EMER 110 Cardiac and Respiratory Theory Flashcards
Deep Vein Thrombosis (DVT)
A thrombosis is a blood clot that remains attached to a vessel wall.
what is the cause of Deep Vein Thrombosis (DVT)
Intimal irritation, roughening, inflammation, traumatic injury, infection, low blood pressures, or obstructions that cause blood stasis Inflammation is the usual cause of DVT
causes of DVT
History of trauma Sepsis Stasis or inactivity Recent immobilization Pregnancy Birth control pillsMalignancy Coagulopathies SmokingVaricose veins
signs and symptoms of DVT
Pain Edema Increase temp extremity Erythema Tenderness
Atherosclerosis
Fatty build up Affects the inner lining of the aorta, cerebral, and coronary blood vessels. Abnormal thickening and hardening of vessel walls
what is Atherosclerosis caused by
Caused by soft deposits of intra-arterial fat and fibrin which harden over time
Risk Factors for atherosclerosis
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
Effects of Arteriosclerosis
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)
Aneurysm
“dilation of a vessel” Artery wall weakness
most common cause for AAA
Atherosclerosis
Signs and Symptoms of a ruptured aneurysm
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
Hypertension
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
Risk Factors of hypertension
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
Pathophysiology of hypertension
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
Treatment Plans Arteriosclerosis Peripheral Vascular Disease Hypertension Deep Vein Thrombosis Aneurysm
*symptomatic only
Endocarditis
Inflammation of the inner lining of the heart, and/or heart valves
causes of endocarditis
Can be caused by either bacteria or virus, bacteria being the most common
risk factors of endocarditis
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
Signs and Symptoms of endocarditis
May involve a number of organ systems Classic findings Fever Cardiac murmur Petechial lesions of skin, conjunctiva, and oral mucosa Chest pain- SOB
myocarditis
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
myocarditis causes
Chest infection Auto immune disease Fungal viral infection
signs and symptoms of myocarditis
Flulike Pain in epigastric region or under sternum (substernal) Dyspnea Cardiac arrhythmias Stabbing chest pain
pericarditis
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.
Signs and Symptoms Pericarditis
Low cardiac output Low SPO2 Chest pain
causes of pericarditis
Trauma Heart attacks
Acute Coronary Syndrome (ACS)
refers to distinct conditions caused by a similar sequence of pathologic events involving abruptly reduced coronary blood flow
Acute Coronary Syndrome (ACS) conditions
Unstable Angina (UANon-ST-segment elevation myocardial infarction (NSTEMI), ST-segment elevation myocardial infarction (STEMI)
Ischemia
Lack of oxygen to the tissues ST depression or T inversion
Ischemic Heart Disease
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
Clinical Features of Ischemic Heart Disease
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
atypical presentation of Ischemic Heart Disease
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
what does schema lead to
Injury prolonged ischemia ST elevation
infarct
death of tissue may or may not show in Q wave
angina Three types:
Stable Angina (Exertional Angina) Unstable Angina (Preinfarction Angina) Prinzmetal’s Angina
Prinzmetal’s Angina
Vasospastic angina: no blockage or clot just spasm of segment of coronary arteryCause: cocaine Treatment: nitro
Angina
Imbalance between myocardial O2 supply and demand choking pain in the chest” Burning Tightness Pressure Crushing heavy
The coronary arteries can spasm as a result of :
Exposure to cold weather Stress Medicines- Anti-migraines, Chemo, Antibiotics Smoking Cocaine use
Myocardial Infarction
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.
If blood flow is not restored to the affected artery
myocardial cells within the sub-endocardial area begin signs of injury within 20 to 40 minutes.
