Low doses: increased renal blood flow Moderate doses: increased renal blood flow, cardiac contractility, cardiac output and blood pressure High doses: vasoconstriction Epinephrine Identify the most prevalent classification of pulmonary hypertension and potential causes. Norepinephrine Dopamine - Effects are dose dependent

Dopamine - Effects are dose dependent

-Anti-muscarinic -Anti-cholinergic drug -Blocks ACh receptor sites - Decreases vagal simulation Describe the mechanism of action for atropine sulfate and provide its classification. Name the complications associated with the administration of nitroprusside (Nipride®) and their treatment. Explain the protocol for using β2-agonists to treat a patient with a severe asthma exacerbation. Provide the most common presenting signs of a pulmonary embolism.

Describe the mechanism of action for atropine sulfate and provide its classification.

Sodium -Removes salt and water Describe brain-type natriuretic peptide (BNP) and the level considered diagnostic for heart failure. Identify the electrolyte imbalances and acid-base abnormality associated with the use of loop diuretics. State indications for the use of RSI. Subdural hematoma

Identify the electrolyte imbalances and acid-base abnormality associated with the use of loop diuretics.

Milrinone -Decreased vascular resistance -Increased contractility Dobutamine -Increased contractility -B1-agonist with some B2 adrenergic activity Explain the role of milrinone and dobutamine in the treatment of congestive heart failure. State indications for the use of RSI. Brainstem: signs and symptoms Identify potential complications associated with prone positioning.

Explain the role of milrinone and dobutamine in the treatment of congestive heart failure.

-Cyanide is formed when the drug is metabolized -Forms methemoglobin -Treatment: Hydroxycobalamin and B12 Name two sedatives that have bronchodilating properties. Epinephrine Name the complications associated with the administration of nitroprusside (Nipride®) and their treatment. Decorticate (Flexor)

Name the complications associated with the administration of nitroprusside (Nipride®) and their treatment.

-Systolic dysfunction is primarily decreased contractility -Diastolic dysfunction prevents ventricles from filling completely due to stiffness Describe the difference between systolic and diastolic heart failure. Identify physiological causes of systolic heart failure Calculate cardiac output given heart rate and stroke volume List five risk factors for developing ARDS.

Describe the difference between systolic and diastolic heart failure.

-Coronary artery disease -Hypertension -Congenital heart disease -Drugs -Diabetes mellitus Recommend treatment options for a patient experiencing a hemorrhagic stroke. State the most common chest injury in children. Describe Cushing's triad and what it is associated with. Identify physiological causes of systolic heart failure

Identify physiological causes of systolic heart failure

Adv Patho Final Objectives Flashcards

Low doses: increased renal blood flow Moderate doses: increased renal blood flow, cardiac contractility, cardiac output and blood pressure High doses: vasoconstriction

-Increased vascular smooth muscle contraction -Increased HR -Increased contractility

-Constricts blood vessels -Increased HR -Dilates bronchioles

-Increased BP -Increased SVR -No change to contractility

-Anti-muscarinic -Anti-cholinergic drug -Blocks ACh receptor sites - Decreases vagal simulation

Sodium -Removes salt and water

Milrinone -Decreased vascular resistance -Increased contractility Dobutamine -Increased contractility -B1-agonist with some B2 adrenergic activity

-Cyanide is formed when the drug is metabolized -Forms methemoglobin -Treatment: Hydroxycobalamin and B12

-Systolic dysfunction is primarily decreased contractility -Diastolic dysfunction prevents ventricles from filling completely due to stiffness

-Coronary artery disease -Hypertension -Congenital heart disease -Drugs -Diabetes mellitus

-Coronary artery disease -Hypertension -Hypertrophic cardiomyopathy -Diabetes mellitus -Restrictive cardiomyopathy -Constrictive pericarditis

-Fatigue -Increase peripheral venous pressure -Ascites (fluid collection in spaces in abdomen) -Enlarged liver/spleen -Distended jugular veins -Anorexia and complaints of GI distress -Weight gain -Dependent edema

-Paroxysmal nocturnal dyspnea -Elevated capillary wedge pressure -Pulmonary congestion (cough, crackles, wheezes, tachypnea, blood tinged sputum) -Restlessness -Confusion -Fatigue - Cyanosis -Tachycardia -Orthopnea (shortness of breath)

