COMPLEX EXAM 1

Heart Tingss (preload, CVP)

Right Sided Preload: - Right Ventricle ◦*Preload (volume) is reflected in the CVP (central venous pressure)* > ◦*Right arterial pressure* > ◦Estimates right heart filling pressure or right ventricular preload > ◦Estimates *volume status/pressure in systemic circulation**, measures volume of circulating blood returning to the heart > ◦*Normal: CVP = 2 - 8 mmHg* Central Venous Pressure (CVP): - *Decreased CVP may indicate hypovolemia or decreased venous return* - *Increased CVP may signify overhydration, increased venous return or right sided heart failure.* - Limitations to CVP readings: §Right ventricle end diastolic pressure (RVEDP) is determined by RV compliance. > Acute or chronic diseases decrease right ventricular compliance: §Ischemia §Hypertrophy §Restrictive Cardiomyopathy §Cardiac Tamponade CVP readings influenced by: - *Right Ventricular Infarct:* ◦Associated w/inferior wall MI ◦*Hypotension* due to RV not functioning properly ◦*JVD* due to blood flow not leaving right side of heart ◦*Tricuspid regurgitation* ◦*A CVP > 11* ◦Brady arrhythmias, heart block ◦*TREAT: with FLUIDS, then inotropes, avoid medications that decrease preload, or decrease peripheral vascular resistance* ◦*Do not give nitroglycerin or morphine as this will decrease preload* (what will happen to patient?) ◦Revascularization with (PCI), may need to pace - Tricuspid Disease ◦Tricuspid Regurgitation - CVP will not be truly reflective of the RVEDP & blood volume changes. ◦Tricuspid Stenosis - impedes blood flow to the RV = increased CVP readings Effect of Intrathoracic Variations on CVP readings: §*Ventilator can cause variations in CVP readings to due positive pressure.* §Intrathoracic cardiovascular structures can increase right atrial pressure and CVP pressures. §This external pressure also interferes with venous return and can decrease CO §Increased PEEP with decreased preload *CPV: (CENTRAL VENOUS PRESSURE) NORMAL 2-8; HAS TO DO WITH RIGHT SIDED PRELOAD AND INFLUENCED BY RIGHT VENTRICULAR INFARCTION* *Left sided Preload:* - Pressure Readings §*Pulmonary Artery Wedge Pressure (PAWP) or Pulmonary Capillary Wedge Pressure (PCWP) reflects LV filling/LVEDP.* §Obtained from the pulmonary catheter (yellow) Swan Ganz/PA catheter when balloon is inflated. §*Estimates LVEDP (after gas exchange) which = preload of LV, systemic fluid status & how well LV is functioning* (Pulmonary Artery Wedge Pressure (PAWP) & Pulmonary Artery Occlusion Pressure (PCWP) mean same thing) > PAWP clinical measurements used to assess "preload" of right and left ventricles > *Normal PAWP/PCWP is 6 - 12mmHg, rises to 15 - 18mmHg in pt's with LV failure* >> *Low values = hypovolemia* >> *High values = hypervolemia, or LV FAILURE/DYSFUNCTION >18 , also seen in mitral valve abnormalities* §PAWP/PCWP & SV both low - hypovolemia likely §PAWP/PCWP high > 18 mmHg but SV is low, LV dysfunction is assumed Left Heart Pressures: - During diastole the *mitral valve* is open and the PAWP/PCWP reflects LVEDP or preload. - When the mitral valve is closed *the pressure reflected is the Left Atrial pressure.* - Provides an estimate of Left Sided Preload *Normal PAWP/PAOP = 6 - 12 mmHg* Significance of PAWP: volume reduction decreases preload & volume increase will increase preload. ◦Normal PAWP/PCWP 6 - 12 mmHg ◦18 - 20 mmHg: Onset of pulmonary congestion ◦20 -25 mmHg: Moderate Congestion ◦25 - 30 mmHg: Severe Congestion ◦*Above 30mmHg: Pulmonary Edema* *PAWP/PCWP: (PULMONARY ARTERY WEDGE PRESSURE) NORMAL 6-12; REFLECTS LEFT SIDE PRELOAD* *To increase preload:* - Increase intravascular volume > *Give fluids* - Increase venous return §Vasoconstricting drugs §Antiembolism stockings §Elevate lower extremities §Fluid response/challenge Clinical problems that increase preload: §CHF, volume overload & renal failure *To decrease preload:* §*Decrease fluids* §Medications §Diuretics §Hydralazine §Nitroglycerine §Morphine §Renal dose of Dopamine *Conditions that Decrease Preload:* §Loss of atrial kick > ◦*Afib, aflutter, Junctional rhythms* §Diuresis §Hemorrhage §3rd spacing §Burns §Fever §*Anaphylactic Shock* §*PEEP & CPAP (due to increased intrathoracic pressure)* Afterload: - *Afterload is the resistance, or pressure the ventricle must overcome to eject its blood volume.* - Stroke volume (SV) is affected by compliance of vascular space into which blood is ejected. > *Left side of the heart afterload = Systemic Vascular Resistance (SVR).* >> SVR can be calculated if the CO, MAP and CVP are known. *Normal = 800-1200* >> Condition of pulmonic valve: stenosis > *Right side of the heart afterload = Pulmonary Vascular Resistance (PVR)* *Normal < 250* >> Condition of aortic valve >> Is the amount of pressure exerted by the blood vessels of the pulmonary vascular bed. - The more resistance, = the harder it is for the heart to pump and blood backs up if it can't move forward: - Contributing factors = vasoconstriction or valvular stenosis. - The less resistance = heart will have easier time pumping; however if afterload is too low there is not enough resistance to keep the blood moving forward §Contributing factor: vasodilation - *To increase afterload:* §*Increase fluids = give volume* qGive drugs: §Inotropics (dopamine) §*Vasopressors (levophed)* - Conditions that increase Afterload: §Hypothermia, cold shock/vasoconstriction §Out of OR patient may need to be warmed to help decrease SVR. - *To decrease afterload* §*Decrease circulating volume = diuretics* qDecrease IV infusion rate q*Give vasodilators:* §*NTG, dobutamine, milrinone, ACE, ARB* qPain medication, anxiolytics qIntra Aortic Balloon Pump (IABP) - Conditions that decrease Afterload: §Hemorrhage, diuresis, 3rd spacing, hyperthermia, sepsis/warm shock.

TYPES OF ANGINA

STABLE ANGINA - Stable - chronic, occurs with activities that involve exertion or emotional stress > Stable pattern of onset, duration, severity, and relieving factors > Typically lasts less than 10 - 15 minutes >> •T-wave inversion on ECG >>> *oTreatment: rest and nitroglycerin* UNSTABLE ANGINA - Unstable (worsening cardiac ischemia) = more often & severe, less relief from Nitro > *May see ST elevation on ECG* > Occurs at rest, even while sleeping, is easily provoked by minimal exertion > lasts longer than 10-15 mins > Women's symptoms usually undertreated/unrecognized > Needs immediate identification & intervention o*Treatment: rest and nitroglycerin; drugs affecting platelets; revascularization (PCI)* - Prinzmetal's (vasospasms) rare but stable §ST elevation during pain episodes §Occurs at rest §*Can be seen in patients with a history of migraine headaches, Raynaud's phenomenon and heavy smoking* §Spasm of a major coronary artery §CAD may or may not be present *oTreatment: Caclium Channel Blocker*

ACS / MI Care

STEMI CARE - *EMERGENT Percutaneous Coronary Intervention (PCI) Cardiac Cath → within 90 minutes* >> Balloon angioplasty + Stents §*Thrombolytic therapy → ONLY for STEMI* in agencies that do not have cath lab oGiven within 30 minutes of ED arrival o2-3 large bore IV lines oComplete invasive procedures BEFORE starting thrombolytics oMonitor for bleeding o*Best possible sign → Return of ST to baseline* - *FYI: Tissue Plasminogen Activator (tPA) is contraindicated in MI because it breaks up the clot and increases risk of stroke → tPA is a thrombolytic (breaks up clot)* - *Alteplase* - Coronary Surgical Revasculation: §When medical management failed in presence of left main coronary artery or 3 vessel disease §Patients who are not candidates for Percutaneous Coronary Intervention (PCI) or failed PCI with ongoing chest pain §Patients with history of diabetes, left ventricle function, chronic kidney disease - CABG (Coronary Artery Bypass Graft Surgery) §Requires sternotomy §Cardiopulmonary bypass (CPB) §Blood is diverted from heart to machine where it is oxygenated and returned to body. Allows surgeon to operate on nonbeating, bloodless heart while perfusion to vital organs is maintained. §Uses arteries and veils for grafts → radial artery, Internal Mammary artery - (Similar to dialysis) - MIDCAB - Minimally Invasive Direct Coronary Artery Bypass: §No sternotomy §No Cardiopulmonary bypass §Faster recovery, shorter hospital stay §Decreased need for blood transfusion COMPLICATIONS OF MI: - *Dysrhythmias:* §Most common complication after an MI §Can be caused by ischemia, electrolyte imbalances, or SNS stimulation §Bradycardias or complete heart block may develop due to key areas of conduction system being damaged or destroyed ØPremature ventricular contractions may precede VTachy/VFib ØVT and VF are most common cause of death in prehospitalization period (life-threatening must be treated immediately) - *Post MI clients are at high risk for:* §Sudden death §Heart failure §Cardiogenic shock §Ventricular aneurysm or rupture - *Papillary muscle dysfunction or rupture:* §Occurs if infarcted area includes or is near the papillary muscle that attaches to the mitral valve *(life-threatening medical emergency)* §New murmur heard at the cardiac apex, *STAT echocardiogram* oDyspnea, pulmonary edema, and decreased cardiac output result from the backup of blood in the left atrium oRequires afterload reduction with nitroprusside/Nipride and/or intra-aortic balloon pump (IABP) therapy, immediate surgery to repair or replace mitral valve. - *Pericarditis - EKG ST elevation ALL leads* §Inflammation of pericardium - Mild to severe pain oIncreases with respiration, coughing, movement of upper body oDull/achy chest discomfort/pain - *Often relieved by sitting forward* oCan lead to cardiac tamponade oProcedures = pericardiocentesis and pericardial window - *Dressler's Syndrome:* §Pericarditis and fever 1-8 weeks after a MI §Chest pain, fever, malaise, pericardial friction rub, arthralgia à more systemic oHigh dose aspirin (NSAID), Colcichine, steroids for refractory pericarditis - *Pericardial Friction Rub:* §ECG changes, continue to monitor for changes §Not heard when holding respirations, pain with inspiration, swallowing, and lying flat, improves sitting up and forward - *Endocarditis is the inflammation of the endocardium:* §caused by various microbes and frequently involves the heart valves §Can result in valvular dysfunction §Assess for new murmur - Types: §Endocardium continuous with valves §Vegetation §Embolization §Valvular dysfunction - *Treatment: antibiotics (IV) 4-6 weeks, rest* •Valve replacement surgery may be indicated - Prevention: antibiotic prescription before treatments (e.g., dentist) or other invasive procedure. - *Heart Failure:* -*Left heart failure:* oDecreased pumping action oBack-up of blood from left ventricle leads to *fluid build-up in lungs* oFailure can progress from left side to right side of heart = *backflow leads to right heart failure* oFail to meet metabolic demands o*Mild dyspnea, restlessness, agitation, slight tachycardia* initially oOther signs indicating the onset of left-sided HF include pulmonary congestion on chest x-ray, S3 or S4 heart sounds on auscultation of the heart, crackles on auscultation of the lungs, paroxysmal nocturnal dyspnea (PND), and orthopnea. - Compensatory mechanisms: §Renin-angiotensin-aldosterone system §Sympathetic nervous system - *Right heart failure:* - Leads to systemic symptoms o*Jugular venous distention, hepatic congestion, lower extremity edema* - *Papillary muscle dysfunction or rupture (life threatening)* §Causes severe mitral valve regurgitation §Aggravates an already compromised LV → rapid clinical deterioration with decreased CO oTreatment includes afterload reduction with nitroprusside (Nipride) and/or IABP therapy, and immediate cardiac surgery with mitral valve repair or replacement. - *Left ventricular aneurysm:* Myocardial wall becomes thinned and bulges out during contraction Leads to HF, dysrhythmias, and angina More common with anterior MIs. Besides ventricular rupture, which is usually fatal, ventricular aneurysms can hide thrombi that can lead to an embolic stroke. *Anticoagulation therapy is recommended for these patients if not contraindicated.*

Systolic vs diastolic HF

SYSTOLIC HF: •HFrEF - *HF with reduced EF <45%* •Inability to pump blood forward caused by: > •Impaired contractile function > •Increased afterload > •Cardiomyopathy > •Mechanical abnormalities •Decreased LV ejection fraction (EF): •The LV in systolic failure loses ability to generate enough pressure to eject blood forward through the aorta. •Over time, the LV becomes dilated and hypertrophied DIASTOLIC HF: •HFpEF - HF with preserved EF *>45%* •Impaired ability of ventricles to: > • relax/Fill during diastole > •resulting in decreased stroke > • volume & Cardiac Output