ACS Management/ Treatment
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
ACS CALL vs NON ACS CALL
ACS CALL Heavy, burning tight NON ACS CALL Sharp pain Increases with palpation Increase with inspiration
angina signs and symptoms
“choking pain in the chest” Burning Tightness Pressure Crushing Heavy Radiates Lasts less than 20 min Sob Occurs with activity Is better with rest
UNSTABLE angina signs and symptoms
Lasts longer than 20mins Can occur at rest
MI: STEMI, NSTEMI signs and symptoms
At rest Doesn’t get better Shock symptoms –Nausea vomiting –Pale cool clammy
Cardiomyopathies
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
Cardiomyopathies are divided into three forms:
Dilated Cardiomyopathy Hypertrophic cardiomyopathy Restrictive cardiomyopathy
cardiac outputstroke volumeFormula
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
Factors that affect CO
- Heart rate 2. Preload: 3. afterload:4. Contractility:
define preload and after load
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
Pulmonary Edema
Swelling within the lungs Sign of left sided CHFDecrease of output to left side of heart
One of the most common causes of pulmonary oedema is
left ventricular failure from an acute MIOther cause are inhaled toxins, infections, and sometimes trauma and altitude changes
Pulmonary Edema Signs and Symptoms
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
Congestive Heart Failure
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.
Left sided CHF
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.
Left-sided heart failure signs and symptoms
Extreme restlessness and anxiety, confusion and agitation Severe dyspnea, tachypnea, tachycardia Hypertension or hypotension Crackles and/or wheezes Frothy pink sputum in severe cases
Right sided CHF
Pumps blood to lungs JVD Pedal edema Pitting edema SOB
Right-Sided heart failure Signs and Symptoms
Jugular vein distention Pedal/pitting edema
Heart Failure Management
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
Pulmonary edema treatment
Crackles: nitro CPAP Wheezing: Ventolin and Atrovent –Call ALS if Combivent doesn’t work
Nitro for pulmonary edema
No chest pain and no nitro prescription –> call med control for orders No chest pain- nitro prescription –>give nitro Chest pain –> give nitro
Causes for pulmonary edema
Cardiogenic Noncardiogenic
Cardiogenic Noncardiogenic
Cardiogenic 1. Left sided failure 2. Systemic hypertension Noncardiogenic -Toxins -Lung infections -Sepsis
Pneumonia Vs Pulmonary Edema
–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
Cardiogenic Shock
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
Signs and symptoms of cardiogenic shock brain
Altered LOC Coma Lethargy Possible stroke
Signs and symptoms of cardiogenic shock lungs
SOB Accessory muscle use Stats less than 90 Tachnyepia
Signs and symptoms of cardiogenic shock heart
Increase HR Decrease BP Arythmias MI
Signs and symptoms of cardiogenic shock skin
Cool Clammy Delayed cap refill
Management of Cardiogenic Shock
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
Frank-starling mechanism
One characteristic of cardiac muscle is that when it’s stretched a contract with greater force
systematic vascular resistance leads to
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
- Changes in contractility may be induced by
medication’s that have a positive or negative inotropic effect
- Nervous system controls regulate the
contractility of the heart from beat to beat
- Positive chronotropic effect
how hard can increase its cardio output by increasing the number of contractions per minute (HR)
- Pacemaker
the area of conduction tissue in which the electrical activity arises at any given time
- AV node
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
- Electric impulses from SA node take how may secs to read AV node
o.o8secs
- The conduction is delayed in the AV node for approximately how many secs
0.12sec
- It takes approx. how many sec for an electrical impulse to spread across the ventricles
0.08
what happens with ions during depolarization
depolarization sodium and calcium ions rush into cell causing inside of cell to be positive
what happens with ions during repolarization
the sodium and calcium channels close and potassium channels open allowing rapid escape of potassium ions from the cell
- Refectory period
period when the cell is depolarized or in the process of repolarizing
- Absolute refractory period
the cell is still highly depolarized and a new action protentional cannot be initialed
- Relative refractory period
the heart is partially depolarized and a new action potential will be inhibited but not impossible
The parasympathetic nervous system
- Sends messages mainly through vagus nerve- Atropine blocks actions of PNS and vagus nerve causing HR to increase
The sympathetic nervous system
- 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
- Alpha 1 receptors
are primarily located on peripheral blood vessels and stimulation results in:o Peripheral vasoconstrictiono Mild bronchoconstrictiono Increased metabolismo Stimulation of sweat glands
