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PRIMARY CARE PARAMEDIC 2021/22 > EMER 110 Cardiac and Respiratory Theory > Flashcards

EMER 110 Cardiac and Respiratory Theory Flashcards

1
Q

Deep Vein Thrombosis (DVT)

A

A thrombosis is a blood clot that remains attached to a vessel wall.

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2
Q

what is the cause of Deep Vein Thrombosis (DVT)

A

Intimal irritation, roughening, inflammation, traumatic injury, infection, low blood pressures, or obstructions that cause blood stasis Inflammation is the usual cause of DVT

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3
Q

causes of DVT

A

History of trauma Sepsis Stasis or inactivity Recent immobilization Pregnancy Birth control pillsMalignancy Coagulopathies SmokingVaricose veins

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4
Q

signs and symptoms of DVT

A

Pain Edema Increase temp extremity Erythema Tenderness

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5
Q

Atherosclerosis

A

Fatty build up Affects the inner lining of the aorta, cerebral, and coronary blood vessels. Abnormal thickening and hardening of vessel walls

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6
Q

what is Atherosclerosis caused by

A

Caused by soft deposits of intra-arterial fat and fibrin which harden over time

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7
Q

Risk Factors for atherosclerosis

A

Hypertension (HTN) Cigarette smoking: thickens vessel walls making it hard for blood to pass through Diabetes High serum cholesterol levels Lack of exercise Obesity Family history of heart disease or stroke Male sex

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8
Q

Effects of Arteriosclerosis

A

loss of elasticity in vessel walls Partial obstruction of vessel lumen (Ischemia) Complete obstruction of vessel lumen (Infarction, Necrosis) Thrombosis Embolism (Obstruction, Infarction (Heart and Brain) —Infarction: complete obstruction Aneurysm (Rupture, Exsanguination) Vessel calcification (Rigidity, Rupture)

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9
Q

Aneurysm

A

“dilation of a vessel” Artery wall weakness

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10
Q

most common cause for AAA

A

Atherosclerosis

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11
Q

Signs and Symptoms of a ruptured aneurysm

A

Shock Pain, usually describe as sharp stabbing in nature. Back pain Difference in blood pressure between arms Absent radial or femoral pulse Mottling of extremities below aneurysm modeling: spider veins, bluish white skin absent radial or femoral pulses

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12
Q

Hypertension

A

Known as lanthanic (silent) disease Characterized by a consistent elevation of systemic arterial blood pressure Often defined by a resting BP consistently greater than 140/90 mm Hg

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13
Q

Risk Factors of hypertension

A

Family history Advancing age Gender (men younger than 55, women older than 74): structural changes of vessels Black race: social status High dietary sodium intake Glucose intolerance: higher cholesterol Cigarette smoking Obesity Heavy alcohol consumption Low dietary intake of potassium, calcium and magnesium

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14
Q

Pathophysiology of hypertension

A

Damages walls of systemic blood vessels Prolonged vasoconstriction and high pressures with in the arteries and arterioles stimulate the vessels to thicken and strengthenEnd result is a permanently narrowed blood vessel

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15
Q

Treatment Plans Arteriosclerosis Peripheral Vascular Disease Hypertension Deep Vein Thrombosis Aneurysm

A

*symptomatic only

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16
Q

Endocarditis

A

Inflammation of the inner lining of the heart, and/or heart valves

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17
Q

causes of endocarditis

A

Can be caused by either bacteria or virus, bacteria being the most common

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18
Q

risk factors of endocarditis

A

Acquired valvular heart disease (mitral valve prolapse) Implantation of prosthetic heart valves Congenital lesions Previous attack Male gender Intravenous drug use: dirty needles Long term indwelling catheterization

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19
Q

Signs and Symptoms of endocarditis

A

May involve a number of organ systems Classic findings Fever Cardiac murmur Petechial lesions of skin, conjunctiva, and oral mucosa Chest pain- SOB

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20
Q

myocarditis

A

Is an inflammation of the heart muscle (myocardium) Results from infection (bacteria or viral) or toxic inflammation (drugs or toxins from infectious agents) Cocaine users are 5x more likely to get it

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21
Q

myocarditis causes

A

Chest infection Auto immune disease Fungal viral infection

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22
Q

signs and symptoms of myocarditis

A

Flulike Pain in epigastric region or under sternum (substernal) Dyspnea Cardiac arrhythmias Stabbing chest pain

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23
Q

pericarditis

A

Inflammation of the pericardium, two thin layers of a sac-like tissue surround the heart, hold it in place and help it work. Normally, a small amount of fluid keeps the layers separate so that there’s no friction between them.

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24
Q

Signs and Symptoms Pericarditis

A

Low cardiac output Low SPO2 Chest pain

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25
Q

causes of pericarditis

A

Trauma Heart attacks

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26
Q

Acute Coronary Syndrome (ACS)

A

refers to distinct conditions caused by a similar sequence of pathologic events involving abruptly reduced coronary blood flow

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27
Q

Acute Coronary Syndrome (ACS) conditions

A

Unstable Angina (UANon-ST-segment elevation myocardial infarction (NSTEMI), ST-segment elevation myocardial infarction (STEMI)

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28
Q

Ischemia

A

Lack of oxygen to the tissues ST depression or T inversion

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29
Q

Ischemic Heart Disease

A

Myocardial ischemia is usually the route of the blockage or gradual narrowing of one or more of the coronary arteries by atheromatous plaque. Narrowing or blockage of a coronary artery can disrupt the oxygen supply to the area of the heart supplied by the affected vessel. If the cause of the ischemia is not reversed and blood flow restored to the affected area of the heart muscle, ischemia may lead to cellular injury and ultimately, cellular death

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30
Q

Clinical Features of Ischemic Heart Disease

A

retrosternal chest pain, pressure, heavinesssqueezing lasting 10 minutes or longer that usually occurs at rest or with minimal exertionCan be accompanied by angina equivalents such as unexplained new-onset or increased exertional dyspnea, unexplained fatigue, diaphoresis, nausea/vomiting, or syncope

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31
Q

atypical presentation of Ischemic Heart Disease

A

may include pleuritic chest pain, epigastric pain, acute-onset indigestion, or increasing dyspnea without chest pain. Atypical presentations are most often observed in younger(25 to 40 years of age) and older(over 75 years) patients, women, and patients with Diabetes Mellitus, chronic renal insufficiency, or dementia

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32
Q

what does schema lead to

A

Injury prolonged ischemia ST elevation

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33
Q

infarct

A

death of tissue may or may not show in Q wave

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34
Q

angina Three types:

A

Stable Angina (Exertional Angina) Unstable Angina (Preinfarction Angina) Prinzmetal’s Angina

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35
Q

Prinzmetal’s Angina

A

Vasospastic angina: no blockage or clot just spasm of segment of coronary arteryCause: cocaine Treatment: nitro

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36
Q

Angina

A

Imbalance between myocardial O2 supply and demand choking pain in the chest” Burning Tightness Pressure Crushing heavy

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37
Q

The coronary arteries can spasm as a result of :

A

Exposure to cold weather Stress Medicines- Anti-migraines, Chemo, Antibiotics Smoking Cocaine use

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38
Q

Myocardial Infarction

A

Sudden and total occlusion or near‐ occlusion of blood flowing through an affected coronary artery to an area of heart muscle Results in ischemia, injury, and necrosis of the area of myocardium distal to the occlusion.

