Understanding the Role of Renewable Energy in Sustainable Development, Exams of Nursing

Download Understanding the Role of Renewable Energy in Sustainable Development and more Exams Nursing in PDF only on Docsity! 1 RNSG 2432 Lecture Exam Review #1 2023-2024 Respiratory Disorders: Pleural and Thoracic Injuries: - Pleural Effusion: an abnormal collection of excess fluid in the pleural space (between lung and chest wall) o Etiology- Congestive Heart Failure (T), Liver Disease (T), Renal Disease(T), Lupus (E), Rheumatoid Arthritis Pneumonia (E), TB (E), Lung Cancer (E), Trauma (E), ARDs (T) o Pathophysiology- ▪ Transudative: caused by changes in pressure (capillary pressure) or decrease in plasma proteins • Non-inflammatory • Trans means movement of fluid due to changes in pressure gradients • Changes in pressure cause fluid from the lungs to leak into pleural space. • Decreased oncotic pressure (from hypoalbuminemia) found in chronic liver or kidney disease o These patients have low serum albumin levels ▪ Exudative: results from inflammatory reaction • Commonly associated with infections and malignancies • Exudate means there is a release of fluids • Due to changes in capillary permeability • The capillaries are inflamed and are not as selective and allow fluid to leak into the pleural space • Empyema- accumulation of pus in pleural space o Clinical Manifestations- ▪ Dyspnea ▪ Pleurisy- inflammation of the lining of the lungs ▪ Decreased breath sounds ▪ Decreased chest wall movement on affected side o Diagnostic Tests: ▪ CXR ▪ CT Scan ▪ ABG’s/ O2 saturation o Interventions: ▪ Thoracentesis- needle aspiration of fluid in pleural space • Usually 1200-1500 ml/time • Don’t want to full too much fluid at once because it can drop BP • Patient will sit up and lean over bedside table ▪ Abx if due to infectious process ▪ Chest tube to drain fluid/air 2 ▪ Pleurodesis- instillation of chemical agent (doxycycline) into pleural space to create inflammatory response to cause the visceral and parietal pleura to stick together so fluid cannot accumulate. ▪ Treat underlying condition that is causing the effusion! - Pneumothorax: o Spontaneous Pneumothorax S/S ▪ Abrupt onset ▪ Pleuritic chest pain ▪ SOB, dyspnea ▪ Increased RR. Tachycardia ▪ Unequal chest excursion ▪ Decreased breath sounds on affected side o Traumatic Pneumothorax: accumulation of air into pleural space due to blunt or penetrating trauma of chest wall/lungs. ▪ Types- • Closed- no opening from external chest o Occurs in crashes, falls, MVAs, CPR, fractured ribs that penetrate the pleura • Open- opening from external chest wall into pleura o Occurs in stabbings, gunshot wounds, impalement injury • Iatrogenic- puncture or laceration of visceral pleura during medical TX o Occurs in central line placement, thoracentesis, lung biopsy, bronchoscopy, mechanical ventilation ▪ S/S- Dyspnea, pleuritic pain, increased RR and pulse, decreased respiratory excursion, absent breath sounds on affected side. o Tension Pneumothorax: air/blood/fluid rapidly enters pleural and unable to escape ▪ Lung collapses ▪ Emergency situation ▪ Patho- • Increase in intrapleural pressure compression of lung to other side compresses against trachea, heart, aorta, and esophagus ventilation and cardiac output greatly compromised ▪ S/S- • Severe dyspnea • Tracheal deviation • Decreased CO • Distended neck veins • Shock ▪ Can result from open or closed pneumothorax • Open- air enters on inspiration but cannot escape 5 -Hypoxemia Respiratory Failure: o Respiratory- ARDS, Pneumonia, Toxic inhalation, Massive PE, PA laceration, PA hemorrhage, Inflammatory state, alveolar injury o Cardiac- Anatomical shunt (VSD), Cardiogenic pulmonary edema, Shock, high cardiac output states o Etiology- 4 physiologic mechanisms- o VQ mismatch (Ventilation/Perfusion) ▪ Most common ▪ Normal Lungs- volume of blood perfusing lungs each minute (4-5 L) is equal to the amount of gas that reaches the alveoli each minute (4- 5L) ▪ 1 ml of air for each 1 ml blood flow (1:1 ratio) ▪ VQ mismatch occurs when it is not 1:1 ▪ Conditions causing VQ mismatch- • Increased secretions are present in the airways (COPD) or alveoli (pneumonia) • Bronchospasms (asthma). • Alveolar collapse (atelectasis) or pain. o These conditions result in limited ventilation to alveoli but no effect on blood flow • Pulmonary embolism affects the perfusion portion of VQ mismatch o Shunt- occurs when blood exits the heart without having participated in gas exchange ▪ An extreme VQ mismatch ▪ Blood passes through an anatomic channel of the heart and does not pass through the lungs ▪ Types- • Anatomic shunt- when blood passes through an anatomic channel in heart (Ventricular septal defect) and bypasses lungs 6 • Intrapulmonary shunt- occurs when blood flow through the pulmonary capillaries without participating in gas exchange. o Seen in conditions in which alveoli are filled with fluid o ARDS, Pneumonia, Pulmonary edema o O2 cannot get passed fluid in alveoli o O2 therapy alone will not be effective o Often require