n325 exam 3 learning objectives

Describe normal venous circulation and compare the structural and functional differences between arteries and veins.

• Normal venous circulation returns oxygen-depleted blood to the heart using one-way valves, skeletal muscle contractions (especially in the calves), and breathing mechanics

• Flow of blood:

  • Right atrium

  • Right ventricle

  • Pulmonary artery

  • Lungs

  • Pulmonary veins

  • Left atrium

  • Left ventricle

  • Aorta

  • Arteries

  • Arterioles

  • Capillaries

  • Venules

  • Veins

  • Central veins (superior/inferior vena cava)

• Arteries

  • OXY BLOOD

  • No valves

  • Away from heart

  • High pressure

  • Very thick, muscular, elastic walls

• Veins

  • DEOXY BLOOD

  • Has valves

  • Toward heart

  • Low pressure

  • Thin, less muscular walls

Identify risk factors associated with venous thromboembolism (VTE) using Virchow’s Triad.

1. Hypercoagulable state

   1. Blood will clot more

   2. Prolonged immobility, clotting disorders, drugs, high altitudes, malignancies, pregnancy, tobacco, polycythemia vera

2. Venous stasis

   1. Blood not moving around = easier to clot

   2. Age, CHF, obesity, orthopedic surgery, pregnancy, prolonged immobility, varicose veins

3. Vessel wall injury

   1. Activates more clotting factors

      1. Surgery, IV therapy, IV meds, drug use, metabolic syndrome, DM, HTN, smoking, trauma

Recognize clinical manifestations of DVT and interpret relevant diagnostic results (D-dimer, ultrasound).

• Clinical manifestations

  • Edema

  • Redness

  • UNILATERAL SWELLING

  • Pain

  • Tenderness

  • Sense of fullness in extremity

  • Temperature (>100.4 F)

• Diagnostic tests

  • D-dimer: (>0.5 mg/L)

    • Elevated in patients who are actively breaking clots down

    • *but high D-dimer doesn’t always mean they have DVT.. just means their body is breaking a clot down

  • Ultrasound: Most common

Implement nursing interventions for DVT prevention and management, including anticoagulant therapy, compression therapy, and early ambulation.

• DO NOT MOBILIZE AN EXISTING CLOT

  • No valsalvas

  • No massage

• Administer anticoagulants

  • Present new thrombi from forming and allows body’s natural clot breaking process to lead the way

  • Factor Xa inhibitors

    • Apixaban (Eliquis)

    • Rivaroxaban (Xarelto)

    • Enoxaparin (Lovenox)

  • Direct thrombin inhibitors

    • Dabigatran (praxada)

  • Vitamin K antagonist

    • Warfarin

  • Avoid aspirin, NSAIDs, certain supplements

  • Report signs of bleeding + bleeding precautions

  • Carry pharmacy card + wear alert bracelet

• Elevate extremities

  • Avoid dependent extremities

• Use SCDs to prevent DBTs

  • Don’t put on leg that has thrombus to not mobilize clot

  • To prevent -> stimulates muscular contraction to push blood back to heart

• Early ambulation

  • Prevents DVTs by moving blood around

• Provide comfort with analgesics

• Monitor for PE

Differentiate between superficial and deep venous thrombosis, and explain the potential complications such as pulmonary embolism.

• SVT

  • Occurs in veins near skin

  • Often lower risk

  • Manage with heat, elevation, NSAIDs, compression stockings

• DVT

  • Occurs in deep veins

  • Higher risk for PE

  • Requires immediate anticoagulation to prevent clots from growing/breaking off

• Pulmonary embolism complications

  • Potentially life-ending event

  • Occurs when one of the arteries in the lungs get blocked by blood clot

  • Can cause right heart failure, pulmonary hypertension

Describe pathophysiology, assessment findings, and evidence-based care for venous stasis ulcers, including compression and wound-healing strategies.

• Cause:

  • Caused by inadequate tissue O2 and nutrient exchange

  • Veins in legs are not moving blood back to the heart well

  • Blood pools in legs instead of moving back to heart

  • Incr venous pressure in lower extremities

  • Extra pressure pushes fluid out of blood vessels and into surrounding vessels -> edema/swelling

  • No good O2 = tissue breaks down easily

  • Small scratch can turn into open sore

• Assessment

  • Lower calf/ankle

  • Dull/aching pain

  • Superficial or deep ulcer

  • Edematous, brown, ruddy tissue

  • Wet wound - serous drainage

  • Irregular edges

• Treatment

  • May take years to develop/resolve

  • Recurrence ~90%

  • Prevent infection -> keep clean, dressed

  • Compression -> unna boot and compression stockings/dressings -> start distally

  • Elevate extremity -> promote venous return

  • Moist dressing -> promote wound healing

  • Wound care referral -> chronic wound

  • Diet -> increase protein, omega-3, zinc, vitamins A, C, D, E

Explain the pathophysiology of peripheral arterial disease (PAD) related to atherosclerosis and reduced perfusion.

• Thickening of artery walls

• Reduced blood flow thru arteries

  • Tissues don’t get as oxygenated

  • Have to increase pressure to push blood thru

• Progressive narrowing of arteries

• Higher risk: diabetes, HTN, hyperlipidemia, smokers

• Most affects the legs -> bc furthest from the heart

• Clinical manifestations not present until ~60-75% occlusion

• #1 cause of PAD = Atherosclerosis

  • Damage to endothelium/arteries

    • d/t high BP to push blood thru

    • Damage and inflammation go together

    • Send platelets amd plaque will form

  • Occlusive thrombus, unstable plaque, microemboli

• Risks:

  • Tobacco, diabetes, HTN, obesity, sedentary lifestyle, stress, age, gender, family history, ethnicity

• Reduced perfusion

  • Assess pulse, temp, cap refill, paresthesia, pain, color and compare sides

• Chronic PAD assessment:

  • No edema

  • Thin & shiny skin w no hair

  • Thick, brittle toenails

  • Numbness, paresthesia, itching

  • Dependent rubor

Correlate clinical manifestations (intermittent claudication, dependent rubor, paresthesia) with ischemic tissue changes.