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39
Q

If blood flow is not restored to the affected artery

A

myocardial cells within the sub-endocardial area begin signs of injury within 20 to 40 minutes.

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40
Q

ACS Management/ Treatment

A

Reduce physical activity, calm reassurance O2 if WOB increased and SPO2 less than 94%, if pale, if SOB If clinically indicated ASA 160-325mg PO –81mg X2= 162mg 3 Lead followed by 12 Lead ECG noted IV BEEFORE NITRO –0.4mg spray –1 every 3-5 mins –At 3 min mark vitals and re assess If clinically indicated, Nitro 0.4mg SL, titrate to effect Consider calling ALS Notify receiving hospital if ST elevation

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41
Q

ACS CALL vs NON ACS CALL

A

ACS CALL Heavy, burning tight NON ACS CALL Sharp pain Increases with palpation Increase with inspiration

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42
Q

angina signs and symptoms

A

“choking pain in the chest” Burning Tightness Pressure Crushing Heavy Radiates Lasts less than 20 min Sob Occurs with activity Is better with rest

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43
Q

UNSTABLE angina signs and symptoms

A

Lasts longer than 20mins Can occur at rest

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44
Q

MI: STEMI, NSTEMI signs and symptoms

A

At rest Doesn’t get better Shock symptoms –Nausea vomiting –Pale cool clammy

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45
Q

Cardiomyopathies

A

Diverse group of diseases that affect the myocardium Most result from underlying disorders In response to injury, the heart may undergo dilation or hypertrophyCardiomyopathies are incurable diseases and the only hope is heart transplantation

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46
Q

Cardiomyopathies are divided into three forms:

A

Dilated Cardiomyopathy Hypertrophic cardiomyopathy Restrictive cardiomyopathy

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47
Q

cardiac outputstroke volumeFormula

A

Cardiac output (CO): amount of blood ejected by each ventricle in 1 minute Stroke volume (SV): amount of blood pumped by each ventricle in 1 beat (mL/beat) CO=SV X HR 70ml/beat x 75 bpm+ 5250mL/min

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48
Q

Factors that affect CO

A
  1. Heart rate 2. Preload: 3. afterload:4. Contractility:
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49
Q

define preload and after load

A

Preload: amount of blood entering ventricles @ diastole (rest) à nitro decreases preload afterload: resistance ventricles have to overcome to circulate blood à decreasing afterload decreases back up into the lungs

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50
Q

Pulmonary Edema

A

Swelling within the lungs Sign of left sided CHFDecrease of output to left side of heart

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51
Q

One of the most common causes of pulmonary oedema is

A

left ventricular failure from an acute MIOther cause are inhaled toxins, infections, and sometimes trauma and altitude changes

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52
Q

Pulmonary Edema Signs and Symptoms

A

In early pulmonary edema you will hear late inspiratory crackles at the lung apices. These crackles are caused by rapid expansion of collapsed alveoli as they reach maximum inflation As pulmonary edema worsens you will hear more proximal crackles in lung fields As fluid migrates into larger more central airways and mix with mucus the crackles become more coarse sounding. As lungs fill up frothy pink sputum may appear, which an ominous sign. Happens acutely

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53
Q

Congestive Heart Failure

A

heart failure may present acutely as a result of acute pump dysfunction from an mi Heart is unable to pump powerfully enough or fast enough to empty its chambers. Blood backs up into the systemic circuit, the pulmonary circuit, or both.

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54
Q

Left sided CHF

A

Pumps blood to body Pulmonary hypertension Back up into the lungs Crackles in lungs SOB Left sided heart failure is most commonly caused by an AMI and chronically by continued hypertension.

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55
Q

Left-sided heart failure signs and symptoms

A

Extreme restlessness and anxiety, confusion and agitation Severe dyspnea, tachypnea, tachycardia Hypertension or hypotension Crackles and/or wheezes Frothy pink sputum in severe cases

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56
Q

Right sided CHF

A

Pumps blood to lungs JVD Pedal edema Pitting edema SOB

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57
Q

Right-Sided heart failure Signs and Symptoms

A

Jugular vein distention Pedal/pitting edema

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58
Q

Heart Failure Management

A

Position of comfort, most often high fowlers If clinically indicated administer nebulized sympathomimetic/anti-cholinergic If clinically indicated initiate Continuous Positive Airway Pressure (CPAP) Consider ALS intercept If clinically indicated administer SL nitroglycerine

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59
Q

Pulmonary edema treatment

A

Crackles: nitro CPAP Wheezing: Ventolin and Atrovent –Call ALS if Combivent doesn’t work

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60
Q

Nitro for pulmonary edema

A

No chest pain and no nitro prescription –> call med control for orders No chest pain- nitro prescription –>give nitro Chest pain –> give nitro

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61
Q

Causes for pulmonary edema

A

Cardiogenic Noncardiogenic

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62
Q

Cardiogenic Noncardiogenic

A

Cardiogenic 1. Left sided failure 2. Systemic hypertension Noncardiogenic -Toxins -Lung infections -Sepsis

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63
Q

Pneumonia Vs Pulmonary Edema

A

–Pulmonary edema: cause by Left heart failure Normal HR Febrile course Crackles Wheeze May or may not be productive cough- punk or white History of CHF Cardiac CP- won’t increase with inspiration —Pneumonia: infection Fast HR Fever thick Crackles Wheeze Productive cough- green or dark yellow History of pneumpnia Sharp CP Cp increase with inspiration/coughing

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64
Q

Cardiogenic Shock

A

Heart is so severely damaged that it can no longer pump a volume of blood sufficient to maintain tissue perfusion. When 25% of the left ventricular myocardium is involved When 40% or more of the left ventricle has been infarcted (tissue death) High mortality rate

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65
Q

Signs and symptoms of cardiogenic shock brain

A

Altered LOC Coma Lethargy Possible stroke

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66
Q

Signs and symptoms of cardiogenic shock lungs

A

SOB Accessory muscle use Stats less than 90 Tachnyepia

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67
Q

Signs and symptoms of cardiogenic shock heart

A

Increase HR Decrease BP Arythmias MI

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68
Q

Signs and symptoms of cardiogenic shock skin

A

Cool Clammy Delayed cap refill

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69
Q

Management of Cardiogenic Shock

A

Focuses on improving oxygenation and peripheral perfusion Secure the airway and administer 100% supplemental oxygen. Advanced airway necessary if the patient is comatose. Place the patient in a supine position. IV with normal saline

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70
Q

Frank-starling mechanism

A

One characteristic of cardiac muscle is that when it’s stretched a contract with greater force

