Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Upon completion, participants will do Weak, winded & woozy – the following without critical error: what’s wrong? Integrate assessment findings in pts who present w/ respiratory distress to form an accurate field impression. This includes developing a list of differential diagnoses using higher order thinking and Connie J. Mattera, MS, RN, EMT-P critical reasoning. NWC EMSS Administrative Director

Upon completion, participants will do What audible sounds indicating airway or the following without critical error: ventilatory impairment can be heard w/o Compare and contrast pts a when inspecting the who present w/ dyspnea, airway? weakness, & possible AMS , gurgling Weigh the indications and Hoarseness contraindications of , sounds possible interventions from larger bronchi and sequence evidence- heard through mouth based EMS care Expiratory grunting

Pulmonary S&S airway impairment pathophysiology Secretions/debris in airway Stridor, snoring, gurgling, grunting All respiratory Restlessness, anxiety, dyspnea problems , agonal ventilations can be Use of accessory muscles; categorized rocking chest motion as impacting Retractions, tracheal tugging . Ventilation Hypoxia, hypercarbia . Diffusion Unable to speak/make age-appropriate snds . Perfusion Faint/absent breath sounds

1 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

What should be assessed Work of about breathing? Muscles used to ventilate

A patent airway does not ensure adequate ventilations or gas exchange

General respiratory rate, depth

Inspection cont. Breathing Diaphragmatic, w/ pursed See Saw, Apical lips breathing? Splinting? Own PEEP

Origins of ventilation dysfunction

Speech: talk test

Sentences or syllables? Pacing of speech and breathing Quality of voice; hoarse or raspy? Airway impairment Stuttering Chest wall impairment

2 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Origins of ventilation dysfunction High SCI

Ventilatory depression or arrest CNS: Trauma, stroke, medical neuro condition

Muscles: Ventilatory depression or arrest Myasthenia Nerves: Polio, Guillain-Barrè syndrome, MS Gravis, muscular dystrophy

Breathing considerations in obese pts Factors that impair diffusion Lungs 35% less compliant Thickening of alveolar walls Weight of chest makes Destruction or collapse of alveoli breathing difficult – ↓ permeability ventilate at 8-10 mL/kg Widened SpO2 unreliable on finger – interspace use central sensor ↓ in blood flow Will desaturate if supine

CO2 retention probable CPAP useful

3 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Atmospheric deficiency Conditions w/ Diffusion cont. Alveolar pathology impaired . Asbestosis High permeability diffusion . COPD . ALI; non-cardiogenic . Inhalation injuries . . Asbestosis Interstitial pathology . Near-drowning . High pressures (HF) . Post-hypoxia . Pulmonary . Inhalation injury hypertension Capillary bed pathology: atherosclerosis

Assess gas exchange/ What factors influence the evidence of hypoxia detection of ?

What info is obtained by assessing skin Rate of blood flow Degree of desaturation (at least 5 Gm) color, temp & moisture? Degree of desaturation (at least 5 Gm) Type of light Observer skill Adequacy of oxygenation Thickness and color of skin Adequacy of peripheral perfusion Evidence of SNS stimulation/compensation Cool, hot, pale, flushed, mottled, ashen, cyanotic, & Skin color unreliable: anemia & diaphoretic skin must be explored for cause peripheral vasoconstriction

Start placing Capnography: Numeric reading + waveform monitors prn

Pulse oximetry

Non-invasive BP after 1 manual reading

ECG rhythm + 12 lead

4 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

What does pulse ox measure? What’s the difference A. Mean arterial pressure

between capnography B. Level of CO2 in the blood C. Amount of O dissolved in plasma & pulse oximetry? 2 D. % of hemoglobin bound with a gas

Problem: Many pts have unrecognized hypoxia by physical exam alone Pulse ox is NOT the same as the pO2! If SpO2 is 90%, the pO2 is…

P Values

P90: SpO2 90 = pO2 60 P75: SpO 75 = pO 40 SpO2 artificially elevates when hyperventilating 2 2 For each 1 Torr pt ↓ pCO2, the pO2 ↑ by 1 Torr P50: SpO2 50 = pO2 27 Hypoxia common in HF & COPD; means severe distress in

Pulse oximetry range guidelines right tool the Ideal: 96%-100% right way! Mild-mod : 90%-95% Use the Severe hypoxia: < 90%