- Alpha 2 receptors
are primarily located on nerve endings and stimulation results in:o Control release of neurotransmitters
- Beta 1 receptors
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)
- Beta 2 receptors
are primarily located on bronchial smooth muscle and stimulation results in:o Bronchodilationo Peripheral vasodilation
Causes of dysrhythmias
- Acid base disturbance- ANS imbalance- CNS damage- Certain poisons- Drugs- Endocrine disorders- Hypothermia- Hypoxemia- Ischemia o infarction- trauma
- disrhythmias happen after an AMI for 2 reasons
- 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
Sodium (Na+)
goes into cell and initiates depolarization
Potassium (K+):
flows out of the cell to initiate repolarization
HypokalemiaHyperkalemia
Hypokalemia: increased myocardial irritabilityHyperkalemia: decreased automaticity/conduction
Calcium (Ca)
has major role in the depolarization of pacemaker cells (maintain depolarization) and in myocardial contractility
Hypocalcemia Hypercalcemia
Hypocalcemia: decreased contractility and increased myocardial irritability Hypercalcemia: increased contractility
Magnesium (Mg)
stabilizes the cell membrane: acts in concert with potassium and opposes the actions of calcium
Hypomagnesemia Hypermagnesemia
Hypomagnesemia: decreased conductionHypermagnesemia: increased myocardial irritability
Absolute Refractory Period
the cardiac muscle cell is completely insensitive to further stimulation Start of the QRS and ends at middle of T wave
Relative Refractory Period
During the relative refractory period, the muscle cell is more difficult than normal to excite, but it can still be stimulated.
Nervous system controlling heart rate
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):
Accelerator nerve (sympathetic NS)
when stimulated, releases neurotransmitter at the SA node to increase heart rate
Vagus nerve (parasympathetic NS)
when stimulated, releases neurotransmitter at the SA node to decrease heart rate
Electrical Conduction System
• Automaticity• Generates its own electrical impulses without stimulation from nerves • Unique feature of the heart• Specialized conduction tissue• Pacemaker
The Sinoatrial (SA)Node
• 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)
Secondary Pacemakers
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
ECGs
- 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
Indications for ECG Monitoring
- 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
Voltage Positive:Negative:
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.
ECG Leads - Bipolar lead*:- Unipolar lead:
- Bipolar lead*:o Two electrodes of opposite polarity. - Unipolar lead: o Single positive electrode and reference point.
Lead Placement
- 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
lead triangle
GO LOOK AT IT - double positive is on the bottom-top right (patients right) double negative-top left (patients left) negative and positive
ECG Graph Paper
- Each Little square is 1mm x 1mm 0.04sec- Each Large square is 5mm x 5mm 0.20 sec
Calibration
- 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
Time Interval
- 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).
- Depolarization
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
- Repolarization
resets charge
- P wave
depolarization of the atriumso Impulse being sent to AV nodeo Positive deflection because its going towards positive
- Q wave
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
- R wave
left ventricle contracting
-QRS
ventricular depolarization
- T
ventricular repolarizationo Reset
PRI IntervalQRS intervalR-R Interval
- 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
Artifact Common causes
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
Rhythm Interpretation 5 Steps
Regularity ratep wavesP-R interval QRS complex
Regularity
- 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
Rate
- 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
P waves significance
- 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?
PRI
- 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)
QRS Complex
- Is there a QRS complex for every P Wave? - IS it Narrow?- a normal QRS complex is less than .12
shockable rhythms
v fibpulseless v tach
starlings law
the greater the stretch the greater the contractions
all sinus rhythms
come from SA node, 4 rhythms - Upright uniform p wave- 1p:1QRS- QRS
Normal Sinus Rhythm
- 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
Sinus Bradycardia
- 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
causes of Sinus Bradycardia
o Medso Hypothermiao Drugs
Sinus Tachycardia
- 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
Sinus Arrhythmia
- 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
Atrial Rhythms come from
atria
Premature Atrial Contractions (PAC’s)
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
Atrial Flutter
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.