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71
Q

systematic vascular resistance leads to

A

a higher after load in the cardiac output can drop or heart rate has to work harder to maintain the same cardiac output which increases oxygen demand

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72
Q
  • Changes in contractility may be induced by
A

medication’s that have a positive or negative inotropic effect

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73
Q
  • Nervous system controls regulate the
A

contractility of the heart from beat to beat

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74
Q
  • Positive chronotropic effect
A

how hard can increase its cardio output by increasing the number of contractions per minute (HR)

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75
Q
  • Pacemaker
A

the area of conduction tissue in which the electrical activity arises at any given time

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76
Q
  • AV node
A

is gatekeeper to the ventricles o In 85-90% of humans blood supply comes from the branch of the RCAo 10-15% of ppl it comes from the left circumflex artery

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77
Q
  • Electric impulses from SA node take how may secs to read AV node
A

o.o8secs

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78
Q
  • The conduction is delayed in the AV node for approximately how many secs
A

0.12sec

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79
Q
  • It takes approx. how many sec for an electrical impulse to spread across the ventricles
A

0.08

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80
Q

what happens with ions during depolarization

A

depolarization sodium and calcium ions rush into cell causing inside of cell to be positive

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81
Q

what happens with ions during repolarization

A

the sodium and calcium channels close and potassium channels open allowing rapid escape of potassium ions from the cell

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82
Q
  • Refectory period
A

period when the cell is depolarized or in the process of repolarizing

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83
Q
  • Absolute refractory period
A

the cell is still highly depolarized and a new action protentional cannot be initialed

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84
Q
  • Relative refractory period
A

the heart is partially depolarized and a new action potential will be inhibited but not impossible

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85
Q

The parasympathetic nervous system

A
  • Sends messages mainly through vagus nerve- Atropine blocks actions of PNS and vagus nerve causing HR to increase
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86
Q

The sympathetic nervous system

A
  • Release norepinephrine ttavels to SA node, AV node and ventricles- every beta agents effects the heart by increases hearts rate, force and automaticity - Vasoconstriction is cause by alpha agent- Vasodilation is caused by beta agent
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87
Q
  • Alpha 1 receptors
A

are primarily located on peripheral blood vessels and stimulation results in:o Peripheral vasoconstrictiono Mild bronchoconstrictiono Increased metabolismo Stimulation of sweat glands

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88
Q
  • Alpha 2 receptors
A

are primarily located on nerve endings and stimulation results in:o Control release of neurotransmitters

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89
Q
  • Beta 1 receptors
A

are primarily located within the cardiovascular system and stimulation results in:o Increased heart rate (positive chronotropic)o Increased strength of cardiac contraction (positive inotropic)o Increased cardiac conduction (positive dromotropic)

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90
Q
  • Beta 2 receptors
A

are primarily located on bronchial smooth muscle and stimulation results in:o Bronchodilationo Peripheral vasodilation

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91
Q

Causes of dysrhythmias

A
  • Acid base disturbance- ANS imbalance- CNS damage- Certain poisons- Drugs- Endocrine disorders- Hypothermia- Hypoxemia- Ischemia o infarction- trauma
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92
Q
  • disrhythmias happen after an AMI for 2 reasons
A
  1. irritability of the ischemic heart muscle surrounding the infarct may cause the damage muscle to generate abnormal cardiac contractions 2. because the infarct damages the conduction
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93
Q

Sodium (Na+)

A

goes into cell and initiates depolarization

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94
Q

Potassium (K+):

A

flows out of the cell to initiate repolarization

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95
Q

HypokalemiaHyperkalemia

A

Hypokalemia: increased myocardial irritabilityHyperkalemia: decreased automaticity/conduction

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96
Q

Calcium (Ca)

A

has major role in the depolarization of pacemaker cells (maintain depolarization) and in myocardial contractility

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97
Q

Hypocalcemia Hypercalcemia

A

Hypocalcemia: decreased contractility and increased myocardial irritability Hypercalcemia: increased contractility

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98
Q

Magnesium (Mg)

A

stabilizes the cell membrane: acts in concert with potassium and opposes the actions of calcium

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99
Q

Hypomagnesemia Hypermagnesemia

A

Hypomagnesemia: decreased conductionHypermagnesemia: increased myocardial irritability

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100
Q

Absolute Refractory Period

A

the cardiac muscle cell is completely insensitive to further stimulation Start of the QRS and ends at middle of T wave

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101
Q

Relative Refractory Period

A

During the relative refractory period, the muscle cell is more difficult than normal to excite, but it can still be stimulated.

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102
Q

Nervous system controlling heart rate

A

Two nerves link the cardiovascular center in the medulla oblongata of brain with the SA node of the heart1. Accelerator nerve (sympathetic NS)2. Vagus nerve (parasympathetic NS):

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103
Q

Accelerator nerve (sympathetic NS)

A

when stimulated, releases neurotransmitter at the SA node to increase heart rate

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104
Q

Vagus nerve (parasympathetic NS)

A

when stimulated, releases neurotransmitter at the SA node to decrease heart rate

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105
Q

Electrical Conduction System

A

• Automaticity• Generates its own electrical impulses without stimulation from nerves • Unique feature of the heart• Specialized conduction tissue• Pacemaker

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106
Q

The Sinoatrial (SA)Node

A

• The Primary Pacemaker - Theoretically, any cell can act as a pacemaker. - Located in the right atrium, near the inlet of the superior vena cava - Receives blood from the Right Coronary Artery in 50-60% of population - Fastest pacemaker in the heart - Inherent rate of 60 to 100 beats per minute(bpm)

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107
Q

Secondary Pacemakers

A

If the SA becomes damaged or is suppressed - AV node inherent rate 40-60 bpm (RCA blood flow in 85-90% of population). - Purkinje fibers 20-40 bpm

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108
Q

ECGs

A
  • The ECG is a graphic representation of the heart’s electrical activity. - It does not provide information regarding mechanical events.- Valuable diagnostic tool for identifying cardiac abnormalities. - For good blood flow the electrical signal must send and the heart must respond
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109
Q

Indications for ECG Monitoring

A
  • Patients at risk for dysrhythmias shall receive continuous ECG monitoring - Known or suspected cardiac patients - Suspected Overdose- Electrical Injuries- Syncope - Elderly patients “feeling unwell”- Issues concerning the Sympathetic System
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110
Q

Voltage Positive:Negative:

A

positive- Seen as an upward deflection on the ECG tracing.negative- Seen as a downward deflection on the ECG tracing. - Flowing backwardsisoelectric- No electrical current detected.- Seen as a straight baseline on the ECG.

