altered mental state PaO2 +PaCO2 acidosis dilatation of cerebral resistance vesseles ICP

Disorientation Headache coma asterixis personality changes Clinical Respiratory compensation Sympathetic stimulation Tissue hypoxia Hemoglobin desaturation cyanosis

Respiratory Failure Laboratory Testing Other tests Hemoglobin

Electrolytes, blood urea nitrogen, creatinine Creatinine phosphokinase, aldolase EKG, echocardiogram Electromyography (EMG) Nerve conduction study Respiratory Failure Laboratory Testing Arterial blood gas PaO2 PaCO2 PH Chest imaging Chest x-ray CT sacn Ultrasound Ventilationperfusion scan Respiratory failure: Interventions

Supportive therapy

Specific therapy Supportive therapy Secure the airway Pulse oximetry Oxygen: by mask, nasal cannula, head box

Proper positioning Nebulization if indicated Blood sampling: Routine, electrolytes, ABG Secure IV line CXR: upright AP & lateral views

Hypoxemic / Non - Hypercapnic respiratory failure

The major problem is PaO2. If due to low V/Q mismatch; oxygen therapy. If due to pulmonary intra-parenchymal shunts (ARDS), assisted ventilation with PEEP may be needed. If due to intracardiac R-L shunt: O2 therapy is of limited benefit. Surgical t/t is needed. Hypercapnic Respiratory failure

Key decision is whether mechanical ventilation is required or not. In Acute respiratory acidosis: Mechanical ventilation must be strongly considered. Chronic Resp acidosis: patient should be followed closely, mech ventilation is rarely required. In acute-on-chronic respiratory failure, the trend of acidosis over time is a crucial factor. Mechanical Ventilation: Indications PaO2< 55 mm Hg or PaCO2 > 60 mm Hg despite 100% oxygen therapy. Deteriorating respiratory status despite oxygen and Nebulization therapy Anxious, sweaty lethargic child with deteriorating mental status. Respiratory fatigue: for relief of metabolic stress of the work of breathing Nursing Management

Note changes suggesting increased work of breathing (tachypnea, diaphoresis, intercostal muscle retraction, fatigue) or pulmonary edema (fine, coarse crackles or rales, frothy pink sputum). Assess breath sounds. Diminished or absent sounds indicate inability to ventilate the lungs sufficiently to prevent Analyze ABG and compare with previous values Determine hemodynamic status (blood pressure, pulmonary wedge pressure, cardiac output) Nursing Management Administer oxygen to maintain Pao2 of 60 mm Hg or Sao2 > 90% using devices that provide increased oxygen concentrations (aerosol mask, partial rebreathing mask, nonrebreathing mask). MIO Provide measures to prevent atelectasis and promote chest expansion and secretion clearance, as ordered (incentive spirometer, nebulization, head of bed elevated 30 degrees, turn frequently, out of bed). Perform chest physiotherapy to remove mucus. Teach slow, pursed-lip breathing to reduce airway obstruction. ARDS clinical syndrome also called noncardiogenic pulmonary edema in which there is severe hypoxemia and decreased compliance of the lungs, which leads to both oxygenation and ventilatory failure

Fulminant form of respiratory failure characterized by acute lung inflammationand diffuse alveolocapillary injury

Sudden and life-threatening deterioration of the gas-exchange function of the lungs

S/S Develop progressively as follows:

Hyperventilation Respiratory alkalosis Dyspnea & Hypoxemia Metabolic acidosis Respiratory acidosis Further hypoxemia Hypotension, decreased cardiac output ,death Diagnostic Evaluation

The hallmark sign for ARDS is a shunt; hypoxemia remains despite increasing oxygen therapy. Decreased lung compliance; increasing pressure required to ventilate patient on mechanical ventilation. Chest X-ray exhibits bilateral infiltrates. Pulmonary artery catheter readings: pulmonary artery wedge pressure >18 mm Hg.

Histopathologic Changes

Diffuse alveolar damage is the descriptive term for the histopathologic findings encountered in acute lung injury.