• Intermittent claudication

  • Ischemia

  • Leg pain with activity d/t lack of O2

  • Continuum of fully compensatory to cell death

  • Fontaine scale

    • I = Asymptomatic

    • IIa = mild claudication

    • IIb = moderate-severe claudication

    • III = ischemic rest pain

    • IV = ulceration or gangrene

• Dependent rubor

  • When leg is down, blood pools in foot and foot turns bright red

  • Gravity forces blood into capillaries that have become permanently dilated due to severe/chronic lack of O2

• Paresthesia

  • Bc bad perfusion, paresthesia occurs -> numbness/tingling in the extremity

Compare and contrast nursing care for venous versus arterial ulcers (elevation vs. dependency, compression vs. none).

• venous ulcers

  • long-term wound care (unna boot, moist dressings)

  • elevate extremity

  • compression hose

  • elevation

  • infection prevention

• arterial ulcers

  • restore circulation

  • prevent trauma and infection

  • don’t elevate extremity

  • no compression devices

Develop a plan of care for patients with chronic PAD emphasizing smoking cessation, exercise therapy, BP and lipid management, and antiplatelet therapy.

• Statins to lower cholesterol

• Antiplatelet (aspirin/clopidogrel)

• Anticoagulation

• Peripheral vasodilators -> incr perfusion to extremity and will lower BP

• BP control -> don’t want hypotension to occur also

• Exercise therapy -> will help BP and blood sugar control

• Smoking cessation

• Angioplasty

  • Insert catheter to occlusion and insert stent

  • Make sure they are on thinners/antiplatelets

• Stents

• Endarectomy -> removes pieces of plaque

• Arterial bypass -> graft blood vessels and create new blood pathway to lower extremity

Differentiate between the clinical manifestations, treatments, management, and plan of care between PVD and PAD

• PVD

  • Peripheral venous disease -> venous insufficiency

  • Blood is not going back to heart well.. Pooling in legs

  • Causing inadequate tissue O2 and poor nutrient exchange

  • Dull, achy, heavy, crampy feeling

  • Brown pigmentation skin

  • Warm to touch

  • Edema

  • Present pulses

  • Ulcers on ankles with irregular borders

• PAD

  • Peripheral arterial disease

  • Blood is not being sent to a lower extremity due to plaque buildup in an artery/thickening… poor oxygenation of tissue

  • Sharp, stabbing, claudication

  • Cool, thin, shiny, hairless, pale

  • No edema

  • Weak pulses

  • Ulcers on feet/toes with punched out look

Differentiate between thoracic, abdominal, and cerebral aneurysms in terms of location, risk factors, and clinical presentation.

• Bulging or ballooning of vessels (usually arteries)

• Thoracic

  • Often asymptomatic until they are pretty large

  • Deep, diffuse pain that may extend to shoulder

  • Hoarseness, difficulty swallowing, persistent dry cough bc putting pressure on laryngeal nerve

  • If rupture, massive hemorrhage

• Abdominal

  • 75% of aortic aneurysms

  • Often asymptomatic until pretty large

  • Pulsatile mass in the periumbilical area

  • Systolic bruit may be heard

  • Gnawing mid-abdominal/lower back pain that is unaffected by movement

  • May mimic abdominal/back disorders

  • Rupture signs: sudden, severe back/abdominal pain and signs of hypovolemic shock - massive hemorrhage

• Cerebral

  • Subarachnoid space

  • Caused by HTN, genetics, smoking

  • Often asymptomatic if not ruptured

  • Can cause headaches

  • If ruptured, really bad HA and neck stiffness/rapid decline in consciousness.. S/S of stroke

Identify signs of aneurysm rupture or dissection and prioritize emergency interventions.

• rupture

  • if AAA or TAA → massive hemorrhage

  • if cerebral → S/S of stroke

• dissection

  • filling of blood in false lumen created between layers of artery

  • bleeding, but not full on rupture

  • if in ascending aortic arch → surgery required, otherwise manage conservatively

• interventions

  • prevent rupture & dissection

  • wellness and education (DM, HTN, obesity, lipid management, exercise)

  • routine monitoring if <5.5 cm

  • surgery if >5.5 cm

    • OAR (open repair)

    • endovascular grafts → cover aneurysms with mesh so it doesn’t rupture

Explain the distinguishing features and management of Raynaud’s Phenomenon and Buerger’s Disease, and educate patients on prevention and symptom control.

• Raynaud’s

  • Common vasospastic disorder causing temporary color changes in digits triggered by cold or stress -> rarely causes permanent damage

  • Episodic, vasospastic disorder of small arteries

  • Involves fingers and toes

  • Vasoconstriction

  • Affects young women (15-40 yrs old)

  • Auto-immune connection?

  • Aggravated by cold/stress

  • Blanching - turn white

  • Cyanosis - turn purple/blue

  • Hyperemia - rubor when blood returns - turns bright red

  • Teach pt to prevent episodes - avoid cold, drugs, tobacco, stress reduction

  • Use warm water when having spasms

  • Use calcium channel blockers to promote vasodilation

  • Sympathectomy -> cut thru nerves that activate vasoconstriction and vasodilation -> have to be severe case

Buerger’s

• Rare, smoking-related condition causing inflammation and blood clots in small/medium arteries -> painful tissue damage and gangrene

• Inflammatory, occlusive, thrombotic arterial disease

• Distal extremities (upper and lower)

• Occurs in more men over 40, smokers, and ppl with hx of periodontal disease

• Cold sensitivity, thrombosis, color/temp change

• STOP SMOKING!!!

• Can lead to amputation

• can use sympathectomy

Define systolic and diastolic blood pressure and describe the physiologic factors that influence each (CO, SVR).

• Systolic BP

  • Pressure during ventricular contraction

  • Influenced by Cardiac output (CO) = volume of blood pumped by heart/min

  • CO = HR x SV

  • Stroke volume = blood pumped per beat

• Diastolic BP

  • Pressure during ventricular relaxation

  • Influenced by systemic vascular resistance (SVR)

  • Constriction vs dilation -> pressure needed to push blood thru vessels

Explain the role of the endothelium in maintaining vascular integrity and summarize how hypertension causes progressive endothelial injury.

