MedSurg 1 final exam 2 Guide With Expert Accurate Answers

MedSurg 1 final exam 2 Guide With Expert Accurate Answers Med Surg Final Neuro: Constricted pupils= miosis dilated pupils= mydriasis Patient has unequal pupils first ask for baseline. Always assume neuro problem until proven otherwise. Assess patients spo2 and glucose levels if patients appears altered. Hypoxia and hypercapnia will affect mental status. Medical management for pt with altered LOC→ ● Airway! -Intubation may be required ● Circulation-Maintaining BP (MAP >60), HR, Perfusion of brain, IV access – IVF, meds ● Nutrition- OGT (oral gastric tube), PEG ● With inc ICP do not want to give hypotonic solutions /D5W only hypertonic such as Mannitol to draw fluid out of cells ● Potential complications of altered LOC→ ○ Pneumonia (aspiration PNA), Aspiration, Pressure ulcer, DVT, Contractures (not using muscles so muscles can shorten) need to do passive ROM to help preserve joint mobility ICP→ ● Monro-kellie hypothesis: Bleeding or swelling within the skull INC the volume of contents within the skull and therefore causes increased ICP. CAN LEAD TO IRREVERSIBLE BRAIN DAMAGE ○ ICP is pressure from the CSF and blood volume and cranial contents (dynamic equilibrium) normal ICP is 5-15mmHg ○ Inc ICP from head trauma (>15mmHg) ○ Whenever there is a shift, it can cause inc ICP ○ Our body compensates by pouring out CSF ○ When body cannot compensate, pressures are elevated above 15 ○ Patient will be in cheyne stokes breathing: very irregular breathing ● Complications→ ○ Compensation to maintain normal ICP is normally accomplished by shifting or displacing CSF ○ With disease or injury ICP may increase ○ Increased ICP ■ decreases cerebral perfusion ischemia, cell death, and (further) edema ○ Brain tissues may shift through the dura (outermost layer of brain and spinal cord) and result in herniation ○ Autoregulation: refers to the brain’s ability to change the diameter of blood vessels to maintain cerebral blood flow (via vasomotor center) ○ CO2 plays a role: ■ decreased CO2 results in vasoconstriction ■ increased CO2 results in vasodilation ○ Chemoreceptors sense CO2, blood acidity, to try to maintain normal cerebral perfusion ● Vasomotor center:○ ANS that regulates SNS and PNS ○ Inc ICP can be injury to vasomotor center that can cause high BP, low HR ○ Baroreceptors are pressure centers that monitor BP ○ If pt is retaining CO2, (COPD, not breathing bc of opioid overdose) causes vessels in brain to dilate, if vessels are dilated it causes more blood flow and volume into cranial vault that only has so much room to take in volume ○ When you blow off CO2 it causes vessels to constrict ● Cerebral edema → ○ Inc ICP= dec perfusion which leads to tissue hypoxia In brain which leads to cerebral edema which worsens ICP ○ One way that brain tries to compensate is the body inc BP to get blood flow to the ischemic brain tissue to try to maintain cerebral perfusion ● ICP and CPP→ ○ CPP (cerebral perfusion pressure) is closely linked to ICP ○ CPP = MAP (mean arterial pressure) – ICP ○ Normal MAP is 70 – 110 mmHg (average pressure within arteries during one cardiac cycle) ○ MAP MAP = SBP + (DBP X 2)/3 ○ Normal ICP is 5 – 15 mmHg ○ Normal CPP is 70 to 100mmHg ○ Heart dysrhythmias can lower CPP. ○ A CPP of less than 50 can result in permanent neurologic damage ■ Dec blood flow to brain tissue ○ Need a CPP > 70 to maintain adequate tissue perfusion ● Increased ICP→ ○ Early signs→ ■ EARLIEST SIGN – CHANGE IN LOC ■ Restlessness, agitation, sudden quietness, disorientation, mental fog (confusion, forgetfulness, repetitive questioning, slowing of speech,) ■ increased resp. effort, purposeless movements, Pupillary changes, impaired EOM (effects of pressure on midbrain/brainstem (CN II, III, IV, VI) ■ Weakness in one extremity or on one side of the body ■ Headache that is constant, increasing in intensity and aggravated by movement or straining ○ Late signs=vasomotor problems→○ ■ Continued deterioration of LOC, Erratic pulse and RR (or may decrease), BP & temp increase, Widening pulse pressure, Altered breathing patterns, Projectile vomiting, Hemiplegia, Abnormal posturing, Bilateral flaccidity before death, Loss of brain stem reflexes: pupillary, corneal, gag, swallowing (their loss is an ominous sign of approaching death) ○ The RAS system is what gives us our alertness and wakeful state ○ Monitor for cushing’s triad = LATE SIGN OF INC ICP→ Dec resp, low HR, systolic hypertension (widening pulse pressure) ■ Monitor CLOSELY for complications: brain stem herniation, DI, SIADH, cerebral edema, hypoxia, hypercapnia, impaired venous return, increases in intrathoracic pressures or abdominal pressures ■ Occurs due to so much pressure building up within cranium that blood and brain tissue needs to go somewhere so it starts to herniate ■ High pressure→ low pressure ■ HR dec bc of reflex bradycardia due to baroreceptors ■ Has widening pulse pressure ■ May have issues with regulating temp bc of hypothalamus ■ If this does not get fixed they can go into autonomic dysreflexia – autonomic dysfunction ● Management for ICP→ ○ Decreasing cerebral edema ■ IV mannitol – osmotic diuretic to dehydrate brain tissue; monitor I&O & serum osmolality to assess hydration ■ Decadron (steroid) - if edema caused by brain tumor ■ Fluid restriction ○ Maintaining CPP ■ manipulating CO with fluidS ■ Inotropics (Dobutamine, Levophed) to maintain CPP >60/ 70 mmHg ○ Reduce CSF & Intracranial Blood Volume ■ CSF drainage via ventriculostomy ■ Keep pCO2 35 – 38 (low pCO2 produces cerebral vasoconstriction (induce hyperventilation) ○ Maintain Oxygenation & Reduce Metabolic Demands ■ Mechanical ventilation – Keep pO2 80-100; pCO2 35-38 ■ Barbiturate Coma – sedation■ Prevent pneumonia by performing routine mouth care. ■ Neuromuscular blockers – paralyze to reduce agitation – NEED SEDATION as well ■ Opioids – decrease agitation; provide analgesia ■ Tape eyes shut, protect eyes, may need artificial tears. ■ No rectal temps will increase pressure, no oral temp, use foley catheter for temp ■ Neuro checks unreliable when sedated – use ICP monitoring, VS, response to mechanical vent; sedation vacation 1x daily ■ Control fever – hypothermia blanket better than Tylenol ■ Perform passive muscle movement to maintain muscle mass and joint movement. ■ Never use restrains can worsen icp ■ Avoid hypotonic saline/ D5W makes cells swell. Bad for increased icp. ● Interventions→ ○ VS q 1-2 hrs. – may need more often depending on acuity ○ Monitor resp. status – maintain patent airway ○ Avoid PEEP ○ Suctioning cautiously – can elevate ICP; pre-oxygenate & limit time ○ HOB elevated at least 30 degrees ○ Maintain head midline neutral position – avoid extreme neck flexion or hyperextension ○ Log roll – avoid hip flexion ○ Avoid/prevent valsalvas, abd. distention ○ Maintain calm atmosphere, space activities, protect pt. from stress ○ Monitor fluid status – I&O q 1 h ○ Monitor ICP - Strict aseptic technique with ICP cath/monitor ● Brain herniation → ○ Results from excessive increase in ICP ■ pressure builds with cranium ■ brain tissue presses down on the brain stem ■ cerebral blood flow ceases → anoxia & brain death ○ Life-threatening brainstem herniation ○ Uncal – shift of one or both areas of temporal lobe ■ Dilated & non-reactive (fixed) pupils ■ Rapid deterioration of LOC ■ Ptosis (eyelid drooping) – pressure on cranial nerve III ■ Causing shifting from high → low pressure■ Uncal herniation causes dilated pupil on the side of the problem ○ Central – downward shift of brainstem & diencephalon ■ Bilateral Dilated pupil (SNS innervation) & non-reactive (fixed) pupils ■ Hyperventilation (Compensating for inc ICP and