Shock

Shock is a syndrome characterized by *decreased tissue perfusion and impaired cellular metabolism. This results in an imbalance between the supply of and demand for O2 and nutrients.* - CATEGORIES: 1. CARDOGENIC 2. HYPOVOLEMIC 3. NEUROGENIC 4. ANAPHYLACTIC 5. SEPTIC 6. OBSTRUCTIVE - STAGES: 1. Initial 2. Compensatory 3. Progressive 4. Refractory - Initial: §First changes at the cellular level §Resulting from decrease in O2 delivery to tissues oIncludes decreased aerobic and increased anaerobic metabolism o*No obvious clinical S/S apparent in this stage of shock* - Compensatory: •Body attempts to compensate for decreases in CO & restore adequate O2 and nutrient delivery to tissues •*SNS activated by hypovolemia and hypotension* •Causes peripheral vasoconstriction and elevation of BP •*Na+ and K+ retention, in conjunction with increased ADH, ACTH, and circulating catecholamine's, effectively increases intravascular volume, HR, and BP, and decreases urine output* •Without vascular volume replacement, intrinsic vasopressors eventually fail as compensatory mechanism •Patient then enters progressive stage - Progressive Stage: •*Characterized by end-organ failure* due to cellular damage from prolonged compensatory changes •Severe hypo perfusion ensures •Impaired O2 delivery to tissues results in multi-organ system failure > •Gastro > •Renal > •Respiratory/Cardiac > •Loss of liver and cerebral function - Refractory Stage: •*Irreversible stage of shock, death is imminent*

mechanical ventilation

absolute indications: - *resp failure- hypoxic or hypercapnic* - neuromuscular disease: when patient cannot protect airway or maintain adequate oxygenaton/ventilation - status asthmaticus - hypoventilation syndrome in a mobidily obese patient - acute head injury GCS <8 - smoke inhalation with burns to mouth and airway potential indications: - bradypnea with resp arrest - tachypnea RR>30 - vital capacity <15 mL/kg - monitor with nueromusclar diesase and spinal cord injuries - minute ventialtion lpm - *increaseing PaCo2 and decreasing pH <7.25* - hypotension - *PaO2 <55 on supplemental oxygen* COMPLICATIONS: Airway: - EET out of poistion - unplanned extubation - laryngeal and tracheal injury - damange to oral and/or nasal muscousa Pulmonary: - Oxygen toxicity - resp alkalosis - dysphagia and asipation - *infection: VAE (VAP) bundle* - trauma: barotrauma volutrauma Cardio: - hypotension - decreased CO GI: - Gastric ulcers - GI bleed What is minute ventilation? (seen on ventilator of mechanically vented patient) - Tidal volume Vt x RR resp. rate - normal is 4L/minute - An increase in minute ventilation indicates an increase in work of breathing Pulmonary perfusion: - Gas exchange, movement of blood past alveoli •A decrease in blood flow past alveoli (pulm. embolus, low cardiac output) will affect the ventilation/perfusion ratio and gas exchange •Normal ventilation/perfusion ratio: 4L- 6L ventilation/min (V) (alveolar ventilation)/ 4L - 6L perfusion/min (Q) (pulm. blood flow) > *0.8 - 1.2 = normal V/Q ratio, ideal 1:1 ratio* •Problem with ventilation or perfusion = V/Q mismatch •With a V/Q mismatch hypoxemia on room air will develop •Provide supplemental O2 and treat underlying cause •Extreme V/Q mismatch, even with 100% FiO2, hypoxemia will NOT be corrected! V/Q Ratio and Shunting: - *A problem with ventilation or with perfusion = V/Q mismatch* > A shunt is: Movement of blood from the right side of the heart to the left side of the heart without getting oxygenated; venous blood to the arterial side §Normal physiologic shunt: thebesian veins of heart empty into left atrium §Anatomic shunt: ventricular or atrial septal defect §ARDS is a pathologic example of a shunt - blood goes through lungs but does NOT get oxygenated resulting in refractory hypoxemia Treatment of a shunt requires more than supplemental O2, as O2 alone will not correct severe hypoxemia > Provide supplemental O2 (FiO2 usually at 100%) > Positive End Expiratory Pressure (PEEP): §PEEP decreases surface tension of alveoli, preventing atelectasis §PEEP increases alveolar recruitment §PEEP maintains pt's airway above atmospheric level by exerting pressure that opposes passive emptying of the lung §With the addition of PEEP to the airway, hypoxemia will be addressed and the FiO2 may be decreased from 100% Diseases/conditions associated with potential for V/Q mismatch §Most common those with increased secretions: §COPD (airways), PNA (alveoli), Asthma (bronchospasm) V/Q mismatch may result from: qPain, alveolar collapse (atelectasis), or pulmonary emboli *S/S: worsening dyspnea, increase in sputum purulence and volume, hypercapnia, hypoxemia* Treatment: §Titrate FiO2 to PaO2 > 60 mmHg or SaO2 > 90% with care not to overcorrect hypoxemia and decrease respiratory drive! §Bronchodilator therapy, corticosteroid therapy, antibiotics (bacterial infections) and use of noninvasive ventilation. §May require intubation and mechanical ventilation if noninvasive ventilation is not sufficient.

endotracheal intubation

insertion of endotracheal tube inot the trachea either thru the nose or mouth indications: - establish airway - assist in sectrion removal - protection from aspiration - provide mechanical ventilatoin nurse role: - know proper equipemtn - -antiipcare HCP needs - Position patient - preoxygenate patient - provide suction PRN - monitor patient - provide info & reassurance post-intubation managment: - confirm placement: *ETT AT 3 cm above the carina* - secure and maintian eet placement - identify and record lip line - *maintain cuff pressure: 20-25 cm H20* - monitor oxygenatoin and ventilation - maintain tube patency - provide oral care - foster comofrt and communicate - *SEDATE!* endotracheal suctioniong: indicated with: - visible secretions - coughing - rhonchi - high PIP on ventilator - ventilator alarm procedure: - determine: open or closed - hyperoxygenate - avoid saline instillation

acute respiratory distress syndrome (ARDS)

§ Sudden progressive form of acute respiratory failure § Alveolar capillary membrane becomes damaged and more permeable to intravascular fluid § *Alveoli fill with fluid* •*Combined: Hypoxemic & Hypercapnic = ARDS, Asthma & COPD* CAUSES: *Most common: Sepsis* - Mutliple organ dysfunction - Either a direct or indirect lung injury causes ARDS. >> Direct: • *Aspiration* of gastric contents or other substances • Bacterial or viral *pneumonia; drowning* >> Indirect: *• Sepsis (especially gram-negative infection)* • Severe massive trauma • Severe TBI • Shock states (hypovolemic, cardiogenic, septic) *Blood transfusions, Pancreatitis* PHASES OF ARDS: *Injury or exudative phase:* - 24 - 72 hours after initial lung injury, or host insult, lasts up to 7 days - Leads to decreased gas exchange capability and lung compliance §↑ Work of breathing (WOB) §*↑ Respiratory rate* §↓ Tidal volume and resp. alkalosis from ↑ in CO2 removal *Classic sign of ARDS = refractory hypoxemia despite receiving higher concentrations of O2* §Patients condition does not improve, patient continues to get worse; Will need mechanical ventilation *Proliferative Phase:* -Begins 1 to 2 weeks after initial lung injury -Influx of neutrophils, monocytes, lymphocytes and fibroblasts continue as part of the inflammatory response -↑ Pulmonary Vascular Resistance (PVR) & Pulmonary Hypertension -Lung compliance continues to ↓ due to interstitial fibrosis -*Hypoxemia worsens due to thickened alveolar membrane* -*V/Q mismatch, diffusion limitations, and shunting* -Airway resistance ↑ from fluid in lungs & secretions in airways -If this phase persists, wide-spread fibrosis results, if it stops the lesions will often resolve *Fibrotic or Fibroproliferative Phase (late/chronic phase)* -Occurs 2-3 weeks after the initial lung injury -Not all patients who develop ARDS enter the fibrotic stage -Survival chances are poor for those who enter fibrotic phase -Lungs completely remodeled by collagenous and fibrous tissues in those who do not fully recover -Marked by diffuse scarring of lungs, interstitial fibrosis, and alveolar duct fibrosis -Results in decreased compliance -Results in reduced surface area for gas exchange = hypoxemia continues -*Typically requires long-term mechanical ventilation* CLINICAL MANIFESTATIONS: Early: §*Dyspnea, tachypnea, cough, restlessness* §Chest auscultation may be normal or may reveal fine, *scattered crackles* §*ABGs show Mild hypoxemia and respiratory alkalosis caused by hyperventilation* §Chest x-ray may be normal or reveal minimal scattered interstitial infiltrates §Edema may not show until 30% increase in fluid content in the lungs Late: §Symptoms worsen with increased fluid accumulation and decreased lung compliance §Pulmonary function tests reveal decreased compliance, lung volumes, and functional residual capacity (FRC) §Tachycardia, diaphoresis, changes in mental status, cyanosis, and pallor §Diffuse crackles and coarse crackles §Hypoxemia despite increased FIO2 §Increasing WOB despite initial findings of normal PaO2 or SaO2 §*Chest x-ray termed whiteout or white lung* because of consolidation and widespread infiltrates, or opacities seen throughout lungs fields As ARDS progresses, ABGs reflect changes in oxygenation and ventilation. *Refractory hypoxemia is the hallmark characteristic of ARDS*. Hypercapnia often signifies that respiratory muscle fatigue and hypoventilation have severely affected gas exchange, and respiratory failure is imminent. DX: CXR ABGs To help evaluate the severity of hypoxemia in ARDS, we can calculate the PaO2/FIO2 (P/F) ratio . This measure reflects the ratio of the patient's PaO2 to the FIO2 that the patient is receiving. COMPLICATIONS: - *Barotramua:* §*Rupture of overdistended alveoli during mechanical ventilation* §TO REDUCE RISK: Ventilate with smaller tidal volumes §Protocol reduces mortality and the number of ventilatory days for patients. §Higher Paco2 - permissive hypercapnia - *Volutrauma:* §*Occurs when large tidal volumes are used to ventilate noncompliant lungs* §Alveolar fracture and movement of fluids and proteins into alveolar spaces §Smaller tidal volumes or pressure-control ventilation is now the standard in ARDS treatment - *Deep Vein Thrombosis* §Susceptible to affects of immobility and venous stasis §At risk for deep vein thrombosis (DVT) and pulmonary emboli §Prophylactic management may include: §LMWH subcutaneous injections §Lovenox §Heparin §TED Stockings §Sequential Compression Devices - *Stress Ulcers* §Bleeding from stress ulcers occurs in 30% of patients with ARDS on mechanical ventilation §Management strategies oCorrection of predisposing conditions oProphylactic Gi/Antiulcer drugs oEarly initiation of enteral nutrition - *Renal Failure* §Occurs from decreased renal perfusion and subsequent decreased delivery of O2 to kidneys §From hypotension, hypoxia, or hypercapnia §May also be caused by nephrotoxic drugs used to treat ARDS-related infections - *Ventilator Associated Pneumonia (VAP) Bundle Strategies for Prevention:* §Good hand washing before, during and after delivery of care §Elevate HOB 30 to 45 degrees §ET tube with subglottic suctioning for secretions §Suction as needed for comfort §Daily assessment of readiness for extubation (weaning trials) §*Twice daily oral care with chlorhexidine* §*Mouth care with antimicrobial every 2 - 4 hours* §Change all oral suction equipment every 24 hours or more often if needed §Rinse disposable apparatus (Yankauer)with sterile water after each use §Stress ulcer prophylaxis, VTE prophylaxis, and turn/reposition every 2 hours (per protocol) CARE: (1) *O2 administration to reduce hypoxia*, (2) *mechanical ventilation*, (3) *low VT ventilation (TIDAL VOLUME)* > 4-8 mL/kg, The delivery of a large VT into stiff lungs is associated with volutrauma and barotrauma. Volutrauma causes alveolar fractures (damage or tears in the alveoli) and movement of fluids and protein into the alveolar spaces. Low VT ventilation has reduced mortality and the risk for volutrauma. (4) *permissive hypercapnia*, As a result of delivering a lower than normal VT to the patient with ARDS, the PaCO2 level will slowly rise above normal limits. This is known as permissive hypercapnia. A PaCO2 of up to 60 mm Hg is acceptable in the early phase of ARDS. (5) *Positive End-Expiratory Pressure (PEEP)*, > *PEEP at 5 cm* H2O compensates for loss of glottic function > Opens collapsed alveoli > Apply *PEEP at 3 to 5 cm H2O increments* > Higher levels of PEEP may be used in patients with ARDS >> However can compromise venous return to right side of heart, *decreases preload, CO & BP* >> Can hyperinflate alveoli, result in barotrauma or volutrauma (6) *prone positioning; takes pressure off the lungs* (7) *extracorporeal membrane oxygenation (ECMO)*; similar to diaylsis: Within the ECMO unit, O2 is delivered into the blood and CO2 removed. SUPPORT: - Maintenance of cardiac output and tissue perfusion §*Hemodynamic monitoring via a central venous or pulmonary artery catheter* > Monitor CO and BP (MAP) mean arterial pressure > Sample blood for ABGs, ScVO2 - *If the CO falls, it may be necessary to administer crystalloid fluids or colloid solutions or to lower PEEP* - *Use of inotropic drugs such as dobutamine (Dobutrex) or dopamine (Intropin)* may also be necessary - *Packed red blood cells* are used to increase hemoglobin and thus the O2-carrying capacity of the blood. NUTRITION / FLUID BALANCE: - *Enteral or parenteral feedings are started once patient hemodynamically stable* > Assess for tolerance, assess for residuals, assess bowel sounds - Monitor hemodynamic parameters (e.g., CVP, stroke volume variation), daily weights, and intake and output to assess the patient's fluid status - The patient is often placed on fluid restriction, and diuretics are used PRN - Increasing pulmonary capillary permeability results in fluid in the lungs and causes pulmonary edema - CVP monitoring/PA Catheter monitoring > At the same time, the patient may be volume depleted > This places the patient at risk for hypotension and decreased CO from mechanical ventilation and PEEP

Angina

§Angina oChronic and progressive disease > •O2 demand > O2 supply → myocardial ischemia •Angina = clinical manifestation >> •Occurs when arteries are blocked 70% or more >> •50% or more for left main coronary artery (LAD) - *Classic characteristics:* •Midsternal pressure •May radiate to arms, neck or jaw •May be associated with related symptoms, such as shortness of breath, diaphoresis and N/V. CHRONIC STABLE ANGINA: §Intermittent chest pain §Occurs intermittently over a long period of time with a similar pattern of onset, duration, and intensity of symptoms §*Often provoked by physical exertion, stress, or emotional upset* §*Usually subsides with rest, sublingual NTG.* §*Pain at rest is unusual and would be a s/s of unstable angina* §EKG findings demonstrate ST segment depression and/or T-wave inversion §Symptoms managed and controlled with drugs TYPES OF CHRONIC STABLE ANGINA: - *Silent ischemia:* §*Ischemia that occurs in absence of any subjective symptoms* §Associated with *diabetic neuropathy* §Confirmed by ECG changes found in routine scans/appointments > Factors causing coronary artery spasm: increased myocardial oxygen demand &nd increased levels of substances (e.g., tobacco smoke, alcohol, amphetamines) - Microvascular angina > Syndrome X §*Chest pain in the absence of significant CAD or coronary spasm of a major coronary artery* §CP is related to myocardial ischemia due to atherosclerosis or spasm of the small distal branch vessels of the coronary microcirculation §More common in postmenopausal women §Prevention and treatment = follow CAD recommendations

Left sided heart failure

•*Most common form of HF* •worse type as the left side is associated with systemic pumping •Results from inability of Left ventricle (LV) to: > •Empty adequately during systole > •Fill adequately during diastole •Further classified as: > •Systolic (emptying) > •Diastolic (Filling) > •Mixed systolic & diastolic (emptying & Filling) •*Blood backs up into left atrium & pulmonary veins which increases pulmonary pressure* > •pulmonary congestion and edema S/S: •Nocturnal dyspnea •Elevated Pulmonary capillary wedge pressure •*Pulmonary Congestion:* > •Blood-tinged sputum > •Cough > •Crackles > •Wheezes > •tachypnea •Orthopnea •Exertional dyspnea •Restlessness •Confusion •Fatigue •Cyanosis •Extra heart sounds (murmur)

kidneys

•*Normal BUN 10-23mg/dL* •Amount of nitrogen in blood from waste product urea (formed from liver) •Dehydration & shock my elevate BUN • •*Best indicator of GFR is 24-hour urine for creatinine clearance.* •*Creatinine 0.8-1.4mg/dL* •Non-protein waste product of creatinine phosphate metabolism by skeletal muscle tissue •Better indicator of renal function (GFR) than BUN

OBSTRUCTIVE SHOCK

•*Physical obstruction to blood flow, occurs with a decreased CO CAUSED BY*: •Restricted diastolic filling of right ventricle from compression •Abdominal compartment syndrome > •Abdominal pressure compresses inferior vena cava = decreasing venous return of blood to the heart - Pulmonary embolism & right ventricular thrombi causes outflow obstruction: •*Decreased CO* •Increased afterload •*JVD* •*Pulsus paradoxus - SBP falls during inspiration >10mmHg* - Quick recognition and treatment help to decrease further hem0dynamic compromise or cardiac arrest TREATMENT: - *based on obstruction:* - Mechanical decompression for pericardial tamponade, tension pneumothorax, and hemopneumothorax may be done by needle or tube insertion. - Obstructive shock from a pulmonary embolism requires immediate anticoagulation therapy or pulmonary embolectomy. - Superior vena cava syndrome, a compression or obstruction of the outflow tract of the mediastinum, may be treated by radiation, debulking, or removal of the mass or cause. - A decompressive laparotomy may be done for abdominal compartment syndrome for patients with high intraabdominal pressures and hemodynamic instability.