MEDICAL MANAGEMENT Primary Focus in the management of ARDS includes: Identification and treatment of the underlying condition. Aggressive, supportive care must be provided to compensate for severe respiratory dysfunction SUPPORTIVE THERAPY Intubation Mechanical ventilation

Circulatory support Adequate fluid volume Nutritional support Monitor ABGs, Pulse Oximetry, bedside Pulmonary Function Test Positive End-Expiratory Pressure (PEEP) is a critical part of the treatment of ARDS. Uses of PEEP-

PHARMACOLOGIC THERAPY (Under Investigation Human Recombinant Interleukin-1 receptor antagonists Neutrophil Inhibitors Pulmonary-specific vasodilators Surfactant Replacement Therapy Antisepsis Agents Antioxidant Therapy Corticosteroids (late in the course of ARDS)

NUTRITIONAL THERAPY

Patients with ARDS require 35-45 Kcal/kg per day to meet caloric requirements. Enteral Feeding is the first consideration; however TPN also may be required.

NURSING MANAGEMENT

General Measures Close monitoring and frequent assessment

Positioning is important to improve ventilation and perfusion in the lungs and enhance secretion drainage. Restrict fluid intake Provide rest Reassurance especially with neuromuscular blocking agents Prepare for intubation and mechanical ventilation using PEEP

Definition Acute Renal failure (ARF)

Inability of kidney to maintain homeostasis leading to a buildup of nitrogenous wastes

Different to renal insufficiency where kidney function is deranged but can still support life ARF Occurs over hours/days Lab definition Increase in baseline creatinine of more than 50% Decrease in creatinine clearance of more than 50% Deterioration in renal function requiring dialysis

ARF Pre renal (functional) Renal-intrinsic (structural) Post renal (obstruction)

ACUTE RENAL FAILURE Stages of ARF OLIGURIC PHASE urine output = < 400cc/day Usually lasts 1-2 weeks BUN, Creatinine, hyponatremia

DIURETIC PHASE Gradual return to glomerular filtration Excretion of fluid: 1-2 liters/ day- 4-5L Usually lasts 2-3 weeks BUN, Creatinine

RECOVERY PHASE Returns to prerenal failure activity level 3-12 months ACUTE RENAL FAILURE Assessment Urine output Ultrasound Azotemia (increased BUN and crea) Hyperkalemia Metabolic Acidosis Anemia Prevention

Drugs taken by client Nephrotoxic drugs NSAIDs

ACUTE RENAL FAILURE Medical Management Fluid maintenance Avoiding fluid excess Dialysis Pharmacologic treatment Kayexalate (sodium polystyrene sulfonate) Retention enema Reduction of drug doses Nutrition: protein- 1g/kg of weight; potassium restriction

ACUTE RENAL FAILURE Maintaning fluid and electrolyte balance High calorie, low protein diet Reducing metabolic rate Promoting pulmonary function Infection prevention Skin care Emotional support

Monro-Kellie Hypothesis because of the limited space for expansion within the skull, an increase in any one of the components causes a change in the volume of the others. (B&S, p. 2169)

What does this mean? Decreased Cerebral Blood Flow What happens to brain cells as blood flow decreases? Early compensatory mechanism: Vasomotor stimulation What assessment findings indicate this? Changes in concentration of CO2 causes cerebral vasodilation causes vasoconstriction Decreased cerebral outflow

Cerebral Perfusion Pressure What is cerebral perfusion?

Steady cerebral perfusion can be maintained if arterial systolic pressure is 50 150 mm Hg and ICP is below 40 mm Hg.

CPP = MAP ICP

Normal CPP is 70 100 mm Hg

Increased ICP Pathophysiology: Acute neurologic condition alters the equilibrium of components within the cranial vault Causes Primary Secondary Regardless of cause, ICP decreases cerebral perfusion, stimulates further swelling, and may cause herniation Background Information The brain is contained within and protected by the rigid cranial vault The cranial vault also contains blood and CSF These components are usually in a state of equilibrium and produce the ICP Usually measured in the lateral ventricles Normal pressure 10 to 20 mm Hg Increased ICP and Cushings Response Increased ICP: Clinical Manifestations Early Indicators: Subtle changes in LOC Pupillary changes Weakness of one extremity or one side Constant headache increasing in intensity and aggravated by movement or straining Late Indicators: Continuing decrease in LOC progressing to coma Bradypnea, bradycardia, hypertension and fever

Altered respiratory pattern Projectile vomiting Hemiplegia, decorticate or decerebrate posturing Loss of brain stem reflexes Diagnostic Tests CT MRI PET SPECT Transcranial Doppler Electrophysiologic monitoring Evoked potential monitoring

Contraindicated Diagnostic Test Which diagnostic test is contraindicated in a patient with increased intracranial pressure?