mechanical ventilation and a high fraction of inspired O2 (FiO2) to improve gas exchange o Diffusion Limitations -occurs when gas exchange across alveolar-capillary membrane is compromised by a process that thickens, damages, or destroys the alveolar membranes ▪ Air cannot get through the membrane or it takes a long time to get through ▪ Thickened- slows gas transport (pulmonary fibrosis, intestinal lung disease, ARDS) ▪ Damaged- toxic gas or chemical or disease process ▪ Destroyed- could be lungs or blood vessels ▪ Worsened by conditions that affect pulmonary vascular bed- emphysema, pulmonary emboli ▪ Classic sign- hypoxemia that is present during exercise but not at rest o Alveolar Hypoventilation- generalized decrease in ventilation that results in an increase in the PaCO2 and decrease in PaO2 ▪ Primarily that result of hypercapnic RF, but mentioned in hypoxemia RF because it causes hypoxia ▪ Common causes- lung disease, CNS disease (ALS), chest wall dysfunction, acute asthma, neuromuscular disease o Clinical Manifestations- o Dyspnea o Tachypnea o Prolonged expiration- o Nasal flaring o Intercostal muscle contractions o Use of accessory muscles o Decreased SpO2 o Paradoxical chest movement (chest moving unevenly) o Cyanosis (late) o Cerebral- agitation, disorientation, restless, delirium, decreased LOC, Coma o Cardiac- tachycardia, hypertension, skin cool, clammy, diaphoretic, dysrhythmias, hypotension (late) o Fatigue o Unable to speak in complete sentences -Hypercapnic Respiratory Failure: o Conditions that cause limitation to ventilatory supply: 7 o Abnormalities of the airway and alveoli- ▪ COPD- alveoli are destroyed, secretions obstruct airflow ▪ Asthma- bronchospasm escalates, edema of bronchial mucosa, plugging of small airways ▪ Cystic Fibrosis- abnormal sodium/chloride transport leads to increased viscous and poorly cleared secretions, clogging of airways over time with copious purulent secretions that obstruct airflow ▪ Increases work of breathing causing muscle fatigue and ultimately respiratory failure o Central Nervous System- ▪ Overdose- respirations slowed by drug effect, insufficient CO2 excreted, resulting in increased CO2, loss in respiratory drive, respiratory depression and failure ▪ Brainstem Infarction- medulla is not altering the RR in response to PaCO2, total loss in respiratory drive, respiratory depression and failure ▪ Head Injury- massive inflammatory state, release of inflammatory mediators and cytokines from dead/dying tissue, causes injury to lung tissue, which interferes with gas exchange ▪ Inadequate gas exchange, increased work of breathing, muscle fatigue and ultimately respiratory failure o Chest Wall- ▪ Soft tissue injury, frail chest, rib fractures, pain- Prevent normal ribcage expansion in inadequate gas exchange ▪ Kyphoscoliosis- changes in spinal configuration compresses lungs and prevents normal expansion resulting in inadequate gas exchange ▪ Morbid Obesity- weight of chest and abdominal contents prevent normal rib cage movement and excursion of diaphragm o Neuromuscular Conditions- ▪ Cervical spinal and phrenic nerve injury- Neural control loss, preventing use of diaphragm, smaller tidal volume on inspiration, increase PaCo2 ▪ ALS, Guillain Barre, muscle dystrophy, MS- respiratory muscle weakness or paralysis, prevent normal CO2 ▪ Toxin exposure- prolonged cholinergic crisis, respiratory weakness/paralysis and hypersecretory state with impaired lung ventilation o Clinical manifestations- o Dyspnea o Decreased RR o Decreased Tidal volume o Decreased ventilation o Cerebral- HA, Disorientation, progressive somnolence (sleepiness), coma o Cardiac- dysrhythmias, HTN, tachycardia, bounding pulse -Nursing Assessment: 10 ▪ Propofol (Diprovan), Lorazepam (Ativan), Midazolam (Versed), Morphine, Fentanyl (Sublimaze) • Diprovan- for ventilated patients o Medical Supportive Therapy- o Treat underlying cause ▪ Monitor treatment effects, monitor ABGs, changes in respiratory status o Maintain adequate CO ▪ Monitor BP (systolic greater than 90) ▪ Monitor MAP (greater than 60 o Maintain adequate Hgb concentration- greater than 9 g/ dl o Nutrition- o High calories and carbohydrate diet o Hypermetabolic state in critical illness increases the caloric requirements needed to maintain body weight and muscle mass o Risk for aspiration- may need parenteral nutrition o Speech therapy- if newly extubated after prolonged intubation o Gerontologic considerations- o Decreased ventilatory capacity, alveolar dilation, larger air spaces, loss of surface air for gas exchange, diminished elastic recoil, decreased respiratory muscle strength -ARDS: sudden and progressive form of acute respiratory failure in which alveolar capillary membrane becomes damaged and more permeable to intravascular fluid o Damage to the alveoli membrane and they are leaking o Symptoms- severe dyspnea, hypoxemia refractory to supplemental oxygen, reduced lung compliance, diffuse pulmonary infiltrates o A-assault to the pulmonary system o R-Respiratory distress o D-decreased lung