Atrial Fibrillation
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
Atrial Fibrillation 2 types
- A-Fib with SVR with slow ventricular response (SVR) below 99bpm- A-Fib with RVR ventricular response (RVR) above 100 bpm
Supraventricular Tachycardia (SVT)
- 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
Paroxysmal Supraventricular Tachycardia (PSVT)
- 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
Bigeminy: Trigeminy:Quadreminy:Couplet:
Bigeminy: every 2nd one is ectopicTrigeminy: every 3rd one is ectopicQuadreminy: every 4th one is ectopic Couplet: 2 in a row
Treatment for atrial rhythms
A-Flutter- treat CP if they have A-Fib- treat CP if they haveSVT- ALS ALWAYS
treatment for sinus rhythms
NSR- Nothing ST- nothingSA- nothingSB- symptomatic- CP- SOB- Pale- Lightheaded- CALL ALS
What Is a 12-Lead ECG?
- 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.
3 lead placement
**white to rightRed to bed (torsoBlack- Smoke over fireGreen- ground
o Contiguous leads
: (Sister leads) Must both be elevated to be important
SALI
septal wallanterior walllateral wallinferior wall
septal wall
o V1, V2o Place Along sternal borders
- Anterior Wall
(left ventricle area)o V3, V4o Placed Left Anterior Chest
- Lateral Wall
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
- Inferior Wall
(looks at bottom of heart- ventricles- CO input/output)o Lead II, III, aVF o Left leg
Placement
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
- Skin Preparation
o Dry/remove oilo Remove excess hair
- Patient Preparation
o Cease movement o Breath normallyo Stop speaking
Obstructive disease
can’t get air out Occurs when the positive pressure of exhalation causes the small airways to pinch shut trapping gas in the alveoli
Signs of obstructive disease
Pursed lip breathing Increased inspiratory to expiratory ratio Abdominal muscle use Jugular venous distention
Asthma Name from Greek work meaning
panting
Asthma is characterized by
an inflammation in the bronchiole airways common chronic inflammatory disease of the airways.
Hallmark of Asthma is
Airway Diameter Reduction
key points of asthma
Reversible Must be triggered
normal levels of C02 in blood
35-45mmhg
CPAP rule
must have neb running
HypoxiaHypoxemia
Hypoxia: area of the body that is short of oxygen Hypoxemia: entire body is short of oxygen
Only way to fix Hypoxemia aka low spo2
02 and PEEP
Bronchospasm/ Bronchoconstriction
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
The primary treatment of bronchospasm
is the administration of bronchodilator medication ex: Ventolin
3 main symptoms of asthma
bronchoconstrictionmucous productioninflammation
Signs and Symptoms of asthma
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
treatment for asthma
Ventolin(Salbutimol) Atrovent(Ipratropium Bromide) epinephrine
Potentially Fatal Asthma
Severely compromised ventilation all of the time Be alert for silent chest syndrome
Potentially Fatal Asthma Ask if pt:
Previous intubation for respiratory failure or respiratory arrest 2 or more admissions to hospital despite oral corticosteroid use 2 or more episodes of pneumothorax
Status asthmaticus
severe prolonged asthmatic attack that cannot be broken with conventional treatment Patient physically tired: accessory muscle use, cyanosis, chest hyperinflatedA despite treatment already given
when is epinephrine used for asthma
silent lungs
Mild asthma
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)
moderate asthma
Can speak few words at a time, tripod position Inspiratory and expiratory wheezes through all 4 lobes O2 immediately
Severe asthma
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
Anaphylaxis
Serious allergic reaction that is rapid in onset and may cause death
Risk factors: Anaphylaxis
Predisposition Substance Route and dosage Time between exposure
AllergenAntibody (immunoglobulin)AntigenHypersensitivity
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
Allergic Reaction vs Anaphylaxis
Allergic Reaction 1 body system Anaphylaxis 2 body systems EPI!!