Why? Complications Brain stem herniation Diabetes insipidus Syndrome of Inappropriate ADH (SIDAH)

What is the cause of these complications? How will they be treated? Medical Management

Increased ICP is a true medical emergency Treatment must be promptly initiated Invasive monitoring of ICP Manipulating one or more cranial vault component Decrease cerebral edema Maintain cerebral perfusion Reduce CSF and intracranial blood volume Controlling fever Maintaining oxygenation Reducing metabolic demands

Nursing Care Maintaining a patent airway Achieving an adequate breathing pattern Optimizing cerebral tissue perfusion Maintaining negative fluid balance Preventing infection Monitoring and managing potential complications cEREBROvaSCULAR ACCIDENT refers to a functional abnormality of the CNS that occurs when the normal blood supply to the brain is disrupted

types Ischemic stroke-little blood flow Thrombotic

Embolic

Hemorrhagic stroke-disrupted blood flow Intracerebral Subdural

types Ischemic stroke-little blood flow 1. Thrombotic formation of a blood clot with coagulation the results in the narrowing of the lumen of a blood vessel with eventual occlusion

2. Embolic occlusion of a cerebral artery by an embolus, resulting in necrosis and edema of the area supplied by the involved vessel types Hemorrhagic stroke-disrupted blood flow 1. Intracerebral hemorrhage stroke-bleeding within the brain caused by a rupture of vessels

2. Subarachnoid hemorrhagic stroke-cause by aneurysm or AV malformation

cEREBROvaSCULAR ACCIDENT Pathophysiology and Etiology Cerebrovascular insufficiency is caused by atherosclerotic plaque or thrombosis, increased PCO2, decreased PO2, decreased blood viscosity, hyperthermia/hypothermia, increased ICP. Carotid arteries, vertebral arteries, major intracranial vessels, or microcirculation may be affected.

Cardiac causes of emboli include atrial fibrillation, mitral valve prolapse, infectious endocarditis, and prosthetic heart valve.

Development of CVA 1.Transient Ischemic attack-brief episodes of neurologic manifestations which clear completely in less than 24 hours 2. Reversible ischemic neurologic deficit-neurologic deficits remain after 24 hours but leaves no residual signs and symptoms after days to weeks 3. Stroke in-evolution-progressing stroke which develops over a period of hours or days; manifestations dont resolve and leave residual neurologic effects 4. Completed stroke- when neurologic deficits remain unchanged over 2-3 day period Risk Factors

Prior ischemic episodes Cardiac disease DM Atherosclerotic diseasae Hypertension, hypercholesterolemia Polycythemia Smoking Oral contraceptives

Emotional stress Obesity Family history of stroke Age Assessment and diagnostic findings Physical and neurologic exams (focus on airway patency and cough and gag reflex) TIA (transient ischemic attack) CT scan ECG Carotid ultra sound Transesophageal echocardiography to rule out emboli from heart.

Tia s/s History of intermittent neurologic deficit, sudden in onset, with maximal deficit within 5 minutes and lasting less than 24 hours. Carotid bruit History of headaches of duration of days before ischemia.