Severely low

SpO2 (< 90%) If low, validate predictor of on another site poor outcomes - use a central sensor

5 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

The affinity of hemoglobin for O2 is altered by conditions in the tissue the blood is flowing through… Which of these will influence the amount of O2 delivered to cells? A. Acid-base status B. Body temperature Capnography C.The amount of hemoglobin Indicates adequacy of ventilations, perfusion, & dead D.All of the above space by detecting how much CO2 is exhaled Gives a numeric value & graphic waveform

HF should have normal, Waveform shape Capnography squared off waveform helps make a differential diagnosis

Shark-fin waveform suggests a Use on intubated pulmonary and non-intubated condition pts with a NC (asthma/COPD) attachment or with delayed mask

Asthma or COPD Capnography findings in HF

Capnography: Incomplete inhalation/ After CPAP started, EtCO2 may briefly rise d/t improved ventilations, before it falls due to exhalation; CO2 does not get completely washed out on inhalation Severely ↑ EtCO2 indicates ↑ pCO2 levels and ventilatory failure

6 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Causes of hypercarbia

Hypoventilation from any cause ■ Airway obstruction ■ Respiratory depression ■ Ventilatory muscle impairment ■ Pulmonary obstructive diseases

Treatment: Correct inciting cause

Breath sound S&S compromised ventilations

Listen Apnea immediately S&S hypoxia for evidence of air entry if Dyspnea; accessory muscle use pt in distress Upright, tripoding; Most ominous Ventilatory efforts weak, sound is shallow, labored, retracting silence Adult RR < 10 or  24/min EtCO2 > 45; change in waveform

O is a drug and must be given to specific 2 Harmed by hyperoxia pts based indications/contraindications and in correct doses by an appropriate route - Uncomplicated Acute MI being vigilant for adverse reactions Post-cardiac arrest Acute exacerbations of COPD Which patients can be Stroke Neonatal resuscitation harmed by hyper oxia

Give O2 to these pts only if evidence of hypoxia and need careful and titrate to dose that relieves hypoxemia without causing hyperoxia (SpO 94%) titration of oxygen? 2 Iscor, S. et al. (2011) Supplementary oxygen for nonhypoxemic patients: O(2) much of a good thing? Crit Care, 15(3), 305

7 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Profound, prolonged hypoxia is also Who should get CPAP? Pulmonary edema COPD/asthma w/ severe distress Flail chest w/o pneumothorax So, who NEEDS O2? Near drowning SpO < 94% (Exception: COPD SpO2 < 94% (Exception: COPD Pneumonia (?) may be best managed w/ SpO 88-92%) 2 Palliative care (?) Actual or potential airway compromise (epiglottitis, airway burns) Diaphragmatic weakness Post-extubation rescue DAI (to increase O2 reserves) Globally poor tissue oxygenation & perfusion (shock)

What do all these conditions have in common? Which is NOT a possible Severe dyspnea & refractory hypoxia complication of using CPAP? Poorly expanded lung fields A. Collapse of the alveoli ↑ WOB (↑ inspiratory muscle work) We’re in B. Decrease in blood pressure ↓ Minute ventilation trouble now! C. Gastric distension and vomiting Inability to remove CO2 from body Hypercarbic ventilatory failure D. Patient anxiety and claustrophobia Narcotic effect on brain  ↓ RR Fatigue + ↓ RR = resp. arrest

Pulmonary circulation (Q) VA/Q ratios Depends on: Adequate blood volume, intact pulmonary vessels & efficient pump Should be 1:1

Q = SV X HR VA = 5,250 mL/min Q = 70 mL X 72 BPM Q = 5,040 mL/min Q = 5,040 mL/min Patients may become hypoxic when ratio is imbalanced

8 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

general rate & quality of pulse: expect strong with HTN; Circulatory/Cardiac status weak if HF or dehydrated  perfusion: general pulse rate, Tachycardia – hypoxia or early shock;  pulse deficit quality, rhythmicity Palpitations or irregular pulse: Ask if hx of AF, PVCs common Establish that BP (SBP  90; underlying cause DBP  60) of respiratory Need MAP of 60 to difficulty is not fill CA cardiac in nature Often high in HF; if low suspect shock

Perfusion impairment Inadequate blood volume Monitor ECG Inadequate hemoglobin: anemia, trauma Bradycardia is Impaired blood flow: pulmonary embolus bad! Capillary wall pathology: pulmonary contusion