MI

•Acute Myocardial Infarction (AMI) •AMI is defined as: •*Non-ST elevation myocardial infarction (NSTEMI):* - NSTEMI or UA usually have transient thrombosis or incomplete coronary occlusion. •Often develop ST depression or T wave inversion on the initial ECG. •Do not develop pathologic Q waves. •Serial ECGs reflect evolution of MI - *Does not require thrombolytic therapy* •*ST elevation myocardial infarction (STEMI):* - STEMI patients usually have a complete coronary occlusion *(EMERGENCY)* •ST elevation is first seen on the 12-lead ECG. Within a few hours to days, T-wave inversion and pathologic Q waves develop. •Thrombolytic (fibrinolytic) therapy indicated when PCI not available •Cause: Imbalance of oxygen supply and demand due to decreased coronary artery perfusion due to atherosclerosis. •The extent of cell death determines the size of the MI. •*Early interventions such as the administration of thrombolytics or early PCI*, can restore perfusion to the ischemic zone and reduce the area of myocardial damage /injury - To limit the infarct size, the artery must be opened within *90 minutes* of presentation to restore blood and O2 to the heart muscle and limit the infarct size. This can be done either by PCI or with thrombolytic (fibrinolytic) therapy. Types - Q wave: total occlusion of coronary artery with thrombus (STEMI) - Non Q wave: partial occlusion of coronary artery (NSTEMI) •*Most infarcts occur in the left ventricle* •Right ventricular infarction commonly occurs in patients with inferior wall infarction. •Abrupt obstruction of blood through coronary artery leads to irreversible myocardial cell death (necrosis of heart muscle) •Right Coronary Artery and Circumflex not as bad → Left is very BAD! CLINICAL MANIFESTATIONS: •Pain: •Severe chest pain, not relieved by rest, changes in position, and nitroglycerin •Heaviness, pressure, tightness, burning, constriction, crushing •*Substernal or epigastric but may radiate to neck, lower jaw, arms, back* •Most often in the early morning •Sometimes no pain in Diabetic neuropathy - *Usually last 20 mins or longer* - Weakness, Nausea, indigestions, SOB, fatigue - *Diaphoreses, cool clammy skin, increased HR and BP.* - BP later drops due to decreased CO - N/V, fever - *Decreased urine output, crackles, s3 , s4, JVD, peripheral edema* - Elevated cardiac enzymes: •*Troponin I & T* •*CK-MB* •*Myoglobin* §Onset of CP < 12 hours §CP of of 30 minutes in duration §CP unresponsive to sublingual (SL) nitroglycerin (NTG)

Chronic HF

•Assessment for Heart Failure FACES → ask patient about these •F -Fatigue •A- Limitation of Activities •C- Chest congestion/Cough •E- Edema •S- Shortness of breath > •Fatigue > •Dyspnea > •Orthopnea (cannot lay down comfortably) > •Paroxysmal nocturnal dyspnea (short of breath at night) > •Tachycardia / Palpitations (A. fib) > •Changes in LOC - decreased Urine output/ nocturia - Skin changes: mottling (blue/ gray), cool, clammy, - sleep apnea - *weight gain (Daily weights)* > *gain of >3 lb (1.4 kg) in 2 days may indicate ADHF, an exacerbation of chronic HF* > If found pretty early on, can be treated at home (take an extra Lasix today and lets see what happens tomorrow) if Left HF: - backs up into left atria and pulmonary system (lungs) •Pulmonary edema, rales, afib, pulsus alternans (every other beat diminished), dyspnea, cough, hyperventilation, dizziness, syncope, fatigue, S3 murmur, increased LV/LA & pulmonary pressures if Right HF: - fluid backs up into systemic circulation •Liver (hepatomegaly), abdominal cavity (ascites), JVD- positive hepatojugular reflex, decreased appetite, N/V, increased RV & RA pressures, S3 (early sign), S4 •Dependent edema, may or may not be pitting DIAGNOSTIC STUDIES: ACUTE OR CHRONIC: •*Echocardiogram Most important* > •Provides information about ejection fraction, heart valves, and heart chambers •ECG, chest X-ray, 6-minute walk test, MUGA scan, cardiopulmonary exercise stress test, right or left heart catheterization, endomyocardial biopsy (EMB) - •*Serum BNP level, normal level of NT-proBNP 100 pg/mL* •< 125 pg/mL for patients aged 0-74 years & < 450 pg/mL for patients aged 75-99 years. - •Brain natriuretic peptide (BNP) Cardiac hormone: •Secreted by ventricular myocytes in response to wall stretch •Often used in assessment of HF. •Reflects severity of heart failure •*In decompensated heart failure, BNP rises* •*As heart failure is treated, BNP will lower* •Good marker for differentiating between pulmonary and cardiac causes of dyspnea TREATMENTS: •*Diuretics* - loop, thiazide > Lasix /Furosemide & Bumex/bumetanide >> Monitor for hypokalemia >>> Metolazone (given as an adjunct 30 minutes prior to Lasix/Bumex) •*ACE inhibitors/ARB's* (decrease afterload) reduces remodeling LV > ACE: (enalapril, lisinopril, ramipril, captopril, benazepril) MUST teach pt to notify physician if dry, persistent cough develops - will switch to ARB. > ARBS: (valsartan, candesartan, losartan, irbesartan (used if ACE's are not tolerated) >> Inhibit the RAAS system *(monitor for hyperkalemia)* •Vasodilators (if further decrease afterload needed) •*Digoxin - improve symptoms, controls ventricular rate HF with afib/aflutter* •*Beta-blockers:* (carvedilol, metoprolol succinate) reduces remodeling LV > heart works smarter - not harder (heart protective) •BNP─nesiritide citrate (Natrecor) manage decompensated HF (diuresis & vasodilation decreases ventricular preload & afterload) •Sacubitril/valsartan (Entresto) newer tx, angiotensin receptor neprilysin inhibitors (ARNI's) used in HF pt's with reduced EF, improves renal blood flow and promotes loss of Na+ = lowers BP & reduces myocardial workload > •Reduces morbidity & mortality, reduces hospital readmissions •*Calcium Channel Blockers:* > •Vasodilates coronary arteries and increases coronary perfusion, reduces cardiac output and afterload > •Ex. Diltaizem/Cardizem and amlodipine/NORVASC - Inotropes are used in clinical areas where patients' hemodynamics can be monitored continuously (MAP, CO, CVP) - Cardiac Assist Devices •Intra-aortic balloon pump •Ventricular Assist Device (LVAD) (RVAD) •Dual chamber Biventricular pacemaker/implantable cardioverter defibrillator (ICD) •Minimally invasive catheter based micro-axial flow ventricular assist device •Ventricular reconstruction •ExtraCorporeal Membrane Oxygenation (ECMO) COMPLICATIONS: •Respiratory -Pulmonary congestion, respiratory muscle weakness, pulmonary hypertension •Dysrhythmias - atrial and ventricular due to changes in normal electrical pathways > •Afib, VT/VF, bradyarrhythmias •Stroke & Thromboembolism •Gastrointestinal - Hepatic congestion & hepatic dysfunction, malabsorption •Musculoskeletal - Muscle wasting •Renal failure due to decreased perfusion •Acute Decompensated Heart Failure (ADHF) "Acute on Chronic HF" *•Cardiogenic shock* *•Sudden Cardiac Arrest* *INTERVENTIONS:* - *daily weights!* - DASH diet (low sodium 2g/day) - fluid restriction (1.5-2L/day) > Ice chips, gum, hard candy, ice pops to help thirst

cardiogenic shock

•Cardiogenic shock: Requires AGGRESSIVE management → High mortality rate •Heart ceases to function effectively as a pump, resulting in decrease in SV and CO •Leads to *decrease in BP and tissue perfusion* •Results in pulmonary capillary pressure increasing = *pulmonary edema* - *Caused by: (anything that affects the heart so that it cannot pump effectively):* •*Myocardial infarction* •*Cardiomyopathy* •*Blunt cardiac injury* •Severe systemic or pulmonary hypertension •Cardiac tamponade •Ventricular hypertrophy •Dysrhythmias •Valvular problems •Ventricular septal defect •Pericardial Tamponade •End-stage HF S/S: •Early Manifestations of Cardiogenic Shock: •*Tachycardia* •*HYPOTENSION!!* •Narrowed pulse pressure •Increase in myocardial oxygen consumptions •There is an increase in oxygen demand but no increase in supply •Physical Assessment for Cardiogenic Shock: •*Tachypnea* •Dyspnea •Pulmonary congestion: CRACKLES •*Pallor, cool, clammy skin* •Decreased capillary refill time •*Anxiety, confusion, agitation (AMS)* •*Increase in pulmonary artery wedge pressure (PAWP) (blood backs up into pulmonary artery)* •Decreased renal perfusion and urinary output •Hypotension •*Narrowing pulse pressure* TREATMENT: •*Remove coronary obstruction* - restore blood flow & O2 to myocardium •Restore balance between oxygen supply and demand •Correct tamponade (if present) •Support ventricular contractility to increase CO - *Cardiac catheterization is done as soon as possible after the initial insult* - Circulatory assist devices • TO Decrease SVR and left ventricular workload: •*Intra-aortic balloon pump* •*Ventricular assist device (VAD)* •Heart Transplant - Drug Therapy •*Nitrates* to dilate coronary arteries •*Diuretics* to reduce preload •*Vasodilators* to reduce afterload •*Beta Blockers* to reduce heart rate

Heart Failure

•Complex clinical syndrome resulting in insufficient blood supply/oxygen to tissues and organs •Chronic HF is progressive disease → heart is just not pumping like it should •Most common and costly cause for hospital admission in adults over age 65 Classifications: •Right or left sided •Systolic or diastolic •Acute or Chronic *HTN (modifiable risk factor) and CAD are the primary risk factors for HF.* - Primary causes: Conditions that directly damage the heart - Precipitating causes: often increase the workload of the heart EJECTION FRACTION: •*Normal EF is 55% to 60%* •Patients with HFrEF generally have an EF less than 45%, can be as low as 5% to 10%. Mixed systolic & diastolic failure: •Seen in disease states such as dilated cardiomyopathy (DCM) •Poor EF's (<35%) •High pulmonary pressures •Biventricular failure (both ventricles may be dilated and have poor filling & emptying capacity) PATHO: •Ventricular failure leads to: oLow Blood pressure oLow cardiac output oPoor renal perfusion > oAbrupt or subtle onset Compensatory Mechanisms of Heart Failure: •*Renin-Angiotensin-Aldosterone System (RAAS):* •Mobilized to maintain cardiac output •Regulates blood pressure, electrolyte balance, fluids •*Causes a retention of sodium and fluid in response to a decrease in cardiac output* > •Causing vasoconstriction to increase BP •The fluid backs up into the body •Short term = Okay... Long term = Very bad •Causes hypertrophy, increased thirst NURSING CONSIDERATIONS: Subjective Data: •Number of pillows used for sleeping •Paroxysmal nocturnal dyspnea •Insomnia •Chest pain or heaviness •*RUQ pain, abdominal discomfort* •Behavioral changes •Visual changes - Objective Data: •Skin color and temperature •*Edema* •Respiratory rate and sounds •*Frothy, blood-tinged sputum* •Heart rate and sounds •Abdominal distention •*Changes in LOC*

acute resp failure (ARF)

•Occurs when oxygenation, ventilation, or both are inadequate •Insufficient O2 transferred to blood > •Hypoxemia > •Decreased PaO2 and SaO2 •Inadequate CO2 removal > •Hypercapnia > •Increased PaCO2 •Assessed by arterial blood gases (ABGs) and pulse oximetry Classification: •*Hypoxemic respiratory failure: (oxygenation failure)* > •Causes involve respiratory or cardiac system disorders or diseases > *is a PaO2 less than 60 mm Hg* when the patient is receiving an inspired O2 concentration of 60% or more. > •Main problem: inadequate exchange of O2 between the alveoli and pulmonary capillaries - Common Causes: Respiratory System : • ARDS • Hepatopulmonary syndrome (e.g., low-resistance flow state, V/Q mismatch) • Massive pulmonary embolism (e.g., thrombus emboli, fat emboli) • Pneumonia • Pulmonary artery laceration and hemorrhage • Toxic inhalation (e.g., smoke inhalation) Cardiac System : • Anatomic shunt (e.g., ventricular septal defect) • Cardiogenic pulmonary edema • Cardiogenic shock (decreasing blood flow through pulmonary vasculature) • High cardiac output states: diffusion limitation *•Hypercapnic respiratory failure: (ventilation failure)* > •Causes involve respiratory system, CNS, chest wall, and neuromuscular system disorders or diseases. > *is a PaCO2 greater than 50 mm Hg* with acidemia (arterial pH less than 7.35).2 The main problem is insufficient CO2 removal. This causes the PaCO2 to be higher than normal. > •Main problem: insufficient CO2 removal; the body is unable to compensate - Common Causes: Respiratory System : • Asthma • COPD • Cystic fibrosis Central Nervous System: • Brainstem injury or infarction • Sedative and opioid overdose • Spinal cord injury • Severe head injury Chest Wall : • Kyphoscoliosis • Pain • Severe obesity • Thoracic trauma (e.g., flail chest) Neuromuscular System : • Amyotrophic lateral sclerosis • Critical illness polyneuropathy • Guillain-Barré syndrome • Muscular dystrophy • Multiple sclerosis • Myasthenia gravis • Phrenic nerve injury • Poliomyelitis • Toxin exposure or ingestion (e.g., tree tobacco, acetylcholinesterase inhibitors, carbamate or organophosphate poisoning)

Right sided heart failure

•Right ventricle fails to pump effectively • → fluid backs up into venous system • → *fluid moves into tissues and organs* - *The most common cause of right-sided HF is left-sided HF.* > As the LV fails, fluid backs up into the pulmonary system, causing increased pressures in the lungs. •Can also be caused by pulmonary embolism or pulmonary disease •Further classified as: > •Systolic > •Diastolic > •Mixed systolic & diastolic S/S: •Jugular venous distention *(JVD)* •*Ascites* (fluid backing up into GI system) •Hepatomegaly/Splenomegaly •Anorexia & complaints of GI distress •*Dependent edema* •Weight gain •Fatigue •Increased Peripheral Venous Pressure •Extra heart sounds (murmur)