Tia s/s Carotid system involvement: amaurosis fugax, homonymous hemianopsia, unilateral weakness, unilateral numbness or paresthesias, aphasia dysarthria. Tia s/s

Vertebrobasilar system involvement: vertigo, homonymous hemianopsia, diplopia, weakness that is bilateral or alternates sides, dysarthria, dysphagia, ataxia, perioral numbness

Warning signs that may precede CVA

Paresthesia Transient loss of speech Hemiplegia Severe occipital or nuchal headaches Vertigo or syncope Motor or sensory disturbances (tingling transient paralysis) Epistaxis Cva S/S Cva S/S Cva S/S Treatment for Ischemic Stroke tPA=Thrombolytic agent Document time of symptom onset. (If awoke with symptoms, must go by time when last seen normal) Immediate head CT (check for blood) Evaluate for tPA administration (review exclusion/inclusion criteria) Treatment for Ischemic Stroke If not a tPA candidate, ASA in ED. Rectal ASA if fails swallow eval. or if swallow eval. not complete. Keep NPO, until a formal swallow eval. is done. Admit as Inpatient and perform diagnostic testing: Carotid US, Echo, TEE, ECG monitoring for a-fib, MRI, fasting Lipid, Clotting disorder blood work (Antiphospholipid, Factor V, Antithrombin III)

Rehabilitation Treatment for Ischemic Stroke Surgery carotid endarterectomy (removal of an atherosclerotic plaque or thrombus from the carotid artery if with TIA symptoms)

tPA Administration Considerations Must be started before 3 hours from onset No blood on head CT Review patients history for other risk factors Accurate weight recorded Foley catheter prior to tPA

tPA Cont Consent explained and signed (BP>185/110) treat with labetolol 10-20mg IV over 1-2 min. May repeat x1 or nitro paste 1-2 inches. If treatment does not lower BP, do not give tPA shows significant deficits to merit treatment.

tPA Contraindications Any recent surgery<14 days/serious head trauma/recent IC surgery or previous stroke within 3 months History of ICH Uncontrolled HTN at time of treatment (BP>185/110) Seizure at the onset of stroke Active internal bleeding (<21 days) Intracranial neoplasm, AV malformation, aneurysm

Use of anticoagulants with PT>15 or INR >1.7 Platelet count <100,000/mm Administration of heparin within 48 hrs preceding the onset of stroke and an elevated PTT at presentation Lumbar puncture <7 days or recent arterial puncture

During tPA Administration Check BP every 15 min for 2 hours Treat hypertension/hypotension as ordered Monitor Neuro status every 30 min x4 Watch for bleeding puncture sites, urine, stool etc. Know signs/symptoms of Intracerebral Hemorrhage: Any acute neurological deterioration, new HA, N/V, sudden HTN Hemorrhage Suspected STOP TPA INFUSION, call MD immediately Stat head CT without contrast Draw blood for PT, PTT, plt ct, fibrinogen, and type and hold Prepare for administration of cryo and or platelets Other Treatment Options for Ischemic Strokes

If symptom onset is greater than 3 hrs consider: Other interventions (IA, corkscrew, stenting) Other trials (thrombolytics, neuroprotective, hyperglycemia)

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke NURSING INTERVENTIONS

Improve Mobility and prevent joint deformities Correctly position patient to prevent contractures Place pillow under axilla Hand is placed in slight supination- C Change position every 2 hours

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke NURSING INTERVENTIONS 2. Enhance self-care Carry out activities on the unaffected side Prevent unilateral neglect Keep environment organized Use large mirror

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke NURSING INTERVENTIONS 3. Manage sensory-perceptual difficulties Approach patient on the Unaffected side Encourage to turn the head to the affected side to compensate for visual loss

CEREBROVASCULAR ACCIDENTS: Ischemic Stroke NURSING INTERVENTIONS 4. Manage dysphagia Place food on the UNAFFECTED side Provide smaller bolus of food

Manage tube feedings if prescribed 5. Help patient attain bowel and bladder control Intermittent catheterization is done in the acute stage Offer bedpan on a regular schedule High fiber diet and prescribed fluid intake

CVA: Hemorrhagic Stroke Normal brain metabolism is impaired by interruption of blood supply, compression and increased ICP Usually due to rupture of intracranial aneurysm, AV malformation, Subarachnoid hemorrhage CVA: Hemorrhagic Stroke Normal brain metabolism is impaired by interruption of blood supply, compression and increased ICP Usually due to rupture of intracranial aneurysm, AV malformation, Subarachnoid hemorrhage CVA: Hemorrhagic Stroke Sudden and severe headache Same neurologic deficits as ischemic stroke Loss of consciousness Meningeal irritation Visual disturbances