CO2) ■ Cheyne-Stokes (erratic breathing patterns, breathing rapidly then slow) ■ Hypotension ■ May push brain through foramen magnum causing instant death ● Assessment for herniation → ○ Head CT – eval cause of ICP, MRI, Cerebral angiography ○ *LP (lumbar puncture-tests CSF) avoided (contraindicated with inc ICP)– 2/2 to sudden release of pressure in the Lumbar region can cause brain to herniate ● Complications→ ○ Brain stem herniation – excessive ICP, Brain tissue presses down on the brain stem ○ DI ■ Dec secretion of ADH ■ Excess UO (FVD, hypovolemic shock) ■ Dec urine osmo (hypernatremia) urine is dilute (low specific gravity) ■ Serum hyperosmo (viscous) ■ To treat we need to give them Desmopressin ○ SIADH ■ Increases secretion of ADH ■ FVO – dilutional hyponatremia (leads to further cerebral edema by causing fluid to shift into cells) ■ Decreased UO (specific gravity is high and concentrated (1.030) ■ Treated with fluid restriction ■ Seizures can occur ○ Problem with posterior pituitary , Normal body osmo is 2x Na ICP monitoring the device needs to be level with the foramen of monro one inch above ear ● Glascow Coma Scale→ ○ a neurological scale which aims to give a reliable and objective way of recording the state of a person's consciousness ○ 15 – 3 (15=alert and responsive, 3= severe impairment) looks at the best eye movement and response (less than 8= intubate) ○ 15 = fully responsive 3 = coma ● Decorticate posturing: CORE arms flex to the CORE of body 3*● Decerebrate posturing: CERE side, arms extended to the side of the body. (considered worse) 2* Brain hemispheres Temporal region: Side of head - hearing (houses auditory cortex) frontal lobe: front of head - memories, emotions, reasoning parietal lobe: top of head - processing sensory, visual, language*, math cerebellum: back bottom of head- balance* and coordination Occipital: above cerebellum-visual process CVA- clinical manifestation, dx tests, treatment guidelines (bp management), T-PA: - Disruption in the cerebral blood flow - Ischemic (from a thrombus) - Hemorrhage (artery ruptures due to uncontrolled BP or trauma) -Embolism -Do not give thrombolytics with hemorrhagic stroke -Document balance and gait to assess for cerebellar stroke Most common blocked artery is MCA middle cerebral artery -Get a CAT scan to see if it is hemorrhagic or ischemic Transient ischemic attack: “mini stroke” temporary block of blood. No brain impairment or neuro deficit. Type S/S TreatmentIschemic (causes) Large artery thrombosis Small penetrating artery thrombosis Cardiogenic embolic Cryptogenic (no known cause) Other – drugs Numbness / weakness of face, arm, or leg ***on one side of the body Change in MS Difficulty speaking Visual changes Gait disturbance *Afib, Valve Dz Anticoagulation Platelet inhibiting medications Thrombotic therapy rt-PA (<60 min GOAL) <3 hours- window) Sx: CEA (carotid enterectomy) Intracerebral Hemorrhage (causes) Subarachnoid hemorrhage Cerebral aneurysm Arteriovenous malformation Meds –AC Intracranial neoplasms yu Headache Sluggish pupil response Decreased LOC (early) Uncontrolled HTN Vomiting focal seizure Bed rest- sedation – prevent agitation, stress, vasospasm Manage ICP Surgery – craniotomy Clips – aneurysms IR- Endovascular tech *hold AC Antidotes if needed Neuro Deficit Manifestation Visual Field Hemianopsia (half the visual loss in one or both eyes) Loss of peripheral vision Diplopia (double vision) Motor Hemiparesis (weakness) Hemiplegia (paralysis) Ataxia (unsteady gait) Dysarthria (difficulty speaking) Dysphagia (difficulty swallowing) Sensory Paresthesias ProprioceptionNeuro Deficit Manifestation Verbal Aphasia Expressive (difficulty speaking) Receptive (inability to understand language) Global (mixture between the 2) Cognitive Memory loss Decreased attention span Can’t concentrate Altered judgment ● When was the onset of the stroke is the most important question ● Balance, eyes, face, arms, speech, time BE FAST ● Dx→ Head CT <25 min of arrival ■ Ischemic – further eval Where is it coming from? ○ EKG /Carotid US – standard tests (a fib, a flutter) ○ CT Angio ○ MRI/ MRA – brain and neck vessels ○ LP (lumbar puncture to assess for blood, subtle hemorrhagic stroke, LAST RESORT ) ● Medical management→ ○ Ischemic stroke- ■ Anticoagulation , Platelet inhibiting medications , Thrombotic therapy ● t-PA (need to assess for bleeding, CONTRAINDICATED) ● These are weight based need accurate patient weight ● Uncontrolled HTN cannot get tpa, Recent stroke cannot get tpa, Recent surgery cannot get tpa ○ Osmotic diuretics ○ Sx: CEA, hemicraniectomy ○ Criteria for TPA→ ■ Age ≥18 years and Time of onset of stroke known and is within center guidelines ■ SBP ≤185 mm Hg; diastolic ≤110 mm Hg ■ No minor stroke or rapidly resolving stroke■ No seizure at onset of stroke ■ Not taking warfarin (Coumadin) , Platelet count ≥100,000/mm3 ■ PT≤15 seconds or international normalized ratio ≤1.7 ■ Not received heparin during the past 48 hours with elevated PTT ■ No prior intracranial hemorrhage, neoplasm, arteriovenous malformation, or aneurysm ■ No major surgical procedures within 14 days ■ No stroke, serious head injury, or intracranial surgery within 3 months ■ No GI or urinary bleeding within 21 days ● Interventions→ ○ Vital signs Q l to 2 hr. HCP > SBP180 mm Hg or diastolic greater than 110 mm Hg ○ Monitor the client’s temperature ■ A fever can cause ICP ■ Cva to hypothalamus may cause the temperature to rise ○ Monitor for changes in the client’s level of consciousness ○ Oxygen therapy ■ to maintain the client’s oxygen saturation level >92%, or if the client’s level of consciousness is decreased ○ Place the client on a cardiac monitor to detect arrhythmias ○ Elevate the client’s head of the bed approximately 30° ■ reduce ICP and to promote venous drainage ○ Avoid extreme flexion or extension of the neck, and maintain the client’s head in the midline neutral position ○ Institute seizure precautions ○ Improve mobility and prevent joint deformities ○ Enhance self-care ○ Managing sensory-perceptual problems ○ Dysphagia – Aspiration precautions ■ Swallow assessment - <24hours of arrival ○ Bowel and bladder control ○ Improve thought process ○ Improve communication ○ Maintain skin integrity ○ If someone is having an ischemic stroke you want BP on higher side bc blood will reach brain faster (permissive hypertension) ○ Contraindicated with hemorrhagic stroke (want BP down in controlled manner)Cerebral hypoxia Decreased cerebral blood flow Extension of the area of injury Oxygenation BP mgmt Avoid hypo/hypertension H/H WNL Maintain CO Adequate hydration Head Injury: ● Nursing management→ ○ Respiratory status – the priority assessment ■ The brain is dependent upon oxygen to maintain function and has little reserve available if oxygen is deprived. ○ Changes in LOC ■ GCS, which provides the earliest indication of neurological deterioration ○ CN function (eye blink response, gag reflex, tongue and shoulder movement) ○ Pupillary changes (PERRLA) ○ Bilateral sensory and motor responses ○ Intracranial pressure (ICP) monitoring ○ Dec ICP ■ HOB > 30 ■ Airway, 02 PRN, hyperventilate to keep normal PaC02 ■ Calm environment ■ Implement measures to prevent complications from immobilization ○ Adequate fluids – to maintain cerebral perfusion Seizure characteristics: SEIZURE TYPE DURATION SYMPTOMS POSTICTAL MEDS PARTIAL SEIZURES Localized or involves one hemisphere of brainSIMPLE PARTIAL 90 sec Abn movement Sensory phenomena No LOC Transient weakness or sensory loss *phenytoin (Dilantin) *carbamazepine (Tegretol) phenobarbital (Luminal) levetiracetam (Keppra) COMPLEX PARTIAL 1-2 min Aura possible Automatisms Wandering, unaware of surrounding +LOC Amnesia