SEPSIS

•SEPSIS - life-threatening response to infection. •May be bacterial, viral, fungal, or on rare occasion rickettsial or protozoal •Associated with a high mortality rate, 1 in 4 patients affected dies •SEPTIC SHOCK - Causes vasodilation, maldistribution of blood flow, and myocardial depression •Characterized by a dysregulated patient response, along with *new organ dysfunction from INFECTION* •Resulting in activation of pro-inflammatory & anti-inflammatory responses and *coagulation abnormalties* •*Persistent hypotension despite adequate fluid resuscitation and inadequate tissue perfusion = tissue hypoxia* •Requiring administration of vasopressors S/S: - Initial: *"lactic acid build up"* > *Normal: 4.5 to 19.8 milligrams per deciliter (mg/dL)* Compensatory stage: - hypotension - Impaired GI mobility - cool clammy skin - *hyperventilation = resp alkalosis* > §*Respiratory failure is common* §Initially hyperventilation = respiratory alkalosis §Once patient can no longer compensate = respiratory acidosis §Respiratory failure seen in 85% of cases, and ARDS in 40% - altered LOC - N/V Progressive: - edema - weak pulse - dysrhythmias - *jaundice* - tachypnea - *elevated BUN & creatinine* - *Risk of DIC* - *crackles* - *metabolic acidosis* - AKI Refractory Period: - Accumulation of lactic acid - profound hypotension - tachycardia - doesn't respond to O2 - organ failure; unlikely recovery S/S: •Monitor for Sepsis - Signs of infection to include: •Fever, hypothermia, tachycardia, hypotension, tachypnea •AMS •New c/o pain •Adventitious breath sounds, increased O2 requirements, new infiltrate on radiograph •Change in appearance of urine, pyuria, bacteria on urine culture •Change in wound appearance or drainage •Leukocytosis, thrombocytopenia on CBC •Elevated blood glucose PATIENTS AT RISK: •Older adults •Immunocompromised •Patients undergoing surgical/invasive procedures •Patients with indwelling catheters •Mechanically ventilated patients CARE: •Collaborate with the health care team to *initiate immediate Volume resuscitation* •*Circulatory support with fluids and vasopressors* •*Empiric antibiotics* •Source of infection control •Monitor and report patient response to treatment •Use *supplemental O2 or lung protective mechanical ventilation as indicated* •Monitor for delirium •Provide *enteral nutrition* to prevent malnutrition and lower risk of bacterial translocation •*Give ulcer prophylaxis* •Administer pharmacologic or mechanical interventions to *prevent venous thromboembolism* PREVENTION: •Hand hygiene •Measures to prevent hospital-acquired infections: •Remove urinary catheters and central lines when no longer indicated •Use aseptic technique when handling lines and catheters •*Facilitate weaning from mechanical ventilation through the sue of spontaneous breathing trials, appropriate care of sedation, and early mobility* •Adhere to transmission based precautions to incluDe use of standard, contact, droplet, and airborne precautions as appropriate TREATMENT OF SEPTIC SHOCK: •CAB (ABC'S) •Supplemental oxygen to maintain PaO2 > 60 - 70 mmHg - *Volume expansion!* •Two large bore IVs with *isotonic crystalloid fluids → VOLUME EXPANSION* •*Isotonic fluids with norepinephrine (vasopressors)* •Keep MAP >60-65 •Monitor: vitals, capillary refill, urinary output, pulses, LOC •*Arterial line and CVP for accurate hemodynamic monitoring* •STRICT I&Os → monitor urine output → >30ml/hr •*Central line for administration of norepinephrine/Levophed, phenylephrine/Neosynephrine, or epinephrine* •*IV Corticosteroids for patients who cannot maintain BP after trying fluids and norepinephrine* •*IV antibiotics in the first hour AFTER blood cultures have been drawn* •Proton Pump Inhibitor *(protonix) for stress ulcer prophylaxis* •*Heparin or Lovenox for DVT prophylaxis* •*NO TRENDLENBURG FOR LOW BP → Elevate legs only* - passive leg raise 45 degrees - Glucose levels should be maintained below 180 mg/dL (10.0 mmol/L) for patients in shock *Systemic Inflammatory Response Syndrome (SIRS):* •Systemic inflammatory response characterized by generalize *inflammation in organs not associated with initial affected area* •Serous, often life-threatening condition •*Can be caused by severe bacterial infection (sepsis), trauma, or pancreatitis* - Can be triggered by mechanical mechanisims such as tissue trauma (burns, crush injuries, surgical procedures), abscesses, ischemic or necrotic tissue, microbial invasion, endotoxin release from invading micro-organisms, post cardiac arrest or shock states/perfusion deficits *Multi Organ Dysfunction Syndrome (MODS):* •*Failure of two or more organ systems*, results from dysregulated systemic inflammatory response •Dysfunction of the kidneys, liver, lungs, heart, genitourinary tract etc. caused by hypo-perfusion and other complications of SIRS •Organ function is not capable of maintaining homeostasis •Homeostasis cannot be maintained without support S/S:• •Signs of impaired organ perfusion: •*Hypotension SBP < 90 mmHg, tachycardia, tachypnea* •If hypertensive, a decrease of 40 mm Hg from baseline is considered severely hypotensive. •*Elevated serum lactate* •*Skin mottling* •Change in capillary refill •Change in renal function - drop in output, elevated creatinine and BUN •Change in liver function - labs to include coagulation studies

lung tings

•Think of compliance as the degree of elasticity of the tissue •A decrease in compliance increases resistance, or stiffness of the lung •*Static Compliance: measures elastic properties of the LUNGS* •Pulmonary problems that involve mainly the lungs *(PNA, ARDS) have a decrease in static compliance*. •Dynamic compliance may also decrease as the lung pressures may transmit up to the airways •*In mechanically ventilated patients: Increased Plateau Pressures = decreased compliance* *•Dynamic Compliance: measures elastic properties of the AIRWAYS* •Patients with pulmonary problems involving mostly airways (asthma) have a decrease in dynamic compliance but static compliance is normal •*In mechanically ventilated patients: Increase in Peak Inspiratory Pressure = decreased compliance* •Decreased compliance = Increased work of breathing! •*Arterial Oxygen: PaO2, normal 80 - 100mm/Hg on room air* > •Less than 80 = hypoxemia •Saturation of Arterial Oxygen: SaO2, normal 95 - 99% on room air > •Direct relationship to PaO2, amount of hemoglobin combined with O2 •*Mixed Venous Oxygen Saturation: SvO2, normal 60 - 75%, directly measured by pulmonary artery* > •Most sensitive indicator of oxygenation at the cellular level •Goal for critically ill patient is to maintain SpO2 at 90% or greater

ECG

•Vertical boxes measure voltage/amplitude •Horizontal boxes measure time •The larger boxes contain 5 smaller boxes on the horizontal line •*5 on the vertical line for a total of 25 per large box.* •Horizontally, one small box = 0.04 seconds each or 40 milliseconds •One large box contains five smaller boxes = 0.20 seconds or 200 milliseconds. •ECG Measurements •When in doubt, do not treat the monitor... CHECK THE PATIENT! •*P wave 0.06 - 0.12* > •Atrial depolarization (contraction of atria) >> •Normally indicates firing of the SA node >> •Always + in NSR in Lead II *•PR Interval: 0.12-0.20 sec* > •Beginning of P wave to beginning of QRS > •Atrial depolarization/delay in AV node •0.12 to 0.20 seconds or 3 - 5 small boxes •Normal is < 0.20 •*Shorter interval = impulse from AV junction* •*Longer interval = first-degree AV block* •*When the PR interval is longer than normal*, the speed of conduction is delayed in the AV node *(brady).* •When the PR interval is *shorter than normal*, the speed of conduction is abnormally fast. *(tachy)* •*QRS between 0.08 & 0.12* *•QRS Interval = < 0.12* > •Contraction of the ventricles (depolarization) > Wide: = slowed conduction >> Bundle branch block (BBB) >> Ventricular rhythm •*QT Interval = 0.34-0.43 sec* > •Amount of time from beginning of QRS to end of T > •Conduction through the ventricles •>> Monitor certain medications because they can cause prolonged QT interval •Measures the total time taken for ventricular depolarization and repolarization. •Abnormal prolongation of the QT interval increases vulnerability to lethal dysrhythmias: > *•Ventricular tachycardia and fibrillation.* •Varies with HR, the QT interval *becomes longer with slower heart rates and shortens with faster heart rates.* •Generally, the QT interval is less than half the RR interval. •Drugs affecting QTI: Zofran, Reglan, Tikosyn, Haldol, Amiodarone (to name just a few) •*ST Segment 0.12* •Look for depression or elevation •*ST elevation = myocardial injury* •*ST depression = ischemia*, associated with reciprocal ECG changes, may be caused by digoxin, anemia, ischemia or blockage •T WAVE •Ventricular repolarization = refractory period (after depolarization to polarization). •*Bigger than a P wave but no greater than 5 small boxes high* •*Inversion = ischemia to myocardium* •Changes in T-wave amplitude or direction can indicate electrical disturbances resulting from an electrolyte imbalance, myocardial ischemia/injury, or pericarditis. •*Hyperkalemia can cause tall, peaked T waves, and ischemia may cause an inverted or upside-down T wave.* U Wave •Repolarization of a small segment of the ventricles. •*Seen after T wave, usually small, rounded & < 2 mm in height* •A final waveform that is occasionally noted on the ECG is the U wave. •May be normal, seen with hyperthyroidism, CNS disease, and long QT syndrome. •*May indicate hypokalemia* •Medications (quinidine, procainamide, disopyramide, amiodarone, digitalis and phenothiazines. •Larger U waves may be present in patients with hypokalemia, cardiomyopathy, and digoxin toxicity. RHYTHM INTERPRETATION *Identify lethal rhythms:* •Second degree - type II •VT without a pulse •Complete heart block •Vfib/Torsades •Idioventricular •PEA Treat the patient "know when to" •Defibrilate •Pace •Medications: • Epinephrine Amiodarone Magnesium • Vasopressin Lidocaine Cardizem • Atropine Adenosine Digoxin •*Shockable rhythm: V-tach without a pulse, V-fib* •Non-shockable rhythms: Asystole (no electrical potential to shock = flat line), pulseless electrical activity (PEA) •*Torsades de points: Responsive to Magnesium IV administration*, occurs when QT interval is too long *ECG POWERPOINTS AND OUT SOURCES*

CAD

*Coronary artery disease (CAD) is a type of blood vessel disorder that we consider in the general category of atherosclerosis (hardening of arteries)* RISK FACTORS: •Age: men >45 years & women > 55 years •Family history •Ethnicity •*Cholesterol:* - total serum > 200 - High LDL > 200, - Triglycerides > 150 & - low levels of HDL <45 *(HDL high = good, LDL low = good)* •Smoking •Hypertension > 140/90 begin lifestyle changes and treat stage 1 or 2 HTN with medications •Inactivity •Overweight •Diabetes •Metabolic syndrome •Substance abuse •Prior hospitalizations fro HF •Shortness of breath, chest pain •*Medications for erectile dysfunction (contraindicated in the administration of nitroglycerin)* •Psychosocial history including stressors DIAGNOSTIC STUDIES - *EKG* - *CXR* - 6 min walk - Holter monitor: •This test is used to detect suspected dysrhythmias. Data are recorded in outpatient/ambulatory setting for 24 to 48 hours while patient logs activities and related signs and symptoms •Loop Recorder/Event Monitor Exercise tolerance test (ETT) or stress test: EKG while exercsing •Echocardiogram/Pharmacologic Echocardiogram •Pharmacological stress testing: Patient's unable to physically exercise are ordered a pharmacological stress test > •Medications such as regadenoson, dipyridamole, or adenosine are used because they cause vasodilation of normal coronary arteries •Trans esophageal echocardiography (TEE) •MRI •Electrophysiology studies (EPS) •CT Angiography with or without calcium scoring •Coronary Angiography LAB DIAGNOSTICS §CBC = Hgb. Hct. Platelets §Serum electrolytes: K+, Mg, Ca, Na+, Phos. - Cardiac enzymes: §CK enzymes found mainly in the heart, brain and skeletal muscle. oCK-MM = skeletal muscle oCK-BB = brain and nervous tissue oCK-MB = the heart oLevels rise in 3 to 6 hours; peak 12 to 24 hours, return to baseline within 12 - 48 hours. §*CK - MB (creatine kinase) or CPK-MB (creatine phosphokinase) is cardiac specific, tests for myocardial cell injury* detectable in 3 to 6 hours, peak 12 - 24 hours, lasts 12 - 48 hours - *Troponin I; MI* - detectable in 3 - 8 hours, peaks in 24 - 48 hours, lasts 3 - 5 days. Negative < 0.03ng/mL, diagnostic for cardiac injury/ischemia. - *Troponin T; MI* - detectable in 3 - 8 hours, peaks in 72 - 100 hours, lasts 5 - 10 days > •Serial sampling required, draw 3 sets of troponins 3-6 hours apart. Negative <0.1ng/mL, diagnostic for cardiac injury/ischemia. - Myoglobin - detectable in 30 minutes to 3 hours after injury, peaks in 6 - 9 hours, lasts one day - C-Reactive Protein (CRP) is associated with unstable plaque and is a risk factor for impending MI. High in bacterial infections and inflammatory disorders. - LDH- Lactate dehydrogenase, onset 24 hours, peak 3 - 6 days, lasts 10 - 14 days - *BNP (b-Type natriuretic peptide) <100pg/mL considered normal, elevated in HF* (ventricles), after nesiritide/Natrecor infusion and for 1 month after cardiac surgery.