General manifestations

Hemorrhagic Stroke Treatment Do not give antithrombotics or anticoagulants Monitor and treat blood pressure greater than 150/100 NPO, until swallow eval is completed Anticipate Neurosurgical consult Possible administration of blood products

CVA: Hemorrhagic Stroke NURSING INTERVENTIONS 1. Optimize cerebral tissue perfusion 2. relieve Sensory deprivation and anxiety 3. Monitor and manage potential complications

Increased Intracranial pressure Intracranial pressure more than 15 mmHg Brunner= Normal intracranial pressure 10-20 mmHg Causes: Head injury Stroke Inflammatory lesions Brain tumor Surgical complications Increased Intracranial pressure Pathophysiology The cranium only contains the brain substance, the CSF and the blood/blood vessels MONRO-KELLIE hypothesis- an increase in any one of the components causes a change in the volume of the other Any increase or alteration in these structures will cause increased ICP Increased Intracranial pressure Pathophysiology Compensatory mechanisms: 1. Increased CSF absorption 2. Blood shunting 3. Decreased CSF production Increased Intracranial pressure Pathophysiology

Decompensatory mechanisms: 1. Decreased cerebral perfusion 2. Decreased PO2 leading to brain hypoxia 3. Cerebral edema 4. Brain herniation

S/s Cushings triad HPN Bradycardia Widening of pulse pressure Decreased cerebral blood flow

Cerebral Edema Abnormal accumulation of fluid in the intracellular space, extracellular space or both. Herniation Results from an excessive increase in ICP when the pressure builds up and the brain tissue presses down on the brain stem Cerebral response to increased ICP Steady perfusion up to 40 mmHg Cushings response Vasomotor center triggers rise in BP to increase ICP Sympathetic response is increased BP but the heart rate is SLOW Respiration becomes SLOW Increased Intracranial pressure

CLINICAL MANIFESTATIONS Early manifestations: Changes in the LOC- usually the earliest Pupillary changes- fixed, slowed response Headache vomiting Increased Intracranial pressure CLINICAL MANIFESTATIONS late manifestations: Cushing reflex- systolic hypertension, bradycardia and wide pulse pressure bradypnea Hyperthermia Abnormal posturing

Increased Intracranial pressure Nursing interventions: Maintain patent airway 1. Elevate the head of the bed 15-30 degrees- to promote venous drainage 2. assists in administering 100% oxygen or controlled hyperventilation- to reduce the CO2 blood

Increased Intracranial pressure Nursing interventions 3. Administer prescribed medications- usually Mannitol- to produce negative fluid balance corticosteroid- to reduce edema

anticonvulsants-p to prevent seizures

Increased Intracranial pressure Nursing interventions 4. Reduce environmental stimuli 5. Avoid activities that can increase ICP like valsalva, coughing, shivering, and vigorous suctioning

Increased Intracranial pressure Nursing interventions 6. Keep head on a neutral position. ACOID- extreme flexion, valsalva 7. monitor for secondary complications Diabetes insipidus- output of >200 mL/hr SIADH

Altered level of consciousness Consciousness Requires: 1. Arousal: alertness; dependent upon reticular activating system (RAS); system of neurons in thalamus and upper brain stem

2. Cognition: complex process, involving all mental activities; controlled by cerebral hemispheres

It is a function and symptom of multiple pathophysiologic phenomena Causes: head injury, toxicity and metabolic derangement Disruption in the neuronal transmission results to improper function Altered level of consciousness Assessment Orientation to time, place and person Motor function Decerebrate Decorticate Sensory function

Altered level of consciousness Patient is not oriented Patient does not follow command Patient needs persistent stimuli to be awake

COMA= clinical state of unconsciousness where patient is NOT aware of self and environment Altered level of consciousness Etiologic Factors Head injury

Stroke Drug overdose Alcoholic intoxication Diabetic ketoacidosis Hepatic failure

Altered level of consciousness ASSESSMENT Behavioral changes initially Pupils are slowly reactive Then , patient becomes unresponsive and pupils become fixed dilated Glasgow Coma Scale is utilized