compliance o S-severe RF o Etiology and Patho- o Direct Lung Injury (common)- ▪ Aspiration ▪ Viral/Bacterial Pneumonia ▪ Sepsis o Direct Lung Injury (less common)- ▪ Chest trauma ▪ Embolism ▪ Toxic inhalation ▪ Near drowning ▪ O2 toxicity 11 ▪ Radiation Pneumonitis o *Inflammatory response in the body o Indirect Lung Injury (common) ▪ Sepsis (specifically gram neg) ▪ Severe massive trauma o Indirect Lung Trauma (less common) ▪ Acute pancreatitis ▪ Anaphylaxis ▪ DIC ▪ Cardiopulmonary bypass o ** Most ARDS caused by indirect o Injury / Exudative Phase: o Primarily characterized by interstitial and alveolar edema and atelectasis o 1-7 days after initial injury (usually 24-48 hours) o Interstitial edema due to engorgement of peribronchial and perivascular interstitial space o Fluid from interstitial space crosses alveolar membrane and enters alveolar space o Intrapulmonary shunt develops b/c alveoli filled with fluid/blood passing through them cannot be oxygenated ▪ Leading to V/Q mismatch o Surfactant dysfunction due to damage of alveolar cells ▪ Leading to atelectasis decrease lung compliance, compromise gas exchange o Fibrosis decreased gas exchange and lung compliance o “Stiff” lungs increasing WOB o Reparative/ Proliferative Phase: o 1-2 weeks after initial injury o Influx of neutrophils, monocytes, and lymphocytes and fibroblast proliferation as part of inflammatory response o Increase pulmonary vascular resistance and pulmonary hypertension o This phase is complete when lung is dense, fibrous tissue o Fibrotic Phase: o 2-3 weeks after the initial injury o “chronic” or “Late phase” o Lung is completely remodeled by collagenous and fibrous tissues o The diffuse scarring and fibrosis result in decrease lung compliance o Surface area for gas exchange reduced o Hypoxemia continues and pulmonary HTN 12 o Early Clinical Manifestations (subtle) o Dyspnea (almost always present), tachypnea, cough, restlessness o Lung sounds- normal or fine, scattered crackles o ABGs- mild hypoxemia and respiratory alkalosis (hyperventilation) o Chest X-ray- may be normal or reveal minimal scattered interstitial infiltrates o Edema- may not show until there is 30% increase in fluid content o Progression of Clinical Manifestations- o Symptoms worsen because of increased fluid accumulation and decreased lung compliance o WOB increases. o Tachypnea and retractions o PFTs reveal decreased compliance, lung volumes, and residual capacity o Tachycardia, diaphoresis, LOC change, cyanosis, pallor o Diffuse widespread crackles and rhonchi o CX reveals diffuse extensive bilateral interstitial infiltrates o PA pressure does not increase in ARDS!! (not cardiac) o Hypoxemia despite increased FiO2 o Hypercapnia due to muscle fatigue and hypoventilation o CXR “white out lungs” o Nursing Goals- o PaO2 patients’ baseline o SaO2 > 90 % 15 o Mode- based on how much WOB the patient should or can perform 16 ▪ How the machine will ventilate the patient in relation to the patient’s own respiratory efforts ▪ Can be used in conjunction with each other ▪ Determines by patient’s ventilation status, respiratory drive, and ABGs ▪ Two types- volume and pressure o Control (CMV) Continuous Mandatory Ventilation- Vent does all the work ▪ Volume and RR are fixed ▪ Used for patient who are unable to initiate a breath ▪ CMV delivers the preset volume or pressure at a preset rate regardless of patients own inspiratory effort ▪ Spontaneously breathing patients must be sedated and/or pharmacologically paralyzes so they don’t breathe out of synchrony with the ventilator o Assist Control (AC)- ▪ Ventilator delivers preset Vt at present frequency (RR) ▪ Will initiate the breath if the patient does not do so within a set amount of time ▪ If patient triggers a breath, the vent will deliver the present Vt ▪ Can breathe faster but not slower ▪ Vent has back up rate ▪ May need sedation to limit the number of spontaneous breaths— can hyperventilate ▪ For patients who can initiate a breath but have a weakened respiratory muscle o IMV o Synchronized intermittent mandatory ventilation (SIMV)- ▪ Present Vt at a preset frequency (RR) while allowing the patient to breathe spontaneously between breaths ▪ Each ventilator breath is delivered in synchrony with the patients’ breaths ▪ The patient is allowed to completely control he spontaneous breaths at their own Vt between mandatory breaths ▪ Used as primary mode and for weaning • Weaning- preset rate gradually reduced • Risk- could increase WOB and cause respiratory muscle fatigue o Settings- o Rate (RR)- number of breaths the ventilator delivers per min (usually 20) o FiO2- fraction of inspired O2 delivered to patient (want this low as possible) o PEEP- Positive pressure applied at the end of expiration of ventilator breaths o Tidal Volume (Vt)- volume of gas delivered to patient during each vent breath (6- 8 usually) o Pressure support- positive pressure used to augment patients’ inspiratory pressure o Pressure Support Ventilation- 17 o Preset pressure that augments patients own inspiratory effort