12-lead IF: Why is AF common in HF? Discomfort (nose to navel, shoulder, arm, back) SOB/HF Palpitations; dysrhythmia (VT/SVT) GI complaint (nausea, indigestion) Diaphoresis; dizziness/syncope Weak/tired/fatigued With hypoxia & distress, many pts can have Why is it a concern? unrecognized ischemia

9 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Ventricular hypertrophy may If HF & ACS suspected: 12-lead ASAP be evident in leads that If acute ischemia; give NTG per ACS overlie affected ventricle 12 L implications If age undetermined, use NTG dosing for R wave may be tall in V5 or pulmonary edema seen in V6, >25 mm high Typically, AMI severe Look for deep S wave enough to cause (>25 mm) in V1 or V2 pulmonary edema, will cause ST depression or T wave hypotension inversioninversion inin thosethose leadsleads suggest ventricular strain

Tall, peaked P waves “P pulmonale” pattern of COPD Cerebral function may be affected by Fatigue Hypoxia; hypercarbia Cardiac status

Assess mental status for: Secondary assessment Alertness, anxiety, apprehension, restlessness SAMPLE history AMS, confusion, disorientation, Full set of VS decreased LOC ROS Dizziness ■ Inspection Headache ■ Palpation Perioral tingling ■ Seizure, syncope, coma ■ Auscultation

10 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Dyspnea on exertion? Chief complaint Ask pt to take a deep breath & ask about pain Dyspnea at rest? Pleuritic may suggest OPQRST of S&S Pleuritis, , Pneumonia (ask about chills or fever) Inflammation of lungs from TB Pulmonary HTN Costochondritis Pericarditis Rib fracture Lung cancer

Coughing? differential Aspiration Smoke inhalation Secretions Irritation Hyperreactive airways Bronchospasm Cough variant asthma is usually caused by airway Productive or irritation and/or constriction. Coughing may increase non-productive? to retching causing bronchospasm & hypoxia.

Sputum quantity, color, Frothy consistency, odor

NOTE due to pulmonary edema Clear (pink-tinged means Yellow/Green surfactant is Rusty/bloody washing out) Quickly look for Pneumonia S&S LV failure Chronic (S3 heart sound)

11 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Allergies to food, meds, plants, pets, bites, stings, environmental triggers, What are all exercise or others? those drugs they are taking?

Medications Meds Cardiac Pulmonary EpiPen prescribed? □ ACEIs: “prils” □ Short/long-acting beta Taken anything to □ ARBs: “sartans” agonists relieve symptoms? □ Beta blockers: “lols” □ Anticholinergics □ Ca Blockers □ Mast cell inhibitors □ Diuretics □ Leukotriene modifiers □ Vasodilators □ Steroids Have they □ Anticoagulants (AF) □ Methylxanthines taken a □ Antiarrhythmics □ Erectile dysf. drugs NEW □ Digoxin □ Home oxygen medication? Time and amount of last dose

Meds – ACE Inhibitors (ACEI) Generic name ends in “pril” What can block Blocks creation of angiotensin II: the SNS? Vasodilates pt, ↓ BP, prevents remodeling Cardio-selective and ↓ the heart’s workload drugs Benzapril / Lotensin Moesipril / Univasc Β-1 blockers: end in “lol” Captopril / Capoten Perindopril / Aceon Enalapril / Vasotec Quinapril / Accupril Fosinopril / monopril Ramipril / Altace Lisinopril / Prinivil / Zestril Trandolapril / Mavik

12 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Acebutolol (Sectral) Beta 1 blockers SOB, cough, dyspnea? Atenolol (Tenormin) Asthma/COPD? …PMH Betaxolol (Kerlone) Other pulmonary conditions? Bisoprolol (Zebeta) Carvedilol (Coreg) CVD: CAD, HTN, ACS, stroke Labetalol HF, dysrhythmias Metoprolol/Lopressor/Toprol Valve disease Nadolol (Corgard) Diabetes Pembutolol Drug abuse Pindolol Propranolol (Inderal) Chronic renal failure Timolol (Blocadren) Gastric surgery Sotalol (Betapace)

Acute vs. Chronic in nature? Past medical history Classified by nature of onset Tobacco use Acute: Rapid onset and short duration Report in pack years Chronic: Slow onset, # of packs smoked/day X persists over time # of yrs they’ve smoked Problems when pack years surpass 20

AP/Lateral diameter Chest palpation Lateral diameter Palpation plays minor role in exam of normal should be 2X chest; lungs covered by ribs & aren’t palpable AP diameter palpable Compress downward on sternum; Increased AP diameter inward on lateral chest wall (gently) (barrel chest) Point of maximum impulse (apical pulse) with diaphragmatic flattening associated w/ emphysema and lung hyperinflation Rib flare?