Cardiac Output = HR x stroke volume

Left heart failure

-Preload -contractility -afterload

-Help the heart handle overload and ventricular stretching Values -Normal: < 100 pg/mL -HF likely: > 400 pg/mL

-bat wing -kerley B lines -increased cardiothoracic ratio -cephalization of vessels -pleural effusion

-Beta blockers (decreased HR and vasodilation) -Carvedilol (Coreg) -Metoprolol (Toprol XL, Zebeta)

Digoxin: - positive inotrope and negative dromotrope -Increases the amount of calcium available for contracting -Enhanced force of contraction -Negative dromotrope 1. Slows conduction through heart 2. Allows for more effecting ventricular filling time -Increased cardiac output -Increased renal perfusion

-SEPSIS -TRAUMA -Aspiration of GI contents -Blood transfusions -Pancreatitis -Drug overdose -Pulmonary contusion -Burns/inhalation injury 85-90% caused by pneumonia, sepsis, aspiration of gastric contents, trauma or blood transfusion.

-Advanced age -Female -Smoking -Alcohol use -Aortic vascular surgery

-Thickened diffusion membrane -Inflamed exudate-filled alveoli -Collapsed bronchioles -Loss of elasticity of the parenchyma -Massive shunt -SEVERE HYPOXIA

-Well-aerated areas of the lung amid the less compliant, atelectatic areas -Located primarily in the non-dependent lung regions

-Asthma -COPD -CHF -Pneumonia* -Pneumothorax -Sepsis* -Pneumonia and sepsis are leading causes of ARDS, but may be present in patients who do not meet the criteria for ARDS

Bilateral diffuse ground glass appearance CT is the gold standard for evaluation

-Lower end-inspiratory (plateu) pressure -Lower Vt -Higher rates -Higher PEEP -4-8 ml/kg -Pplat < 30

-Creates a more even distribution for gas delivery -More homogenous distribution of the mechanical stress & strain secondary to mechanical ventilation -Improved V/Q ratio -Lower mortality rates

-Absolute contraindication Unstable spine fracture -Relative contraindication Recent sternotomy -High BSA of anterior burns -Unstable pelvic or long bone fractures -Elevated ICP -Massive hemoptysis

-Skin breakdown -Line dislodgement -Unplanned extubation -Back pain

A large thrombus detaches, passes through the right heart and becomes lodged in the bifurcation of the pulmonary artery

-Blockage of the pulmonary system -Pulmonary infarction -Atelectasis -Alveolar consolidation -Bronchospasm

-Patients with malignancy -Pregnant women -Acute stroke -Hospitalized patients -Acute spinal cord injury -Joint replacement -Inherited clotting disorders -Any major surgery -Higher in males

-Most common is sudden onset of chest pain and shortness of breath -Cough -Shock - PE is number one cause of obstructive shock - test question -Dysrhythmia -Syncope, lightheadedness, and confusion -Tachypnea* -Calf or thigh swelling, erythema, edema, and/or tenderness* -Tachycardia -Rales; wheezes

Sudden onset of chest pain and shortness of breath

-Also known as the fibrinogen test -Looks for an increased level of the protein fibrinogen (part of the clotting process) -Values > 500 ng/mL are considered positive -Use clinical correlation -Just identifies that a clot is being formed somewhere in the body

-CT angiogram -Becoming the preferred method for diagnosing PE -V/Q scan and pulmonary angiogram

ANTICOAGULATION -Safer and more effective than high-molecular weight heparin -Enoxaparin, dalteparin, and tinzaparin -Coumadin (Warfarin) Thrombolytic agents -Streptokinase (Streptase®) -Urokinase (Abbokinase®) -Alteplase (Activase®) -Reteplase (Retavase®) Preventive measure -IVC filter (Greenfield filter & TrapEase filter) -Pneumatic compression -Pulmonary embolectomy (last resort)

-Defined as an increase in mean pulmonary artery pressure ≥ 25 mmHg at rest or > 30 mmHg during exercise -Normal range is 10 - 20 mmHg at rest -Done in cath lab

-Class II is the most prevalent classification Causes by: -Systolic dysfunction (can't squeeze) -Diastolic dysfunction (can't fill) -Valvular disease

-dyspena -lightheadness -fatique -hemoptysis -hoarsness -syncope -chest pain -ascites -raynauds disease -peripheral edema -cyanosis