COMMON DRUGS:

*Norepinephrine (LevoPhed):* §Stimulates Alpha and Beta 1 receptors §*Especially helpful in management of massive vasodilation in septic shock patients.* - Adverse Effects: Tachyarrhythmias, Myocardial ischemia, tissue necrosis, hypertension - Nursing Considerations: §*Infuse in central line when available* §Monitor infusion site frequently §*Monitor vital signs closely, every 5 min when titrating* §*Monitor ECG* §Obtain titration parameters §*Correct hypovolemia* §Extravasation treated with Regitine *Phenylephrine (Neosynephrine):* §Stimulates Alpha receptors causing vasoconstriction without inotropic effects §Adverse effects: increased cardiac workload, decreased organ perfusion, tissue necrosis, reflex bradycardia - Nursing Considerations: §Infuse in central line §Monitor infusion site closely §Monitor vitals, ECG §Titrate down to off slowly due to longer half life *Vasopressin (Pitressin):* §Normally acts as antidiuretic hormone, but when given in septic shock becomes potent vasopressor. §*Shown to restore the mean arterial pressure in septic shock patients.* §*Typically takes 15 mins to see increase in MAP and SVR.* - Nursing Considerations: §*DO NOT titrate according to BP, use low, fixed dose.* §*Monitor vitals at least Q15min x4 after initiation of gtt.* §May be able to reduce other pressors once vasopressin is on board. *Dopamine (Intropin):* §Nursing Considerations: §Not as effective as Levophed in septic shock. §Titrate by 1-4mcg/kg/min every 3-4 min until desired BP achieved. §Infuse per central line. §Monitor vital signs every 5 min while titrating. §*Monitor for tachyarrhythmias.* *Dobutamine (Dobutrex)* §Stimulates Beta 1 receptors (Positive Inotrope). §*Increases CO through increased contractility, decreases preload and afterload, may increase HR.* - Nursing Considerations: §Monitor for tachyarrhythmias and ventricular ectopy. §*Monitor electrolytes, especially potassium* §Document response to therapy. Improvement based upon improvement in HR symptoms and ScvO2 greater than 70%. *MILRINONE (PRIMACOR):* §*Used with HF patients.* §Relaxes smooth muscle and has dilating effects, may have effects on *BP (low).* - Nursing Considerations: §*Do not give Lasix in same line as Milrinone, it will precipitate.* §*Monitor BP, signs of hypotension and ECG.* §Document response to therapy, should see improved S/S of HF.

acute coronary syndrome

*When ischemia is prolonged and not immediately reversible, acute coronary syndrome (ACS) develops* - Acute Coronary Syndrome = UNSTABLE angina!!! - Relationship between Coronary Artery Disease (CAD) and Acute Coronary Syndrome (ACS): - CAD → "Impending thrombus" → Chronic Stable Angina > Example: Mowing the lawn, chest starts to hurt, sits down and feels better in a few minutes - ACS → STEMI & NSTEMI → Rupture of clot that was once stable > NSTEMI: Partial occlusion of the coronary artery >> Non-occlusive thrombus > STEMI: Total occlusion of the coronary artery *(MUCH WORSE)* >> Occlusive Thrombus - *Acute coronary syndrome (ACS) includes:* - stable angina - unstable angina (UA) - acute myocardial infarction (AMI) ACS TREATMENT: •*Short-acting nitrates NITROGLYCERIN* •Dilate peripheral and coronary blood vessels •Given sublingually •*If symptoms are unchanged or worse in 5 minutes, call EMS; if some relief, repeat every 5 minutes for maximum 3 doses (call EMS if symptoms have not resolved completely)* •Patient teaching, store tablets away from light/heat sources to prevent degradation, comes in an airtight container - once opened replace every 6 months. •Can use prophylactically 5 -10 minutes prior to beginning activity. •Pt. should be seated when taking, tingling sensation when administered sublingually (if not may be outdated). •Common side effects include H/A, dizziness, or flushing. •Change positions slowly to avoid orthostatic hypotension. •*Long-acting nitrates:* •Reduce angina incidence •Main side effects: H/A, orthostatic hypotension •Methods of administration •Oral - isosorbide dinitrate (Isordil) and isosorbide mononitrate (Imdur) •Nitroglycerin (NTG) ointment (Nitro-paste 2%) dosed by the inch > oPlaced on the upper body or arm, over a flat muscular area that is free of hair and scars > oOnce absorbed, it produces anginal prophylaxis for 3 to 6 hours > oIt is especially useful for nighttime and UA > oThe ointment should be wiped off to allow for a 10-14-hour nitrate free interval in order to prevent nitrate tolerance •Transdermal controlled-release NTG - silicone gel and polymer matrix > oThese systems allow timed release of NTG over a 24-hour period •These preparations should also be removed in the evening to allow for a 10-14-hour nitrate free interval

Ventilator weaning

- Adequate oxygenation - *Spo2 >90* - *FIO2 < 4-50* - *pH > 7.25* - pt ability to initiate inspiratory effect - stable hemoglobin - *core temp < 100.4* - mental status easily arousable Breathing Trials: - Spontaneous awakening and breathing trial done prior to exubation > Muscle strength (NIF test) and endurance tested - *SBT length: 30-120 min MAX* - Sedation held - Performed with CPAP support, T-peice, or low PSV Stop weaning process if: - RR > 35 or < 8 - low spontaneous VT < 5 - labored resp, use of accessory muscles - low Spo2 <90 - HR or BP changes > 20% from baseline - Dysrhythmias (PVCs, ST-segment elevation) - Decreased LOC - Anxiety SBT Failure: - *Sedation returned to 50%* - Placed back on full ventilator suport - Reattempted the next day - Goal: allow rest and decrease WOB aiming for success the next day Extubation: - *Equipment: Oral suction, 100% NRB. BMV* - hyper oxygenate - loosen ETT securement - oral and ETT suction - instruct pt to take deep breath - at peak inspiration deflate ET cuff and pull ETT - *Immediately place pt on NRB* - *Closey monitor pt status for 1 hr post extubation*

What influence hemodynamics

- Intrinsic Controls: Heart rate, contractility, preload and afterload - Extrinsic Controls: Autonomic nervous system (SNS and PNS) - Nervous Influences: the ANS which regulates vital functions via reflex and CNS control > ◦The two opposing branches keep balance - Sympathetic Nervous System (SNS) ◦Neuro Transmitter: nor-epinephrine ◦Influences both the atria and the ventricles. ◦Producing an increase in rate, conduction, force of contraction and irritability caused by anger, pain, fright, caffeine, nicotine or amphetamines. - Parasympathetic Nervous System (PNS) §Neuro Transmitter - Acetylcholine ◦Activates cholinergic receptors ◦Influences primarily the atria §Response: ◦Decreased HR, conduction, and irritability ◦ Caused by vomiting, coughing, straining (vaso vagal response). ◦Stimulates the GI tract §Slows things down. §Has a negative chronotropic, inotropic & dromotropic effect. §Responsible for mundane things such as digestion.

Heart Defenitions

- Systole = when preload (stretch) overcomes afterload (resistance) ◦Semi-lunar valves are forced open ◦Ventricles eject their contents - Diastole = period of time when heart relaxes after contraction →ventricle fills passively - *Preload (Volume)* §*Volume of blood that exerts a force or pressure (stretch) on the ventricles during diastole (filling phase)* §Filling pressure of the ventricles at the end of diastole §Amount of blood that fills the ventricles during diastole oToo much preload causes ventricular contraction to be less effective (more stretch, less recoil) - *Afterload (Resistance)* §Amount of pressure or resistance the ventricles must overcome to open the aortic and pulmonic valves and pump blood into the systemic and pulmonary vasculature Coronary Artery Profusion: - *Coronary Artery Profusion occurs during diastole* > Heart muscle receives greatest amount of freshly oxygenated blood during this time - Increasing diastolic blood pressure and time, can increase coronary artery blood flow > An example of this would be the use of Intra Aortic Balloon Pump (IABP) - *Tachycardia decreases diastolic time* = decreased coronary artery blood flow > Increases myocardial O2 demand → ischemia & decreased cardiac contractility = CP - Preload (think volume) - Afterload (think resistance) - Contractility (think ability to pump) - Cardiac Output (think perfusion status) The heart is a pump that must adjust to the amount of blood it receives. Cardiac Output: CO = HR X SV - Stroke Volume (SV) - amount of blood ejected by the ventricle with each beat - *Cardiac Output (CO) - Amount of blood ejected from the heart into the systemic circulation each minute* - *Normal CO is: 4 - 8 L/min.* -*Effects on Cardiac output* > If HR and PRELOAD (volume) increases, CO increases > If HR and PRELOAD (volume) decreases, CO decreases > If contractility decreases or increases, cardiac output will follow - Stroke Volume (SV) = the amount of blood ejected from the heart into systemic circulation with each contraction. Normal = 60-100 MAP: Reflects changes between CO and Systemic Vascular Resistance (SVR). - Normal 70 - 110 - indictaor of LV function - low = decreased blood flow to organs - high = increased cardaic workload

Heart

- The heart has electrical components that dictate the mechanical movements of the heart; this includes 3 pacemakers: •Primary - *SA node pacemaker of the heart, generates an impulse at 60-100 bpm, located at the top of the RA* •Secondary - *AV node/junction , generates an impulse at 40-60 bpm, located in the base of the RA* •Tertiary - *Ventricular, generates an impulse at 20-40 bpm, only seen if SA and SVJ failure* > Bundle of His/ Purkinje fibers/Ventricles = 20 to 40 beats/min - Depolarized - loss of electrical charge, impulse spreads across the myocardial tissue to each cell and then relaxes > Depolarization leads to contraction - Repolarized - regaining the electrical charge, getting charged up, impulses spread from cell to cell > Repolarization leads to resting and filling of ventricles from atria - ECG is evidence of electrical activity, not contraction

ans D

1. 1. Certification in critical care nursing (CCRN) by the American Association of Critical-Care Nurses indicates that the nurse a. is an advanced practice nurse who cares for acutely and critically ill patients. b. may practice independently to provide symptom management for the critically ill. c. has earned a master's degree in the field of advanced acute and critical care nursing. d. has practiced in critical care and successfully completed a test of critical care knowledge.

c

1. A patient admitted with syncope has continuous ECG monitoring. An examination of the rhythm strip reveals the following: atrial rate 74 beats/min and regular; ventricular rate 62 beats/min and irregular; P wave normal shape; PR interval lengthens progressively until a P wave is not conducted; QRS normal shape. The priority nursing intervention would be to a. give epinephrine 1 mg IV push. b. prepare for synchronized cardioversion. c. observe for symptoms of hypotension or angina. d. apply transcutaneous pacemaker pads on the patient.

d

1. A patient has a spinal cord injury at T4. Vital signs include falling blood pressure with bradycardia. The nurse recognizes that the patient is experiencing a. a relative hypervolemia. b. an absolute hypovolemia. c. neurogenic shock from low blood flow. d. neurogenic shock from massive vasodilation.

b c. d

1. In teaching a patient about coronary artery disease, the nurse explains that the changes that occur in this disorder include (select all that apply) a. diffuse involvement of plaque formation in coronary veins. b. abnormal levels of cholesterol, especially low-density lipoproteins. c. accumulation of lipid and fibrous tissue within the coronary arteries. d. development of angina due to a decreased blood supply to the heart muscle. e. chronic vasoconstriction of coronary arteries leading to permanent vasospasm

d

1. RIFLE defines the first 3 stages of AKI based on changes in a. blood pressure and urine osmolality. b. fractional excretion of urinary sodium. c. estimation of GFR with the MDRD equation. d. serum creatinine or urine output from baseline.

ans: 3

1. The client has experienced an increased preaload, which supports an increase in cardaic output. What nursing action contributes to an increased preload? 1. Diureitc admin 2. Intotrope admin 3. Increased fluid admin 4. Calcium Channel blocker admin

ANS: A B D

1. Which signs and symptoms distinguish hypoxemic from hypercapnic respiratory failure? (select all that apply) a. Cyanosis b. Tachypnea c. Morning headache d. Paradoxical breathing e. Use of pursed-lip breathing

a b c e

1. Which statements accurately describe heart failure with preserved ejection fraction (HFpEF)? (select all that apply) a. Uncontrolled hypertension is the primary cause. b. Left ventricular ejection fraction may be within normal limits. c. The pathophysiology involves ventricular relaxation and filling. d. Multiple evidence-based therapies have been shown to decrease mortality. e. Therapies focus on symptom control and treatment of underlying conditions.

a

10. A kidney transplant recipient has had fever, chills, and dysuria over the past 2 days. What is the first action that the nurse should take? a. Assess temperature and initiate workup to rule out infection. b. Reassure the patient that this is common after transplantation. c. Provide warm covers to the patient and give 1 gram oral acetaminophen. d. Notify the nephrologist that the patient has manifestations of acute rejection.

The answer is D. A pulmonary artery wedge pressure measures the left atrial pressure. A pulmonary catheter is "wedged" with a balloon in the pulmonary arterial branch to measure the pressure. If the reading is less than 18 mmHg it indicates this is NOT a cardiac issue but most likely ARDS. Therefore, the pulmonary edema is due to damage to the alveolar capillary membrane leaking fluid into the alveolar sac....NOT a heart problem ex: heart failure.

10. A patient is experiencing respiratory failure due to pulmonary edema. The physician suspects ARDS but wants to rule out a cardiac cause. A pulmonary artery wedge pressure is obtained. As the nurse you know that what measurement reading obtained indicates that this type of respiratory failure is NOT cardiac related? A. >25 mmHg B. <10 mmHg C. >50 mmHg D. <18 mmHg

ans : a d e

2. 2. What are appropriate nursing interventions for the patient with delirium in the ICU? (select all that apply) a. Use clocks and calendars to maintain orientation. b. Encourage round-the-clock presence of caregivers at the bedside. c. Silence all alarms, reduce overhead paging, and avoid conversations around the patient. d. Sedate the patient with appropriate drugs to protect the patient from harmful behaviors. e. Identify physiologic factors that may be contributing to the patient's confusion and irritability.

b

2. A 78-yr-old man with a history of diabetes has confusion and temperature of 104°F (40°C). There is a wound on his right heel with purulent drainage. After an infusion of 3 L of normal saline solution, his assessment findings are BP 84/40 mm Hg; heart rate 110; respiratory rate 42 and shallow; CO 8 L/min; and PAWP 4 mm Hg. This patient's symptoms are most likely indicative of a. sepsis. b. septic shock. c. multiple organ dysfunction syndrome. d. systemic inflammatory response syndrome.

b

2. After teaching about ways to decrease risk factors for CAD, the nurse recognizes that further instruction is needed when the patient says a. "I can keep my blood pressure normal with medication." b. "I would like to add weight lifting to my exercise program." c. "I can change my diet to decrease my intake of saturated fats." d. "I will change my lifestyle to reduce activities that increase my stress."

ans: D

2. An important consideration in selecting an O2 delivery device for the patient with acute hypoxemic respiratory failure is to a. always start with noninvasive positive pressure ventilation. b. apply a low-flow device, such as a nasal cannula or face mask. c. be able to correct the PaO2 to a normal level as quickly as possible. d. base the selection on the patient's condition and amount of FIO2 needed.

b d

2. During the oliguric phase of AKI, the nurse monitors the patient for (select all that apply) a. hypotension. b. ECG changes. c. hypernatremia. d. pulmonary edema. e. urine with high specific gravity.

d

2. The ECG monitor of a patient in the cardiac care unit after an MI shows ventricular bigeminy with a rate of 50 beats/min. The nurse would a. perform defibrillation. b. administer IV amiodarone. c. prepare for temporary pacemaker insertion. d. assess the patient's response to the dysrhythmia.

d

2. What compensatory mechanism involved in both chronic heart failure and acute decompensated heart failure leads to fluid retention and edema? a. Ventricular dilation b. Ventricular hypertrophy c. Increased systemic blood pressure d. Renin-angiotensin-aldosterone activation

ans: 1 2 3 4

2. Which of the following conditions cause a decreased central venous pressure CPV? SATA 1. Sepsis 2. Hypovolemia 3. Dehydration 4. HF 5. Fluid volume overload

C

3. 3. The critical care nurse recognizes that an ideal plan for caregiver involvement includes a. having a caregiver at the bedside at all times. b. allowing caregivers at the bedside at preset, brief intervals. c. a personally devised plan to involve caregivers with care and patient needs. d. restriction of visiting in the ICU because the environment is overwhelming to caregivers.

b

3. A hospitalized patient with a history of chronic stable angina tells the nurse that she is having chest pain. The nurse bases his actions on the knowledge that ischemia a. will always progress to myocardial infarction. b. can be relieved by rest, nitroglycerin, or both. c. is often associated with vomiting and extreme fatigue. d. indicates that irreversible myocardial damage is occurring.