Sensitization
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
Anaphylaxis Common causes
Drugs Foods and Additives Hymenoptera Stings
Chemical Mediators cause and result in
Causes inflimation, bronchonstriction and mucous These substances result in bronchoconstriction, peripheral vasodilation and increased capillary permeability.
Mediators that are stored include
*histamine, heparin and chemotactic factors. Other mediators are formed during degranulation such as prostaglandins, leukotriene’s, bradykinins and interleukins.
Histamine Receptors H1
Bronchospasm increased peristalsis Vessel dilation Post capillary venule permeability Increases heart rate
Histamine Receptors H2
Gastric acid secretion
Anaphylaxis Presentation initial response
which occurs within the first 30 minutes after exposure and resolves within one hour consists of vasodilation, vascular leakage, and smooth muscle spasm
Anaphylaxis Presentation delayed response
which can occur hours later and last for days consisting of more intense infiltration of tissues with inflammatory cells and more severe symptoms
Anaphylaxis Presentation skin
Urticaria (Hives) Pruritus(itching) Angioedema (Swelling)
Criteria for anaphylaxiss exist when one of the following are met:
- 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
COPD
General term (umbrella term): contains emphysema and chronic bronchitis
copd spo2
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
copd CO2
CO2 is always higher 50-60 mmhg
Common Pathologies of COPD
Airflow obstruction Bronchospasm/bronchoconstriction Increased mucous production Impaired elasticity of airways
Emphysema
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.
Pulmonary Emphysema (Pink Puffers)
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
Emphysema Pathologies
Destruction of alveoli walls Weakening and destruction of bronchioles Decreased alveoli surface area Decreased gas exchange
Emphysema – Signs and Symptoms
“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
Chronic Bronchitis
Inflammation, swelling and excessive mucous production in the bronchial tree. Minimal alveoli involvement Decreased ventilation of alveoli due to airflow obstruction
Chronic Bronchitis - Signs and Symptoms
“blue bloater”- respiratory distress: inhalation Cyanotic Sweating Leaning forward Use of accessory muscles Tachypnea Distended neck veins
COPD with right heart failure
Very difficult to push the patients thick blood through lungs destroyed by emphysema and through capillaries squashed by hyperinflated alveoli
COPD with right heart failure Signs and symptoms
Peripheral edema JVD End inspiratory crackles
Hypoxic Drive
Rare phenomenon that affects only a very small percentage Pts whose respiratory drive can be decreased by high levels of oxygen
Bagging someone with COPD
Pts who have severe asthma or copd should be ventilated 4-6 breaths per pin to avoid bagging them to death
Management of COPD
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
Pleural effusion
is when fluid collects between the visceral and parietal pleura.
Effusions can be caused by
infections, tumors, CHF, trauma
what do pleural Effusions cause
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.
where do P effusions happen
Happens in pleural space
what will you hear with a pleural effusionwhat will the spo2 be
When you listen you won’t hear anything SPO2 will be low (hypoxemic)
P effusions Treatment
Prehospital treatment should consist of proper positioning, high fowlers most often, aggressive supplemental oxygen if required.
Bronchitis
Is an inflammation of the mucous membranes of the bronchi
bronchitis Is characterized by
development of cough or small sensation in the back of the throat, with or without production of sputum
bronchitis Divided into two categories:
Acute Chronic
bronchitis treatment
treat symptomatically
Laryngitis
inflammation of voice box due to overuse, irritation or infection
Croup
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
symptoms and cause of croup
symptoms include loud harsh barking cough, fever, noisy inhalations, hoarse voice and dyspnea caused by a virus
Pneumonia
Is an inflammatory condition of the lung, affecting primarily the alveoli
Viral Pneumonia
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)
Pneumonia signs and symptoms systemic:skin:lungs;muscular:centralvascularheartgastricjoints
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
Pneumonia treatment
treat symptomatically
V:Q normals and normal ratio
Ventilation 4l/min Perfusion 5l/min 0.8 is normal VQ ratio
Pulmonary Embolism
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).