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111
Q

ECG Leads - Bipolar lead*:- Unipolar lead:

A
  • Bipolar lead*:o Two electrodes of opposite polarity. - Unipolar lead: o Single positive electrode and reference point.
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112
Q

Lead Placement

A
  • White (upper right), black (upper left), green (lower right), red (lower left)- Between ribs, does not conduct well on bone - Positive always at the bottom
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113
Q

lead triangle

A

GO LOOK AT IT - double positive is on the bottom-top right (patients right) double negative-top left (patients left) negative and positive

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114
Q

ECG Graph Paper

A
  • Each Little square is 1mm x 1mm 0.04sec- Each Large square is 5mm x 5mm 0.20 sec
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115
Q

Calibration

A
  • The sensitivity of the 12-lead ECG machine is standardized - When properly calibrated, a 1-mV electrical signal produces a 10-mm deflection (two large squares) on the ECG tracing
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116
Q

Time Interval

A
  • Denoted by short vertical lines on the ECG graph paper. - At standard speed, the distance between each short vertical line is 75 mm (3 seconds).
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117
Q
  • Depolarization
A

The sinoatrial (SA) node on the wall of the right atrium initiates depolarization in the right and left atria, causing contraction, which corresponds to the P wave on an electrocardiogramo Discharge of the impulse

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118
Q
  • Repolarization
A

resets charge

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119
Q
  • P wave
A

depolarization of the atriumso Impulse being sent to AV nodeo Positive deflection because its going towards positive

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120
Q
  • Q wave
A

polarization of right ventricle (may not have)o Bigger the Q wave the bigger the injuryo If you can fill it with water its important

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121
Q
  • R wave
A

left ventricle contracting

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122
Q

-QRS

A

ventricular depolarization

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123
Q
  • T
A

ventricular repolarizationo Reset

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124
Q

PRI IntervalQRS intervalR-R Interval

A
  • PRI should me 0.12-0.20 sec how long it takes impulse to get from sa node to av node- QRS less than 0.12 sec - R to R interval: top of R wave to next
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125
Q

Artifact Common causes

A

o Improper grounding of the ECG machine o Patient movement o Loss of electrode contact with the patient’s skin o Patient shivering or tremors o External chest compressions

126
Q

Rhythm Interpretation 5 Steps

A

Regularity ratep wavesP-R interval QRS complex

127
Q

Regularity

A
  • Is the rhythm regular? - To analyze ventricular rhythm, compare R-R intervals (time between each contraction) systematically from left to right - Certain rhythms will never be regular- Sinus tach will rarely be over
128
Q

Rate

A
  • SVT has no p waves ever- Anytime its wide means its going slowo Should be less than 0.4 (1.2) Six Second method: Count number of QRS complexes in a 6-second interval and multiply number by 10
129
Q

P waves significance

A
  • Are P waves present? o If there are no p waves it means SA node is not working- Are the P waves regular? - Is there one P wave for each QRS complex, and is there a QRS complex following each P wave? - Are they upright or inverted? - Do they all look alike?
130
Q

PRI

A
  • Represents the amount of time it takes for the atria to depolarize and for the impulse to travel through AV node. - It includes the slight delay that normally occurs when the impulse is slowed AV node. - This delay allows for ventricular filling Normal PRI is 0.12-0.20 sec - Normal PR Interval (PRI) - 0.12sec – 0.20sec (3-5 little boxes long)
131
Q

QRS Complex

A
  • Is there a QRS complex for every P Wave? - IS it Narrow?- a normal QRS complex is less than .12
132
Q

shockable rhythms

A

v fibpulseless v tach

133
Q

starlings law

A

the greater the stretch the greater the contractions

134
Q

all sinus rhythms

A

come from SA node, 4 rhythms - Upright uniform p wave- 1p:1QRS- QRS

135
Q

Normal Sinus Rhythm

A
  • P Wave o Normal and upright; one in front of every QRS - PRIo .12 - .20 - QRS o Less than .12 o narrow- Sinus node fires regularly at 60-100 bpm with each beat conducted normally through to the ventricles
136
Q

Sinus Bradycardia

A
  • Regularity o Regular- Rate o Less than 60 bpm- P Wave o Normal and upright; one in front of every QRS- PRI o .12 - .20 and constant - QRS o Less than .12 - Sinus node fires regularly at less than 60 bpm with each impulse conducting normally through to the ventricles
137
Q

causes of Sinus Bradycardia

A

o Medso Hypothermiao Drugs

138
Q

Sinus Tachycardia

A
  • Regularity o Regular- Rate o 100 - 160 bpm (above)- P Wave o Normal and upright; one in front of every QRS- PRI o .12 - .20 and constant - QRS o Less than .12
139
Q

Sinus Arrhythmia

A
  • Regularity o Irregularo Commono Has to do with respirations —As you breath in it goes faster, breath out slows down- Rate o 60 - 100 bpm (usually)- P Wave o Normal and upright; one in front of every QRS- PRI o .12 - .20 and constant - QRS o Less than .12 - Sinus node fires in an irregular pattern with each impulse conducting through to the ventricles. Rate increases as patient breathes in and decreases as patient breathes out
140
Q

Atrial Rhythms come from

A

atria

141
Q

Premature Atrial Contractions (PAC’s)

A

Ectopic - Just comes earlier than it should, looks like all the others- Regularity o Depends on underlying rhythm- Rateo Usually, normal - P Wave o Upright uniform P waveo P wave of early beat differs from sinus P wave- PRIo .12-.20- QRS o Less than .12 - Pacemaker is an irritable focus in atrium that fires prematurely and produces a single ectopic beat with conduction through to the ventricles

142
Q

Atrial Flutter

A

comes from one place in the atriaRegularity - Atrial rhythm regular; o Ventricular rate reg/irreg - Rate o Atrial rate 250 -300; o Ventricular rate varies - P Wave o Characteristic Saw tootho Shark fino They look like this because they are coming from atria and not SAo Each time it happens they look the same- PRI o Unable to determine- QRS o Less than .12 - A single irritable focus in the atria issues impulse conducted in a rapid, repetitive fashion. AV node blocks some of the impulses from being conducted.

143
Q

Atrial Fibrillation

A

comes from all parts of atria and sends impulses - Regularity o Grossly irregular - Rate o Atrial greater than 300; Ventricular varies greatly - P Wave o No discernible P Waves - PRIo Unable to measure - QRS o Less than .12- The atria are so irritable that a multitude of foci initiate impulses causing atria to depolarize. AV node blocks most of the impulses so there is only limited conduction to ventricles

144
Q

Atrial Fibrillation 2 types

A
  • A-Fib with SVR with slow ventricular response (SVR) below 99bpm- A-Fib with RVR ventricular response (RVR) above 100 bpm
145
Q

Supraventricular Tachycardia (SVT)

A
  • comes from one place in atria and goes around so fast you cant see p waves- Regularity o Regular- Rateo greater than 150 bpm- pwaveo Upright, uniform, however rarely seen d/t rate, one in front of every QRS - PRI o .12 - .20 – when seen - QRS o Less than .12 - Tachycardia that originates from a pacemaker above the ventricles, that overrides the SA node.- ALS call- Try Vagul
146
Q

Paroxysmal Supraventricular Tachycardia (PSVT)

A
  • A rhythm changes from something to SVT- Regularityo Regular- Rateo greater than 150 bpm- Pwaveo Upright, uniform, however rarely seen d/t rate, one in front of every QRS - PRIo .12 - .20 – when seen - QRS o Less than .12 - Paroxysmal means “occurring in spasms”. PSVT is a specific rhythm reflecting its tendency to begin and end abruptly
147
Q

Bigeminy: Trigeminy:Quadreminy:Couplet:

A

Bigeminy: every 2nd one is ectopicTrigeminy: every 3rd one is ectopicQuadreminy: every 4th one is ectopic Couplet: 2 in a row

148
Q

Treatment for atrial rhythms

A

A-Flutter- treat CP if they have A-Fib- treat CP if they haveSVT- ALS ALWAYS

149
Q

treatment for sinus rhythms

A

NSR- Nothing ST- nothingSA- nothingSB- symptomatic- CP- SOB- Pale- Lightheaded- CALL ALS

150
Q

What Is a 12-Lead ECG?