Mild/mod confusion *Phenytoin *Carbamazepine Levetiracetam GENERALIZ ED SEIZURE Bilateral & symmetric – nonspecific point of origin TONIC CLONIC Grand mal 1-2 min Cry, fall, cyanosis, Tonic – muscle contraction Clonic – jerking motion Amnesia Confusion Deep sleep *Phenytoin ABSENCE 2-15 sec Brief LOC; blank staring/daydreaming look *common in PEDS Amnesia No confusion *valproate (Depakote) ethosuximide (Zarontin) clonazepam (Klonopin)STATUS EPILEPTICU S Acute prolonged seizure occurring w/o full recovery of consciousness between attacks - Life threatening emergency STATUS EPILEPTICU S > 5 - 10 min or repeated seizures over course of 30 min. prolonged seizure occurring w/o full recovery of consciousness between attacks Confusion, Loss of bowel/bladder control, Irregular breathing, Difficulty speaking Diazepam Ativan *Phenytoin Phenobarbital, Cerebryx IVF – D5W or NS Status epilepticus→ is an emergency because the pt is not breathing fully which causes decreased oxygen to the brain. ● Establish an airway – intubate & oxygenate ● Start IV – NS or D5W if cause is hypoglycemia ● Stop seizures – IV push Ativan or Valium followed by IV Dilantin (phenytoin) or Cerebyx (fosphenytoin)loading dose; phenobarb if need to help maintain seizure-free ● Protect from injury ● Neuro checks & VS ● Monitor serum levels of anti seizure meds Phenytoin (dilantin) 10-20 ug/ml Nursing management→ ● Observation and documentation of patient signs and symptoms before (pre-ictal), during, and after seizure (postictal) ● Nursing actions during seizure for patient safety and protection – risk for injury, hypoxia, & aspiration ● After seizure care, prevent complications as above Myasthenia Gravis→ Chronic autoimmune neuromuscular disorder characterized by: fatigue & severe weakness in skeletal muscles (caused by autoantibody attack on AcH receptors in the muscle end-plate membrane)● Remissions & exacerbations ● Incidence: Age 20 – 30 yrs, Women 3:1 s/s→ ○ Ocular – ptosis, diplopia ○ Facial – dysarthria (difficulty of speech), dysphagia (difficulty swallowing), difficulty chewing, altered facial expression ○ Musculoskeletal ■ Weakness and fatigue ■ Decreased function - hand, arm, leg & neck muscles; impaired fine motor movements of hands appear early ○ Respiratory ■ Weakened intercostal muscles & decreased diaphragm movement ■ Dyspnea ○ Bladder & bowel incontinence ● Nursing management→ ○ Promote rest & energy conservation ○ Respiratory support – maintain effective airway clearance ○ Assist with communication ○ Maintain nutritional support –impaired swallowing – aspiration precautions; dysphagia diet; SLP & nutritional consult ○ Eye protection ○ Patient/Family TeachingMultiple Sclerosis→ autoimmune demyelination of CNS, onset 25-35 years common in females, may be due to virus exposure, periods of remissions and exacerbations, risk greater when first degree relative affected. Temperature extremes hot or cold can exacerbate symptoms. ● s/s→ ○ Sensory loss ○ Visual deficits – blurred vision/ red-green color distortion ○ Weakness ○ Paresthesias ○ Ataxia ○ Vertigo ○ Fatigue ○ Depression ○ Stiffness, slowness ○ bladder and bowel dysfunction, (May be on anticholinergic meds to help with urination) ● RN interventions→ ○ Maintain mobility ○ Proper nutrition ○ Pain management ○ Collaborate with PT ■ Active ■ Resistive ■ Stretching ■ *maintain muscle tone, joint mobility, dec spasticity, improve coordination ○ Emotional stability ■ Daily routine ○ Medications: no cure only disease modifying therapy, interferon beta 1a (avonex & Rebif) anti inflammatory interferon beta 1b (betaseron) immunosuppressive drugs Copaxone: patient on long term steroids is at high risk for infection Parkinson’s Disease→ too little dopamine ● a slow progressive neurologic movement disorder that eventually leads to disability ● 4th most common neurodegenerative disease● M > F ● s/s→ ○ Resting Tremors – resting tremors (prominent at rest - hands at sides or on lap) subside with intentional motion; commonly “pill-rolling” motion; increase with concentration or anxiety ○ Rigidity – resistance to passive movement; “lead-pipe” (total& constant) or “cogwheel” (jerky) rigidity; mask-like face ○ Bradykinesia – slow “shuffling” gait; difficulty turning over in bed or rising from chair; reduced fine motor coordination – smaller handwriting; reduced automatic movements - arm swing, blinking, swallowing, chewing, uncontrolled drooling ○ Postural instability – flexed posture (forward tilt/flexed trunk); difficulty pivoting; impaired balance; propulsive gait ○ Autonomic symptoms – excessive and uncontrolled sweating, paroxysmal flushing, orthostatic hypotension, gastric and urinary retention, constipation, sexual dysfunction ○ Psychosocial changes – depression, dementia, delirium, and hallucinations; personality changes, rapid mood swings, psychosis, and acute confusion, sleep disturbances ○ Auditory and visual hallucinations may occur ○ Dysphonia (soft, slurred, low-pitched, monotonous, and less audible speech) occurs ● Nursing interventions→ ○ Improving Mobility & Enhancing Self-Care ■ Progressive daily exercise program ■ ROM/joint mobility, stretching exercises ■ Postural exercises ■ Walking techniques for safety and balance ■ Proper shoes ■ Warm baths; massage ■ Consultation with PT & OT ■ Modify environment ■ Use of assistive devices ■ Frequent rest periods ○ Improving Swallowing & Nutrition ■ Prevent aspiration – upright during meals ■ Semisolid diet; thickened liquids ■ Small, frequent meals ■ Chewing & swallowing techniques ■ Adaptive utensils■ Supplements as needed ■ Nutritional consult ■ Monitor weekly weights ○ Improving Communication ■ Speech therapy consult ■ Speak slowly, pause frequently ■ Electronic amplifier ○ Improving Bowel Elimination ■ Establish regular bowel routine ■ Increased fluids & fiber ■ Raised toilet seat ○ Support Coping Abilities & Promote Independence in Daily Activities ■ Observe for depression, dementia ■ Assess family coping ■ Community resources & support groups; respite care CN assessment→ ● OOOTTAFAGVAH→ ○ I=olfactory (smell) ○ II=optic (snellen chart 20 feet) ○ III=oculomotor (eye movement) test III, IV, VI together ○ IV=trochlear (eye movement) ○ V=trigeminal (sensation to the skin of the face and controls the muscles of mastication) ○ VI=Abducens (eye movement) ○ VII=facial (controls muscles of facial expression and is involved in taste) ○ VIII=vestibulocochlear (involved in the process of hearing and balance) ○ IX=glossopharyngeal (oral sensation, taste and salivation) ○ X=vagus (controls muscles of the larynx and pharynx) ○ XI=accessory (responsible for shoulder shrugging and head turning) ○ XII=hypoglossal (tongue movement)Respiratory: Pulmonary embolism Risk factors- trauma, pregnancy, HF, hypercoagulable states, immobility (virchow’s triad- blood stasis, blood vessel injury and hypercoagulable state (factor 5, birth control)) Major s/s- pleuritic pain, anxiety, cough, edema, low O2, dyspnea Pathophysiology- due to a blood clot or thrombus, hemodynamic consequences- increase in pulmonary vasculature due to vasoconstriction and decreased size of vein, increase pulmonary arterial pressure → increased right ventricular work → decreased cardiac output Dysrhythmias = poor blood flow (more at risk for PE) FVE leading cor pulmonale (backing up of fluid) s/s rt sided HF= dependent edema (blood pooling and going backwards into systemic circulation), JVD, hepatomegaly (congestion in liver) PE can cause pulmonary infarction (ischemia) Assessment- Inspection- diaphoretic, anxious, can’t complete a full sentence, dyspnea, cough, leg swelling, pleuritic pain, feeling of impending doom Palpation- bounding pulse Auscultation- crackles, decreased