c

3. If a patient is in the diuretic phase of AKI, the nurse must monitor for which serum electrolyte imbalances? a. Hyperkalemia and hyponatremia b. Hyperkalemia and hypernatremia c. Hypokalemia and hyponatremia d. Hypokalemia and hypernatremia

b

3. In the patient with supraventricular tachycardia, which assessment indicates decreased cardiac output? a. Hypertension and dyspnea b. Chest pain and palpitations c. Abdominal distention and tachypnea d. Bounding pulses and a systolic murmur

ans: A

3. The most common early clinical manifestations of ARDS that the nurse may see are a. dyspnea and tachypnea. b. cyanosis and apprehension. c. respiratory distress and frothy sputum. d. bradycardia and increased work of breathing

c d

3. The nurse is caring for a patient with acute decompensated heart failure who is receiving IV dobutamine. Why would this drug be prescribed? (select all that apply) a. It dilates renal blood vessels. b. It will increase the heart rate. c. Heart contractility will improve. d. Dobutamine is a selective β-agonist. e. It increases systemic vascular resistance.

a c

3. Treatment modalities for the management of cardiogenic shock include (select all that apply) a. dobutamine to increase myocardial contractility. b. vasopressors to increase systemic vascular resistance. c. circulatory assist devices such as an intraaortic balloon pump. d. corticosteroids to stabilize the cell wall in the infarcted myocardium. e. Trendelenburg positioning to facilitate venous return and increase preload.

ans: 1 2 4

3. Which of the following clinical findings are associated with an elevated pulmonary artery occlusive pressure (PAOP)? SATA 1. Dyspnea 2. S3 or S4 heart sounds 3. Flat neck veins 4. Crackles

C

4. 4. To establish hemodynamic monitoring for a patient, the nurse zeros the a. cardiac output monitoring system to the level of the left ventricle. b. pressure monitoring system to the level of the catheter tip in the patient. c. pressure monitoring system to the level of the atrium, or the phlebostatic axis. d. pressure monitoring system to the level of the atrium, or the midclavicular line.

a

4. A patient is admitted to the hospital with chronic kidney disease. The nurse understands that this condition is characterized by a. progressive irreversible destruction of the kidneys. b. a rapid decrease in urine output with an elevated BUN. c. an increasing creatinine clearance with a decrease in urine output. d. prostration, somnolence, and confusion with coma and imminent death.

a b

4. A patient with chronic heart failure and atrial fibrillation is treated with low-dose digitalis and a loop diuretic. What does the nurse need to do to prevent complications of this drug combination? (select all that apply) a. Monitor serum potassium levels. b. Teach the patient how to take a pulse rate. c. Withhold digitalis if pulse rhythm is irregular. d. Keep an accurate measure of intake and output. e. Teach the patient about dietary potassium restrictions.

ans: C D E

4. Interventions used in managing the patient with ARDS include (select all that apply) a. IV injection of surfactant. b. aggressive IV fluid resuscitation. c. giving adequate analgesia and sedation. d. elevating the head of bed 30 to 45 degrees when supine. e. monitoring hemodynamic parameters and daily weights.

d

4. The most accurate assessment parameters for the nurse to use to determine adequate tissue perfusion in the patient with MODS are a. blood pressure, pulse, and respirations. b. breath sounds, blood pressure, and body temperature. c. pulse pressure, level of consciousness, and pupillary response. d. level of consciousness, urine output, and skin color and temperature.

b

4. The nurse is caring for a patient who is 2 days post MI. The patient reports that she is experiencing chest pain when she takes a deep breath. Which action would be a priority? a. Notify the provider STAT and obtain a 12-lead ECG. b. Obtain vital signs and auscultate for a pericardial friction rub. c. Apply high-flow O2 by face mask and auscultate breath sounds. d. Medicate the patient with as-needed analgesic and reevaluate in 30 minutes.

d

4. The nurse prepares a patient for synchronized cardioversion knowing that cardioversion differs from defibrillation in that a. defibrillation delivers a lower dose of electrical energy. b. cardioversion is a treatment for atrial bradydysrhythmias. c. defibrillation is synchronized to deliver a shock during the QRS complex. d. patients should be sedated if cardioversion is done on a nonemergency basis.

b c d e

5. 5. The hemodynamic changes the nurse expects to find after successful initiation of intraaortic balloon pump therapy in a patient with cardiogenic shock include (select all that apply) a. decreased SV. b. decreased SVR. c. decreased PAWP. d. increased diastolic BP. e. decreased myocardial O2 consumption.

d

5. A barrier to hospice referrals for patients with stage D heart failure is; a. family member refusal. b. scarcity of hospice facilities. c. history of pacemaker placement. d. difficulty in estimating prognosis.

a b e

5. A patient is admitted to the ICU with a diagnosis of NSTEMI. Which drugs(s) would the nurse expect the patient to receive? (select all that apply) a. Oral statin therapy b. Antiplatelet therapy c Thrombolytic therapy d. Prophylactic antibiotics e. Intravenous nitroglycerin

a b d e

5. Nurses can screen patients at risk for developing chronic kidney disease. Those considered to be at increased risk include (select all that apply) a. older black patients. b. patients more than 60 years old. c. those with a history of pancreatitis. d. those with a history of hypertension. e. those with a history of type 2 diabetes.

ans: C

5. Which intervention is most likely to prevent or limit volutrauma in the patient with ARDS who is mechanically ventilated? a. Increasing PEEP b. Increasing the inspiratory flow rate c. Use of low tidal volume ventilation d. Suctioning the patient via endotracheal tube hourly

b c d

5. Which patient teaching points should the nurse include when providing discharge instructions to a patient with a new permanent pacemaker and the caregiver? (select all that apply) a. Avoid or limit air travel. b. Take and record a daily pulse rate. c. Obtain and wear a Medic Alert ID device at all times. d. Avoid lifting arm on the side of the pacemaker above shoulder. e. Do not use a microwave oven because it interferes with pacemaker function.

c

6. A patient is recovering from an uncomplicated MI. Which rehabilitation guideline is a priority to include in the teaching plan? a. Refrain from sexual activity for a minimum of 3 weeks. b. Plan a diet program that aims for a 1- to 2-lb weight loss per week. c. Begin an exercise program that aims for at least 5 30-minute sessions per week. d. Consider the use of erectile agents and prophylactic NTG before engaging in sexual activity.

c

6. Important teaching for the patient scheduled for a radiofrequency catheter ablation procedure includes explaining that a. ventricular bradycardia may be induced and treated during the procedure. b. catheter will be placed in both femoral arteries to allow double-catheter use. c. the procedure will destroy areas of the conduction system that are causing rapid heart rhythms. d. general anesthetic will be given to prevent the awareness of any "sudden cardiac death" experiences.

b c e

6. Patients are at risk for which complications in the first year after heart transplantation? (select all that apply) a. Cancer b. Infection c. Rejection d. Vasculopathy e. Sudden cardiac death

a b d

6. Patients with chronic kidney disease have an increased incidence of cardiovascular disease related to (select all that apply) a. hypertension. b. vascular calcifications. c. a genetic predisposition. d. hyperinsulinemia causing dyslipidemia. e. increased high-density lipoprotein levels.

a

6. The purpose of adding PEEP to positive pressure ventilation is to a. increase functional residual capacity and improve oxygenation. b. increase FIO2 to try to help wean the patient and avoid O2 toxicity. c. determine if the patient can be weaned and avoid pneumomediastinum. d. determine if the patient is in synchrony with the ventilator or needs to be paralyzed.

a b c

7. Nutritional support and management are essential across the entire continuum of chronic kidney disease. Which statements are true related to nutritional therapy? (select all that apply) a. Sodium and salt may be restricted in someone with advanced CKD. b. Fluid is not usually restricted for patients receiving peritoneal dialysis. c. Decreased fluid intake and a low-potassium diet are part of the diet for a patient receiving hemodialysis. d. Decreased fluid intake and a low-potassium diet are part of the diet for a patient receiving peritoneal dialysis. e. Decreased fluid intake and a diet in protein-rich foods are part of a diet for a patient receiving hemodialysis.

C

7. The most common finding in people at risk for sudden cardiac death is a. aortic valve disease. b. mitral valve disease. c. left ventricular dysfunction. d. atherosclerotic heart disease.

c

7. The nursing management of a patient with an artificial airway includes a. maintaining ET tube cuff pressure at 35 cm H2O. b. routine suctioning of the tube at least every 2 hours. c. observing for cardiac dysrhythmias during suctioning. d. preventing tube dislodgment by limiting mouth care to lubrication of the lips.

a

8. An ESRD patient receiving hemodialysis is considering asking a relative to donate a kidney for transplantation. In helping the patient decide about treatment, the nurse informs the patient that a. successful transplantation usually provides better quality of life than that offered by dialysis. b. if rejection of the transplanted kidney occurs, no further treatment for the renal failure is available. c. hemodialysis replaces the normal functions of the kidneys, and patients do not have to live with the continual fear of rejection. d. the immunosuppressive therapy after transplantation makes the person ineligible to receive other treatments if the kidney fails.

c

8. The nurse monitors the patient with positive pressure mechanical ventilation for a. paralytic ileus because pressure on the abdominal contents affects bowel motility. b. diuresis and sodium depletion because of increased release of atrial natriuretic peptide. c. signs of cardiovascular insufficiency because pressure in the chest impedes venous return. d. respiratory acidosis in a patient with COPD because of alveolar hyperventilation and increased PaO2 levels.

c d e

9. To assess the patency of a newly placed arteriovenous graft for dialysis, the nurse should (select all that apply) a. monitor the BP in the affected arm. b. irrigate the graft daily with low-dose heparin. c. palpate the area of the graft to feel a normal thrill. d. listen with a stethoscope over the graft to detect a bruit. e. assess the pulses and neurovascular status distal to the graft.

HYPOVOLEMIC SHOCK

= *Low circulating fluid volume caused by bleeding or fluid loss BY:* •Hemorrhage •GI bleed •Vomiting •Diarrhea •Fistula drainage •Diabetes insipidus •Hyperglycemia •Diuresis •SIGNS AND SYMPTOMS OF HYPOVOLEMIC SHOCK: •Increased HR (tachycardia) •Increased RR (tachypnea) •*Decreased BP (hypotension)* •Decreased stroke volume •*Decreased PAWP* •*Decreased urinary output <25ml/hr* •Anxiety •Cold clammy skin •Restless/agitation •*Ascites (third spacing seen with relative hypovolemia)* TREATMENT: - *Fluid/Volume Replacement:* •Pulmonary Arterial Pressure: PAOP low ( < 8 mmHg) •RAP low ( < 5 mmHg) •Right ventricular end-diastolic volume index low • *Type and cross-match for blood type* > •If blood loss is >30% then blood volume is replaced > •Two large bore IVs > •*Isotonic fluids (volume expanders), initiate vasoactive therapy - Keep MAP >60-65* >> •Monitor: vitals, cerebral pressures, abdominal pressures, capillary refill, urinary output, pulses, LOC >> •*STRICT I&Os → monitor urine output → want >30ml/hr* •*Vasopressors - phenylephrine, vasopressin & Inotropic/Vasopressors - norepinephrine, epinephrine, dopamine* - Nutrition •*Start enteral nutrition within 24 hours* •Slow drips of small amounts → increase as tolerated •Monitor protein, albumin, prealbumin, BUN, glucose, electrolytes •*NO TRENDLENBURG FOR LOW BP → Elevate legs only* •*Passive leg raise* may be used to assess preload responsiveness by using the patient's own blood volume to mimic a fluid bolus. • Position the patient in the semi-recumbent position with the head and torso elevated at 45 degrees. •Obtain a baseline measurement (i.e. baseline CO). •*Lower the patient's upper body and head to the horizontal position and raise and hold the legs at 45 degrees for one minute.* •Obtain subsequent measurement - a 10% increase in CO has been shown to predict fluid responsiveness. *We often calculate the initial fluid resuscitation using a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss)*

DISTRUBITUVE SHOCK

= ANAPHYLACTIC SHOCK & NEUROGENIC SHOCK ANAPHYLACTIC SHOCK: •*Acute allergic reaction to sensitizing substance (drug, chemical, vaccine, food, insect venom)* •Contact, inhalation, ingestion, or injection with antigen (allergen) previously sensitized to S/S: *Rash, chest pain, sense of impending doom, chest pain, wheezing/stridor, swelling lips, tongue, angioedema, respiratory distress* TREATMENT OF ANAPHYLACTIC SHOCK •Supplemental O2 to maintain PaO2 > 60 - 70 mmHg •CAB's - monitor and maintain hemodynamic status - *epinephrine & fluids* •Administer fluid volume expanders *NS, Lactated Ringers* large, via rapid bolus •One or two large bore IVs •Keep MAP >60-65 •Monitor: vitals, abdominal pressures, capillary refill, urinary output, pulses, LOC •STRICK I&Os → monitor urine output → >30ml/hr > •*Epinephrine immediate injection of 1:1, 000 aqueous solution, 0.1 to 0.5 ml, repeated every 5 to 20 minutes* > •*Maintain patent airway (assess for s/s narrowing airway - supplemental O2→ Bronchodilators, aerolized epinephrine* > •Anticipate need for advanced airway or mechanical ventilation > •*Diphenhydramine (Benadryl)* > *•Ranitidine (zantac)* > •IV corticosteroids if significant hypotension persists after 1-2 hours NEUROGENIC SHOCK: NEUROGENIC/DISTRIBUTIVE SHOCK: •*Hemodynamic condition that can occur within 30 minutes of a spinal cord injury at the 5th thoracic (T5) vertebra or above, can last up to 6 weeks.* •*Dysfunction directly related to level of spinal cord injury (cervical or high thoracic)* •Leads to pooling of blood in the vessels, tissue hypo-perfusion •Can also occur with certain medications (opioids, benzodiazepines). S/S: •*Profound Hypotension* •*Bradycardia!!!* •Difficulty regulating body temperature •*Skin is warm* due to massive vasodilation, may become cool as heat disperses resulting in *hypothermia* •Bowel & bladder dysfunction •*Flaccid paralysis and loss of reflexes below level of lesion* TREATMENT: •Maintain patent airway •Provide supplemental O2 •Intubation/mechanical ventilation if needed •Monitor body temperature •Minimize spinal cord trauma with stabilization •*Cautious! administration of fluids because hypotension is NOT related to fluid loss* •Vasopressors (phenylephrine) •*Atropine for bradycardia* - If the cause is spinal cord injury, general measures to promote spinal stability (e.g., spinal precautions, cervical stabilization with a collar) are initially used.