13 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Must have significant disease before How can EMS miss findings or asymmetry ofPalpation expansion can be identified on exam misdiagnose? Point tenderness: Investigate painful areas Poor equipment Deformity, instability Poor auscultation technique Misinterpret cause of wheezes Crackles isolated to 1 lobe Diminished lung sounds not detected Lack of adequate history

DIANA:hf-3-08

Sit pt up (if able) How to listen? Technique: Turn supine patient to assess back Where should you listen? Ask pt to breathe normally All lobes, front and back through open mouth Stethoscope on skin – not over clothes Front

Back

Where to start? Anterior: Start at apex, move down Auscultatory triangle in back to bases - compare Medial/lower scapula; less side to side muscle mass; easy to hear snds TIPS Lower diaphragm attachment Lasissimus dorsi Have pt cough if in back; fluid accumulates sounds difficult there first to hear Move up from posterior bases - Exhale forcefully to compare side to side – accentuate wheezing one breath at each site that is faint when breathing normally

14 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

What are List 2 conditions that may adventitious sounds? List 2 conditions that may present with crackles Sounds that are super-imposed on LV failure w/ pulmonary edema normal breath sounds Poorly ventilated areas of atelectasis Crackles Localized over early or non-consolidating pneumonia Wheezes Pulmonary fibrosis Stridor Tubercular lung cavities Pleural friction rub Lung abscess Terminally ill w/ depressed cough reflex

Brother O’Mara

Harmonic, musical sounds Wheezes Wheezes produced by turbulence when air Sibilant (asthma/emphysema) passes through bronchi that fluctuate between closed & barely open Sonorous (formerly called rhonchi) Louder/longer on expiration Describe according to location, pitch, duration, Severity does not correlate timing, complexity well w/ degree of airway obstruction – assess capnography Wheezes dissipate with bronchodilator therapy No wheezing if severe airway obstruction – assess ability to move air

All that wheezes is not asthma Consider other causes Bilateral wheezes in cardiac conditions A: Asthma . May be caused by external airway S: Stasis: Pulmonary embolism compression from interstitial water T: Toxins/inhaled irritants . Fluid in alveoli irritating bronchioles causing H: Heart: HF; “cardiac asthma” bronchospasm M: Mechanical obstruction, FB, cancer . Other mechanisms not well understood A: Allergy/aspiration TIC: Trauma, infection, chronic (COPD)

DIANA:hf-3-08

15 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Differential Pleural friction rub Pleural friction rub Pericardial friction rub Quality: Loud & grating, Quality: Hard & grating, creaking or squeaking scratching or crunching Location: Low axilla; Location: Lower L sternal anterior, lateral, or post. border bases Timing: Occurs in relation Produced by inflamed pleurae moving over Timing: one another - associated w/ pleuritic pain Timing: Late inspiration/ to heartbeat; most early expiration; ceases noticeable during deep May be heard in pulmonary if pt holds breath; inspiration; continues if pt thromboembolism, pneumonia, persists during coughing holds breath and pulmonary vasculitis

Decreased or Stridor absent sounds Fluid may move into pleural space, causing a pleural effusion Loss of surfactant → atelectasis

Heart sounds S3: Ventricular gallop 3rd sound occurs early in diastole immediately after “dub” with cadence like “Ken-tuck-y” Caused by early, rapid filling of a dilated LV Most audible at apex with pt on L side Abnormal > 30 years of age Present in 70% of pts > 40 yrs w/ EF < 30% S1 (lub): Beginning of systole; closure of mitral and tricuspid valves. Most audible at apex & lower sternal border S2 (dub): Beginning of diastole; closure of aortic & pulmonic valves Most audible at base