o Decreases WOB o Used for stable patients with SIMV to overcome resistance of breathing through ventilator tubing o Patient completely controls rate and volume o For stable patient o Inverse Ration Ventilation- o Inspiratory/expiratory ratio set at 2:1 or greater max 4:1 ▪ Normal inspiratory/expiratory is 1:2 o Longer inspiratory time ▪ Increased the amount of air in the lungs at the end of expiration (FRC) ▪ Improves oxygenation by re-expanding collapsed alveoli ▪ Acts like PEEP o Shorter expiratory time ▪ Prevents alveoli from collapsing again o Very uncomfortable, sedation required o For patients with continuing refractory hypoxemia despite high levels of PEEP (occur sin ARDS) -Ventilatory Alarms: o Low Pressure- o Circuit Leaks o Airway Leaks o Chest tube leaks o Patient disconnection o High Pressure- o Coughing o Patient biting tube o Fighting ventilator o Secretions or mucus in the airway o Airway problems o Reduced lung compliance o Water in the circuit o Kink o **ASSESS PATIENT NOT ALARM! o NEVER TURN ALARM OFF -Complications of PPV: o Cardiovascular- o Increased intrathoracic pressure compresses thoracic vessels o Decreased venous return to the heart o Decreased preload, CO, BP o Increased mean airway pressure if PEEP > 5 cm H2O 20 o Psychosocial- o Physical/ emotional stress due to inability to speak, eat, move, breathe normally o Pain, fear and anxiety related to tubes o Ordinary ADLS are complicated or impossible o Provide sedation and or/analgesia to facilitate optimal ventilation -Extracorporeal Membrane Oxygenation (ECMO)- alternative form of pulmonary support for patients with severe RF o Modification of cardiopulmonary bypass—involves partially removing blood through use of large-bore catheters, infusing oxygen, removing CO2, and returning blood back to patient -Properties of Cardiac Cells: Cardiac Rhythm Disorders: o Automaticity- the ability to spontaneously generate an impulse o Excitability- the ability to respond to an electrical impulse o Conductivity- transmission of the electrical impulse to another cardiac cell o Contractility- the ability to contract after an electrical impulse is received o * You need both the mechanical and electrical functions of the heart for it to pump properly! -Most Important Labs to monitor: o Potassium (K+)- plays an important role in repolarization o Magnesium (mg+) o Calcium (Ca+) o Sodium (Na+) -Nervous System Control of the Heart: o Autonomic Nervous system controls- o Parasympathetic nervous system- (Vagus nerve) ▪ Decrease rate of SA node ▪ Slows impulse conduction of the AV node o Sympathetic nervous system- ▪ Increases rate of SA node ▪ Increased impulse conduction of AV node ▪ Increases cardiac contractility -Dysrhythmias: o Disorder of impulse formation, conduction of impulses, or both o SA Node- normal pacemaker of heart (60-100 beats/min) o Secondary pacemakers- o AV node (40-60 b/m) o His-Purkinje fibers (20-40 b/m) -Ectopic Foci: abnormal site out of normal conduction pathway that was the ability to generate an impulse which isn’t normal for these cells to do 21 o You can have multiple foci o Biggest reason of this is electrolyte imbalance -Electrocardiogram (ECG) Monitoring: o Graphic tracing of electrical impulses produced by the heart o Waveforms on ECG represent activity of charged ions across membranes of myocardial cells o Depolarization- contract o Repolarization- relax o P wave: Atrial depolarization o PR interval- time it take the impulse to spread from the atria the Purkinji fibers right up to ventricular depolarization o QRS complex- Ventricular depolarization o ST segment- between ventricular depolarization and repolarization (should be flat, MI come into play here) o T wave- ventricular repolarization o Q T interval- time it takes from the entire electrical depolarization and repolarization of ventricles. o Things to consider- o Factors that can affect how the patient’s heart rhythm looks in monitor- placement, patient moving, leads not sticking well, breathing pattern, sweaty/hairy patient o Change electrodes every 24 hours o Communicate to Telemetry monitor tech when patient is showering, discharged, going off the floor, specific meds -ECG Time and Voltage: o One big box- 0.2 seconds o One small box- 0.04 seconds o 1 big box= 5 small boxes 22 -Calculating HR: o The number of R waves in 6 seconds, and multiply by 10 o Small-block method: number of small squares between one R-R interval, and divide this number into 1500 o Big-block method: number of large squares between one R-R interval, and divide this number into 300 -Assessment of Heart Rhythm: o Interpret the rhythm and assess the clinical status of the patient o Is the patient hemodynamically stable? BP, shortness of breath? Change in LOC? Chest pain? o Determine cause of dysrhythmia o Assess and treat the patient not the monitor! -Steps in assessment of heart rhythm: o Is the rhythm regular or irregular? o Equal distance between R waves o Is the QRS complex wide or narrow? o Wide- coming from atria o Narrow- coming from ventricles o