AKI

AKI can develop over hours or days with progressive elevations of blood urea nitrogen (BUN), creatinine, and potassium with or without a reduction in urine output. CAUSES: - Prerenal: > *The oliguria is caused by a decrease in circulating blood volume* (e.g., severe dehydration, heart failure [HF], decreased cardiac output). Prerenal oliguria is readily reversible with appropriate treatment - Intrarenal: > *conditions that cause direct damage to the kidney tissue*. prolonged ischemia, nephrotoxins (e.g., aminoglycoside antibiotics, contrast media), hemoglobin released from hemolyzed red blood cells (RBCs), or myoglobin released from necrotic muscle cells. > *Acute tubular necrosis (ATN)* is the most common intrarenal cause of AKI in hospitalized patients. It is primarily the result of ischemia, nephrotoxins, or sepsis. •Potentially reversible •Post-infectious (strep, hepatitis, varicella) •Common causes while hospitalized: major surgery, shock, sepsis, blood transfusion reaction, muscle injury from trauma, and prolonged hypotension - Postrenal: •*Causes include mechanical obstruction of outflow*: •Benign prostatic hyperplasia (BPH) •Prostate cancer •Calculi (stones) •Trauma •Extrarenal tumors •Bilateral ureteral obstruction S/S: •RIFLE classification: describes stages of AKI •Risk (R) •Injury (I) •Failure (F) •Loss (L) •End-stage renal disease (E) Clinically, AKI may progress through phases: oliguric, diuretic, and recovery. When a patient does not recover from AKI, CKD may develop. OLIGURIC PHASE (1): - Urinary changes- oliguria •*Urinary output less than 400 mL/day* •Occurs within 1 to 7 days after injury •Lasts 10 to 14 days •Urinalysis may show casts, RBCs, WBCs - Fluid volume: •Hypovolemia may exacerbate AKI •Decreased urine output → *fluid retention:* > •Neck veins distended > •Bounding pulse > •Edema > •Hypertension •Fluid overload can lead to heart failure, pulmonary edema, and pericardial and pleural effusions - *Metabolic acidosis:* •Impaired kidney cannot excrete hydrogen ions •Serum bicarbonate production is decreased •Severe acidosis develops •*Kussmaul respirations* - Sodium balance •Increased excretion of sodium •*Hyponatremia* can lead to cerebral edema - *Potassium excess:* •Impaired ability of kidneys to excrete potassium •Increased risk with massive tissue trauma •Usually asymptomatic •ECG changes = peaked T waves - Hematologic disorders •Leukocytosis (High WBC) - Waste product accumulation •*Elevated BUN and serum creatinine levels* - Neurologic disorders •Fatigue and difficulty concentrating •Seizures, stupor, coma DIURETIC PHASE: *•Daily urine output is 1 to 3 L* •May reach 5 L or more •Monitor for *hyponatremia, hypokalemia, and dehydration* RECOVERY PHASE: •May take up to 12 months for kidney function to stabilize *The recovery phase begins when the GFR increases, allowing the BUN and serum creatinine levels to decrease.*

acute decompensated heart failure

Acute Decompensated Heart Failure (ADHF) *•Sudden onset of signs and symptoms of HF* •Requires urgent medical care •Pulmonary and systemic congestion due to ↑ left-sided and right-sided filling pressures •Early → increased pulmonary venous pressure > •*Increase in the respiratory rate* > •*Decrease in PaO2* •Later → interstitial edema > •*Tachypnea* •Further progression → *alveolar edema* > •*Respiratory acidemia* •Life-threatening situation - alveoli fill with fluid -most commonly associated with left-sided HF S/S: •Increasing Shortness of breath •Changes in level of consciousness •*Pulmonary edema → when they breathe → may hear Crackles in all lung fields* •Early → from increased pulmonary venous pressure > •Increase in respiratory rate *(tachypnea)* > •*Decrease in PaO2* (normal 80-100) •Later → Interstitial edema > •Tachypnea > •Alveolar edema > •Respiratory Acidemia *(resp. acidosis)* •*Can manifest as flash pulmonary edema (Extreme ADHF)* •Life-threatening situation → alveoli fill with blood (like drowning) •*Most commonly associated with left sided heart failure* *Classic symptoms of Pulmonary edema:* - *JVD* •Anxious, agitated •Cyanosis, cool clammy skin •Dyspnea, decrease in oxygen saturation •*Orthopnea (cannot lay down)* •Tachypnea, abdominal breathing (use of accessory muscles) •*Cough with frothy, blood-tinged sputum (fluid from alveoli)* •Crackles and wheezes •Tachycardia •Hypo or hypertension •Abnormal Heart sounds > •S1 (lub) and S2 (dub) are normal heart sounds > •*S3 and S4 are abnormal (extra) heart sounds → Like a gallop* Patients with ADHF are categorized into 1 of 4 groups based on hemodynamic and clinical status: dry-warm, dry-cold, wet-warm, and wet-cold. The most common presentation in patients with ADHF is the wet and warm patient. A patient is "wet" due to volume overload (e.g., congestion, dyspnea) but "warm" due to adequate perfusion (warm skin, positive pulses). CARE: •Continuous monitoring and assessment: > •Vital signs > •Oxygen saturation > •Urinary output (foley catheter insertion) >> •*Diuretics to help get rid of some of the extra fluid* •*Hemodynamic monitoring (arterial line, CVP, PA catheter)* •Supplemental oxygen > •Keep oxygen saturation 94%, or as ordered > •Mechanical ventilation if unstable •High-Fowlers position > •*High-Fowlers is good but if you can sit them on end of bed if legs dangling its best* •*Ultrafiltration - Continuous Renal Replacement Therapy (CRRT) help to remove excess fluid* •Care for ADHF & Chronic Heart Failure: •Oxygen therapy > •For dyspnea and fatigue relief > •Support to get the pulse Ox above 94% •Physical and emotional rest > •Conserve energy and decrease oxygen needs •Structured exercise program > •Cardiac Rehabilitation is associated with better outcomes •Cardiomems system > •Implantable monitoring device •Implantable cardioverter defibrillator (AICD)

Aneuyrsm

Aneurysm is a diseased area of an artery causing dilation and thinning of the wall. - Several types can be viewed in the image to the right - Aortic aneurysms •Thoracic aortic •Thoraco-abdominal aortic •Abdominal aortic •Treatment based on size and symptoms •False versus true - need diagnostic evaluation •Pseudoaneurysm - blood vessel wall is injured, leaking blood collects in surrounding tissue - sometimes causing a false aneurysm •*True aneurysm causes the artery or vessel to weaken and bulge, which may form a blood-filled sac* vRisk of rupture, requires monitoring until it reaches the size that negates surgical intervention. - Abdominal Aortic aneurysm §¾ occur in abdominal aorta (most occur below the renal arteries) §¼ occur in thoracic area §Outpouching or dilation of arterial wall §Common problem involving aorta but may occur in other locations §Occur in white men most often; Increase incidence with age Appearances of Aortic Aneurysms: - Sacular - bulges or balloons out only on one side of the blood vessel - Fusiform → (more common) bulges or balloons out on all sides of the blood vessel (like old garden hose with bubble) - Dissection → Torn layers of the blood vessel wall allows blood to flow between the layers causing them to separate further. > When the aortic wall separates, blood cannot flow freely, this may cause the aortic wall to burst. COMPLICATIONS: *•Rupture- Serious complication (Life threatening)* > Rupture into retroperitoneal space: •Bleeding may be tamponade by surrounding structures, preventing exsanguination and death •Severe back pain •*Grey Turner's Sign → Back/flank bruising (ecchymosis) (classic NCLEX question)* - Rupture into thoracic or abdominal cavity: •Massive hemorrhage > •Hypovolemic shock with tachycardia, hypotension, pale clammy skin, decreased urine output, altered level of consciousness, abdominal tenderness •Most do not survive long enough to get to the hospital → Bleeding out results in hypovolemic shock INDICATIONS OF RUPTURE: •Diaphoresis •Pallor •Weakness •Tachycardia •*Hypotension* •Abdominal, back, groin, or periumbilical pain •Changes in level of consciousness *•Pulsating abdominal mass → NEVER palpate!* •Nausea/vomiting - Pain •Sudden intense severe chest or back pain •*Sharp, worst pain ever (tearing, ripping, or stabbing)* •Does not respond to medications •*STAT CT* - Aortic Dissection •Blood is leaking in intima (inner and outer layers of the artery) can be sudden or gradual •Ascending aorta or aortic arch •*EMERGENCY/Life-threatening → Can progress rapidly* •Immediate surgical intervention •Chronic Hypertension hastens the process TYPE A ANEURYSM: •Involved aortic arch → High cardiac output area •Cardiac tamponade → Blood can leak into pericardial sac and put pressure on heart, restricts contraction •Heart will still get electrical impulse but will not be able to pump •*Needle in pericardial sac to drain fluid OR Pericardial window* TYPE B: •Thoracic and abdominal aneurysm TREATMENT: - •Aneurysms < 5 cm in diameter and no symptoms: = monitor regularly oUltrasound or CT scan oTreat hypertension: drug of choice is beta blockers, which may slow growth oIndividuals diagnosed with Marfan's syndrome are treated sooner than later - Thoracic aneurysm causing symptoms or > *6 cm:* oSurgical repair o*Dissection: immediate surgery* oAggressive tx of HTN and heart rate control: Labetalol IV infusion - Post-Operative: Evaluation for Abdominal Aneurysm graft procedure •Patent graft •Distal perfusion → hands and feet > oTemp > oColor > oCap refill > oSensation and movement •Adequate urine output •Monitor for infection •Assess all systems routinely •Encourage turning, coughing and deep breathing while splinting the incision.

Modes of mechanical ventilation

Assist Control (AC) / Continous Mandartory Ventilation > Volume Mode: - *Total mechanical ventilation, each breath is delivered at the present volume* - if pt triggers own breath, set TV is delivered to pt - this mode is used to decrease the work of breathing and considered a resting mode AC/ CMV : - set tidal voume will not vary - peak airway pressure will vary - set RR - all breaths will be delivered at the presnt volume - no pressure support - can have PEEP - peak flow sensitivity set by the respiratory Synchronized Intermittent Mechnical Ventilation (SIMV) > Volume Mode: - Pt will receive preset number of breaths by the ventilator at a preset tidal volume - *pt is able to breathe spontanously on their own* - TV will vary for spontanous breaths, dependent on pt resp effort and lung compliance - *ventilator will sync pt spontanoues breaths with set RR* Pressure Support: - used in SIMV, CPAP, or during breathing trial pre-extubation - Inspiratory positive pressure - As the ventilator sense the pt taking a spontanous breath the preset amount of pressure support will be delivered to augment the patients spontanois breath - pressure supoprt should be set to acheive a spontanoues tidal volume of 5-6 mL/kg Noninvasive Positive-Presure Ventilation: CPAP - *a set amount of pressure remains in the lungs at all times* - this mode is totally spontanoues. no set rate or tiddal volume - the patient breaths at their own spontanoues tidal volumes - used is OSA, COPD, pulmonary edeam, early hypoemxia

CAD Continued

CARE: Aging adult considerations with CAD: §Especially when symptomatic or hospitalized •The need to modify physical activity: •Longer warm, up •Longer periods of low-level activity •Longer rest periods - Avoid extremes of temperature •Promote physical fitness, weight reduction •Reduction of > 10% of systolic blood pressure •Decrease LDL and increase HDL •Decrease saturated fats & cholesterol •Increase complex carbohydrates and fiber •Decrease consumption of red meat, egg yolks, whole milk •Increase consumption of Omega-3 fatty acids DRUG THERAPY: Lipid lowering drug therapy - used when diet & exercise ineffective - Inhibits synthesis of cholesterol in the liver oStatins - inhibit cholesterol synthesis, decrease LDL, increase HDL > *Simvastatin (Zocor): Increased risk for rhabdomyolysis when used with fibric acid derivatives (e.g., gemfibrozil [Lopid]), niacin (Niaspan), or erythromycin.* • *Manifestations of rhabdomyolysis include high creatine kinase levels and muscle pain.* oMonitor liver function (lipid profile) for damage and for myopathy - Niacin - lowers LDL & triglyceride by inhibiting synthesis, increases HDL. oS/E - *flushing, pruritus, GI, orthostatic hypotension* > Premedicate with aspirin or NSAID 30 minutes before taking to reduce flushing. - Fibric acid derivatives gemfibrozil (Lopid) - decreases triglycerides and increases HDL oS/E - GI N/V hypoglycemia - Increase Lipoprotein Removal - Bile Acid Sequestrants - Decrease Cholesterol Absorption -ezetimbe (Zetia) - Antiplatelets: lower the risk of heart attack, stroke, blood clot formation, or occlusion of stents. *(Aspirin)*

CKD

CKD has many different causes. *The leading ones are diabetes (about 50%) and hypertension (about 25%)* *CKD as either the presence of kidney damage or a decreased GFR less than 60 mL/min/1.73 m2 for longer than 3 months.* The last stage of kidney disease, end-stage renal disease (ESRD), occurs when the GFR is less than 15 mL/min. At this point, RRT (dialysis or transplantation) is required to maintain life. S/S: - *Uremia* is a syndrome in which kidney function declines to the point that symptoms may develop in multiple body systems: *GFR IS 15 OR LESS* - As the GFR decreases, the BUN and serum creatinine levels increase. Significant increases in BUN contribute to nausea, vomiting, lethargy, fatigue, impaired thought processes, and headaches. - hyperkalemia - met acidosis - anemia - defect in platelet function - infection - CVD - Kussmaul breathing - *Stomatitis with exudates and ulcerations, a metallic taste in the mouth, and uremic fetor (a urinous odor of the breath)* - weight loss, malnutrition, constipatoin - lethargy, apathy, decreased ability to concentrate, fatigue, irritability, and altered mental ability. - hypocalcemia DIAGNOSTIC STUDIES: - UA - GFR DRUG THERAPY: • Calcium supplementation, phosphate binders, or both • Antihypertensive therapy • ACE inhibitors or ARBs • Erythropoietin therapy (ANEMIA) • Lipid-lowering drugs (STATINS) - Acute hyperkalemia may need treatment with IV glucose and insulin or IV 10% calcium gluconate. > Sodium polystyrene sulfonate NUTRITION: - resitrct sodium & potassium & phosphate -

ARF clinical manifestations

CLINICAL MANIFESTATIONS: •Sudden or gradual onset > •*A sudden decrease in PaO2 or rapid increase in PaCO2 implies a serious condition or life-threatening emergency* •Signs of respiratory failure are related to: > •Extent of changes in PaO2 or PaCO2 > •Speed of change > •Ability for compensation to occur •Failure of compensatory mechanisms leads to respiratory failure > •Frequent assessment is a priority Lack of O2: > decreased LOC > sodoum retention > peripheral edema > AKI > mental changes >> Restlessness, confusion, and agitation suggest inadequate O2 delivery to the brain. >> a morning headache and slow respiratory rate with decreased level of consciousness may indicate problems with CO2 removal. > Tachycardia, tachypnea, slight diaphoresis, and mild hypertension are early signs of ARF > Cyanosis (late) HYPOXEMIA: (Shallow breathing pattern) Respiratory : Dyspnea *Tachypnea* Prolonged expiration Nasal flaring Intercostal muscle retraction Use of accessory muscles in respiration ↓ SpO2 (<90%) Paradoxical chest or abdominal wall movement with respiratory cycle (late) Cyanosis (late) Tachycardia Hypertension *Skin cool, clammy, and diaphoretic* HYPERCAPNIC: (slower resp rate) Dyspnea Use of tripod position Pursed-lip breathing Limited chest wall movement *↓ Respiratory rate or rapid rate with shallow respirations* ↓ Tidal volume ↓ Minute ventilation Hypertension Tachycardia Bounding pulse Muscle weakness ↓ Deep tendon reflexes Tremors, seizures (late) •First sign of respiratory failure is a change in mental status AFTER looking at PaO2 and PaCO2 •*Decreased O2 = restlessness, confusion, agitation* •*Increased CO2 = morning headache, decreased RR, and decreased LOC* •Priority: immediate assessment of ability to breathe and provide assistive measures •May require intubation and mechanical ventilation Auscultate breath sounds: •Fine crackles: pulmonary edema •Coarse crackles: fluid in airways •Absent or diminished: atelectasis, pneumonia, or hypoventilation •Bronchial: consolidation •Pleural friction rub: pneumonia involving pleura

