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PRIMARY CARE PARAMEDIC 2021/22 > EMER 111 Cardiac Care > Flashcards

EMER 111 Cardiac Care 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

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.

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.

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

56
Q

Right sided CHF

A

Pumps blood to lungs JVD Pedal edema Pitting edema SOB

57
Q

Right-Sided heart failure Signs and Symptoms

A

Jugular vein distention Pedal/pitting edema

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

59
Q

Pulmonary edema treatment

A

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

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

61
Q

Causes for pulmonary edema

A

Cardiogenic Noncardiogenic

62
Q

Cardiogenic Noncardiogenic

A

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

63
Q

Pneumonia Vs Pulmonary Edema

A

–Pulmonary edema: cause by Left heart failure Normal HR Febrile 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 Crackles Wheeze Productive cough- green or dark yellow History of pneumpnia Sharp CP Cp increase with inspiration/coughing

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

65
Q

Signs and symptoms of cardiogenic shock brain

A

Altered LOC Coma Lethargy Possible stroke

66
Q

Signs and symptoms of cardiogenic shock lungs

A

SOB Accessory muscle use Stats less than 90 Tachnyepia

67
Q

Signs and symptoms of cardiogenic shock heart

A

Increase HR Decrease BP Arythmias MI

68
Q

Signs and symptoms of cardiogenic shock skin

A

Cool Clammy Delayed cap refill

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

70
Q

Frank-starling mechanism

A

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

71
Q
  • Arise and systematic vascular resistance leads to
A

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

72
Q
  • Changes in contractility may be induced by
A

medication’s that have a positive or negative inotropic effect

73
Q
  • Nervous system controls regulate the
A

contractility of the heart from beat to beat

74
Q
  • Positive chronotropic effect
A

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

75
Q
  • Pacemaker
A

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

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

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

o.o8secs

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

0.12sec

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

0.08

80
Q

what happens with ions during depolarization

A

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

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

82
Q
  • Refectory period
A

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

83
Q
  • Absolute refractory period
A

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

84
Q
  • Relative refractory period
A

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

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
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
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

88
Q
  • Alpha 2 receptors
A

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

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)

90
Q
  • Beta 2 receptors
A

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

91
Q

Causes of dysrhythmias

A
  • Acid base disturbance- ANS imbalance- CNS damage- Certain poisons- Drugs- Endocrine disorders- Hypothermia- Hypoxemia- Ischemia o infarction- trauma
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
93
Q

Patient Assessment

A
  • Most common reports are chest pain, dyspnea, fainting, palpations, nausea and fatigue
94
Q

Scene assessment

A
  • Anticipate the need for resources- Look for any clues that may help identify what might’ve brought on the problem such as meds alcohol cigarettes drug paraphernalia or living conditions
95
Q

General appearance

A
  • Serve patient’s general parents as you approach him or her and assess for apparent life threats
96
Q

ABCs and skin

A
  • Determine the patency of patient’s airway if the patient is talking to you the airway is patent- Note the rate, quality and effort of breathing and consider initiating oxygen therapy at this time - Assessment of circulation is done primarily by checking the patient’s pulse note the rate regularity and overall quality- Is the skin pink warm and dry is there edema poor turgor or skin tentingo Shiny waxy skin lacking hair indicates vascular disease
97
Q

Transport decision

A
  • The primary assessment ends with making a load and go transport decision for your patient based on your findings
98
Q

dyspnea questions

A

o When did it starto Paroxysmal nocturnal dyspnea: acute episode of sob in which patient suddenly wakes up from sleep feeling suffocated o Did it come on gradually or suddenlyo Is it continuous or intermittento Does it happen during activity or while at resto Does any position make the shortness of breath better or worseo Have you ever had shortness of breath like this beforeo Dissipation have a cough is a dry productive

99
Q
  • Fainting questions
A

o Under what circumstances did this episode occur what were they doingo Were there any warning feelings before the episode or did it occur suddenly and unexpectedlyo What position was the patient in when here she faintedo Has this happened beforeo Were there other symptoms

100
Q
  • Palpations questions
A

o Refer to sensation of abnormally fast or irregular heartbeato Ask about presence of associated symptoms such as chest pain, dizziness and dyspnoea

101
Q

Past medical history, medications and allergies

A
  • Ask if they’ve ever been diagnosed with the following:o Coronary artery diseaseo Atherosclerotic heart disease: angina, previous MRI, hypertension, heart failureo Valvular diseaseo Aneurismo Pulmonary diseaseo Diabeteso Renal diseaseo Vascular diseaseo Inflammatory cardiac diseaseo Previous cardiac surgery- Is the patient taking any medication’s- Does the patient have known allergies to foods or medication’s and what type of reaction
102
Q