16 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

S4: Atrial diastolic gallop Rapidly assess abdomen Forceful ejection of blood into stiff ventricle  for ascites – chronic RV heart failure Most audible at apex Hepatojugular reflux – neck veins distend Occurs late in diastole and may be caused by when liver palpated (sign of hepatomegaly) pulmonic stenosis or any condition that affects left ventricular compliance, e.g., aortic stenosis, hypertension, MI, cardiomyopathy

Peripheral edema New-onset HF <25% of pts; rarely have peripheral edema Causes: . Ischemia or MI . HTN crisis . Arrhythmia – tachy, brady . Pulmonary embolus Acute decompensation of chronic Rt HF ~75% of pts (RV involved) Often have recent wt gain (fluid) & dependent edema (sacral or feet/ankles)

911 called for a 68 y/o m w/ breathing problems Look OK right now? Pt confused but able to speak in short phrases Exam: ↑ WOB w/ diffuse wheezes; no crackles VS: BP 148/89; P 87; RR 32 & labored; SpO2 84% on RA Glucose: 145 12 L ECG as follows:

17 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

HPI: ↑ SOB for past 24 h w/ mild cough and confusion What’s wrong? Denies fever/chest pain Meds: metformin, Benicar, Crestor, albuterol, ipratropium Unsure if he took meds PMH: CAD, HTN, high cholesterol, bypass surgery, HF, t2DM, chronic bronchitis

Differential Consider cause: Treat based on etiology ALI Heart failure AMI Panic disorders Pleural effusion Anaphylaxis Pulmonary edema Aspiration Pneumonia Asthma Pneumothorax COPD Pulmonary embolism

Common causes of Lt HF Path to pulmonary edema LV systolic dysfunction When patient has an MI, uncontrolled (60% of pts) HTN, valve disease, or dysrhythmia, HTN (75% of pts) LV becomes CVD, CAD damaged and Hx: MI does not pump Faulty valves effectively Myocardial disease (myopathies, myocarditis) Diabetes, renal failure

18 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Compensatory mechanisms SNS tries to compensate… ↓ LV stroke volume sensed by receptors - Norepi from nerve trigger series of compensatory responses endings Baro receptors in aortic arch, Epi from adrenal carotid sinus glands and kidneys ↑ heart performance Osmoreceptors & maintain MAP in brain Epi activates β receptors Norepi activates α receptors

Fight or flight response SNS Actions Goal: Provide energy, O2, & ability to react to stress α β Pupils dilate Arterioles constrict ↑ rate, force, Leg arteries dilate Heart automaticity, ↑ HR, contractility, BP conduction Bronchodilation, Lungs Constricts Dilates ↑ RR ATP stimulated Sweating Vessels Constricts Dilates

Nor-epi adds to afterload from atherosclerosis LV must work harder to overcome afterload Kidneys sense & pump blood to systemic circulation drop in perfusion ↑ workload =

O2 demand enlarged heart Heart becomes stiffer & more rigid, ↓ elasticity Secrete renin…

19 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Circulatory RAAS 10% Tissue RAAS 90% Secondary Angiotensinogen compensatory mechanisms Renin Angiotensin I Endothelin from vascular lining results in Angiotensin converting enzyme vasoconstriction – helps perpetuate failure (ACE) Angiotensin II ADH acts on renal collecting ducts to Angiotensin receptors hold water and Vasoconstriction Sympathetic stimulation vasoconstrict pt Remodeling •Heart •Blood vessels

Aldosterone Sodium and water retention with edema Secretion Increase in interstitial fibrosis

Increased preload activates Cardiac muscle cells lengthen & thin Starling’s law Inflammatory response forms scar tissue to create greater contraction Ventricle remodels to a spherical shape – RIGHT heart receives changing mass, composition, volume & blood from body & cardiac function pumps it into lungs Over time, ventricles become overstretched & weak (chronically overinflated balloon)

Fluid dynamics in LV HF Blood cannot move Ventricular filling &/or emptying is impaired forward from lungs to LV ↑ blood remains in LV after systole Pulmonary vessels LV & LA overfill until they cannot hold more engorge with blood ↑ hydrostatic pressure leads to venous congestion in lungs

20 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

End result – In HF, fluid accumulates faster than Pressure problem in lungs removed = interstitial edema Pressure in vessels > pressure in tissues → fluid leaks to interstitial spaces Bronchovascular cuffs can hold ~500 mL Lymph system can remove 10-20 mL/ hr in healthy lung; under stress, can remove more through ↑ flow Gas exchange impaired; O2 demand ↑ 500% leading to ↑ WOB Pt experiences dyspnea & wheezes