Determine the heart rate—is it fast or slow? o Evaluate the P wave- is there one P wave for every QRS complex? o Determine the PR interval—normal or prolonged? o Determine the duration of the QT interval—normal? o Any ectopic beats or other abnormalities? o Determine the cardiac rhythm -Normal Interval Ranges: o PR Interval- 0.12-0.20 seconds o QRS interval- 0.04-0.12 seconds 25 o Contraction starting from an ectopic focus in the atrium in a location other than SA node o Travels across atria by abnormal pathway, creating distorted P wave o May be stopped, delayed or conducted normally at the AV node o Causes- stress, fatigue, caffeine, tobacco, alcohol, hypoxia, electrolyte imbalance, valve disease or heart disease o Manifestations- palpations, heart “skips a beat” o Treatment- o Monitor for more serious dysrhythmias o Withhold source of stimulation o Beta Blockers ▪ If having increased P waves -Paroxysmal Supraventricular Tachycardia (PSVT): o A dysrhythmia starting in an ectopic focus anywhere above the bifurcation of the bundle of His. o PAVT occurs because of a reentrant phenomenon (reexcitation of the atria when there is a one-way block) o Reentrant phenomenon: PAC triggers a run of repeated premature beats o Paroxysmal refers to an abrupt onset and termination o Associated with overexertion, stress, deep inspiration, stimulants, disease, digitalis toxicity o HR is between 150-220 o P wave is often hidden o PR interval may be shortened or normal 26 o QRS complex is usually normal o Manifestations- o HR greater than 180 leads to decreased CO and stroke volume o Palpitations o Dizziness and/ or lightheadedness o Hypotension o Dyspnea o Angina o Treatment: o Is the patient stable? Symptomatic? If so then treat o Drug therapy- 1st ▪ IV adenosine (DRUG OF CHOICE)—IV Push • MOA- Interrupts electrical pathway made by ectopic foci • Expected response- reset heart and allow SA node to take over — restore normal sinus rhythm • Safe dose- 6-12 mg; IV Push • Nursing consideration- Monitor HR, apical pulse, continuous EKG, crash cart at bedside o Can cause patient to feel hot, flushed, dizzy, chest pain, palpations ▪ IV Beta blockers ▪ Calcium channel blockers ▪ Amiodarone- antiarrhythmic o Vagal stimulation o Cardioversion- if other TX is ineffective and patient is hemodynamically unstable ▪ Goal- reset electrical pathway; SA node take over -Atrial Flutter: o Is an atrial tachydysrthymia identified by recurrent, regular, sawtooth-shaped flutter waves that originate from a single ectopic focus in the right atrium (most common) or left atrium. o Single ectopic foci in right atrium that is firing multiple times but only being conducted the 4th time 27 o Typically associated with heart disease (CAD, CMP, valvular disorders, HF, other cardiac surgery) o Symptoms result from high ventricular rate and loss of “kick” decreased CO heart failure o Shortness of breath, chest pain, dizzy, light headedness, change in LOC o Atrial HR is 200-350 b/m o Rhythm is regular o Atrial flutter waves represent atrial depolarization followed by repolarization o ORS complex is usually normal o Increased risk of stroke because of the risk for thrombus formation in the atria from the stasis of blood o Coumadin is given to prevent stroke o Very high risk for re-occurrence o Treatment: o Goal- slow the ventricular response by increasing AV block, prevent blood clots/stroke o Drugs- ▪ Calcium channel blockers ▪ Beta blockers ▪ Anti-dysrhythmias ▪ Common meds- • amiodarone (Cordarone) • sotalol (Betapace) • ibutilide (Corvert) • dofetilide (Tikosyn) • flecainide (Tambocor) • dronedarone (Multaq) • digoxin (Lanoxin) • warfarin (Coumadin) • apixaban (Eliquis) • dabigatran (Pradaxa) o Electrocardioversion- to convert atrial flutter to sinus rhythm in emergency o Radiofrequency ablation (PRIMARY TX)- ▪ Involves placing catheter in right atrium and ablating ectopic foci causing the end of the dysrhythmia and normal sinus rhythm ▪ Patient care after- cont. EXG, check pulses, monitor site (radial or femoral), watch for bleeding, hematomas, typically on bed rest, monitor for numbness or tingling, monitor LOC -Atrial Fibrillation: o Characterized by total disorganization of atrial electrical activity because of multiple ectopic foci, resulting in loss of effective atrial contraction 30 o Associated with stimulants, electrolyte imbalance, hypoxia, heart disease (MI, HF, CMP, CAD) o Not harmful with normal heart but CO reduction, angina, HF in diseased heart o Assess apical-radial pulse deficit o Wide, distorted QRS complex o Can come in different shapes and from different ectopic foci o Multifocal PVCs- arise from different foci appear different in shape o Ventricular bigeminy- every other beat is PVC o Ventricular trigeminy- every third beat is a PVC o Ventricular tachycardia (VT)- occurs when there are three or more consecutive PVCs o Treatment- o Correct cause of the PVCs (O2 therapy for hypoxia, electrolyte replacement) o Drug therapy- BB first, amiodarone 31 -Ventricular Tachycardia (VT): o Three or more PVCs in a row is called a “run of VT” o Occurs when an ectopic focus or foci fire repeatedly and the ventricle takes control as a pacemaker o Ventricular rate is 150-250 b/m o Associated with heart disease, electrolyte imbalance, drug toxicity, CNS disorder o Can be stable (patient has pulse) or unstable o Sustained VT causes decrease in CO o Hypotension, pulmonary edema, decreased cerebral blood flow, cardiopulmonary arrest. 