-Right heart catheterization is the gold standard for diagnosing PH -Only test that directly measures pulmonary artery pressures

-Oral calcium channel blockers (diltiazem) -Prostaglandins (Iloprost, epoprostenol, Treprostinil) - nebulized medication -Endothelin receptor antagonist -Inhaled nitric oxide -Phosphodiesterase inhibitors - viagra

B- Beards O- Obesity O- Old T- Toothless S- Snoring

-Assess oral opening -Intercisor gap: 2-3 fingers or 40 mm -Adequate room for laryngoscope

-Minimum of 3 fingers or > 6.5 cm -Predicts the ability to lift the tongue into the mandible

-Patient's with a gag reflex -Facial trauma -Esophageal trauma -Suspected foreign body airway obstruction -Non-fasting patient -Poor lung compliance

-Positive gag reflex -Known esophageal injury, surgery, or disease -History of laryngectomy with stoma -Any circumstance where airway edema is suspected or could develop -Ingestion of a caustic substance -Allergic/anaphylactic reaction

-Impending respiratory failure secondary to cardiopulmonary disease states -Acute injury that threatens airway patency -Head injury -Burns with inhalation injury -The inability to maintain or protect the airway -CVA -Overdoses

-Esophageal >>>Confirmation Bradycardia>>>Atropine -↑ ICP>>>Adequate pre-treatment -Trauma>>>Sedation/technique -Pneumo>>>Proper tidal volume -R.mainstem>>>Proper depth -Aspiration>>>Suction -Laryngospasm>>>Paralytic/positive pressure -Hypotension>>>Proper drug/tidal volume

Preparation - Pre-oxygenation - Pre-intubation optimization -Paralysis and/or sedation -Positioning with protection -Placement (intubation) with proof - Post-intubation management

-Midazolam -Lorazepam -Propofol -Etomidate -Ketamine

Dexmedetomidine (Precedex) - not used as induction agent -Propofol

-Propofol -Ketamine

Depolarizing -Mimics acetylcholine but remains on receptor sites longer -Prolongs depolarization -Paralysis results because muscles cannot repolarize Non-depolarizing -Block acetylcholine receptor sites -Acetylcholine cannot transmit the impulse -Muscles cannot contract -Paralysis begins

-Progressive pulmonary dysfunction -Pneumonia -ARDS

-Persistent cough, stridor, or wheezing -Hoarseness -Deep facial or circumferential neck burns -Singed nasal hairs -Carbonaceous sputum -Blistering or edema in the nasopharynx -Depressed mental status

Increased risk of severe hyperkalemia

-Paralyzed right -side hemiplegia -Impaired speech and language -Slow performance -Visual field deficits -Aware of deficits, depression, anxiety -Impaired comprehension -Left side brain damage = right side body weakness

-Paralyzed left side hemiplegia -Spatial-perceptual deficits -Tends to minimize problems -Short attention span -Visual field deficits -Impaired judgment -Impulsive-Impaired time concept -Right side brain damage = left side body weakness

-Decreased LOC -Nausea and vomiting -Eye movement abnormality -Double vision -Dysconjugate gaze -Decreased mobility on one of both sides -Dysarthria -Dysphagia -Abnormal respirations -Vertigo, dizziness -Hearing loss Locked in syndrome

-Ipsilateral ataxia -DiscoordinationT -runcal or gait ataxia -imbalance

Atrial fibrillation

-Anticonvulsants -Antihypertensives -Beta-blockers -ACE inhibitors -Nicardipine -Hydralazine -Nitroprusside (can increase ICP) -Osmotic diuretics

-ABCs -Establish time of onset -Rule out mimics -Noncontrast CT/MRI -Glucose -Manage BPIV tPA if initiated within 4.5 hours of symptom onsetIntra-arterial fibrinolytic therapy within 3-6 hours of symptom onset -Mechanical thrombectomy within 24 hours of symptom onset -Antithrombotic therapy -DVT and PE prophylaxis -Statins

-Facial droop -Arm drift -Abnormal speech -If any one of these three signs is present as a new event, the probability of stroke is 72%

-Direct impact Acceleration/deceleration -Penetrating brain injury -Blast waves

-Electrolyte imbalance -Inflammation -Vascular injury -Cerebral vasospasm

occur when the person's head slams against a stationary object.