breath sounds, heart murmur (S3, S4), pleural friction rub Vital signs- decreased BP (seen because of ventricular failure → blood pooling → decreased venous return), increased HR, increased RR, low grade temp, decreased O2 satDiagnosis- ABG (initial low PaCO2), CBC (HgB and Hct), D-dimer (increased level= suspicion for clot), chest CT, VQ scan, pulmonary angiography (ABG → resp alkalosis → resp acidosis). ABG- low pCO2 because you're blowing it off (tachypnea) initially. Going to be in resp Alkalosis Then when body starts decompensating it will go into resp acidosis (bradypnea) Changes on EKG with pt with PE Intervention and treatment- O2 therapy, high fowler’s, anticoagulants, exercise, pain management, IVC filter, ambulation, anti-embolism stockings, initiate/maintain TV access), avoid vitamin K food, embolectomy, monitor for decrease in BP, tachycardia and JVD. Pneumothorax: •Parietal or visceral pleura is breached & the pleural space is exposed to + atmospheric pressure –*intra-thoracic (neg pressure – needed for lung inflation) •When air enters pleural space –Lung or portion of lung collapses Types of pneumothorax: •Simple Pneumothorax – spontaneous –Healthy, atraumatic(underlying connective tissue disorders) •Traumatic pneumothorax •Stab wound chest wall ● Invasive procedures -Central line placement (jugulars, apices of lung are right above clavicle) ● May have secondary -Open pneumothorax -Hemothorax -accumulation of blood in pleural space •Tension pneumothorax (one way valve where air cannot escape out) –air is drawn into the pleural space through a small opening in the chest wall. –Air enters the chest with each inspiration and becomes trapped – cannot be expelled during expiation •Think one way valve •With each breath (+ pressure / tension) will cause an increase in pleural space •Causes lung to collapse & heart great vessels, & trachea to shift toward the unaffected side (mediastinal shift) Hyperresonance heard on percussion with pneumothorax (air) Dullness heard on percussion with hemothorax (blood)•Thoracotomy(hemothorax where they go into space and evacuate blood to try and find out where pt is bleeding from) May give chest tube with pneumo or hemo COPD→ Emphysema- loss of lung compliance, hyperinflation of lung tissue (think air trapping); chronic bronchitis- increased resistance due to inflammation of the bronchioles, inflammatory response due to chronic exposure to irritants → sputum production, airflow elimination problem, decreased tidal volume and decreased pulmonary compliance. -As COPD advances, the forced expiratory volume to forced vital capacity decreases. -COPD pts drive to breathe is hypoxic, too much given O2 can cause O2 toxicity ● Blue bloater (chronic bronchitis) → overweight and cyanotic, elevated hemoglobin, peripheral edema, rhonchi and wheezing. ● Goblet cells producing excess mucus, lack of macrophages leading to increased risk for dz, push vaccinations such as the flu and pneumonia. Decreased vital capacity and decreased FEV1/fvc ratio. Avoid being around people who are sick due to decreased immunity. Pink puffers (emphysema) older and thinner (hurts to eat), severe dyspnea, hyperinflation of lungs with distended diaphragm. Patient will be in respiratory acidosis. Sat of 80 maybe normal, paco2 of 47 maybe nor Assessment: inspection- clubbing of fingers, use of accessory muscles, barrel chest, cyanosis ● Palpation- decreased fremitus, decreased chest expansion ● Percussion- hyperresonance ● Auscultation- crackles/wheezing ● Vital signs- increased RR, shallow breathing, decreased O2 satmal. May have high levels of bi carb in the blood to compensate. Don't leave copd patient on oxygen too long, patient can stop breathing. Chronic hypercarbia: usually only 1-2 L/min via NC hypoxic drive: brain become sensitized to constant increased Co2 state. Copd will lead to right sided heart failure. Cor pulmonalePneumonia→ ● CAP→ ○ Community acquired pneumonia- one of us that gets it in the community ○ Strep pneumoniae (affects younger population that is healthy) ○ Pts who are older that are unhealthy tend to get different types of organisms that cause their -pneumonia (h. flu) ○ Children tend to get viral pneumonias ○ Treatment is antibiotics, clean equipment, mouth care ● HAP→ ○ Hospitals-pt gets pneumonia while in the hospital ○ exposed to plethora of different bacteria ○ harder to treat bacteria ○ bad hand hygiene by HCP ○ contaminated equipment ○ Treatment is antibiotics, clean equipment, mouth care ABGs→ Partial compensation- all three values are changed Full compensation- pH is within normal range but CO2 and HCO3 are changed No compensation- only one (HCO3 or CO2) and pH are different pH- 7.35-7.45 CO2- 35-45 HCO3- 22-26 Pleural effusion→ ● Risk factors- PNA, TB, trauma to chest, PE, CA, HF, renal pts, thoracotomy, Those with underlying lung infections, lung diseases, heart failure or renal failure (fluid volume overload) ● Pathophysiology- fluid accumulates in the pleural space secondary to an underlying disease process. 20cc or 20ml is normal fluid in the pleural space. Problem with capillary permeability and fluids cant drain out of this space. Increase in capillary permeability ● Permeability=leakability ● Fluid characteristics: Clear, bloody, purulent ● Thoracentesis (assist): Put pt sitting up right leaning over bedside table to expand lungs ○ Get culture and equipment ○ 4th or 5th intercostal space midaxillary line is where you draw it from ○ Hemothorax is another call for thoracentesis ○ Pneumothorax is 2ndintercostal space (air) ● Assessment- Inspection- breathing pattern, body posture, use of accessory muscles PNA pts: fever, chills, pleuritic chest pain CA pts: SOB, difficulty lying flat, coughing, hemoptysisPalpation- DECREASED tactile fremitus “99”, chest excursion-asymmetric Percussion- dullness where fluid is, resonance where air is Auscultation- decreased breath sounds, increased voice sounds ● Abnormal pressures at the capillary membrane that causes a lack of fluid to leak out of that space, therefore fluid tends to build up. ● S/S → chest pain, dyspnea, dry cough. ● Diagnostics → culture for pleural fluid, chest x-ray, chest CT, thoracentesis, pleural fluid analysis, pleural biopsy ● Interventions and treatment → discover the underlying condition, analgesics for pain, thoracentesis (CA pts may cause fluid to reaccumulate (pleural cath may be given)), chest tube management, pulmonary edema may result from removal of too much fluid too quickly (FVD) ● Pulmonary edema- fluid is INSIDE the lung ● Pleural effusion- fluid is OUTSIDE the lung Simple pneumothorax: spontaneous, healthy tall and skinny Hemothorax: blood in the pleural space, S/s tachycardia, dullness, pallor, anxiety. thoracentesis Tension pneumothorax: tracheal shift to the unaffected side, need chest tube Cardiac tamponade: distant heart sounds, JVD, decreased BP. pericardiocentesis removal of blood from around the heart. Pulmonary Embolism: blockage in the pulmonary artery, either air or embolism patient with long bone fractures. Flail chest: 3 or more fractured ribs, paradoxical chest movement. patient splinting affected side. Pleurisy (pleuritis) sharp stabbing pain. Worse on inspiration. Place patient on affected side to minimize expansion of lung. Cardiac: How blood flows through the heart: vein= blood going towards the heart artery= away Aorta sends blood to the body Blood ends up in the right atrium from superior and inferior vena cava→ goes through tricuspid valve to right ventricle → passes through the pulmonary valve → to right and left pulmonary ARTERIES (deoxygenated) → to the lungs where the blood becomes oxygenated → to the left atrium → goesinto