P embolism most commonly results from
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)
Pulmonary embolism Risk Factors
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
Signs and Symptoms of pulmonary embolism
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
pulmonary embolism treatment
symptomaticallyhigh O2
Normal co2 levels
35-45 mmhg
Acute Respiratory Failure
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.
hypoxemia
A drop in blood oxygenation
hypercapnia
a rise in arterial carbon dioxide level
Type 1 Respiratory Failure
Oxygenation Failure hypoxia without hypercapnia, and indeed the PaCO2 may be normal or low
ventilation/perfusion (V/Q) mismatch
; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs
the 5 causes of Type 1 Respiratory Failure
- V:Q mismatch 2. Low inp fiO2= 21% 3. Alveolar wall disease 4. Low resp rate 5. Shunt
Type 1 Respiratory Failure treatment
oxygen
conditions that affect oxygenation
Parenchymal disease (V/Q mismatch) Diseases of vasculature and shunts: right-to-left shunt Pulmonary embolism Interstitial lung diseases: ARDS, pneumonia, emphysema
Type 2 Acute Respiratory Failure
Ventilation CO2 Failure to compensate: hypercapnia They will be breathing like 35 times per minute but their end tidal will still be high
inadequate ventilation defined
the build up of carbon dioxide levels (PaCO2) that has been generated by the body
Type 2 Acute Respiratory Failure underlying causes include
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.
Respiratory failure resulting from hypoventilation
Conditions and impair lung function Conditions that impair mechanisms of breathing Conditions are impaired the neuromuscular apparatus Conditions that reduce respiratory drive
Acute Respiratory Distress Syndrome
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
Acute Respiratory Distress Syndrome death rate
This condition has a 90% death rate in untreated patients
Acute Respiratory Distress Syndrome symptoms
People usually present with shortness of breath, tachypnea leading to hypoxia and providing less oxygen to the brain, occasionally causing confusion
Aspiration
Is the inhalation of either oropharyngeal or gastric contents into the lower airways
Aspiration Pneumonia
Migration of fluids and inflammatory cells into the area of irritation Fever, productive cough, radiographic findings Immunocompromised patients may not present the inflammatory response
most common area if aspiration occurs in the sitting position Aspiration in supine position
Right lower lobemay produce infection in any lobe
The severity of the symptoms of Aspiration Pneumonia is related to :
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
Aspiration Pneumonia Management Acute symptomatic Aspiration
Remove airway obstruction Monitor CO2/SpO2 Correct hypoxia Ventilate as required Bronchodilators –Aspiration-induce bronchospasm Bronchoscopy
Aspiration Pneumonia Treatment
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
BVM: ROMAN
restrictionobesitymask sealage over 55 (loss of muscle tone/ increase risk for disease)no teeth
SGA: RODS
restrictionobesitydeformed anatomystiff neck
nasal O2
1-6lpm24-44%
simple o2
6-12lpm24-50%
nrb o2
10-15lpm90-100%
bvm 02
15lpm100%
o2 consumption constantDEH
D= 0.16E= 0.28H= 3.14
o2 consumption formula
psi in tank x constant—————————— flow rate
fiO2
fraction of inspired oxygen
Hyperventilation
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.
Hyperventilation Signs and symptoms
Palpation Chest pain Paresthesia hand and muscle Light headed Weak Dizzy Carpo-pedal spasm
- CPAP
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%
- The overall goal of CPAP
CPAP is to increase Functional Residual Capacity(FRC)
- Functional Residual Capacity(FRC
is the volume of air present in the lungs at the end of passive expiration.
How does CPAP work?