A
  • Each ECG lead looks at the heart from a different angle - One lead may see a normal myocardium, while another may be looking at major damage.
151
Q

3 lead placement

A

**white to rightRed to bed (torsoBlack- Smoke over fireGreen- ground

152
Q

o Contiguous leads

A

: (Sister leads) Must both be elevated to be important

153
Q

SALI

A

septal wallanterior walllateral wallinferior wall

154
Q

septal wall

A

o V1, V2o Place Along sternal borders

155
Q
  • Anterior Wall
A

(left ventricle area)o V3, V4o Placed Left Anterior Chest

156
Q
  • Lateral Wall
A

o V5 and V6o Lead I and aVL o Left Armo Placed Left Lateral Chest o elevation in 2 or more (doesn’t have to be all) its important

157
Q
  • Inferior Wall
A

(looks at bottom of heart- ventricles- CO input/output)o Lead II, III, aVF o Left leg

158
Q

Placement

A

V1- 4TH intercostal (R sternum)V2- 4th intercostal (L sternum)V3- in between V2 and V4V4- midclavicular 5th intercostal (L side)V5- in between V4 and V6V6- mid axillary 5th intercostal

159
Q
  • Skin Preparation
A

o Dry/remove oilo Remove excess hair

160
Q
  • Patient Preparation
A

o Cease movement o Breath normallyo Stop speaking

161
Q

Obstructive disease

A

can’t get air out Occurs when the positive pressure of exhalation causes the small airways to pinch shut trapping gas in the alveoli

162
Q

Signs of obstructive disease

A

Pursed lip breathing Increased inspiratory to expiratory ratio Abdominal muscle use Jugular venous distention

163
Q

Asthma Name from Greek work meaning

A

panting

164
Q

Asthma is characterized by

A

an inflammation in the bronchiole airways common chronic inflammatory disease of the airways.

165
Q

Hallmark of Asthma is

A

Airway Diameter Reduction

166
Q

key points of asthma

A

Reversible Must be triggered

167
Q

normal levels of C02 in blood

A

35-45mmhg

168
Q

CPAP rule

A

must have neb running

169
Q

HypoxiaHypoxemia

A

Hypoxia: area of the body that is short of oxygen Hypoxemia: entire body is short of oxygen

170
Q

Only way to fix Hypoxemia aka low spo2

A

02 and PEEP

171
Q

Bronchospasm/ Bronchoconstriction

A

Caused by the construction of smooth muscle that surrounds the larger bronchi in the lungs When air is forced through the constricted tubes it causes them to vibrate which creates wheezing

172
Q

The primary treatment of bronchospasm

A

is the administration of bronchodilator medication ex: Ventolin

173
Q

3 main symptoms of asthma

A

bronchoconstrictionmucous productioninflammation

174
Q

Signs and Symptoms of asthma

A

SOB Increase Work of Breathing Accessory Muscle use SPO2 abnormalities Adventitious lung sound, especially wheezing Decreased air entry Pallor or cyanosis ETCO2 reveals signs of bronchoconstriction

175
Q

treatment for asthma

A

Ventolin(Salbutimol) Atrovent(Ipratropium Bromide) epinephrine

176
Q

Potentially Fatal Asthma

A

Severely compromised ventilation all of the time Be alert for silent chest syndrome

177
Q

Potentially Fatal Asthma Ask if pt:

A

Previous intubation for respiratory failure or respiratory arrest 2 or more admissions to hospital despite oral corticosteroid use 2 or more episodes of pneumothorax

178
Q

Status asthmaticus

A

severe prolonged asthmatic attack that cannot be broken with conventional treatment Patient physically tired: accessory muscle use, cyanosis, chest hyperinflatedA despite treatment already given

179
Q

when is epinephrine used for asthma

A

silent lungs

180
Q

Mild asthma

A

Can form sentences Lungs: clear -Expiratory wheezes 2.5-5.0mg Ventolin -Contra: tachy arrythmia 250-500mcg Atrovent *won’t do anything after 2 doses (1000mcg)

181
Q

moderate asthma

A

Can speak few words at a time, tripod position Inspiratory and expiratory wheezes through all 4 lobes O2 immediately

182
Q

Severe asthma

A

Stridor —Upper airways already 50% closed wheezing upper lobes, silent lower lobes 02 5.0/500 Combivent- Atrovent and Ventolin CPAP: must have neb running 0.5mg EPI when you hear Silent chest —Call ALS

183
Q

Anaphylaxis

A

Serious allergic reaction that is rapid in onset and may cause death

184
Q

Risk factors: Anaphylaxis

A

Predisposition Substance Route and dosage Time between exposure

185
Q

AllergenAntibody (immunoglobulin)AntigenHypersensitivity

A

Allergen: antigen Antibody (immunoglobulin): attach to surface of mast cell and Antigen: proteins found on surface of cells Hypersensitivity: results from immune response to antigens

186
Q

Allergic Reaction vs Anaphylaxis

A

Allergic Reaction 1 body system Anaphylaxis 2 body systems EPI!!

187
Q

Sensitization

A

over production of IgE (antibodies) First exposure Antibodies attach to MAST cells and basophils –Mast cell: part of immune system and fights off stuff Release of chemical mediators

188
Q

Anaphylaxis Common causes

A

Drugs Foods and Additives Hymenoptera Stings

189
Q

Chemical Mediators cause and result in

A

Causes inflimation, bronchonstriction and mucous These substances result in bronchoconstriction, peripheral vasodilation and increased capillary permeability.

190
Q

Mediators that are stored include

A

*histamine, heparin and chemotactic factors. Other mediators are formed during degranulation such as prostaglandins, leukotriene’s, bradykinins and interleukins.