left ventricle through bicuspid (mitral) valve → goes through aortic valve → aorta → the rest of the body Cardiac biomarkers: CK-MB normal range 3-5 % evident 3 days , TROPONIN I any elevation levels are bad (most accurate) , myoglobin earliest marker (not specific) , BMP brain natriuretic peptide- maker for heart failure. Dysrhythmias→ Normal sinus rhythm- ● Rhythm: Regular ● V/A Rate: 60 to 100 beats/minute ● P waves: Normal in size, shape, direction; positive in lead II; ● PR interval: Normal (0.12 to 0.20 second) ● QRS complex: Normal (0.12 second or less) ● P: QRS complex 1:1 ratio Rhythm: Regular Rate: 80 Sinus Bradycardia- Sinus node generating impulses slower than 60 beats per minute (Even tho its not “normal” some people normally have low HR, Runners, athletic people often have lower HRs, can be their normal) ● Causes → Low metabolic need – sleep, hypothermia, hypothyroidism ○ Vagal stimulation- vomiting, suctioning, pain or bearing down ○ Medications: beta blockers (olol), calcium channel blockers (dipines) ○ Increased intracranial pressure ○ Myocardial infarction- inferior wall ● S/S → dizzy/weak, confusion, syncope, hypotension, diaphoresis, SOB, anginal pain ● Management → limit vagal stimulation, if hemodynamically unstable; hold meds that slow pulse *test, take steps to inc HR, Atropine 0.5-1mg IV push (blocks vagal stimulation) parasympatholytic, prepare for pacing ● Rhythm: Regular ● Rate: < 60 beats/minuteSinus tachycardia- Sinus node generating impulses faster than 100 beats per minute ● Causes → Blood loss, anemia ○ Shock, hypovolemia, hyperkalemia, ○ Increased metabolic demands, fever ○ Exercise, Stress, and Anxiety ○ sympathomimetic drugs ● S/S → can be asymptomatic or weak, fatigued, SOB, DOE, orthopnea, JVD, restlessness, anxiety, anginal pain and palpitations ● Management → look for s/s of dec CO, shock, pulmonary edema ○ Fever, basic first aid ○ Meds: CCBs, Beta blockers ● Rhythm interpretation: Regular ● Rate: 100 to 120 beats/minuteHR is 110 because last R wave isn’t full QRST Sinus arrhythmia- sinus node impulse created an irregular rhythm ● Rate often ○ INCREASED with inspiration ○ DECREASED with expiration ● Non- Respi Causes ○ Heart disease ○ Valvular disease ● Usually not treated ● Usually does not cause hemodynamic decompensated states, if pt is decompensated check with them again, look for another explanation ● Rhythm interpretation: Irregular ● Rate: Normal (60 to 100 beats/minute) or slow (< 60 beats/minute; often seen with bradycardia) Rate- 50 bpm 1:1 ratio Rhythm – irregularPremature atrial contraction-Atrial ectopic beat (extra beat coming from a point other than the SA node) ● An impulse originating from the Atrium before next normal impulse of SA node ○ PAC depolarizes the SA node early ● Irritable site in atria-that take over for pacemaker for one or more beats ● s/s → “skip beat”, pulse deficit from apical to radial sites ● Stimulants → caffeine, nicotine, chocolate, OTC cold medication (Sudafed), alcohol, hypokalemia, anxiety, hypervolemia, inc metabolic states, atrial ischemia or infarction ● Management → usually not treated if infrequent ○ Greater than 6 per minute may signal worsening disease or more serious arrhythmia ○ Treat underlying cause → limit stimulants, coffee, hypoK ○ If frequent may lead to a fib ● Rhythm interpretation: irregular with PACs – SHORTER P-P INTERVAL (underlying rhythm may be regular) *early P wave ● Rate: That of underlying rhythm (ST) ● P waves: Premature and abnormal in size, shape or direction; abnormal P wave is often found hidden in preceding T wave, distorting T wave contour – MAY BE HIDDEN IN T WAVE Rhythm- irregular Rate- 90 bpm P wave- abnormal with PAC; some lost in previous T waves – hidden at complex 2, 4 and 6 Not a 1:1 ratio Atrial flutter- Atrial rate much faster than what AV node can conduct. Many impulses not conducted to ventricles ● *If all impulses did travel to ventricle would lead to V-Fib – LETHAL! ● Causes → COPD, valvular heart disease, CAD, pulmonary disease, hypertension, hyperthyroidism, holiday heart syndrome-ETOH excess ● A flutter has a lot of P waves (or “F” waves)● s/s → palpitations, weakness, fatigue, SOB, angina, hypotension, evidence of HF ● Management → first try vagal maneuvers (having pt bear down) ○ Medications to slow and convert rate ○ Rhythm control ■ Pharmacological Cardioversion ■ Adenosine (sympathetic block → slow conduction) 6-12-12 ■ Electrical Cardioversion (shocks to the heart to redirect impulses) – TEE, coumadin pre & post ■ Pacemaker implantation, catheter ablation, or surgical ablation (maze procedure), may be indicated for patients who do not respond to medications. ○ Rate control ■ Beta-blocker (propranolol [Inderal], atenolol [Tenormin], metoprolol [Lopressor], or esmolol [Brevibloc]) blocks beta 1 which dec HR ■ Calcium channel blockers (diltiazem or verapamil) – not with impaired vent. Function ○ Anticoagulation therapy- coumadin ● Rhythm interpretation: (Atrial) Regular ●● P waves: Sawtooth wave deflection affecting the entire baseline ● PR interval: Not measurable ○ QRS complex: Normal (0.10 second or less Rhythm- irregular Rate- 60 bpm P wave- not measurable PRI- not measurable T wave- unmeasurable Atrial fibrillation- disorganized twitching of atria (most common) ● Therefore no real p waves ● Impairs CO → rapid ventricular response, impaired ventricular filling, dec SV ● Chronic or paroxysmal(comes and goes)● Causes → COPD, valvular heart disease, CAD, pulmonary disease, hypertension, hyperthyroidism, holiday heart syndrome-ETOH excess ● s/s → asymptomatic or experiencing significant hemodynamic collapse ○ Altered LOC, hypotension, chest pain, pulmonary edema, especially with heart disease ● Management → ○ Rhythm control ■ Electrical Cardioversion – TEE, coumadin ■ Pharmacological Cardioversion ■ amiodarone, dofetilide (Tikosyn), ibutilide, flecainide, norpace, sotalol ■ Pre-op: beta blockers , amiodarone ■ Pacemaker implantation, catheter ablation, or surgical ablation (maze procedure), may be indicated for patients who do not respond to medications. ○ Rate control ■ Beta-blocker (propranolol [Inderal], atenolol [Tenormin], metoprolol [Lopressor], or esmolol [Brevibloc]) ■ Calcium channel blockers (diltiazem or verapamil) – not with impaired vent. Function ○ Anticoagulation therapy- coumadin ● Want to target rate first ● High risk of developing blood clots → DVT, PE, CVA ● Rhythm interpretation: Grossly irregular (unless ventricular rate is very rapid, in which case the rhythm becomes more regular) ● Rate: ● Atrial: 400 beats/minute or more; not measurable on surface ECG ● Ventricular: Varies with number of impulses conducted through atrioventricular node to ventricles; ● ventricular rate is controlled if rate is less than 100 beats/minute, uncontrolled if it is greater than 100 beats/minute ● P waves: Wave deflections that affect entire baseline ● PR interval: Not measurable ● QRS complex: Normal (0.10 second or less) ● “irregularly irregular → wavy baseline” Rhythm- irregularRate- 120 bpm P waves- absent PRI- unmeasurable Irregular, no P waves = automatically A FIB Premature ventricular contraction- ventricular ectopic beat → originates in ventricle before next normal sinus impulse ● Causes → in healthy people- stimulants, alcohol ○ Myocardial ischemia, infarction ○ CHF ○ Digitalis toxicity, hypoxia, acidosis, electrolyte disturbances ● s/s → “skipped beat” or palpitations ● Management → wait and see if less than 6 per minute, unifocal, not in pairs ○ Amiodarone or sotalol ○ Lidocaine IV push or drip ○ *Caution may be precursor to lethal dysrhythmia if persistent ● Rhythm interpretation: Underlying rhythm usually regular; irregular with