• Endothelium regulates vasodilation.. When vessels dilate -> lower BP and improve flow

• Endothelium acts as gatekeeper -> controls movement of fluids, electrolytes, and macromolecules from the blood into surrounding tissues

• Endothelium prevents clotting, ensuring blood remains fluid

• Endothelium controls inflammation

• Hypertention causes progressive endothelial injury as there is mechanical shear stress overtime -> causes cells to become disorganized, swollen, and eventually detached

  • When cells are damaged, vessels can’t relax properly and increases resistance -> increases BP more

  • HTN triggers inflammatory response and causes endothelium to become sticky to pick up LDL and white blood cells

  • Gatekeeper functions fail -> causes atherosclerosis

Differentiate between primary, secondary, and hypertensive crisis classifications according to AHA guidelines.

• Normal BP = <120 SBP and 60-80 DBP

• Elevated BP = 120-129 SBP or < 80 DBP

• Stage 1 HTN = 130-139 SBP or 80-89 DBP

• Stage 2 HTN = >140 SBP or > 90 DBP

• Primary HTN

  • Develops overtime without a single known cause

  • Most common form

  • Driven by genetics, aging, lifestyle factors, and inactivity

  • Treatment focused on long-term lifestyle changes and maintenance meds

• Secondary HTN

  • HTN caused by an identifiable underlying medical condition, medication, substance, rather than lifestyle factors

  • Affects 5-10% of patients and appears suddenly

  • Often more severe than primary HTN

  • Can sometimes be cured by treating root cause

  • ex) pregnancy-induced HTN, sleep apnea, endocrine disorders

• Hypertensive crisis

  • Urgency: BP > 180/120, no S/Sx TOD

  • Emergency: BP > 180/120, S/S TOD

  • Clinical manifestations:

    • S/Sx of TOD

    • Retinal: papilledema, hemorrhage

    • Neuro: HA, seizures, confusion, coma

    • CV: chest pain, SOB, dysrhythmias

  • Goals of treatment

    • Lower BP: 2-4 hrs later, BP reduction of 25%

    • Stabilize to 160/100 mmHg over next 2-6 hours

  • Treatment

    • Confirm reading

    • IV vasodilators

  • Complications

    • Cerebral bleed, heart failure, renal failure

    • Too-rapid reduction in BP can lead to ischemia

Identify modifiable and non-modifiable risk factors contributing to hypertension.

• Modifiable

  • Smoking

  • Obesity

  • Sodium

  • Caffeine

  • Alcohol

  • Stress/anxiety

  • Lack of physical activity

• Non-modifiable

  • Age

  • Genetics

  • Ethnicity

  • Sex

Interpret common diagnostic assessments (e.g., BP measurement technique, renal studies, echocardiogram) and determine their relevance to patient status.

• EKG

• CXR

  • Can show cardiomegaly

• Arteriography

  • Radiopaque dye is injected into arteries under Xray

  • Identifies exact location and % of arterial blockage

  • Identifies if pt is candidate for stent/bypass graft

• Ophthalmic exam

  • Can directly visualize small blood vessels to look for systemic vascular damage

• BP measurement technique

  • Taken after 5 mins of rest, feet flat, back supported, arm at heart level with correctly sized cuff

• Renal studies (BUN/creatinine)

  • Elevation suggests intrinsic kidney damage from chronic hypertension

• Echocardiogram and/or ultrasound

Compare pharmacologic classes used to treat hypertension (diuretics, beta blockers, ACE inhibitors, ARBs, CCBs) and explain key nursing considerations and patient teaching for each.

• Diuretics

  • Class: thiazide diuretics

  • ex) hydrochlorothiazide (HCTZ)

  • MOA: inhibits Na+ reabsorption in kidneys which promotes diuresis. Reduces blood volume

  • Cautions: orthostatic hypotension, electrolyte imbalances, can cause nephrotoxicity

• Beta-blockers

  • Class: beta blockers

  • ex) metoprolol

  • MOA: blocks beta adrenergic stimulation that increase BP (heart and peripheral vascular system)

  • Cautions: orthostatic hypotension, contraindicated with asthma, bradycardia

• ACEis

  • Class: ACE inhibitors (ACEIs)

  • ex) lisinopril

  • MOA: inhibits conversion of angiotensin I to angiotensin II; dilates arteries and veins

  • Cautions: orthostatic hypotension, dry cough, dizziness, hyperkalemia

• ARBs

  • Class: angiotensin receptor blockers (ARBs)

  • ex) losartan

  • MOA: blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II

  • Cautions: orthostatic hypotension, angioedema, hyperkalemia

• CCBs

  • Class: calcium channel blockers (CCBs)

  • ex) amplodipine

  • MOA: blocks Ca+2 entry into smooth muscle cells

  • Cautions: peripheral edema, constipation

• Alpha blockers

  • Ex) prazosin

  • MOA: blocks alpha-1 receptors on peripheral blood vessels

  • Potent periphal vasodilation; reduces SVR

  • Cautions: first dose syncope

• Alpha-2 receptor agonists

  • ex) clonidine

  • MOA: stimulates alpha-2 receptors in the brain

  • Reduces sympathetic outflow, slowing HR and dilating vessels

• Vasodilators

  • ex) nitroglycerin

  • MOA: direct relaxation of vascular smooth muscle

  • Reduces SVR

Evaluate the effectiveness of lifestyle modifications (DASH diet, sodium reduction, weight control, stress management, physical activity) in lowering blood pressure.

• Weight reduction: 5-20 mmHg per 10 kg weight loss

• DASH diet: ~11 mmHg

• Physical activity: 4-9 mmHg

• Sodium reduction: 2-8 mmHg

• Decrease ETOH: 2-4 mmHg

• Avoid tobacco

• Stress management

Differentiate between hypertensive urgency and emergency based on clinical presentation and prioritize appropriate nursing interventions.