32 o Precipitating causes must be identified and treated (hypoxia) o VT with pulse treated with antidysrhythmic or cardioversion o Pulseless VT treated with CPR and rapid defibrillation o Rhythm may be regular or irregular – depends on QRS configuration o Monomorphic- regular (QRS complex same shape, size, and direction) o Polymorphic- irregular o Sustained- longer than 30 seconds o Non-sustained- less than 30 seconds o Torsades de Pointes: polymorphic VT associated with a prolonged QT interval o Considered life-threatening because of decrease CO and the possibility of deterioration to ventricular fibrillation -Ventricular Fibrillation- ventricles “quivering” o Severe derangement of heart rhythm characterized on EKG by irregular waveforms of varying shapes and amplitude o Firing of multiple ectopic foci in the ventricles o Associated with MI, ischemia, disease states, procedures o Unresponsive, pulseless, and apneic o If not treated rapidly, death will result o Treat with immediate CPR and ACLS o Defibrillation and drug therapy (epinephrine, vasopressin, amiodarone) 35 o What to do if ICD fires o Medic Alert ID o ICD identification card o Caregivers to learn CPR -Pacemakers: o Used to pace the heart when the normal conduction pathway is damaged o Provides cardiac stimulation to the myocardium when natural cardiac stimulation fails o Pacing circuit consist of- o Programmable pulse generator (power source) o One or more conducting (pacing) leads to myocardium o Helps stimulate ventricles at a set rate o Pace atrium and/or one or both of ventricles o *Most pace on demand, firing only when HR drops below preset rate o Sensing device inhibits pacemaker when HR adequate o Pacing device triggers when no QRS complexes within set time frame -Transcutaneous Pacing (TCP): o For emergency pacing needs o Noninvasive o Bridge until transvenous pacer can be inserted o Use lowest current that will “capture” o Patient may need analgesia/sedation -Permanent Pacemakers: o ECG monitoring for malfunction o Failure to sense – pacemaker is firing when not needed o Fails to recognize spontaneous atrial or ventricular activity o Causes inappropriate firing o Causes- batter failure lead dislodgement, tip of lead itself becomes fibrous o Failure to capture – firing but myocardium is failing to respond o Lack of pacing when needed leads to bradycardia or asystole o Electrical charge sent to the myocardium is insufficient to produce contraction o Causes- battery failure, tip of lead fibrous o Monitor for other complications: o Infection o Hematoma formation o Pneumothorax o Atrial or ventricular septum perforation o Lead misplacement o * CXR for misplacement or pneumothorax, WBC for infection, Fever, check for bleeding, cont. EKG o Post-op Orders: o CBC with diff in AM (WBC count, platelets due to risk for bleeding and infection) 36 o BMP in AM (monitor electrolytes and need to replace, checking creatinine, making sure they are hydrated, no kidney issues) o VS Q15 minutes x2, q30 min x4, then q4 hours o Elevate HOB at 45 degrees o Keep incision site dressing clean and dry o May shower on POD #3 (cannot submerge site) o Interrogation by company representative in AM prior to discharge (functioning properly) o Review lifting restrictions (no higher than shoulder, shouldn’t be lifting, driving restrictions, activity restrictions-– no sports) o Place sling to affected extremity o XR Chest upon arrival to unit o XR Chest in AM (look at lead placement and pneumothorax) -Radiofrequency Catheter ablation therapy: o For atrial flutter and sometimes atrial fib o Electrode-tipped ablation catheter “burns” accessory pathways or ectopic sites in the atria, AV node, and ventricles o *Non-pharmacologic treatment of choice for atrial flutter, atrial fibrillation, & SVT o Post care similar to cardiac catheterization o ECG Adult 12 Lead Routine, (Obtain as soon as possible post procedure) o Bed rest x 3 hours o VS q15min x 4, q30min x 4, q1h x 4, then q8h if stable o Neurovascular Assessment Lower Extremity: q15min x 1 hour, q30min for 2 hours, then q1hr x 4 hours o Check puncture site and pedal pulses AND document results in the Medical Record o Notify Provider for Systolic BP less than 100 mmHg or greater than 160 mmHg o Notify Provider for Bleeding, Hematoma, Absent pulse, and/or Sensory/Motor deficits of the affected extremity o CBC with diff in AM o BMP in AM o esomeprazole (Nexium) 20 mg PO daily x4 weeks Heart Failure: -Heart failure: results from the inability of the heart to provide sufficient blood to meet O2 needs of tissue and organs o Defect in either ventricular filling (diastolic