PVC ● Rate: That of the underlying rhythm ● P waves: None associated w PVC ● PR interval: Not measurable w PVC ● QRS complex: Premature and wide (0.12 second or greater) Rhythm- irregular Rate- 120 bpm with PVCs P wave- not measurable PRI- not measurable PVC at complex 1, 7 and 11Ventricular tachycardia- Three or more PVCs in a row at a rate of greater than 100 beats per minute ● May be precursor for v-fib!! ● Ineffective pumping = dec CO ● Treatment determined by whether stable or unstable (determine by looking at hemodynamics) ● Etiology- as for PVCs ○ CAD, MI, ischemia ○ Cardiomyopathy ○ Electrolyte imbalance (esp K, Mg) ○ Meds (digoxin) ○ Reperfusion ● Management → PULSELESS VT treated same as VF – DEFIBRILLATE ○ •STABLE VT WITH PULSE – asymptomatic (cannot shock) ■ Continuing ■ assessment, especially obtaining a 12-lead ECG, may be the only action necessary. ○ IV amiodarone is the medication of choice for a patient with impaired cardiac function or acute MI. ■ Procainamide (Pronestyl) in patients who do not have acute MI or severe HF. ■ Sotalol – beta blocker ○ UNSTABLE VT WITH PULSE - symptomatic ■ CARDIOVERSION (can shock) – regular & monomorphic VT in a symptomatic patient ○ EF > 35% --- AMIODARONE ○ EF < 35% --- AICD (automatic implantable cardiac defibrillator) ● Rhythm interpretation: Regular ● Rate: 140 to 250 beats/minute ● P waves: None associated ● PR interval: Not measurable ● QRS complex: Wide (0.12 second or greater) Rhythm- regularRate- 180 bpm P waves- absent QRS- wide, 6 or 7 boxes Ventricular fibrillation- Complete electrical disorganization ventricular quivering instead of pumping ● Absence of atrial activity ● Causes → untreated v tach, myocardial ischemia and infarction, untreated electrolyte disturbances, hypoxia, acidosis, electrical shock ● Chaotic- pulseless (usually unconscious, no pulse) ● Management → v fib = de fib!! ○ No coordinated cardiac activity ○ CPR (Until de-fib) ○ Antiarrhythmics → amiodarone or lidocaine (caution CNS a/e) ○ Support BP ● Rhythm interpretation: Chaotic, irregular deflections ● Rate: 0 (P waves and QRS complexes absent) ● P waves: Absent; wavy, irregular deflections are present that vary in size, height, and shape ● PR interval: Not measurable ● QRS complex: AbsentAsystole- ● “Flat-line” ● Absence of electrical activity in myocardium ● Possible causes: ○ Power off ○ Leads or electrodes not attached ● CHECK PT. – LOC? PULSE? ● ALWAYS CHECK IN 2 LEADS to R/O fine V Fib ○ If V Fib → DEFIBRILLATE ● Asystole/PEA (Pulseless Electrical Activity – electrical activity with no pulses) – NONSHOCKABLE ○ CPR, Epinephrine Cardioversion- usually synched on pts R wave or counter shocked to pts underlying rhythm ● During ventricular depolarization ● Used during a-fib, a-flutter, v-tach with pulse ● Use a lot less jules (energy used when de-fibing) more beneficial and efficient to the heart Defibrillation- ● Use higher jules (200-300) ● V-fib, v-tach with no pulse ● Not synched Pacing- ● To control HR as a temporary measure Make sure nobody is touching pt when sending shock -safety Hemodynamics: ● Preload→ amount of blood in ventricles at end diastole ○ HF pts have inc preload (FVO) → diuretics lower, NTG lowers, morphine (venodilators) ○ Shock state pts want to inc preload○ RAP = CVP ● Afterload → resistance ventricles must push against to eject blood ○ Inc resistant = HTN → give ACE inhibitors (prills) to dec afterload ○ Resistance not enough → shock states → give vasopressor to inc afterload ○ Systemic vascular resistance is measurement of afterload ○ Afterload reduction → vasodilators ■ Nitroglycerine, nitroprusside, CCBs, ACE inhibitors, hydralazine ■ Dec afterload = improve workload of heart ○ Afterload increaser → vasopressors ■ Used in shock states → Epinephrine and norepinephrine, vasopressin, dopamine ● CO → amount of blood pumped in liters per min ○ CO = SV x HR ○ Normal is 4-8 Lpm ○ SV = amount of blood pumped with one ejection ○ MAP= mean arterial pressure ● Contractility → force of myocardium ○ Positive inotrope → inc HR and the strength of contractility (Epinephrine) ○ Negative inotrope → dec HR and the force of contractility (antiHTN) Contractility manipulation: ● Positive inotropes → directly stimulate the force of heart contraction (making heart pump more efficiently) e.g. digoxin ○ Beta 1 adrenergic- endogenous- catecholamines ■ Epinephrine and dopamine ○ Synthetic catecholamines ■ Dobutamine ○ Calcium → inc intracellular Ca+ = inc cellular contraction ■ Calcium gluconate and calcium chloride ○ Cardiac glycosides → inc influx of Ca+ into cardiac cells = inc contraction ■ Digoxin ● Always look at NA, K and Ca ● Negative inotropes → dec cardiac O2 demand (weaken force of contraction, antihypertensives) ○ Beta blockers → block epinephrine and NE → dec HR and BP ■ Metoprolol, atenolol, labetalol ○ Calcium channel blockers → block entry of Ca+ → dec workload of heart, relax blood vessels (dilate) → improve perfusion and dec BP ■ Diltiazem, verapamil, amlodipine, nifedipine Arterial pressure: AP = CO x PR ● Inc in PR (peripheral resistance) or CO will inc AP● Dec in PR or CO will dec AP ● PR is regulated by → constriction and dilation (of arterioles) Diastole → ventricles relax ● AV valves (mitral and tricuspid) open and blood flows from higher pressure atria to relaxed ventricles ● Atria contract → atrial kick ○ Aortic and pulmonic valves are closed allowing ventricles to fill Systole → ventricles contract ● Aortic and pulmonic valves open, and blood flows from the ventricles into the aorta and pulmonary artery ○ Mitral and tricuspid valves are closed ANS → responds rapidly (in seconds or mins) to acute changes in BP (baroreceptors), provides steady-state control ● in carotids and aortic arch ● When you drop HR, BP drops ● inhibit sympathetic nervous system response ● This is how BP maintains to be less than 120/80 RAAS → responds slowly, taking hours or days to influence AP ● Decreased BP or perfusion to kidneys during sympathetic response → causes renin aldosterone system ● 1. Kidneys then produce renin (a protein) that converts angiotensinogen (produced by liver), to hormone angiotensin 1 ● 2. Angiotensin 1 → angiotensin 2 (via the lungs) ● 3. Angiotensin 2 stimulate adrenal medulla to secrete aldosterone (stimulation of aldosterone retains sodium and water) whenever you have sodium, you have water increase volume into the kidney that isn’t being used during a stress response or blood vessel constriction by angiotensin 2 ● 4. Increased blood pressure ● High BP: prescriber may order an ACE inhibitor Kidneys → responsible for long-term control and may take days or weeks to adjust AP Drug terms that effect CO: ● Chronotropic → effect HR ● Inotropic → effect force of contraction ● Vasopressor → vasoconstriction → inc afterload (resistance in LV will inc) → inc BP ● Vasodilator → dec afterload → dec BP (antihypertensives are afterload reducers) Good volume = good CO ● Inc preload- FVO (HF pts) ● Dec preload- FVD (give isotonic fluids) Volume reducers → venodilators and diuretics ● Venodilators- morphine and nitroglycerin given to cardiac pts with chest pain● Diuretics- ○ Loop diuretics-inhibit reabsorption of Na ○ Osmotic diuretics ○ Thiazides- interferes with Na and Cl, H2O moves out ○ K sparing diuretics- aldosterone antagonists- reduce K excretion S3 fluid volume overload S4 noncompliant LV Heart failure: Heart failure: → heart is too weak to pump efficiently so it cannot provide proper CO to maintain metabolic needs Left sided HF → lungs, DROWNING Dyspnea..rales..orthopnea..weakness..nocturnal paroxysmal dyspnea(at night they will wake up with extreme difficulty breathing)..inc HR (trying to get blood to organs)..nagging