191
Q

Histamine Receptors H1

A

Bronchospasm increased peristalsis Vessel dilation Post capillary venule permeability Increases heart rate

192
Q

Histamine Receptors H2

A

Gastric acid secretion

193
Q

Anaphylaxis Presentation initial response

A

which occurs within the first 30 minutes after exposure and resolves within one hour consists of vasodilation, vascular leakage, and smooth muscle spasm

194
Q

Anaphylaxis Presentation delayed response

A

which can occur hours later and last for days consisting of more intense infiltration of tissues with inflammatory cells and more severe symptoms

195
Q

Anaphylaxis Presentation skin

A

Urticaria (Hives) Pruritus(itching) Angioedema (Swelling)

196
Q

Criteria for anaphylaxiss exist when one of the following are met:

A
  1. Acute onset symptoms involving hives, flushing, swelling of the mouth and throat, with at least one of the following: Respiratory concerns or distress, including difficulty breathing or speaking or decrease peak expiratory flow Declining blood pressure Symptoms of end organ disfunction2. Rapid occurrence of two or more of the following after exposure to likely Allergan: Skin and mucosal tissue symptoms including hives itchy and flushed skin and or swelling of the face and body respiratory concerns or distress including difficulty breathing or speaking or decreased peak expiratory flow Declining blood pressure Symptoms of an organ disfunction Severe gastrointestinal symptoms 3. Exposure of known allergin causing a decline in blood pressure
197
Q

COPD

A

General term (umbrella term): contains emphysema and chronic bronchitis

198
Q

copd spo2

A

Spo2 always lower than normal Goal is 94 but COPD pts goal is 90-92 Do not get COPD pt into 98Too much O2 will lower respiratory rate

199
Q

copd CO2

A

CO2 is always higher 50-60 mmhg

200
Q

Common Pathologies of COPD

A

Airflow obstruction Bronchospasm/bronchoconstriction Increased mucous production Impaired elasticity of airways

201
Q

Emphysema

A

is a long-term, progressive disease of the lungs that primarily causes shortness of breath due to over-inflation of the alveoli. Emphysema patients have damage to lung tissue in alveoli, which causes thickening and delays, or block entirely, the oxygen/carbon dioxide exchange.

202
Q

Pulmonary Emphysema (Pink Puffers)

A

Abnormal, permanent enlarged air spaces distal to terminal bronchiole Usually a non-productive cough Increased Anterior/Posterior diameter (barrel chest) due to hyperinflation and increased lung volume

203
Q

Emphysema Pathologies

A

 Destruction of alveoli walls Weakening and destruction of bronchioles Decreased alveoli surface area Decreased gas exchange

204
Q

Emphysema – Signs and Symptoms

A

“pink puffer”- respiratory distress: exhalation Pink color Pursed lip breathing Leaning forward Use of accessory muscles Tachypnea Distended neck veins Barrel chest Tachypneic Thin because they burn calories trying to breath

205
Q

Chronic Bronchitis

A

Inflammation, swelling and excessive mucous production in the bronchial tree. Minimal alveoli involvement Decreased ventilation of alveoli due to airflow obstruction

206
Q

Chronic Bronchitis - Signs and Symptoms

A

“blue bloater”- respiratory distress: inhalation Cyanotic Sweating Leaning forward Use of accessory muscles Tachypnea Distended neck veins

207
Q

COPD with right heart failure

A

Very difficult to push the patients thick blood through lungs destroyed by emphysema and through capillaries squashed by hyperinflated alveoli

208
Q

COPD with right heart failure Signs and symptoms

A

Peripheral edema JVD End inspiratory crackles

209
Q

Hypoxic Drive

A

Rare phenomenon that affects only a very small percentage Pts whose respiratory drive can be decreased by high levels of oxygen

210
Q

Bagging someone with COPD

A

Pts who have severe asthma or copd should be ventilated 4-6 breaths per pin to avoid bagging them to death

211
Q

Management of COPD

A

Primary goal is to reverse airflow obstruction through bronchodilation This is accomplished through use of sympathomimetics and anticholinergics. CPAP, if indicated, helps with medication administration PEEP: Positive End Expiratory Pressure

212
Q

Pleural effusion

A

is when fluid collects between the visceral and parietal pleura.

213
Q

Effusions can be caused by

A

infections, tumors, CHF, trauma

214
Q

what do pleural Effusions cause

A

can contain several litres of fluid, which can decrease lung capacity and cause dyspnea. They impair breathing by limiting lungs expansion and can cause partial or complete lung collapse.

215
Q

where do P effusions happen

A

Happens in pleural space

216
Q

what will you hear with a pleural effusionwhat will the spo2 be

A

When you listen you won’t hear anything SPO2 will be low (hypoxemic)

217
Q

P effusions Treatment

A

Prehospital treatment should consist of proper positioning, high fowlers most often, aggressive supplemental oxygen if required.

218
Q

Bronchitis

A

Is an inflammation of the mucous membranes of the bronchi

219
Q

bronchitis Is characterized by

A

development of cough or small sensation in the back of the throat, with or without production of sputum

220
Q

bronchitis Divided into two categories:

A

Acute Chronic

221
Q

bronchitis treatment

A

treat symptomatically

222
Q

Laryngitis

A

inflammation of voice box due to overuse, irritation or infection

223
Q

Croup

A

is the inflammation of the larynx and airwaves just below it it primarily affects children five years or younger it comes on strongest in the night time in the last 3 to 7 days

224
Q

symptoms and cause of croup

A

symptoms include loud harsh barking cough, fever, noisy inhalations, hoarse voice and dyspnea caused by a virus

225
Q

Pneumonia

A

Is an inflammatory condition of the lung, affecting primarily the alveoli

226
Q

Viral Pneumonia

A

In adults, viruses account for approximately a third and in children for about 15% of pneumonia cases Commonly implicated agents include rhinoviruses, coronaviruses, influenza viruses, respiratory syncytial virus (RSV)

227
Q

Pneumonia signs and symptoms systemic:skin:lungs;muscular:centralvascularheartgastricjoints

A

Systemic: -High fever -Chills Skin: -Clamminess -Blueness Lungs: -Cough with sputum or phlegm -SOB -Pleuritic chest pain -Hemoptysis Muscular: -Fatigue -Aches Central: -Headaches -Loss of appetite -Mood swings Vascular: -Low bp Heart: -High hr Gastric: -Nausea -Vomiting Joints: -Pain

228
Q

Pneumonia treatment

A

treat symptomatically

229
Q

V:Q normals and normal ratio

A

Ventilation 4l/min Perfusion 5l/min 0.8 is normal VQ ratio

230
Q

Pulmonary Embolism

A

is a blockage of the main artery of the lung or one of its branches by a substance that has travelled from elsewhere in the body through the bloodstream (embolism).