Then… Alveolar walls damaged Basic problems… Pressure in tissues > pressure in alveoli Too much fluid (pressure) in lung Fluid floods into alveoli, washes out surfactant = atelectasis & alveolar pulmonary edema vessels and tissues Alveoli only open with Loss of surfactant, atelectasis & considerable ventilatory effort alveolar flooding Gas exchange impaired, Impaired ventilations & gas exchange crackles & hypoxia develop ↑ myocardial workload

↑ O2 demand

How may they present? BNP Tachypnea w/ ↑ WOB Released from Accessory muscle use; damaged atria  for retractions and ventricles, position (tripod?) causes excessive Orthopnea, PND, freq. neuroendocrine nocturia: fluid returns to stimulation – lungs & kidneys vasodilates pt Prolonged expiration Breathing w/ pursed lips – own PEEP

21 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Assess for hypoperfusion & cardiorespiratory compromise Differentiate HF from COPD/ asthma by: History Meds Capnography S&S

Emphysema Chronic Obstructive Pulmonary Disease? Destruction of alveolar walls (distal to terminal C O P D bronchioles) & pulmonary capillaries Fundamental problems: So, could it be his Loss of elastic recoil causes bronchioles to collapse on expiration Decreased ability to oxygenate blood

Pathophysiology cont. Large blebs cause alveolar collapse Lungs become Reduces surface for gas exchange more compliant Alters V /Q ratio (stretchy) and Alters VA/Q ratio distend Alveolar walls enlarge and decrease in #

22 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

As disease Pathophysiology cont. progresses, Compensates O levels fall w/ ↓CO & 2 Stimulates RBC Limited blood flow production thru relatively well (polycythemia) oxygenated lung Better ABGs = w/ normal ABGs “Pink puffer” & lung pressures

Pink Puffer - emphysema With low CO - rest of body suffers BP: Pulsus paradoxus hypoxia & P: Tachycardia pulmonary RR: Tachypnea cachexia 1-2 word dyspnea Muscle wasting & Increased WOB weight loss Pursed lip breathing Little/no cough

Chronic bronchitis Tripod position Mucous glands enlarge Chest: Airway walls infiltrated with inflammatory cells Barrel shape Bronchi thicken & become rigid (vasodilation, congestion, edema) Hyperresonant; wheezing; Cilia don’t clear bacteria & mucous HS distant Inflammation & secretions cause obstruction Suprasternal Relatively undamaged retractions pulmonary capillary bed

23 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Pathophysiology Body responds by What form of COPD ↓ventilation & ↑ CO is more likely to develop Rapid circulation in a poorly ventilated Cor Pulmonale? lung = hypoxemia, CO2 retention Emphysema or

↑ pCO2 causes AMS, headaches, and Chronic Bronchitis personality changes

Causes of Cor Pulmonale “Blue bloater” Chronic bronchitis Increased RV strain due to pulm HTN Peripheral edema? (Pulmonary embolism) Cor Pulmonale, HF, renal RV hypertrophy, venous congestion failure, metastatic cancer Cyanosis May be obese Accessory muscle use common Poor peak flow (<150-200 mL)

COPD comparisons

Chronic bronchitis Emphysema “Blue bloater” “Pink puffer”

Productive cough Long hx of progressive Assess for JVD Progression over time to dyspnea intermittent dyspnea Late onset non- Cause: Elevated RA pressure productive cough or inability to drain blood into RA Frequent/recurrent pulmonary infections Occasional mucopurulent May not be present with acute LV failure Progressive cardiac/ relapses + JVD if right HF respiratory failure w/ Eventual weight loss & edema & weight gain respiratory failure

24 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Acute hypoxic ventilatory failure Decision tool if patient is wheezing

SpO2 < 92 w/ FiO2 > 60% PMH Restlessness, anxiety Cardiac Pulmonary Lightheaded □ CVD: HTN; ACS; HF □ Asthma/COPD Disorientated, confused □ Stroke or TIA □ Pulmonary embolus □ Dysrhythmias risk factors □ PVD □ Pneumothorax □ Valve disease □ Diabetes; renal dx □ Pleural effusion □ Drug abuse □ TB, lung cancer □ No Hx resp problem □ Smoking; inhalation □ + cardiac risk factors exposure