dysfunction) or ventricular ejection (systolic dysfunction) -Key Terms: o Cardiac Output- Stroke volume x heart rate o Normal value is 4-8 Liters/min 37 o Stroke Volume- Amount of blood pumped from the heart with each heartbeat o Preload- the volume of blood in the ventricles at the end of diastole, before the next contraction. o Afterload- the peripheral resistance that the left ventricle pumps against o Ejection Fraction (EF)- is a measurement of the percentage of blood leaving your heart each time it contracts. o The heart contracts and relaxes. When your heart contracts, it ejects blood from the two pumping chambers (ventricles). When your heart relaxes, the ventricles refill with blood o Diastole- heart relaxes, ventricle filling o Systole- heart contracts, ventricle emptying o EF dependent on contractility of the heart and preload (amount of blood in chamber) -Causes of HF: o HF is a response to myocardial injury o Leads to remodeling of the cardiac structure and function o Anything that causes stress to the heart can lead to HF o Interference with CO may cause HF o Preload o Afterload o Contractility o HR o Impacts the stroke Volume o CO=SV x HR o Primary causes- o Coronary Artery Disease (CAD) including MI ** o Hypertension ** o Myocarditis o Cardiomyopathy o Valve problems o Congenital Heart Disease o Rheumatic heart disease o Hyperthyroidism o Pulmonary HTN o Precipitating causes- increase the workload of the heart o Dysrhythmias o Pulmonary Emboli o Endocarditis o Hypervolemia o Anemia o Obstructive sleep apnea o Genetic 40 o Results in increase cardiac workload, progressive LV dysfunction, remodeling of the ventricles o Ventricular Adaptations o Dilation of chambers of the heart ▪ Chambers of the heart get larger ▪ Increase in stretch of muscle fibers due to increase in blood volume ▪ The greater the stretch, the greater the force of contraction (Frank- Starling Law) ▪ Initially, causes increase in cardiac output. After time, muscle fibers are overstretched and contraction decreases ▪ **heart can double size with dilation and hypertrophy ▪ **increase muscle fibers to increase blood volume ▪ Initially causes increase CO and then overtime decreases CO o Hypertrophy ▪ Increase in muscle mass of heart ▪ Increases contractility at first ▪ However, hypertrophic muscle doesn’t work as well, needs more oxygen, greater risk for rhythm problems, and has poor circulation ▪ **Heart is pumping so heart muscles get bigger o Counter regulatory Mechanisms o Natriuretic Peptides: ▪ Atrial natriuretic peptide (ANP) & b-type natriuretic peptide (BNP) • Hormones produced by the heart that promote vasodilation (decreasing preload and afterload) • Increase glomerular filtration rates • Block effects of RAAS—respond to fluid • **If BNP is high, we know that the body is struggling with fluid -Clinical manifestations: o Acute decompensated HF: o Often associated with CAD/ MI o Often presents as pulmonary edema o Pale, anxious, dyspnea, possibly cyanotic, o Crackles, wheezing, rhonchi, pink frothy sputum ▪ Pink sputum- when blood enters the lungs; tine capillaries in the lung have busted due to high pressures in the lungs o Increased HR, S3 heart sound o BP high or low –depends on severity o Chronic HF: o Depends on right vs left sided failure o Often has signs/ symptoms of biventricular failure ▪ Fatigue (early sign) ▪ Dyspnea ▪ Nocturnal Dyspnea 41 -Complications: ▪ Tachycardia ▪ Edema ▪ Nocturia- increase urination at night ▪ Chest pain ▪ Weight changes- fluid retention, edema renal failure ▪ Behavioral changes- head not perfusing (could be dizzy) o Pleural Effusion- fluid buildup into pleural cavity of lungs secondary to increased pressure in pleural capillaries o Dysrhythmias- enlargement of heart can cause changes to electrical pathway o Thrombus o Cardiogenic Shock- if patient is not perfusing o Hepatomegaly- more likely in RV failure o Renal Failure (Cardiorenal syndrome) o Anemia -Classification: o NYHA classification based on classes o These patients have been diagnosed with some degree of HF o ACC/AHA classification on stages o Patients who are at risk (DM, HTN) o We want to help before HF -Diagnostic Tests: o History and Physical o CBC, BMP, cardiac enzymes (Troponin, CK, CKMB), liver function tests, BNP, PT/INR o CBC- monitor cardiac enzymes o BMP- tells us if there is a fluid issue and going into HF o Chest x-ray- can show heart infiltrates o 12- lead ECG o Echocardiogram***- best test for HF o Shows the pumping of the heart, chamber size, EF and determines if it’s a systolic or diastolic issue o Nuclear imaging studies o Stress testing o Hemodynamic monitoring- in critical situation o Heart catheterization (right and/ or left) -Treatment goals: o Symptom Relief o Correct volume status o Support oxygenation, ventilation, CO and end organ perfusion o Address the cause o Avoid complications o Patient teaching and Discharge planning 42 o Decrease Intravascular Volume- decreases venous return, decreases preload, more efficient contraction and increased cardiac output o Decrease