231
Q

P embolism most commonly results from

A

deep vein thrombosis (a blood clot in the deep veins of the legs or pelvis) that breaks off and migrates to the lung, a process termed venous thromboembolism (VTE)

232
Q

Pulmonary embolism Risk Factors

A

Estrogen-containing hormonal contraception Cancer (due to secretion of pro-coagulants) Alterations in blood flow: immobilization after surgery, injury, pregnancy, obesity (also procoagulant), cancer (also procoagulant) Smoking Travel

233
Q

Signs and Symptoms of pulmonary embolism

A

Dyspnea Short of breath but clear and equal lung sounds think pulmonary embolism Pleuritic chest pain on inspiration Pin point chest pain Low oxygen saturation Cyanosis Tachypnea Hemoptysis Usually clear sounding lung sounds About 15% of all cases of sudden death are attributable to PE Severity of symptoms depend on the vessel size and location

234
Q

pulmonary embolism treatment

A

symptomaticallyhigh O2

235
Q

Normal co2 levels

A

35-45 mmhg

236
Q

Acute Respiratory Failure

A

Respiratory failure is inadequate gas exchange by the respiratory system, with the result that levels of arterial oxygen, carbon dioxide, or both cannot be maintained within there normal ranges.

237
Q

hypoxemia

A

A drop in blood oxygenation

238
Q

hypercapnia

A

a rise in arterial carbon dioxide level

239
Q

Type 1 Respiratory Failure

A

Oxygenation Failure hypoxia without hypercapnia, and indeed the PaCO2 may be normal or low

240
Q

ventilation/perfusion (V/Q) mismatch

A

; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs

241
Q

the 5 causes of Type 1 Respiratory Failure

A
  1. V:Q mismatch 2. Low inp fiO2= 21% 3. Alveolar wall disease 4. Low resp rate 5. Shunt
242
Q

Type 1 Respiratory Failure treatment

A

oxygen

243
Q

conditions that affect oxygenation

A

Parenchymal disease (V/Q mismatch) Diseases of vasculature and shunts: right-to-left shunt Pulmonary embolism Interstitial lung diseases: ARDS, pneumonia, emphysema

244
Q

Type 2 Acute Respiratory Failure

A

Ventilation CO2 Failure to compensate: hypercapnia They will be breathing like 35 times per minute but their end tidal will still be high

245
Q

inadequate ventilation defined

A

the build up of carbon dioxide levels (PaCO2) that has been generated by the body

246
Q

Type 2 Acute Respiratory Failure underlying causes include

A

Increased airway resistance( COPD, Asthma, Suffocation) Reduced breathing effort (drug effects, brain stem lesion, extreme obesity) A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis). Neuromuscular problems (GB syndrome., myasthenia gravis, motor neurone disease)  Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest.

247
Q

Respiratory failure resulting from hypoventilation

A

Conditions and impair lung function Conditions that impair mechanisms of breathing Conditions are impaired the neuromuscular apparatus Conditions that reduce respiratory drive

248
Q

Acute Respiratory Distress Syndrome

A

Is a life-threatening reaction to injuries or acute infection to the lung.nflammation of the lung parenchyma leads to impaired gas exchange with systemic release of inflammatory mediators, causing inflammation, hypoxemia and frequently multi organ failure

249
Q

Acute Respiratory Distress Syndrome death rate

A

This condition has a 90% death rate in untreated patients

250
Q

Acute Respiratory Distress Syndrome symptoms

A

People usually present with shortness of breath, tachypnea leading to hypoxia and providing less oxygen to the brain, occasionally causing confusion

251
Q

Aspiration

A

Is the inhalation of either oropharyngeal or gastric contents into the lower airways

252
Q

Aspiration Pneumonia

A

Migration of fluids and inflammatory cells into the area of irritation Fever, productive cough, radiographic findings Immunocompromised patients may not present the inflammatory response

253
Q

most common area if aspiration occurs in the sitting position Aspiration in supine position

A

Right lower lobemay produce infection in any lobe

254
Q

The severity of the symptoms of Aspiration Pneumonia is related to :

A

Volume of aspirant Amount of bacterial contamination Oropharyngeal contents with anaerobic bacteria pH of material pH less than 2.0 are associated with a much higher mortality rate

255
Q

Aspiration Pneumonia Management Acute symptomatic Aspiration

A

Remove airway obstruction Monitor CO2/SpO2 Correct hypoxia Ventilate as required Bronchodilators –Aspiration-induce bronchospasm Bronchoscopy

256
Q

Aspiration Pneumonia Treatment

A

Aggressively reduce the risk of aspiration by avoiding gastric distension when ventilating and by decompressing the stomach with an NG tube whenever appropriate Aggressively monitor the patient’s ability to protect his or her own airway and seek to protect the patient’s airway with an advanced airway if this is impossible Aggressively treat aspiration to suction and airway control if steps one and two fail

257
Q

BVM: ROMAN

A

restrictionobesitymask sealage over 55 (loss of muscle tone/ increase risk for disease)no teeth

258
Q

SGA: RODS

A

restrictionobesitydeformed anatomystiff neck

259
Q

nasal O2

A

1-6lpm24-44%

260
Q

simple o2

A

6-12lpm24-50%

261
Q

nrb o2

A

10-15lpm90-100%

262
Q

bvm 02

A

15lpm100%

263
Q

o2 consumption constantDEH

A

D= 0.16E= 0.28H= 3.14

264
Q

o2 consumption formula

A

psi in tank x constant—————————— flow rate

265
Q

fiO2

A

fraction of inspired oxygen

266
Q

Hyperventilation

A

Hyperventilation Syndrome is a respiratory disorder, psychologically or physiologically based, involving breathing too deeply or too rapidly. The hyperventilation is self-promulgating as rapid breathing causes carbon dioxide levels to fall below healthy levels, and respiratory alkalosis (high blood pH) develops.

267
Q

Hyperventilation Signs and symptoms

A

Palpation Chest pain Paresthesia hand and muscle Light headed Weak Dizzy Carpo-pedal spasm

268
Q
  • CPAP
A

is a respiratory modality which can assist patients in their breathingdistends alveoli preventing collapse on expirationallows for greater surface area, which improves gas exchangeincreases medication distribution when used for COPD is very effective in reducing the amount of fluid in the alveoli and increase the FiO2 (Fraction of Inspired Oxygen) of the inhaled air up to 100%

269
Q
  • The overall goal of CPAP
A

CPAP is to increase Functional Residual Capacity(FRC)

270
Q
  • Functional Residual Capacity(FRC
A

is the volume of air present in the lungs at the end of passive expiration.

271
Q

How does CPAP work?

A
  • CPAP mask forms a tight seal around patients mouth and nose. - CPAP system pressurizes the patients airway while still allowing them to spontaneously inhale and exhale on their own
272
Q

What is CPAP?