• Urgency: BP > 180/120, no S/Sx TOD

• Emergency: BP > 180/120, S/S TOD

• Clinical manifestations

  • S/Sx of TOD

  • Retinal: papilledema, hemorrhage

  • Neuro: HA, seizures, confusion, coma

  • CV: chest pain, SOB, dysrhythmias

• Goals of treatment

  • Lower BP: 2-4 hrs later, BP reduction of 25%

  • Stabilize to 160/100 mmHg over next 2-6 hours

• Treatment

  • Confirm reading

  • IV vasodilators

• Complications

  • Cerebral bleed, heart failure, renal failure

  • Too-rapid reduction in BP can lead to ischemia

Develop patient-centered education plans that promote medication adherence, home BP monitoring, and recognition of complications.

• Routine assessment (Q 3-6 months)

  • History

  • Home BP logs

  • Physical assessment

  • Taking meds?

  • Med SEs?

  • Lifestyle mods

• Education

  • Pt and family teaching

  • Med compliance

  • Home monitoring

  • When to call

  • When to come back in

Apply the Clinical Judgment Model to a case scenario by recognizing cues of early hypertension, analyzing cues to identify risk, prioritizing hypotheses for intervention, and evaluating outcomes.

• Early HTN often asymptomatic

• But can include: frequent morning headaches, dizziness, blurred vision, nosebleeds, and fatigue or confusion

• integrate lifestyle mods and preventative meds early on

Define ventilation, gas exchange, oxygen transport, and perfusion.

• Ventilation

  • Movement of air in and out of the lungs

• Gas exchange

  • Diffusion of O2 and CO2 across the capillary membranes

• Oxygen transport

  • Delivery of O2 to tissues via hemoglobin and circulation

• Perfusion

  • Flow of oxygenated blood to tissues and cells

Identify normal respiratory structure and function including lung compliance, resistance, and control of breathing.

• Compliance

  • Ability of the lungs to expand

  • How easy/hard it is for the lungs to expand

  • ex) thick vs thin rubber band

• Resistance

  • Obstacle to airflow during inspiration and/or expiration

  • Affected by the diameter of the airways

  • ex) bronchoconstriction or mucus buildup

• ANS respiratory control centers

  • Medulla and pons in brainstem

  • Autonomic nervous system -> respiratory centers

  • Respond to chemical/mechanical signals to continue resp processes

Explain how PaCO₂ and pH regulate respiratory rate.

• PaCO2 is the main driver of respiration -> buildup of CO2 = let’s breathe now

• More PaCo2 = lower pH = breathe more

• Chemoreceptors sense the increased CO2 and prompt the respiratory system to promote you to breathe

Interpret ABG abnormalities (acidosis, alkalosis) to oxygenation status.

• Normal ABGs

  • pH = 7.35 - 7.45

  • PaCO2 = 35 - 45 mmHg

  • PaO2 = 80 - 100 mmHg

  • HCO3- = 22-26 mmHg

  • SaO2 = 94 - 100%

Differentiate between ventilation problems & gas-exchange problems.

• Ventilation problems

  • Problem with moving air in and out of lungs

  • ex) stiff lungs, over sedation, damage to brain stem, pain, obesity, chest injury, COPD

• Gas exchange problems

  • Problem with exchanging O2 and CO2 at alveoli

  • ex) pneumonia, COPD, ARDs, fibrosis, atelectasis

  • Can eventually lead to ventilation problems because muscles that work harder to facilitate breathing are gonna get tired and worn out

Explain the oxyhemoglobin dissociation curve and how shifts to the right or left affect oxygen loading and unloading in the tissues.

• Shows relationship between PaO2 and SaO2

• Cooperative binding -> binding of one O2 molecule makes it easier for the next to bind -> S-shaped curve

• Right shift

  • Hemoglobin has lower affinity for oxygen

  • Enhanced unloading of O2 to tissues

  • Will occur in active states when you need more O2 -> low pH, high CO2, fever, increased metabolic rate

  • Will need higher PaO2 to have same SaO2… -> blood is unloading O2 and has less affinity for each O2 ir unloads

  • ex) running with tiger

• Left shift

  • Hemoglobin has higher affinity for oxygen

  • Greater for when picking up O2 in the lungs

  • But harder to release O2 in tissues

  • Caused by increased pH, decreased CO2, hypothermia

  • Needs lower PaO2 to have same SaO2 -> blood is picking up O2 easily

  • ex) resting and digesting

Apply age-related changes in respiratory structure, defense mechanisms, and acid-base compensatory capacity

• Alteration in structure

  • Stiffer chest wall/mobility of rib cage

  • Decreased elastic recoil and compliance

• Alteration in defense

  • Decreased immune function

  • Weaker cough

  • Decreased ciliary action

• Alteration in respiratory control

  • Decreased response to rises in PaCO2

• Renal function

  • Decreased ability to compensate for acid-base

Differentiate respiratory distress from early respiratory failure across lower respiratory conditions and prioritize timely, condition-specific nursing actions.

• Early respiratory distress S/Sx

  • Anxiety

  • Increased HR & BP

  • Increased RR

  • Decreased UOP

  • Restlessness

  • Dyspnea w/exertion

  • Fatigue

  • Maybe accessory muscle use

  • Tripoding

• Late respiratory distress S/Sx = RESPIRATORY FAILURE

  • Confusion/lethargy

  • Decreased HR and BP

  • Decreased RR

  • Decreased UOP

  • Cyanosis

  • Dyspnea at rest

  • Fatigue

  • Significant accessory muscle use

  • Pause for breathe between sentences/words

  • Breathing muscle fatigue

Prioritize interventions appropriately for respiratory distress & respiratory failure.

• 1. Optimize ventilation

  • RAISE HOB

  • Tripod position

  • Stop exertion

• 2. Oxygenate

  • Stay with patient

  • Nasal cannula (1-6 L, 22-44% O2)

  • Venti mask (5-10 L, 35-60% O2)

  • Partial rebreather (10-15 L, 50-60% O2)

  • Nonrebreather (10-15 L, 65-95% O2)

  • Positioning -> sit up

  • PURSED LIP BREATHING

• 3. Make notifications

Evaluate patient response to oxygen therapy and when to escalate care

• Measure SpO2, look at respiratory effort, observe mental status -> reslessness, agitation, or confusion is one of the earliest signs of hypoxia

• Check skin color for any blue tint, esp on lips and nail beds

• Escalate care when SpO2 continues to drop/fails to rise, significantly increased work of breathing, and altered LOC

• Assess ABGs, RBCs and hemoglobin, sputum culture/cytology to identify if there is an underlying infection hindering gas exchange

Integrate diagnostic findings (CBC, chest x-ray, sputum cultures, peak flow, PaO₂/FiO₂ ratio) with assessment data and identify the nursing implications associated with diagnostic processes (bronchoscopy, thoracentesis, etc.)