More cardiac tings

Central Venous Oxygen Saturation (ScVO2) - *ScVO2: measures O2 saturation of venous blood* §Demonstrates the relationship balance between O2 delivery & O2 consumption (supply & demand). §A decreased ScVO2 % indicates increased O2 consumption, or decreased O2 supply - *Normal ScVO2 is 60 - 80%*, *< 60% = impaired tissue oxygenation!* - ScVO2 < 30% results in anaerobic metabolism and lactic acidosis (very useful in septic shock patients) •Influenced by: acid base imbalance, hemorrhage, hypoxia and decreased CO > *•Blood gas analysis* of mixed venous blood sample from distal port of the *pulmonary artery (PA) catheter (yellow port).* > •Can also be obtained from CVP in superior vena cava or right atrium is Decreased with: Anemia §Anxiety §Hypovolemia §Cardiogenic Shock §CHF §Fever, hyperthermia, shivering §Suctioning *TREATMENT FOR LOW Low ScVO2:* §Optimize preload/volume - *give fluids* §Optimize afterload/vascular resistance §Optimize oxygen content - *intubate/mechanically ventilate or increase hemoglobin via RBC transfusion.* §Optimize contractility - *start inotropic agent (improves systemic venous & pulmonary congestion)* - is Increased with: §Anesthesia §Hypothermia §Neuromuscular blockade §Sepsis §Sleep §Vasodilation *TREATMENT High ScvO2:* §Maintain optimal preload, afterload, contractility and oxygen content. §Most common cause is maldistribution of blood flow related to sepsis, and inability to use O2 at the cellular level. STROKE VOLUME: •*Stroke Volume (SV) = the amount of blood ejected from the heart into systemic circulation with each contraction.* •Stroke Volume Index (SVI) = stroke volume adjusted to the body surface area. • *If low, indicates pump performance (LV dysfunction), or hypovolemia (preload)* •Individuals with LV dysfunction (contractility), a slow HR can produce decrease in CO > •Bradycardias & tachycardia's are potentially dangerous as they may result in decreased CO if adequate SV is not maintained •Increased systemic vascular resistance (afterload) and cardiac valve dysfunction can cause decreased SV/SVI •*If high, vascular resistance is low (sepsis, use of vasodilators, neurogenic shock, and anaphylaxis)* •*Normal Stroke Volume (SV): 60 - 100 ml/beat (CO / HR x 1000)* EJECTION FRACTION: •Ejection - the amount of blood pumped out of the left ventricle during each heart beat. •Fraction - refers to the fact that some blood remains in the ventricle with each heart beat. •*Ejection Fraction (EF) = the % of blood within the chamber that is pumped out with each beat.* *•LEVF 55% - 75% is considered normal* •LVEF 40% - 49% mild disfunction •LVEF 30% - 39% moderate disfunction •LVEF less than 30% severe dysfunction MAP: •Reflects changes between CO and Systemic Vascular Resistance (SVR). *•Normal 70 - 110* •*SBP and MAP are indicators of LV function.* •The MAP reflects the arterial pressure in the vessels that is perfusing the organs. •*Low MAP - decreased blood flow to organs.* •*High MAP - increased cardiac workload.* ARTERIAL LINE (A-LINE) •*Most common site is radial*, although femoral may be used. •*Pt BP continuously monitored through A-Line, real-time monitoring.* •ABGs and other labs can be drawn off A-Line. •Uses a pressurized system. •*Ensure Modified Allen's Test performed prior to insertion.* •Monitor for 5 P's •A VAMP may or not be in use. ZEROING AN A LINE •The phlebostatic axis marks *the atria of the heart.* *•Placing the transducer ABOVE phlebostatic axis causes falsely LOW blood pressure.* *•Placing the transducer BELOW the phlebostatic axis causes falsely HIGH blood pressure.* •The transducer is "zeroed" to atmospheric pressure to reduce the influence on the tubing and transducer. •*Zeroing occurs: upon placement of A-line, pressure cable disconnection, or in determining of accuracy of BP.* •*Must be leveled if patients position changes.* Pulmonary Artery Catheter (Swan-Ganz): INDICATIONS: - Assessment of repsonse to therapy in patients with pulmonary HTN and mixed types of shocks - Cardiogenic shock - MI w complications - HF

Ventilator Tings

Common Ventilator Alarms: *High peak pressure:* triggered when pressure increases, stop inspiration to prevent barotrauma > *assess for kinks in system* > *assess patient for anxiety* , biting, coughing, decreased lung compliance, pneumothorax > assess for water trapped in system > *obstruction* *Low Pressure*/ Low PEEP/CPAP Triggered when pressure decreases in circuit > * First assess for leak or ventilation disconnection* > *THEN ! if persists, ventilate pt with bag valve attached to EET* *Low Exhaled Tidal Volume:* *Volume exhaled is 10% below set VT* > *assess for circuit disconnection* > *assess for leak in ETT cuff* > if has chest tube assess for increase in air leak in system > assess lung compliance *High Exhaled Tidal Volume:* *Volume exhaled is 10% above set VT* > *assess pt for increased RR - anxiety, pain, hypoxemia, metabolic acidosis* > *assess for excess water in tubing*

Hemodynamic Monitoring

Common indications for hemodynamic monitoring: §*Shock states (Sepsis, Hypovolemic, Cardiogenic, Anaphylaxis)* §*MI with significant right and/or left ventricular failure* §Hypotension or hypertension §Cardiac Tamponade §(Acute Respiratory Distress Syndrome (ARDS)* §Post Open Heart Surgery/Post operative care §Guide fluid resuscitation §Evaluate Cardiac Output (CO) Physical parameters indicative of low CO: §*Change in LOC or AMS* §Mean Arterial Pressure - MAP < 60 -65% (>60% to perfuse organs adequately §*JVD* §*Crackles* §*SOB* §*Peripheral edema* §Tachycardia or Bradycardia §Decreased urinary output §Decreased pulses §Cool extremities §Pallor §*Decreased capillary refill* §Markedly reduced bowel sounds Physical Assessment: How does the nurse assess circulation? - Neurological: LOC/AMS, confusion, feeling of doom, obtunded - Cardiac: Systolic BP < 90 or MAP < 65 * needs to be addressed ◦MAP < 65 decreased tissue perfusion & *MAP < 60 inadequate tissue and organ perfusion* ◦MAP = 2 x Diastolic + Systolic / 3 Ex. 120/60 = 240/3 = MAP 80 Pulse Pressure - difference between SBP & DBP, normal 40-60mm/Hg ◦Narrow/decreased - shock state or HF (insufficient preload leading to reduced CO) ◦Wide/increased - may occur during exercise or in those with atherosclerosis of larger arteries; increased ICP > ◦Jugular Vein Distension (JVD) > ◦Tachycardia or Bradycardia may be seen - Pulmonary: Abnormal or adventitious breath sounds - Gastro Intestinal: ◦Hypoactive or absent bowel sounds ◦Nausea or vomiting ◦Paralytic Ileus - Renal: *Urine output less than 0.5mL/kg/hr (average 30mL/hr)* - Integumentary: ◦Blood shunting from skin in low cardiac states ◦Breakdown ◦Capillary refill > 3 seconds ◦Diminished or absent pulses ◦Cold, clammy, cyanotic ◦Peripheral edema

MI Continued

DIAGNOSTIC STUDIES: - *Coronary angiography* •*For patients with a STEMI (urgent need)* •Not for patients with unstable angina or NSTEMI (stabilize then treat) - Pharmacologic stress testing: •For patients with abnormal but non-diagnostic ECG and negative biomarkers - Cardiac Catheterization for CAD •Diagnostic •Interventional > •*Percutaneous coronary intervention (PCI)* > •*Balloon angioplasty* > •Stent >>>> oPost stent placement anticoagulant & antiplatelet as stent is a foreign body and blood will try to collect on it. INITIAL INTERVENTIONS FOR MI §*12 lead EKG* (compare to previous EKG if possible) §Baseline physical & neurologic assessment §Upright position, *NPO (except for meds) Then Low salt, low saturated fats, low cholesterol diet* §*Oxygen → JUST enough to keep O2 above 93%* §*IV access (2) large bore = 20 gauge or 18 preferred* §*Nitroglycerin (sublingual) and ASA (chewable) 324mg* §*Statin* §*Morphine - opioid analgesic = given for pain, air hunger* §Nitroglycerin (SL) (use cautiously with RCA/Inferior wall MI) > Decreases preload and afterload while increasing the myocardial O2 supply, may cause hypotension *STEMI → Within 90 minutes DOOR TO BALLOON (cardiac Cath lab)* ONGOING INTERVENTIONS FOR MI §Frequent monitoring of vital signs §Treat dysrhythmias §*Complete bed rest for 12-24 hours* §Anxiety reduction §*ASA (chewable) 325mg, then daily 325 - 81 mg Antiplatelet (loading dose) clopidogrel/Plavix, or ticagrelor/Brilinta* Unstable Angina or NSTEMI o*Dual antiplatelet therapy and heparin* oWhen stable → Cardiac catheterization w/ percutaneous coronary intervention (PCI) oReperfusion therapy Drugs affecting platelets: oASA oGlycoprotein IIb/IIIa inhibitors prevent platelet aggregation and thrombus formation, mainly used during and after coronary artery angioplasty > abciximab/ReoPro > eptifibatide/Integrilin > tirofiban/Aggrastat •Beta-blockers = metoprolol tartrate, end in -olol •Nitrates •ACE inhibitors = end in -pril, S/E = dry cough, angioedema - switch to ARB if not tolerating •Anti-dysrhythmics CARE FOR CARDIAC CATH: - Preprocedure: •*Assess for allergies, especially contrast dye.* •Assess patients home medications •Perform baseline assessment *which systems? •*NPO 6-12 hours prior* •Assess baseline laboratory diagnostics * which values? •Provide education about procedure and post procedure •Administer medications as ordered •Complete preprocedural checklist will include, EKG, CXR, H&P, Lab values, consents etc - Postprocedure: •Perform assessment and compare to baseline •Assess pulses, color, sensation, warmth of extremity •*Observe access insertion site for hematoma and bleeding every 15 minutes for the 1st hour, then follow protocol.* •Monitor patient for chest pain •Maintain bedrest as ordered after femoral access, no closure 6 hours, with a closure device OOB in 2 hours, may turn side to side with assistance •*Affected extremity is kept straight and HOB no greater than 30 degrees until hemostasis is adequately achieved!!!* •Maintain IV and/or oral fluid intake and monitor urinary output •Provide discharge education

ARF

DIAGNOSTIC STUDIES: Most common: •*Chest x-ray* •*ABG analysis/pulse oximetry* Others: •CBC, serum electrolytes, urinalysis •12-lead ECG •Blood and sputum cultures •CT scan or V/Q scan •End tidal CO2 ( with mechanical ventilation) CARE: > Respiratory Therapy: >> *O2* >> Secretions can be mobilized by *proper positioning, effective coughing, chest physiotherapy, suctioning, humidification, hydration, and, when possible, early ambulation.* >> *Positioning: good lung down,* allows for improved V/Q matching in the affected lung. Pulmonary blood flow and ventilation are better in dependent lung areas. This position allows secretions to drain out of the affected lung so they can be removed with suctioning. For example, place a patient with right-sided pneumonia on the left side. This will maximize ventilation and perfusion in the "good" lung and aid in secretion removal from the affected lung (postural drainage). >> CPAP/BIPAP >> *Intubation, mechanical ventilation if supplemental O2 cannot maintain acceptable PaO2 & PaCO2 levels* DRUG THERAPY: > *Corticosteroids (e.g., IV methylprednisolone [Solu-Medrol]) *are often used in combination with other drugs, such as bronchodilators, for relief of inflammation and bronchospasm. (monitor potassium) > *short-acting bronchodilators (e.g., albuterol)*, may be given at 15- to 30-minute intervals until a response occurs. Give these drugs using a hand-held nebulizer or a metered-dose inhaler with a spacer. Side effects include tachycardia and hypertension. > Use of *IV diuretics (e.g., furosemide [Lasix]), morphine, or nitroglycerin can decrease pulmonary congestion caused by HF.* > IV antibiotics are often given to treat infection. > Benzodiazepines (e.g., lorazepam, midazolam), and opioids (e.g., morphine, fentanyl) may decrease anxiety, restlessness, and pain.

AKI CONT

DX: •Thorough history •Serum creatinine increased •Urinalysis •Kidney ultrasonography •Renal scan •CT scan •Renal biopsy - Contraindicated: •*MRI with gadolinium contrast medium* •Magnetic resonance angiography (MRA) with gadolinium *contrast* medium > •Nephrogenic systemic fibrosis > •Contrast-induced nephropathy (CIN) CARE: •Accurate intake and output •Daily weights •Assess for signs of hypervolemia or hypovolemia •Assess for potassium and sodium disturbances •Meticulous aseptic technique •Careful use of nephrotoxic drugs •Skin care measures/mouth care •Ensure adequate intravascular volume and cardiac output > •Force fluids > •Loop diuretics (e.g., furosemide [Lasix]) > •Osmotic diuretics (e.g., mannitol) •Closely monitor fluid intake during oliguric phase - *Hyperkalemia:* > Insulin and sodium bicarbonate > Calcium carbonate > Sodium polystyrene sulfonate (Kayexalate) - Indications for renal replacement therapy (RRT): •Volume overload •Elevated serum potassium level •Metabolic acidosis •BUN level > 120 mg/dL (43 mmol/L) •Significant change in mental status •Pericarditis, pericardial effusion, or cardiac tamponade •Peritoneal dialysis (PD) = Not frequently used •*Intermittent hemodialysis (HD)* •Continuous renal replacement therapy (CRRT) > •Cannulation of artery and vein NUTRTIONAL: •Maintain adequate caloric intake •*Primarily carbohydrates and fat* •Recommended protein intake •0.8 to 1.0 g of protein per kilogram of desired body weight •*Restrict sodium* •Increase dietary fat •Enteral nutrition

Terms r/t mechanical ventilation

FIO2 = fractional inspired oxygen *(21%-100%)* Rate: *the set number of breaths* the ventilation will deliver to the patient in volume control and pressure conrolled ventilation Tidal Volume (VT/TV) = determined by height and ideal body weight. *7-9 mL/kg of ideal body weight for normal lungs.* PEEP = Positive End Expiratory Pressure; is a set amount of pressure that remains in the lungs at the end of expiration; used to imporve oxygenation; *3-5 cm H2O pressure* I:E ratio = Inspiratory:Expiratory Ratio; Represents the length of inspiratory time to expiratory time. *Normal ratio is 1:2*; a longer expiratory time is needed by patients who have COPD because of the decreased elasticity of their lungs; can be inversed in pressured controlled ventilation and APRV Sensitivity = a set parameter that determines how much effort the patient must exert to trigger the ventilatior to deliver a breath; can be set by pressure or flow; setting may need to be adjusted for high spine injuries Flow patterns = determine how the breath is delivered by the ventilator Inspiratory Time (I Time) = length o time allowed for inspiration; Can be set in the following modes of ventilation: pressure control ventilation, VC mode, Bilevel