Altered level of consciousness Nursing Intervention 1. Maintain patent airway Elevate the head of the bed to 30 degrees Suctioning 2. Protect the patient Pad side rails Prevent injury from equipments, restraints and etc. Altered level of consciousness Nursing Intervention 3. Maintain fluid and nutritional balance Input an output monitoring

IVF therapy Feeding through NGT 4. Provide mouth care Cleansing and rinsing of mouth Petrolatum on the lips Altered level of consciousness Nursing Intervention 5. Maintain skin integrity Regular turning every 2 hours 30 degrees bed elevation Maintain correct body alignment by using trochanter rolls, foot board 6. Preserve corneal integrity Use of artificial tears every 2 hours Altered level of consciousness Nursing Intervention 7. Achieve thermoregulation Minimum amount of beddings Rectal or tympanic temperature Administer acetaminophen as prescribed 8. Prevent urinary retention Use of intermittent catheterization Alteration In Metabolism DKA HHNK TERMS

Gluconeogenesis is a metabolic pathway that results in the generation of glucose from non-carbohydrate carbon substrates such as lactate, glycerol, and glucogenic amino acids. Glycogenolysis takes place in the muscle and liver tissues, where glycogen is stored, as a hormonal response to epinephrine (e.g., adrenergic stimulation) and/or glucagon, a pancreatic peptide triggered by low blood glucose concentrations, and produced in the alpha cells of the islets of Langerhans. Lipolysis is the breakdown of lipids and involves the hydrolysis of triglycerides into free fatty acids followed by further degradation into acetyl units by beta oxidation. The process produces Ketones, which are found in large quantities in ketosis, a metabolic state that occurs when the liver converts fat into fatty acids and ketone bodies, which can be used by the body for energy. Lipolysis testing strips such as Ketostix are used to recognize ketosis. Role of Insulin Required for transport of glucose into Muscle Adipose Liver Inhibits lipolysis

Absence of insulin Glucose accumulates in the blood Liver Uses amino acids for gluconeogenesis Converts fatty acids into ketone bodies Acetone, Acetoacetate, -hydroxybutyrate Increased counterregulatory hormones

Diabetes Mellitus group of metabolic diseases characterized by elevated levels of glucose in the blood (hyperglycemia) resulting from defects in insulin secretion, insulin action, or both ((American Diabetes Association )

Classification of Diabetes

DM1- IDDM

- formerly insulin dependent diabetes mellitus of insulin

- near absolute/ absolute deficiency - juvenile onset -if insulin is not given,fats are metabolized ,resulting into

ketonemia(acidosis)

DM2- NIDDM formerly non-insulin dependent DM resistance to action of insulin

- relative lack of insulin or

-usually sufficient to stabilize fat and protein metabolism ,but not to deal with carbohydrate metabolism - adult-onset

Risk Factors Family History Diet Obesity Sedentary lifestyle Age Stress 4 Cardinal Signs Polyuria Polydipsia Polyphagia

Weight Loss

Diabetic Ketoacidosis acute, life-threatening hyperglycemic crisis

Develops when severe/ absolute insulin deficiency occurs

Complication of DM 1

main characteristics: hyperglycemia over 300 mg/dL (300-800) low bicarbonate level (<15 mEq/L), and acidosis (pH <7.30) with ketonemia and ketonuria.

DKA Precipitating Factors Failure to take insulin Failure to increase insulin Illness/Infection Pneumonia MI Stroke Acute stress Trauma Emotional

Medical Stress Counterregulatory hormones Oppose insulin Stimulate glucagon release Hypovolmemia Increases glucagon and catecholamines Decreased renal blood flow Decreases glucagon degradation by the kidney Diabetic Ketoacidosis Due to: Severe insulin deficiency Excess counterregulatory hormones Glucagon Epinephrine Cortisol Growth hormone 3 Lines of defense against Acidosis 1st Line: Immediate buffering (converts H ions-CO2& H2O) Lungs: excrete CO2 Kidneys: excrete acetoacetate in urine

2nd Line:

Resp.: acetone & CO2 exhaled depth & rate Kussmauls fruity/ acetone breath

3rd Line:

Renal System: excretes 30-100g ketones/day ammonia mechanism is activated -excretion of excess hydrogen

Inadequate insulin

Clinical manifestations

Management

Goals:

Correct fluid & electrolyte imbalancesRestore normal circulating blood volume

Shift from a state of fat catabolism to a state of carbohydrate catabolism by providing insulin

Identify and correct those factors that precipitated ketoacidosis

Management Correct Fluid and Electrolyte Imbalances:

Intravenous infusion of Isotonic saline (0.9% or 0.45% NaCl) started immediately usually 1000 ml/first hour- then 2000-8000ml over the next 24 hours

Dextrose is added (D5NSS or D5 0.45 saline) when blood glucose level reaches 250-300 mg/dl Clients with compromised cardiac function may require slower intravenous fluid replacement

Potassium Administration Hypokalemia occurs Once Intervention begins due to re-entering of potassium back to the cells along with insulin

Nursing Intervention

Monitor Vital signs, neurovital signs ( ICP)

2.

Assess weight, skin turgor, and hematocrit

3.Administer Oxygen therapy

Start Intravenous line; (0.9% PNSS/ 0.45% NSS)

Client Education Take insulin or oral antidiabetic medications as prescribed

Monitor blood glucose frequently

Monitor urine ketones when blood glucose levels rise (above 250mg/dl)

Schedule regular appointments with the physician for regular review of blood glucose tests, weight gain or losses, and general health and well-being.

Recognize signs/symptoms of infection ( a major cause of DKA)

Call the physician/ seek consultation if any of the following develops: Anorexia Nausea, vomiting or diarrhea Ketonuria persisting for more than 8 hours A febrile illness or infection Any sign or symptom of acidosis

Hyperosmolar Nonketotic Syndrome Extreme hyperglycemia and dehydration Unable to excrete glucose as quickly as it enters the extracellular space Maximum hepatic glucose output results in a plateau of plasma glucose no higher than 300-500 mg/dl When sum of glucose excretion plus metabolism is less than the rate which glucose enters extracellular space. HHNK Hyperglycemic, HyperOsmolar, NonKetotic Coma

Occurs in DM2 (NIDDM) Extreme hyperglycemia 800-2000 mg/dl No ketosis and no acidosis Polyphagia, polydipsia, glycosuria,hypotension, shock

Major difference of DKA and HHNK is LACK of KETONURIA in HHNK

Treatment is similar with DKA Hyperosmolar Nonketotic Syndrome Extreme hyperglycemia and hyperosmolarity High mortality (12-46%) At risk Older patients with intercurrent illness Impaired ability to ingest fluids Urine volume falls Decreased glucose excretion

Elevated glucose causes CNS dysfunction and fluid intake impaired No ketones Some insulin may be present Extreme hyperglycemia inhibits lipolysis

Hyperosmolar Nonketotic Syndrome Presentation Extreme dehydration Supine or orthostatic hypotension Confusion coma

Neurological findings Seizures Transient hemiparesis Hyperreflexia Generalized areflexia Hyperosmolar Nonketotic Syndrome Presentation Glucose >600 -1200mg/dl Sodium Normal, elevated or low Potassium Normal or elevated Bicarbonate >15 mEq/L Mental status changes Seizures neurological deficts Treatment of HHS Hydration!!!

Even more important than in DKA Find underlying cause and treat! Insulin drip Should be started only once aggressive hydration has taken place. Switch to subcutaneous regimen once glucose < 200 and patient eating. Serial Electrolytes Potassium replacement.

Hyperosmolar Nonketotic Syndrome Treatment Fluid repletion NS 2-3 liters rapidly Total deficit = 10 liters Replete in first 6 hours Insulin Make sure perfusion is adequate Insulin drip 0.1U/kg/hr Treat underlying precipitating illness Clinical Errors Fluid shift and shock Giving insulin without sufficient fluids Using hypertonic glucose solutions Hyperkalemia Premature potassium administration before insulin has begun to act Hypokalemia Failure to administer potassium once levels falling

Recurrent ketoacidosis Premature discontinuation of insulin and fluids Hypoglycemia Insufficient glucose administration when ketones still present