• Blood

  • Do CBC to look at RBCs and WBCs

  • This is to check if there is an infection causing problems

  • Look at ABGs

• X-ray

  • CXR

  • Patient position (AP vs lateral)

  • Portable vs standard

• Sputum

  • Culture and sensitivity

  • Cytology -> to identify the origin, structure, function, and pathology of cell

  • Acid bacillus: to identify presence of TB

  • Early morning is best time to collect sputum

  • Cough up from bronchial tree

  • Get respiratory to induce if possible

• Endoscopic bronchoscopy

  • Allows practitioner to visualize lungs and air passages

  • Partial intubation -> consciously sedated

  • Go in with scope and look at bronchial tree + some alveolar sacs to get tissue samples

  • NPO 6-12 hrs before

  • Consent

  • GAG/SWALLOW REFLEX MONITORING

  • Monitor VS, breath sounds & LOC during and post-procedure

• Biopsy

  • Diagnostic sampling for culture or cell analysis

  • May be done by endoscopy, needle aspiration, or surgical procedure

  • Ask if pt is taking blood thinners since we’re poking holes in someone

• Thoracentesis

  • Taking pleural fluid sample or draining to remove excess

  • Can stil have hypotension d/t this

  • Assess for resp. Distress

  • Can poke a lung, be careful

  • Before the procedure, educate patient, get consent, and work on positioning

  • After procedure, get x-ray, patient will cough as lung expands, assess for respiratory distress & hypotension

• Peak flow

  • measures how well air moves out of your lungs

  • max exhalation speed to monitor asthma or chronic breathing conditions

  • helps detect narrowing in the airways before symptoms appear

• PaO2/FiO2 Ratio

  • critical clinical metric used to evaluate lung oxygenation efficiency and severity of hypoxemia

  • calculated by dividing PaO2 by fractional inspired O2 (FiO2)

  • normal is 300-500

  • <100 is severe ARDs

  • <200 is moderate ARDs

  • <300 mild ARDs

acute bronchitis

• Inflammation of bronchi

• Viral cause

• Primarily affects bronchi and not alveoli

• Manifestations:

  • Coughing

  • Clear mucoid sputum; may become purulent

  • Fever

  • Dyspnea

  • Headache & malaise

  • Violent coughing

  • Hoarseness, myalgia, chest pain

• Diagnosis:

  • Listen to crackles d/t mucus build up and wheezes on exhalation with exertion

  • Chest x-ray to r/o pneumonia

• Tx goals:

  • Symptom relief w tea, honey, cough drops, menthol

  • Prevent pneumonia

• Interventions:

  • Droplet precuations

  • VS

  • TCDB Q2H

  • PO fluids to loosen mucus

  • Prevent spread

  • Antitussives

  • Expectorants

  • Bronchodilators -> levalbuterol and albuterol

pneumonia

• Infection that spread from bronchioles to alveoli -> more dangerous

• Bacterial infection cause

• Organism reaches lung thru aspiration, inhalation, or hematogenous spread

• Community acquired/nosocomial

• infection/fluid in lung tissue

• Swelling in alveoli and consolidation of debris, fibrin, fluid = impaired gas exchange

• Assessment

  • Fever

  • Chills

  • Cough

  • Sputum

  • Chest pain

  • Crackles

  • Rhonchi

  • Decreased SaO2

• Diagnostics

  • CXR

  • C&S

  • CBC

  • Pulse ox

  • Blood cultures if increased fever

• Interventions

  • TCDB, IS

  • O2 to treat hypoxemia

  • Hydration

  • I&O

  • Analgesics for pain

  • Antipyretics for fever

  • Antibiotics for infection

  • Comfort with cough suppressants, mucolytics, bronchodilators, corticosteroids

pertussis

• Highly contagious bacterial disease with violent whooping cough

• Symptoms:

  • Initial: similar to acute bronchitis

  • Severe coughing, worse at night

  • Vomiting may occur with coughing

  • Runny nose

  • Fever (102 F or lower)

• Stages

  • Stage 1 (1-2 weeks): low-grade fever, runny nose, watery eyes, general malaise, nonproductive cough

  • Stage 2 (2-10 weeks): violent coughing

  • Stage 3 (2-3 weeks): less severe cough, weak

• Diagnosis:

  • Initially based on symptoms

  • Sputum culture

  • CBC

• Rx:

  • Airborne precautions

  • Antibiotics -> macrolides -> erythromycin, zithromax

  • Fluids

  • Expectorants & suppressants are NOT helpful are are not recommended

• Prevention:

  • DPT vaccination for children

  • All adults should have TDAP

  • Children under 2 months cannot be vaccinated

tuberculosis

• Infectious disease spread by airborne droplets

• Lungs are most commonly infected

• ¼ of world’s population has TB

• Travel, work in hospital, living in group settings is a risk

• Classification:

  • Exposure to TB thru inhalation, but contained with immune response

  • Active TB -> immune response fails and bacteria duplicate & disease emerges within 2 years

  • Latent TB -> positive skin test but asymptomatic and non-transmissible, 5-10% risk of developing active TB

• Manifestations:

  • Latent TB:

    • No S/S

    • Doesn’t feel sick

    • skin/blood test (+)

    • (-) sputum smear

    • Normal CXR

  • Active TB:

    • Coughing > weeks

    • Chest pain

    • Weakness, fatigue

    • Weight loss, anorexia

    • Chills

    • Fever

    • Night sweats

    • Feels sick

    • Skin blood test (+)

    • Sputum smear (+)

    • Abnormal CXR

• Diagnostics

  • H&P

  • Skin test

  • QuantiFERON-TB gold test

  • CXR

  • Bacteriologic studies

  • Sputum smear for acid fast bacilli

  • Sputum culture

• Interventions:

  • Active TB:

    • Restrict visitors + public exposure

    • Hand hygiene and oral hygiene

    • Aggressive antibiotic therapy (4-9 months)

    • Direct observed therapy is preferred but is controversial

  • Latent:

    • Antibiotic therapy (4-9 months)

atelectasis

• Alveolar collapse - lung not expanding

• Decreased surfactant

• Secretions occlude alveoli and make them collapse

• Caused by shallow breathing, sedation, decreased mobility, post-op

• Easier to anticipate/prevent than to treat

• Assessment:

  • RR and rhythm

  • WOB

  • Dyspnea

  • Cough

  • Breath sounds decreased or absent

• Diagnostic test:

  • O2 sat

  • CXR

  • ABGs

• Interventions:

  • Re-expand alveoli with cough, suctioning, CPT

ARDs

• A life-threatening, severe inflammatory lung injury that causes fluid to build up in the alveoli (air sacs), preventing oxygen from reaching the bloodstream

  • Damage to alveoli and pulmonary capillaries

  • Increased permeability of alveolar blood vessels

  • Fluid accumulates in alveolar spaces

  • Alveoli becomes airless, damaged, decr surfactant, less compliance, less ventilation, so hypoxia occurs

  • Respiratory failure

• Caused by pneumonia, sepsis, trauma, inhalation injury

• Risk factors of smoking, alcohol abuse, high-risk surgeries

• Assessment:

  • Early -> increased RR, dyspnea, restlessness, cough

  • Late -> diaphoresis, increased SOB, cyanosis

• Diagnostics:

  • CXR, CT

  • ABGs

  • SaO2

• Interventions:

  • mechanical ventilation

  • Positioning -> prone position

  • Pursed lip breathing

  • Strict I&O

  • Keep patient euvolemic

  • Serial ABG monitoring

pulmonary fibrosis

• progressive scarring or thickening of the lung tissue surrounding the alveoli

• no good expansion of lungs or alveoli

• caused by environmental things/chronic inflammatory processes or unknown cause

• assessment:

  • SOB

  • DOE

  • dry cough

  • weakness/fatigue

  • clubbing of fingers or toes

  • chest discomfort

• diagnostics:

  • imaging

  • PFTs to measure lung volume/capacity

  • biopsy

• interventions:

  • monitor respiratory status

  • administering meds

  • educate abt energy conservation

  • promote adequate nutrition

  • encourage smoking cessation

  • facilitate emotional support

chronic obstructive pulmonary disease (COPD)

• Group of pulmonary disorders with S&S of chronic cough and expectoration, dyspnea, and impaired expiratory airflow

• Combo of 3 diseases that limit airflow and it isn’t fully reversible:

  • Emphysema

  • Chronic bronchitis

  • Asthma

• Pathophysiology

  • Irreversible airflow limitations during forced exhalation d/t loss of elastic recoil

  • Airflow obstruction r/t mucous, bronchospasm, mucosal edema

  • Primary initiation is inflammation -> inhalation of noxious particles, mediators released cause damage to lung tissue, airways inflamed, parenchyma destroyed

  • Supporting structures of lungs are destroyed -> air goes in easily but remains in the lungs.. Bronchioles tend to collapse and this can cause barrel-chest look

• Complications

• Hypoxemia, hypoxia, hypercapnia, respiratory acidosis

  • Inflammation of airways -> destruction of alveoli -> restricted flow of O2 -> hypercapnia -> respiratory acidosis

• Respiratory tract infections

  • More likely to catch colds and infection can damage lung tissue

• Cardiac dysrhythmias

  • r/t respiratory and heart failure, HTN, coronary disease

• Pulmonary hypertension -> cor pulmonale and cardiac failure

  • Constriction of pulmonary blood vessels d/t alveolar hypoxia.. Increased blood viscosity

Prioritize nursing interventions specific to individual conditions including positioning, controlled oxygen therapy, pursed-lip breathing, and infection prevention.

• For oxygenation & respiratory conditions like COPD and pumonary HTN

  • Pursed lip breathing

  • Positioning -> high fowler’s or tripod

  • Controlled oxygen therapy

  • Infection prevention -> bc higher risk of developing a respiratory tract infection

• Circulatory conditions (right-sided heart failure/cor pulmonale)

  • Positioning -> elevate HOB

  • O2 therapy -> to maintain adequate oxygenation is vital to reduce pulmonary artery pressure

Recognize clinical patterns of pulmonary fibrosis and ARDS and determine priority interventions to optimize oxygenation and prevent worsening respiratory failure.

• ARDs

  • Hypoxemia

  • tachypnea , dyspnea, dry cough, restlessness

  • Cyanosis, diaphoresis, increase WOB

• Pulmonary fibrosis

  • Progressive scarring leads to stiff lungs that are difficult to inflate

  • Chronic dry cough, dyspnea on exertion, fatigue, weakness

  • Clubbing of fingers/toes

• Interventions!

  • Optimize ventilation with raise HOB, tripod position, high fowler’s

  • Energy conservation to reduce body’s demand of O2

  • Pursed lip breathing

  • Escalate O2 therapy

  • mechanical ventilation for ARDs to keep alveoli open with positive pressure

  • Prone positioning for ARDs

  • Maintain fluids

  • Continually monitor ABGs

Explain the pathophysiology of chronic bronchitis and emphysema and how they contribute to airflow limitation.

• Chronic bronchitis

  • “Blue bloater”

  • Airway problem -> inflammation and excessive mucus

  • Chronic exposure to irritants causes hypertrophy of mucus-secreting glands -> thick mucus that can’t be effectively cleared

  • Airway narrowing bc bronchial walls become thick and inflamed

  • Mucus plugs form to block smaller airways

  • Increased resistance to airflow which can lead to hypoxemia and cyanosis

• Emphysema

  • “Pink puffer”

  • Alveolar problem -> destruction of lung parenchyma

  • Irritants trigger breakdown of elastin in alveolar walls

  • Alveolar septa destroy and the grapes become one conglomerate -> lose valuable SA

  • Loss of elastic recoil - > air can’t be effectively pushed in and out

  • Hyperinfaltion of lungs -> barrel chest

Recognize cues distinguishing COPD baseline status from an acute exacerbation (increased dyspnea, sputum change, wheezing, SpO₂ decline).