is a type of brain injury that causes tears in the brain's long connecting nerve fibers, called axons. -This injury occurs due to a blunt injury that causes the brain to rotate and shift rapidly inside the skull

"Lemon" - rapidly expanding with arterial blood -Skull fracture -Torn middle meningeal artery -Dura pushed away by hematoma

-"Banana"-slowly expanding with venous blood -Superior sagittal sinus -Torn bridging vein -Dura is attached to the skull, so cannot cross falx, tentorium

-Frequent VS -Neuro exam including GCS and pupillary movement -Serial neuro exams to monitor for clinical deterioration -Evaluation and management of increased ICP -Cerebral herniation -Labs (CBC, lytes, BGL, coag, BAC, urine toxicology)

-Bradycardia -Hypertension -Irregular RR

-Arms are like C's -Moves in toward the cord -Problems with cervical spinal tract or cerebral hemisphere

-Arms are like e's -Problems within midbrain or pons -Decerebrate posturing is usually indicative of more severe damage lower in the brainstem.

-Prevent or control secondary injury -Manage ICP -Maintain adequate cerebral perfusion pressure -Optimize oxygenation and BP -Manage temperature, glucose, and seizures -Anti-seizure medications to prevent and treat post-traumatic seizures -Prevent fever -Fever shown to ICP and worsen secondary brain injury in patients with severe TBI

-Be cautious with ETCO2 -Acute hypercarbia may increase ICP (vasodilation) -Acute hypocarbia may cause cerebral ischemia (vasoconstriction) -Recommendation: Keep > 30 mmHg -Target PaO2 > 60 mmHg -PEEP 15- 20 cmH2O or APRV is safe (neither impacts ICP)

-HOB at 30° to permit adequate venous drainage -External ventricular drain (EVD) -Keep ICP < 22 mmHg-Sedation (Propofol) -Decompressive craniectomy

-Air trapped in the pleural space -Anxiety -Cyanosis -Increased dyspnea -Tracheal deviation -Hypotension -Tachycardia -JVD -Unequal chest rise -Subcutaneous emphysema

-JVD -Hypotension -Muffled heart sounds

Pulmonary contusion

-Most common blunt trauma injury -Pain with breathing, coughing, or pressing on the chest -Crepitus common over fracture site -Ribs 4 to 10 most fractured -Fractures of ribs 8 to 12 look for -Diaphragmatic tears -Liver or spleen injury -Great force required to break 1st and 2nd ribs -Associated with myocardial contusion, bronchial tears, and vascular injury

-Bruising -Seatbelt sign -Crepitus

-Oxygen therapy -Chest tube -Thoracotomy -Video-assisted thoracoscopy (VATS) -Mechanical ventilation

-Talks in words -Leans forward -Is agitated -Uses accessory muscles to breathe -RR > 30 breaths/min -HR > 120 beats/min -Room air SpO2 < 90% -PEF 33-50% of their best or predicted value

-Increases in dyspnea and wheezing -increases in the frequency of nocturnal awakenings -increased use of SABA rescue medications -increased diurnal variability in PEFR -hospitalization or ED visits in the past year -recent or current use of oral glucocorticoids

Severe airflow resistance due to bronchial mucosal inflammation and edema, constriction of bronchial smooth muscle, and mucus in the bronchial lumen

depressed/flattened diaphragm -hyperinflation -translucent fields

2.5- 5 mg nebulized every 20 minutes for three doses then every 1-4 hours - For severe exacerbations, 10-15 mg can be administered via continuous nebulization over 1 hour - May also give 4-8 puffs MDI every 20 minutes for three doses, then taper

Combined β2-agonist/ipratropium: - One vial (ipratropium 0.5 mg and albuterol 2.5 mg) every 20 minutes for three doses and then as needed for up to 3 hours Corticosteroids:- Methylprednisolone 40 - 60 mg IV- Prednisone 60 mg PO - Magnesium sulfate 2 grams IV over 20 minutes

Optimal mode not known; volume limited is recommended - Caution with pressure modes - varying Vt - Rate 10-12 - Vt 6-8 mL/kg IBW - MV < 115 mL/kg/min - PEEP 5 cmH2O... check for intrinsic PEEP - FiO2 start at 100% and titrate to maintain SpO2 > 90% or PaO2 > 60 mmHg

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Adv Patho Final Objectives

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