- 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
What is CPAP?
- 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
protocol criteria for CPAP
- 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
Indications for CPAP
- 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
CPAP Contraindications
- Pneumothorax or chest trauma - Hemodynamically unstable patients - Altered mental state- Patient has a tracheotomy- Patient is actively vomiting- Patient has an upper GI bleed
why do we put end tidal on everyone
- Want to see whats going on in the lungs (bronchoconstriction) 2. Want to see the effects of treatments
- Capnography (capnometry)
The measurement of carbon dioxide in exhaled breath
- Capnometer
The numeric measure of CO2
- Capnogram
The wave form produced with inspiration & expiration
- ETCO2 define
the level of partial pressure of carbon
-PaCO2
Partial pressure of CO2 in arterial blood
3 things needed for 02
- Cardiac output - Ventilation: gas exchange at the alveoli wall - Metabolism: what the cells need to use oxygen
- CO2
is the “Gas of Life” produced from “The fire of life” metabolism
ETCO2
- 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.
SPO2
- Delayed, SpO2 can show high saturations for several minutes- SPO2 will not show immediate apnea- Directly related to oxygenation of the pt.
What else can ETCO2 tell us?
Not only can ETCO2 measure ventilation but . . . . - It also indirectly measures metabolism & circulation
- An increased metabolism will
increase the production of carbon dioxide & increasing levels on the monitor
- A decreased metabolism will
decrease the amount of CO2 delivered to the lungs & decreases levels on the monitor
Intubated Capnography Patients
- EtCO2 is directly related to the ventilation status & can be used in intubated as well as non-intubated pt.’s
- Capnography in Intubated pt.’s can be used to:
o Verify ETT placement o Monitor ETT position o Assess ventilation and treatments o Evaluate resuscitative efforts during CPR
Non-Intubated Capnography Patients
- Asthma & COPD - CHF/Pulmonary Edema - CPAP pt.’s - Pulmonary Embolus - Head Injury
Capnography Values Hyperventilation / Hypocapnia
- > 45mmHg - Respiratory Acidosis
In-accurate readings may be due to;
- Poor positioning of NC capnofilters - Obstructed nares - Mouth breathers - O2 by mask may lower reading by 10% or more
Increased ETCO2
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
Decreased ETCO2
Decreased CO2 production- Hypothermia- Sedation- Paralysis Decreased delivery to the lungs - Decreased cardiac output
Normal Waveform
- Straight boxes are good- Length of wave = Time- Height of wave = CO2 Level
- CO2 is a result of
Metabolism
Hyperventilation Waveform
CO2 goes down - Wave forms start getting lower- Anxiety- Bronchospasm- PE- Increased ventilation - Remember to look at the trend not just the number
Causes for CO2 going down
- Hypothermia- Decreased Metabolism- Decreased Pulmonary perfusion
Hypoventilation Causes
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
High CO2 Waveform
Causes for CO2 going up - Decrease in respiratory rate - Decrease in tidal volume - Increase in metabolic rate - Rapid rise in body temperature (hyperthermia)
Bronchospasm Waveform
- 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.
what type of shape is bronchospasm
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
Emphysema Waveform
- 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
Cardiac Asthma & ETCO2
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.
Pulmonary Embolus
- PE will cause an increase in dead space in the lungs decreasing the alveoli available to off load CO2 - The ETCO2will go down.
- A zero reading from intubated pt
may indicate the ETT is in the esophagus, prolonged down time prior to CPR, or massive PE
Ventilating Pt.’s With ICP
- Finding a Balance - Hyperventilation = Hypocapnea = Cerebral Ischemia - Hypoventilation = Hypercapnia = Dialation bleed & pressure - Keep C02 value of aprox 30 (>35 & not <25 mmHg)
“Bucking” the Tube - “Curare Cleft”
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
Capnography & Cardiac Output
- Increased Cardiac Output = Increased CO2 - Decreased Cardiac Output = Decreased CO2