A
  • CPAP increases pressure in the lungs and holds open collapsed alveoli, pushes more oxygen across the alveolar membrane, and forces interstitial fluid back into the pulmonary vasculature. - This improves oxygenation, ventilation and ease of breathing. - The increased intrathoracic pressure decreases venous return to the heart and reduces the overwhelming preload (pressure in the ventricles at the end of diastole). - This lowers the pressure that the heart must pump against (afterload), both of which improve left ventricular function. - CPAP alters the pressure gradient
273
Q

protocol criteria for CPAP

A
  • Patient must be alert and able to follow commands (GCS >13) - Be able to maintain an open and patent airway on their own - Patient is over 12 years of age and must be able to fit the CPAP mask - PCP’s may apply CPAP to adult patients with severe respiratory distress - Severe Respiratory distress as per Paramedic Clinical Practice protocols is RR greater than 25,SPO2 less than 92%, use of accessory muscle use. - If the CPAP is on, try to keep it on. Alveoli can collapse again within seconds. - It may take hours to reopen alveoli again
274
Q

Indications for CPAP

A
  • Hypoxemia secondary to congestive heart failure - Acute cardiogenic shock - Pulmonary edema - Asthma/COPD - Respiratory distress (A respiratory rate >25bpm, SpO2 <92%, accessory muscle use during
275
Q

CPAP Contraindications

A
  • Pneumothorax or chest trauma - Hemodynamically unstable patients - Altered mental state- Patient has a tracheotomy- Patient is actively vomiting- Patient has an upper GI bleed
276
Q

why do we put end tidal on everyone

A
  1. Want to see whats going on in the lungs (bronchoconstriction) 2. Want to see the effects of treatments
277
Q
  • Capnography (capnometry)
A

The measurement of carbon dioxide in exhaled breath

278
Q
  • Capnometer
A

The numeric measure of CO2

279
Q
  • Capnogram
A

The wave form produced with inspiration & expiration

280
Q
  • ETCO2 define
A

the level of partial pressure of carbon

281
Q

-PaCO2

A

Partial pressure of CO2 in arterial blood

282
Q

3 things needed for 02

A
  • Cardiac output - Ventilation: gas exchange at the alveoli wall - Metabolism: what the cells need to use oxygen
283
Q
  • CO2
A

is the “Gas of Life” produced from “The fire of life” metabolism

284
Q

ETCO2

A
  • Provides an immediate, real time, picture of the pt.’s condition- Capnography will show immediate apnea- Directly related to the ventilatory status of the pt.
285
Q

SPO2

A
  • Delayed, SpO2 can show high saturations for several minutes- SPO2 will not show immediate apnea- Directly related to oxygenation of the pt.
286
Q

What else can ETCO2 tell us?

A

Not only can ETCO2 measure ventilation but . . . . - It also indirectly measures metabolism & circulation

287
Q
  • An increased metabolism will
A

increase the production of carbon dioxide & increasing levels on the monitor

288
Q
  • A decreased metabolism will
A

decrease the amount of CO2 delivered to the lungs & decreases levels on the monitor

289
Q

Intubated Capnography Patients

A
  • EtCO2 is directly related to the ventilation status & can be used in intubated as well as non-intubated pt.’s
290
Q
  • Capnography in Intubated pt.’s can be used to:
A

o Verify ETT placement o Monitor ETT position o Assess ventilation and treatments o Evaluate resuscitative efforts during CPR

291
Q

Non-Intubated Capnography Patients

A
  • Asthma & COPD - CHF/Pulmonary Edema - CPAP pt.’s - Pulmonary Embolus - Head Injury
292
Q

Capnography Values Hyperventilation / Hypocapnia

A
  • > 45mmHg - Respiratory Acidosis
293
Q

In-accurate readings may be due to;

A
  • Poor positioning of NC capnofilters - Obstructed nares - Mouth breathers - O2 by mask may lower reading by 10% or more
294
Q

Increased ETCO2

A

Due to Increased CO2 Production - Fever - Burns - Hyperthyroidism - Seizure - Bicarbonate Tx - Return Of Spontaneous Circulation - (ROSC) - Release of Tourniquet / Reperfusion - Decreased ETCO2 - Increased CO2 Clearanceo Hyperventilation - Exercise- Sick

295
Q

Decreased ETCO2

A

Decreased CO2 production- Hypothermia- Sedation- Paralysis Decreased delivery to the lungs - Decreased cardiac output

296
Q

Normal Waveform

A
  • Straight boxes are good- Length of wave = Time- Height of wave = CO2 Level
297
Q
  • CO2 is a result of
A

Metabolism

298
Q

Hyperventilation Waveform

A

CO2 goes down - Wave forms start getting lower- Anxiety- Bronchospasm- PE- Increased ventilation - Remember to look at the trend not just the number

299
Q

Causes for CO2 going down

A
  • Hypothermia- Decreased Metabolism- Decreased Pulmonary perfusion
300
Q

Hypoventilation Causes

A

Hypoventilation Causes – CO2 goes up, wave form slows - Wave forms start getting bigger- Decreased ventilation- OD/Intoxication/Sedation - CNS Dysfunction- Tiring respiratory pt. Remember to look at the trend not just the number

301
Q

High CO2 Waveform

A

Causes for CO2 going up - Decrease in respiratory rate - Decrease in tidal volume - Increase in metabolic rate - Rapid rise in body temperature (hyperthermia)

302
Q

Bronchospasm Waveform

A
  • This wave form can occur in Asthma, COPD, Incomplete Airway Obstruction, Tube kinked or obstructed o CO2 that is transferred to the alveoli from the bloodstream may take longer to exhale because of the narrowed bronchi. o This delayed emptying of the alveoli varies in different parts of the lungs. o This results in the sloping plateau on the capnograph trace, CO2 from parts of the lungs with more severe bronchial narrowing is exhaled later than those parts with less severe narrowing.
303
Q

what type of shape is bronchospasm

A

o This represents struggling to exhale & un- even emptying of alveoli o The pt. hyperventilates to compensate, CO2 drops to below 35 o Asthma worsens, the C02 levels will rise to normal

304
Q

Emphysema Waveform

A
  • The slope of phase III can be reversed in patients with emphysema where there is marked destruction of alveolar- capillary membranes and reduced gas exchange
305
Q

Cardiac Asthma & ETCO2

A

Decrease in airway diameter caused by pulmonary congestion, not bronchoconstriction. - If the wave form is upright, there is no constriction, the wheezing is caused by the CHF, not the COPD, you might want to withhold the neb treatment.

306
Q

Pulmonary Embolus

A
  • PE will cause an increase in dead space in the lungs decreasing the alveoli available to off load CO2 - The ETCO2will go down.
307
Q
  • A zero reading from intubated pt
A

may indicate the ETT is in the esophagus, prolonged down time prior to CPR, or massive PE

308
Q

Ventilating Pt.’s With ICP

A
  • Finding a Balance - Hyperventilation = Hypocapnea =  Cerebral Ischemia - Hypoventilation = Hypercapnia = Dialation  bleed & pressure - Keep C02 value of aprox 30 (>35 & not <25 mmHg)
309
Q

“Bucking” the Tube - “Curare Cleft”

A

Sedated Intubated Pt.’s - A notch in the wave form indicates the pt. is starting to arouse from sedation, breathing on their own & may need additional medication

310
Q

Capnography & Cardiac Output

A
  • Increased Cardiac Output = Increased CO2 - Decreased Cardiac Output = Decreased CO2

PRIMARY CARE PARAMEDIC 2021/22 (12 decks)

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