cough(frothy blood tinged sputum)..gaining weight(2-3 lb in 5 weeks) ● Blood back flows through LA → lungs ● Crackles, SOB, orthopnea, pulm s/s ● Can inc pressure in RV, can cause pt into right sided HF ● Left systolic dysfunction → low ejection fraction (<40%) ○ Systolic = squeezing (contracting) ○ Fills normally ○ Amount of blood contracted out of LV ○ Normal EF is more than 50% ○ Can be diagnosed with echo, heart cath and nuclear stress test ● Left diastolic dysfunction → issue w ventricle being able to fill properly ○ Contraction in normal (EF is normal) Right sided → systemic, SWELLING Swelling of hands, legs, liver..weight gain..edema (pitting)..large neck vein (JVD)..lethargic..irregular HR(a fib)..nocturia(lying down allows fluid to go to kidneys)..girth ● Blood goes back through superior and inferior vena cava → systemic circulation ● Peripheral edema, excessive weight gain, JVD, ascites, hepatomegaly ● Not as common as left sided HF ○ Caused by cor pulmonale and left sided HF Labs: BNP will be ordered, CBC, BMP(biomarker that is released when pressure on heart) <100 is good Chest x ray, echo, heart cath, nuclear stress test Exacerbation of HF: ● High Na and fluid intake ● Infection ● Uncontrolled a fib ● Renal failure Nursing interventions: ● Assess symptoms ○ Presenting worse than before?○ Assess pts responsiveness to meds, asses edema ○ Watch BP (ACE, ARBs, vasodilators) ■ Risk for ortho hypo ○ Watch volume status ■ Diuretics ○ Monitor daily weights/ I&Os ○ Monitor K levels ○ Make sure pt is compliant with cardiac diet and fluid restriction ○ Put pt in high fowlers position ○ safety→ ortho hypotension, swelling feet → risk for falls ● Educate pt → follow low Na diet (no more than 2 g a day), fluid restriction (no more than 2L a day), need to get annual flu vaccine and need to be up to date on pneumococcal vaccine, aerobic exercise, daily weights (3 lbs per day or 5 lbs per week is bad), smoking cessation and limit EOTH Meds→ ● Angiotensin-converting enzyme (ACE) inhibitors ○ Vasodilation ○ monitor for hypotension, hyperkalemia, altered renal function; cough ● Hydralazine and isosorbide dinitrate ○ alternative to ACE inhibitors ● Beta-blockers ○ prescribed in addition to ACE inhibitors; may be several weeks before effects seen; use with caution in patients with asthma ● Diuretics ○ decreases fluid volume, monitor serum electrolytes ● Digitalis (pos inotrope) ○ improves contractility ○ monitor for digitalis toxicity especially if patient is hypokalemic ● IV medications ○ indicated for hospitalized patients admitted for acute decompensated HF ● Milrinone: decreases preload and afterload; causes hypotension and increased risk of atrial fib post cardiac surgery ● Natrecor: (vasodilator) recombinant BNP; vasodilator; useful to relieve dyspnea at rest/minimal activity; SE - prolonged hypotension Pericarditis→ ○ inflammation of the pericardium, acute or chronic, can reoccur ○ Causes: ■ usually viral ■ pericarditis can occur 10 days - 2 months after MI ■ chest trauma: injury, surgery, catheterization, pacemaker implantation ■ radiation therapy of chest/ upper torso ■ connective tissue disease (RA, SLE, Scleroderma) ■ Kidney injury (build up of waste products bc kidney is in failure and cannot function and excrete properly, which can cause pericarditis)○ Complications: ■ pericardial effusion (fluid accumulates in pericardium space) ■ cardiac tamponade from unrelieved pericardial effusion (builds up & causes tension) ○ Clinical manifestations: ■ Precordial chest pain (under clavicle, neck, scapula) ■ Increased by: breathing, coughing, swallowing, lying supine, turning, moving, flexing, rotation ■ Patient will say relief comes from sitting up and leaning forward ■ Fever ■ other: nonproductive cough, dyspnea, hiccups, tachycardia ○ Pericardial friction rub: characteristic and diagnosis sign ■ scratchy or creaky sound auscultated most clearly at left lower sternal border, 4th ICS, louder at the end of exhalation & heard better when patient is sitting up and leaning forward ■ know the difference from pleural friction rub by telling the patient to hold their breath, if its pericardial friction rub it will be heard when patient holds their breath ○ Diagnosis: S&S, echo, CT ○ Management: ■ bed rest is a very important measure ■ assist with activity ■ analgesics and rest for pain relief, NSAIDS, colchicine (very effective), corticosteroids ■ treat underlying cause ■ monitor S&S of HF ■ assist with pericardiocentesis (needle to relieve pressure & take out fluid if any) ■ ALERT FOR S&S OF CARDIAC TAMPONADE - falling systolic BP, narrowing pulse pressure, JVD, distant/muffled heart sounds CAD: Risk factors (that inc arteries of becoming atherosclerotic)- smoking, obesity, high cholesterol, sedentary lifestyle, diabetes, family hx Lifestyle changes- smoking cessation, diet (low fat, low calorie), losing weight, exercise, monitoring BP and HR, s/s when to seek help (chest pain) HDL- good lipoprotein LDL(what causes the plaque build up)- lousy lipoprotein ● Antiplatelets: keep plaque from forming and growing ○ Aspirin- watch for GI bleeding ○ Plavix- (if pt had stent placed or cannot take aspirin) ■ watch for TTP- thrombotic thrombocytopenic purpura: clotting disorder where small clots form in blood vessels → limits blood flow to vital organs… will see neuro changes in pt, renal failure, fever, bruising, low platelets and anemia ■ *will need to be discontinued 5-7 days before surgical procedure ● Nitroglycerine: dilates vessels to allow blood to get to the heart muscle○ Taken sublingual (tablet pill or spray) ○ Want pt to take when they are getting chest pain, take one tab 3x for every 5 mins, if not relieved → unstable angina → call 911!! ○ Do NOT give these to pts if they take phosphodiesterase inhibitors (viagra, levitra, or cialis) → hypotension ● Cholesterol meds “statins” → lipitor, zocor, crestor ○ Goal is to dec LDL to less than 100 mg/dl ○ Lower LDL, lower cholesterol, lower triglycerides and increase HDLs ○ Notify HCP if feeling muscle pain or weakness immediately ○ Watch CPK levels → med can inc CPK levels causing muscle weakness ○ Monitor liver function Stable angina: ● Not a medical emergency → needs evaluation ● May progress to unstable ● s/s → chest pain with activity (heaviness on chest), SOB, fatigue ● Relieved by rest or NTG ● Will order stress test, EKG, 24-48 hr holter monitor, blood tests (lipoprotein) Unstable angina: ● Chest pain at rest not relieved with NTG ● Medical emergency → treated immediately PCI- percutaneous coronary intervention: ● Balloon angioplasty → Inflate a balloon in clogged artery → compresses plaque on the artery wall and a stent is placed in to help keep it open...if artery is too occluded they will need CABG ● Artherectomy → removal of plaque from artery ● Post op assessment: temperature, infection, bleeding? Coronary artery bypass graft- CABG (open heart surgery): → A surgical procedure in which blood vessel is grafted to the occluded coronary artery so blood can flow beyond occlusion ● Commonly used vessels are internal mammary arteries & the greater and lesser saphenous vein. ● The vein is grafted to ascending aorta and coronary artery distal to the occlusion ● Indicated with someone has multivessel disease (When 3 main coronaries are occluded), alleviation of angina that cannot be controlled with meds, signs of impending MI after PTCA ● ECMO (post arrest – bridge device to transplant or LVD). ● Mid sternal incision; connect pt to CPB machine ○ Cannula is placed in rt atrium, vena cava or femoral vein. Blood removed from body is filtered, oxygenated, cooled or warmed by machine, and then returned to body. Return cannula is located in ascending