Decision tool: Adult wheezing Decision tool: Adult wheezing

Clinical presentation Vital signs Cardiac Pulmonary Cardiac Pulmonary □ Pain: non-pleuritic □ Pain: may be pleuritic □ Cough: frothy □ Cough: mucoid, yellow, Hyper/hypodynamic state BP WNL unless very □ DOE green Pulse deficits if fast HR or hypoxic / dehydrated □ Orthopnea; PND □ Chills, fever, ectopics □ Freq. nocturia night sweats Weak pulse w/ hypotension Upright, (tripod?) position Tachypnea w/ ↑ WOB Accessory muscle use; retractions ↓SpO2; evidence of hypoxia Breathing w/ pursed lips – own PEEP ↑EtCO2; hypercarbia; shape of waveform Right heart failure? Pulsus paradoxus if air trapping/real trouble

Here’s our patient Consider possible causes of S&S

Stridor: F/B aspiration, croup, epiglottitis PaCO2 > 50 mmHg at FiO2 > 50% Wheezing: Asthma/COPD, HF, ACS Crackles: pneumonia (isolated), HF (diffuse) Hypotension: Shock - rate, volume, vessel, pump or rhythm problem Urticaria: Infection, anaphylaxis Unconscious: AEIOU-TIPS; vasovagal syncope

25 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Meld theory to practice: Main treatment goals If ventilatory effort is good, how should O be applied first if both are available? ↓ cardiac workload 2 ↓ fluid pressure in pulmonary vessels ↓ lung water ↓ WOB

↓ O2 demands Keep alveoli open

↑ O2 & CO2 diffusion; ↑ pulse ox; ↑ FRC ↑ cardiac output CPAP IS their oxygen delivery device

Why is the EMS goal to avoid Vascular access needed? intubating a patient in HF or with COPD/severe asthma? A. Intubated pts cannot be given PEEP B. To avoid barotrauma, over sedation & infection C. EMS personnel can rarely place the tube correctly D. They are more likely to go into cardiac arrest after intubation

While prepping CPAP equipment, Must decide which meds if suspect HF, quickly give ASA ASPIRIN 324 mg (4 tabs 81 mg) PO unless contraindicated AMI cause of acute HF HF pts at ↑ risk for thromboembolic events AF promotes stasis & ↑ risk of thrombus formation May give small sip of water to swallow ASA prior to NTG

26 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

Gently place head straps and gradually tighten Why is NTG so If HF: Lift mask every 3-5 min to give NTG unless contraindicated important for HF? If asthma/COPD: Albuterol/ipratropium neb in- line w CPAP

Dilate veins = ↓ RV preload (↓ lung water) Dilate CA = ↓ ischemia; ↑ pump function Dilate arteries = ↓ LV afterload NTG 0.4 mg SL –give 1st dose right before CPAP applied Net benefit: ↓ workload & Onset 1-3 min; half life 5 min ↑ CO If SBP ≥ 90: Repeat NTG q. 3-5 min Give even if NO dose limit - no chest Need continuous action pain to ↓ pulmonary congestion & maintain other benefits Lift CPAP mask to give more

May give NTG if HR >100 in HF HA, dizziness, light-headedness, Different from ACS syncope, blurred vision, ringing in ears ↓ BP Benefits of NTG outweigh risk if ↓ BP Bradycardia/tachycardia, palpitations patient in HF is tachycardic Burning under tongue; flushed skin N / V; abdominal pain, dry mouth

NTG side effects

27 Weak, winded & woozy - Connie J. Mattera MS, RN, PM

What about furosemide? Anticipated outcomes No ETI

Stabilized FiO2 requirements ↓ WOB; ↓ RR

↑ SpO2, ↓ CO2 retention Improved breath sounds Improved chest excursion Improved patient comfort; ↓ dyspnea & verbal impairment No longer indicated for acute No ICU admit, ↓ length of stay pulmonary edema BP stable

Bottom line Patients rarely Suddenly deteriorate; healthcare professionals suddenly notice! Emcrit REASSESS FREQUENTLY Patient really needs to be in a cardiac cath lab!

So we need an action plan… Predetermine a course of action based on best practice models Always put patients first Work as a team Head into action Expect problems; solve them as they come Always point to success (but learn from our failures) Daily, give thanks for the privilege of serving those who need our care & expertise.

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