Preload- vasodilator, positioning o Decrease Afterload- decreases pressure against which LV must pump o Increase Contractility- inotropes increase cardiac output -Drug therapy: o Diuretics: reduce preload o Furosemide (Lasix)** - PO or IV, loop diuretic. o Spironolactone (Aldactone)- PO, potassium sparing diuretic o Metolazone (Zaroxolyn)- PO, when extra diuresis necessary (thiazide diuretic) o ** we need to monitor K o ** this is to decrease fluid o Ace-Inhibitors- reverses remodeling of the heart o lisinopril o first line therapy in chronic HF o block conversion of angiotensin I to angiotensin II, o decrease aldosterone o Decrease afterload. Increase cardiac output. o Major SE- nagging cough and angioedema o Vasodilators: o Nitrates- directly dilate vessels, decrease preload, vasodilate coronary arteries. o Nitroprusside (Nipride)- reduces preload and afterload o Nesiritide (Natrecor)- arterial and venous dilation o Morphine ▪ Trps fluid in peripheral in order to decrease preload of the heart o B- Blockers- Carvedilol (Coreg), Metoprolol (Lopressor) o Block negative effects of SNS system (such as increased HR) o Can reduce myocardial contractility o Improves patient survival o Positive Inotropes: Increase contractility o Digoxin- increases contractility, decreases HR ▪ Watch for hypokalemia ▪ Reduces symptoms, but not shown to prolong life o Dopamine o Dobutamine o Milrinone (Primacor) – IV only (can cause dysthymias) o Angiotensin II Receptor Blockers (ARBs)- for patients who cannot tolerate ACE o Mostly for patients unable to tolerate Ace Inhibitors o Similar effects to Ace Inhibitors o Isosorbide dinitrate and hydralazine (BiDil) o Combination drug o ARNI- Angiotensin receptor- neprilysin inhibitor 45 o Heart Transplant List- o Each patient has a Status ranking o Status 1a: critically ill, hospitalized o Status 1b: require IV medications (inotropes) or heart assist device o Status 2: not hospitalized, do not require IV medications o Status 7: Temporarily inactive o Surgery involves removing the recipient’s heart, except for the posterior right and left atrial walls and their venous connections o Recipient’s heart is replaced with the donor heart o Donor sinoatrial (SA) node is preserved so that a sinus rhythm may be achieved postoperatively o Immunosuppressive therapy usually begins in the operating room and continues o Infection is the primary complication followed by acute rejection in the first year after transplantation o Endomyocardial biopsies are obtained from the right ventricle weekly for the first month, monthly for the following 6 months, and yearly thereafter to detect rejection o Beyond the first year, malignancy (especially lymphoma) and coronary artery vasculopathy are major causes of death o One year survival rate is 85-90% o Three year survival rate is 79% Hemodynamic Monitoring: o Measuring pressures in the heart o Assess patient and get baseline. o Getting information from catheter to determine pressures o Looking at pressure and fluid levels in the heart o Baseline data obtained o General appearance o Level of consciousness o Skin color/temperature o Vital signs o Peripheral pulses o Urine output o Baseline data correlated with data obtained from technology (e.g., ECG; arterial line, CVP, PA, and PAWP pressures) o Look at trends!! o Purpose: o Evaluate cardiovascular system ▪ Pressure, flow, resistance ▪ Assess heart function, fluid balance, effect of treatments o Establish baseline values and evaluate trends 46 ▪ Determine presence and degree of dysfunction 47 o Implement and guide interventions early to prevent problems o Both invasive (internally placed) and non-invasive measures o Heart Rate o O2 Saturation o Blood Pressure and MAP o Central Venous Pressure CVP o Pulmonary Artery Pressures o Systemic Vascular Pressure (SVR) o Pulmonary Vascular Pressure (PVR) o Cardiac Output/ Cardiac Index o Stroke Volume o Types of Invasive Pressure Monitoring: o Continuous arterial pressure monitoring for the following: ▪ Acute hypertension/hypotension ▪ Respiratory failure ▪ Shock ▪ Neurologic shock ▪ Coronary interventional procedures ▪ Continuous infusion of vasoactive drugs ▪ Frequent ABG sampling o Atrial Pressure Monitoring: ▪ High and low pressure alarms based on patient’s status ▪ High pressure alarm caused by- clot? ▪ Low pressure alarm caused by- disconnection ▪ Risks: • Hemorrhage • infection • thrombus formation • neurovascular impairment • loss of limb (Assess 5 P’s- Pain, Paralysis, Paresthesia, Pulse, Pallor) o Want to assess the site distal from the insertion site to check for circulation o Pulmonary Artery Pressure Monitoring: ▪ Guides management of patients with complicated cardiac, pulmonary, and intravascular volume problems ▪ PA diastolic (PAD) pressure and PAWP: Indicators of cardiac function and fluid volume status • PAWP- gives fluid volume status ▪ Monitoring PA pressures allows for therapeutic manipulation of preload ▪ Complications- • Infection and sepsis o Asepsis for insertion and maintenance of catheter and tubing mandatory