• An acute exacerbation has:

  • Dyspnea at rest

  • Sputum that increases in volume, thickness, and change in color

  • Increase in wheezing

  • SpO2 decline

Evaluate complications such as cor pulmonale and CO₂ narcosis.

• Cor pulmonale:

  • Right-sided heart failure

  • d/t air trapping, airway collapse, inelastic alveolar walls -> right ventricle of heart has to work harder to push blood into the pulmonary arteries

  • Over time, RV enlarges… and can cause right-sided heart failure

  • Hypoxia and high CO2 cause pulmonary vasoconstriction -> increases resistance in the pulmonary arteries -> RV has to work harder to push blood thru narrowed vessels -> overtime, RV muscle enlarges and can fail

    • Cues:

      • Peripheral edema

      • JVD

      • Hepatomegaly

      • Weight gain

• CO2 narcosis (CO2 retention)

  • Pts drive to breathe is disrupted by inappropriate O2 therapy

  • In chronic COPD, brain becomes used to high CO2 and stops responding to it

  • Instead, the body relies on low O2 levels to trigger breathing

  • If giving pt supplemental oxygen, their brain senses high O2 and won’t be prompted to breathe

  • This leads to CO2 buildup

    • Cues:

      • Altered mental status -> lethargy/drowsiness

      • Confusion & agitation

      • Shallow, slow respirations

    • TITRATE O2 TO 88-92%

Describe the normal pH range of arterial blood (7.35–7.45) and explain its importance for enzyme activity, oxygen delivery, and cellular function.

• Normal pH is 7.35-7.45

• At that pH, enzymes work, muscle contraction, and O2 delivery

• When pH is off, cardiovascular changes occur bc all the muscle in the heart

• Build up of acid in body makes hemoglobin carry less O2

Define acids and bases and identify primary sources of acids in the body.

• Acids are CO2 or H+ or metabolism byproduct

• Cellular metabolism -> carbonic acid (H2CO3)

• Anaerobic metabolism -> lactic acid

• Fat metabolism -> ketoacids

• Stomach -> hydrochloric acid (HCl)

Explain the concept of acid-base balance and differentiate between acidosis and alkalosis.

• Acids and bases have to be balanced to maintain normal body pH to keep functions going

• Acidosis is too much acid in body or too little buffer

• Alkalosis is too little acid in the body or too much buffer

Summarize how buffer systems (carbonic acid–bicarbonate, phosphate, protein, hemoglobin) maintain short-term regulation of pH.

• Carbonic acid-bicarbonate buffer:

  • Main buffer that is most efficient and works the quickest

  • Buffers change strong acids into weaker ones and bind to them to neutralize

  • CO2 + H2O ←→ H2CO3 ←→ HCO3- + H+

  • We can also balance by breathing out the CO2 that carbonic acid breaks down into

  • If buildup of CO2, it’ll bind to water to create carbonic acid -> turns into bicarb and H+ -> get rid of bicarb thru kidneys

• Phosphate buffer

  • Active in the ICF and renal tubules

  • Consists of sodium dihydrogen phosphate and sodium monohydrogen phosphate

  • Highly effective in the kidneys, where it buffers H+ ions in the urine, preventing the urine from becoming too acidic and allowing for the safe excretion of “trash” acids

• Protein buffer

  • Most abundant buffer system bc proteins are everywhere

  • Proteins can act as either acid or base

  • Amino acids can release H+ if pH is too high and can release an amino acid that binds to H+ if pH is too low

• Hemoglobin buffer

  • Hemoglobin can bind to H+ to help excrete them from the body, but that means less O2 able to bind to hemoglobin instead

Explain how the respiratory system regulates acid-base balance through control of CO₂ and ventilation rate.

• Respiratory center in brainstem senses changes in CO2 and H+ and will adjust rate/depth of respirations to restore balance

• Acts within minutes

• Fast but temporary!

• When pH low (acidic) -> breathe faster and deeper to get out CO2

• When pH high (alkalosis) -> breathe slower to retain more CO2

Describe the renal system’s role in maintaining long-term acid-base balance by controlling H⁺ and HCO₃⁻ levels.

• Slowest compensatory system

• Responds in hours - days

• But provides long-term regulation

• Kidneys regulate HCO3- and H+

• When pH low (acidic) -> pee out more H+ and increase production of bicarb

• When pH high (alkalosis) -> retain more H+ and decrease production of bicarb

Compare and contrast the speed and effectiveness of respiratory vs. renal compensation mechanisms.

• Respiratory

  • Works faster - within minutes

  • Temporary compensation

• Renal

  • Works slower - hours to days

  • Long-term regulation

Analyze how compensation attempts to restore pH toward normal in both acute and chronic imbalances.

• Respiratory compensation = control breathing

  • High pH (alkalosis) -> retain CO2 -> slow/shallow breathing

  • Low pH (acidosis) -> get rid of CO2 -> faster/deeper breathing

• Renal compensation = control what you pee out + produce

  • High pH (alkalosis) -> retain more H+ and produce less bicarb

  • Low pH (acidosis) -> get rid of CO2 -> pee out more H+ and make more bicarb

respiratory acidosis

• Causes:

  • Hypoventilation

  • COPD -> can’t exhale air fully

  • Pneumonia -> fluid in lungs so harder to breathe

  • Pulmonary edema -> fluid overload in lungs

  • Airway obstruction

  • opioids/sedatives

  • Chest wall injury

  • Pain

  • Neuromuscular weakness

• Manifestations:

  • Dyspnea

  • Headache

  • Hyperkalemia

  • Dysrhythmias (increased K+)

  • Drowsiness, dizziness, disorientation

  • Muscle weakness

  • Hyperreflexia

  • Decreased BP with vasodilation

• Compensatory responses:

  • Kidneys -> pee out more H+ and produce more bicarb

respiratory alkalosis

• Causes:

  • Hyperventilation

  • Anxiety

  • Fear

  • Pain

  • Fever

  • Hypoxia

  • Brain injury

  • Mechanical over-ventilation

• Manifestations: - activation of sympathetic nervous system

  • Tachycardia

  • Decreased BP

  • Hypokalemia + hypocalcemia - alkaLOWsis

  • Numbness & tingling of extremities

  • Hyperreflexes and muscle cramping

  • Seizures

  • Increased anxiety + irritability

  • Numbness in lips/fingertips

• Compensatory responses:

  • Kidneys -> retain H+ and produce less bicarb

metabolic acidosis

• Causes:

  • Too much acid

    • Diabetic ketoacidosis -> body doesn’t produce enough insulin, breaks down fat for energy, ketones are acidic

    • Lactic acidosis -> byproduct of anaerobic metabolism

    • Sepsis -> hypoxia and metabolic dysfunction force cells to produce lactate instead of energy -> lactic acidosis

    • Shock -> hypoperfusion causes anaerobic metabolism -> lactic acidosis

  • Not enough base

    • Acute kidney injury -> kidney stop doing their job well -> doesn’t make enough bicarb and doesn’t get rid of H+

    • Chronic kidney disease -> kidney stop doing job well -> doesn’t make enough bicarb or get rid of H+

    • Diarrhea -> lose base from butt

• Manifestations:

  • Headache

  • Decreased BP

  • Hyperkalemia

  • Muscle twitching

  • Warm, flushed skin

  • Nausea, vomiting, diarrhea

  • Changes in LOC -> confusion and drowsiness

  • KUSSMAUL RESPIRATIONS -> compensatory fast and rly deep breathing to blow off CO2

• Compensatory responses:

  • Respiratory!

  • Breathe more rapidly and deeper to get out CO2

metabolic alkalosis

• Causes:

  • Too much base or not enough acid

  • Excess bicarb intake -> antacids, IV sodium bicarb, Ca+2 supplements

  • Diuretics -> Increase renal bicarb reabsorption and H+ loss -> raises blood pH

  • GI acid loss -> vomiting, NG suctioning

  • Hypokalemia -> drives K+ out of cells -> H+ moves into cells and decr blood pH

• Manifestations:

  • Restlessness followed by lethargy

  • Dysrhythmias (tachycardia)

  • Confusion (decreased LOC, dizzy, irritable)

  • Nausea, vomiting, diarrhea

  • Tremors, muscle cramps, tingling of fingers/toes

• Compensatory responses:

  • Respiratory!

  • Decreases rate and depth of respirations - slower and more shallow

Recognize clinical signs and expected ABG changes for each imbalance.

• Respiratory acidosis:

  • pH < 7.35

  • PaCO2 > 45 mmHg

  • Clinical signs:

    • Hypoventilation

    • Drowsiness, confusion

    • Headache

    • Cyanosis (late)

    • Tachycardia

• Respiratory alkalosis:

  • pH > 7.45

  • PaCO2 < 35 mmHg

  • Clinical signs:

    • Hyperventilation

    • Anxiety, irritability

    • Lightheadedness

    • Paresthesia

    • Muscle cramps/tetany

• Metabolic acidosis:

  • pH < 7.35

  • HCO3- < 22 mEq/L

  • Clinical signs:

    • Kussmaul respirations - deep and rapid

    • Confusion/lethargy

    • Weakness

    • N/V

    • Warm, flushed skin

    • Hyperkalemia -> dysrhythmias

• Metabolic alkalosis:

  • pH > 7.45

  • HCO3- > 26 mEq/L

  • Clinical signs:

    • Muscle cramps/tetany

    • Hyperreflexia

    • Weakness

    • Dizziness

    • Hypokalemia - dysrhythmias

    • Shallow respirations - compensation

Prioritize nursing interventions to correct or support compensation (oxygen therapy, rehydration, electrolyte replacement, etc.).

• Respiratory acidosis

  • Improve ventilation -> elevate HOB, deep breathe, IS

  • O2 therapy -> 88-92%

  • Airway clearance with chest physiotherapy or suctioning

• Respiratory alkalosis

  • Slow rate of breathing by encouraging paper bag breathing/rebreather

  • Anxiety management

  • Calm environment

• Metabolic acidosis

  • Fix root cause..

    • DKA -> IV insulin & fluids

    • Diarrhea -> rehydration, antidiarrheals

    • Sepsis -> antibiotics & IV fluids

    • Shock -> IV fluids, vasopressors

    • Renal failure -> dialysis

  • Could admin sodium bicarb but it isn’t gonna fix it

  • Support ventilation & oxygenation

• Metabolic alkalosis

  • Fix root cause..

    • Vomiting -> antiemetics

    • Hypokalemia -> K+ replacement, avoid K-wasting diuretics

    • Excess bicarbonate -> discontinue or reduce intake

  • Support ventilation & oxygenation

    • Since breathing is slowing down, might need external O2 source

Explain potential complications of untreated acid–base disorders (e.g., dysrhythmias, altered LOC, hemodynamic instability).

• Cardiac dysrythmias due to movement of K+dysrhythmias

  • Acidosis = high K+ -> peaked T-waves and can lead to v-fib or astyole

  • Alkalosis = low K+ -> U-waves, flattened T-waves, increased cardiac irritability

• Altered LOC

  • Acidosis = narcosis/metabolic coma -> excessive CO2 acts as a CNS depressant

  • Alkalosis = neuromuscular excitability

• Respiratory failure

  • Body’s attempt to respiratory compensate will eventually lead to exhaustion

Identify normal ABG values

• pH: 7.35-7.45

• PaCO2: 35 - 45 mmHg

• PaO2: 80-100 mmHg

• HCO3-: 22-26 mEq/L

• SaO2: 94-100%

Interpret ABG results in the context of clinical scenarios to determine the type of imbalance.

• Look at pH first -> acidosis or alkalosis?

• Respiratory or metabolic?

  • ROME method

    • Respiratory, opposite -> pH and PaCO2 should be opposite trending

    • Metabolic, equal -> pH and HCO3 - should be same trend

Differentiate between uncompensated, partially compensated, and fully compensated states.

• Uncompensated:

  • Compensating lab value remains within normal range -> hasn’t changed to try to fix anything

• Partially compensated:

  • Compensating lab value shifts to correct the imbalance, but pH isn’t back to normal

• Fully compensated:

  • Compensating value shifts to correct imbalance and pH has returned back to normal range