aorta. Heart is stopped by injection of high potassium solution into coronary arteries. ● Maintain hypothermia to decrease met. Rate.Post-op care: ● LOC, Neurological assessment - pupils, reflexes, facial symmetry, hand grip ● V/S, temps (hypothermia, infection); HR & rhythm ● Respiratory status: - assess hypoxia- ATRIA; cyanosis, chest movement, breath sounds, ventilator settings, chest tube drainage (ALERT for cardiac tamponade), ABG’s; ● May be extubated 2-4 hrs after procedure - deep breathing coughing, incentive spirometry. T&P ● Hemodynamic monitoring – PA pressures, CVP, CO, CI ● Pain – location (incisional pain differentiated from angina); use PCA,NSAIDS oral or IV ● F/E status – FVE, FVD; Assess neck veins for distension; monitor K, Ca, Mg levels, I&O, urine specific gravity (know sodium, potassium and calcium) ● Assess for bleeding – monitor CBC, incisional, retroperitoneal, leg graft site ○ Do not apply pressure unless area is bleeding ● Peripheral vascular - assess pulses, color, temp, capillary refill, lips, earlobes, DVT prevention ● Prevent skin breakdown ● AMBULATE asap (either later that day or the following day) ● Look at pts K and Mg levels Hemorrhage , dysrhythmias, and MI USUALLY WANT A MAP > 70 --- LESS THAN 70 DEC TISSUE PERFUSION MAP = average pressure in a patient’s arteries during one cardiac cycle. BEST indicator of perfusion to vital organs than systolic blood pressure (SBP). 5 headaches- ● Hypothermia (or hyperthermia) any significant drop can inc metabolic demand and inc workload on heart ● Hypovolemia ● Hypotension ● Hypertension ● Hemorrhage 5 T’s for dysrhythmiasTamponade, tension pneumo, thrombus (cardiac and pulm), toxins, trauma Intra-arterial pressure monitoring via radial artery line: RN assessment: ● Allen's test → make sure pt has good blood perfusion ● MAP = (systolic x 2 x diastolic) / 3 ● Check for 5 P’s → pulselessness, pallor (perfusion problem), pain, paresthesia, paralysis ● Direct arterial pressure monitoring ● Cath is placed and sutured into radial artery to get continuous BP monitoring ● Can get arterial blood ● Get second to second fluctuations to BP ● Make sure there is sensation to fingertips MI: ● Patho → limited blood supply to myocardial tissue that causes it to die or become necrotic ● Causes → blockage in coronary artery (CAD), coronary spasm (drug use (cocaine) or uncontrolled HTN), damage to artery due to coronary artery dissection (tear in artery) which causes blood to leak into tunica media → common in women and can happen spontaneously● Job of coronary arteries is to supply fresh blood to heart muscle ● NSTEMI → (non ST segment elevation MI) ○ Thrombus partially/intermittently occludes coronary artery ○ Elevated bio-marker TI = cardiac cells have died ○ ST depression or T wave inversion = ischemia ● STEMI → (ST segment elevation MI) ○ Thrombus completely occludes coronary artery ○ EKG evidence of acute MI= injury ○ Ischemia and necrosis→ emergency → 90 mins to get to cath lab!! ○ LAD (left anterior descending) → supplies RV, LV and septum ■ Most common site for blockages ■ Can cause worst damage ■ LV is the biggest area to get blood pumped → will get LVF (a lot of damage in the heart) When artery is 100% blocked heart muscle cells die → irreversible after approximately 30 mins and cannot be replaced!! ○ Early s/s → no physical changes to the heart yet until 6-8 hrs after injury ■ Myoglobin is released 1 hr post injury (not heart selective) ■ Troponin levels → released 2-4 hrs post injury ■ CKB → released 4-6 hrs post injury ■ EKG changes (ST segment elevation and depression, T wave inversion or hyperacute) ● 24-36 hrs: inflammation and neutrophils come onto the scene at site of injury → risk for pericarditis ○ pericarditis → s/s pt may complain of pain when coughing or lying on their back, relief when leaning forward, may hear pericardial friction rub on auscultation ■ Pump failures, risk for cardiogenic shock and arrhythmias ● 10 days: granulation of injured tissue w/ macrophages on the scene. (WBCs that clean up dead cells → tissue unstable → complication cardiac rupture) ● 2 months: scarring which affects heart size and function of heart, inc collagen ● s/s of MI: CRUSHING ○ Chest pain → intense and heavy ○ Radiating chest pain → radiate to left arm, jaw or back ○ Unrelieved by NTG or resting ○ Sweating → cold sweat○ Hard to breath → SOB because of intensity of pain ○ Inc HR or BP ○ Nausea/ vomiting ○ Going to be anxious and scared ■ Women present differently → may not have heaviness, but will be SOB, pain in the lower part of chest and extremely fatigued (will just feel like they have the flu) ■ Diabetics → silent MI, no pain (diabetic neuropathy all over) ● Dx tests: ○ Troponins- most effective ■ Typically drawn in series (every 6 hrs x 3 sets) ○ Myoglobin- early marker (not specific to heart) ○ CK- released whenever there is muscle damage (not just specific to cardiac) ○ CKMB- 4-6 hrs after injury (more specific to heart) ○ Echocardiogram- ultrasound of heart ○ Heart cath- femoral or radial artery, injecting dye, taking x ray to see if there is any blockages to see if they can put a stent in there ○ Stress test with myocardial perfusion injury (MPI)- physical or chemical ○ EKG- any time pt has chest pain ■ Assess for any changes → notify HCP immediately ■ Compare to previous EKGs of pt ■ Lateral- circumflex and LAD blockage ■ Inferior- RCA blockage ■ Septal- LAD blockage ■ Anterior- LAD blockage ○ Zone of injury = ST segment elevation, death of tissue ○ ST segment depression = ischemia ○ Hyperacute T waves = ischemia ○ Zone of Ischemia = Inverted T waves ○ Zone of infarction, Pathological Q wave = current or prior MI ● Nursing interventions: ○ TIME IS MUSCLE ○ Assess pts chest pain and evaluate it ■ Asses CV system → EKG ○ Continuous cardiac monitoring at bedside ■ Risk for dysrhythmias ○ Monitor BP and HR ○ Place on O2 nasal cannula 2-4 L ○ Have a working IV (at least one) ○ Monitor resp sounds ■ Crackles → HF ○ Strict bedrest ○ Collect cardiac enzymes (troponin levels)○ Administering meds as ordered → side effects of meds, pt response, pt education and how they work, typical meds given ■ MONA → morphine, O2, NTG, aspirin ■ Anticoagulants → antithrombotics and antiplatelets ● Antithrombotics → prevent formation of clot ○ Lovenox- subq injection, monitor for bleeding (assess gums, stool, urine, drop in BP and inc HR) ■ Watch for bleeding on gums ○ Heparin- (drip, subq) monitor bleeding, watch platelet levels → heparin induced thrombocytopenia (HIT) → discontinue ■ Drop in platelets → dec several days while being on heparin ■ Collecting PTT (how long it takes a clot to form) (normal 25-35 seconds), on heparin is generally (60-80 sec) ■ Protamine sulfate is the antidote for Heparin ● Antiplatelets → dec platelet aggregation thrombus formation ○ Aspirin → low dose, dec clot from forming ■ Watch for GI bleeding ○ Plavix → if pt cannot take aspirin ■ Thrombotic thrombocytopenic purpura → dec platelets, neuro changes, renal failure, fever, cannot pee ■ Need to stop 5-7 days before surgical procedure ● Morphine → acute situations w chest pain when NTG does not work ○ Given IV ■ Watch for hypotension and resp depression ● Nitrates → NTG ○ Ointment, SL, IV, transdermal ○ vasodilates→ inc blood flow to heart ■ Monitor BP, assess chest pain, VS, watch EKG, continuous bedtime monitoring ■ s/s headache, flushing, dizzy ● ACE inhibitors → “prils” ○ Block angiotensin 1 → angiotensin 2 ■ s/s dry cough, Inc K levels ● Beta blockers → “olol” ○ Dec HR, dec BP ■ Monitor HR ○ Can mask symptoms of hypoglycemia○ CI with COPD and asthma ○ Do not take with grapefruit juice ● ARBs → “sartan” ○ In place of ACE inhibitors ○ Blocks angioten