Pulse

A
  • Best to assess both radio pulses- Pulsus paradoxus: excessive drop in systolic blood pressure with each inspired breath- Pulsus alternans: alternates in strength from one beat to the next
103
Q

Blood pressure

A
  • High 130/80- A very low blood pressure may indicate a drop in systemic vascular resistance due to causes such a septic shock anaphylaxis or sedative drug- Bilateral upper limb bps should be obtained in all patients with chest paino A difference of greater than 20 should be considered abnormal and brought to the attention of receiving facility personnel
104
Q

Respirations

A
  • Note the rate and quality of patients respirations- Is the rate rapid is the patient labouring to breathe yes
105
Q

Cardiac monitoring and pulse oximetry

A
  • Treat as a set of vitals
106
Q

Secondary Assessment

A
  • Focussed physical assessment
107
Q

Physical Examination

A
  • Assess neck for JVD, trachea positioning- Look listen and feel to chest
108
Q

Reassessment

A
  • Once the history and vital signs have been obtained and physical examination complete continue treatment of the patient initiate transport reassess on route begin with repeated initial assessment vital signs every 5 to 15 minutes repeat physical examination if any changes occur assess effectiveness of all interventions
109
Q
  • Digoxin
A

prescribe for treatment of chronic heart failure or certain rapid atrial dysrhythmiaso Ask by increasing strength of cardiac contractions improve in cardiac output and slowing conduction through the AV junction allowing fewer impulses to be conducted slowing the heart rate

110
Q

Nitrates

A
  • The first medication to be used for relief vagina- Failure of nitro to relieve anginal pain can occur because the pain is not cardiac, the pain is extra ordinary severity, the pain is from infarction rather than angina or the nitroglycerine has been open too long and is no longer effective- If the patient experienced a throbbing headache but no relief from chest pain suspect that the patient is having an AMI
111
Q

Beta blockers

A
  • Vacations that block beta sympathetic receptors are prescribed for patients with hypertension angina and chronic heart failure- they work by decreasing the rate and strength of cardiac contractions decreasing the hearts demand for oxygen
112
Q

calcium channel blockers

A
  • Block the influx of calcium ions into cardiac muscles they relieve angina in two ways one by preventing spasm of coronary arteries and two by decreasing the force of a cardiac contraction thereby decreasing myocardio oxygen demand- Diltiazem and verapamil
113
Q

Antidysrhythmic medications

A
  • Used to control chronic disturbances in cardiac rhythm
114
Q

Antihypertensive medications

A
  • Are used to treat high blood pressure- they work by relaxing the arteries reducing both blood pressure and afterload
115
Q
  • Orthostatic hypotension
A

patients who take these agents may have symptoms of hypertension including weakness and dizziness lightheadedness with a change of position

116
Q

‘Management of Symptomatic Bradycardia and Tachycardia’

A
  • Focussed assessment- Assess and manage any reversible causes before considering if rhythm is the cause of any hypoxia hypothermia hypervolaemia toxins or other clinical disorders- Have a full set of vitals - complete a primary assessment - identify the rhythm and considerate if its the problem or just a symptom
117
Q

Management of symptomatic bradycardia

A
  • Hypoxia is a common cause of bradycardia and should be corrected- Symptomatic and stable bradycardia’s do not require management in the field it should be monitored on route and can wait for the treatment and hospital- Unstable bradycardia’s will require management which starts with atropine then proceeds to TCP1. Ensure patent airway, assist ventilation’s if needed and ensure adequate oxygenation 2. Measure vital signs identify rhythm and perform a 12 lead establish IV normal saline 3. Search for and manage any reversible causes4. For symptomatic but stable bradycardia is no further treatment required
118
Q

Management of tachycardia

A
  • Security oxygenation and ventilation- vital signs and initiate cardiac monitoring- Determine whether this rhythm is causing the symptoms or whether the tachycardia is the response to another condition- Unstable tachycardia’s were required synchronize cardioversion where stable symptomatic tachycardia treatment depends on the rhythm and requires rhythm interpretation
119
Q

Defibrillation

A
  • Surge of electric energy delivered to the heart - Delivers a current to the heart powerful enough to depolarize - Needs to be carried out as soon as possible in VF or pulseless VT - Not useful in asystole
120
Q

Monophasic

A

delivers shock to the heart from one vector

121
Q

Biphasic

A

delivers a shock from two vectors, therefore allowing for lower joule settings.

122
Q

Sequence for Manual Defibrillation

A

• One paramedic should ready the monitor-defibrillator while the other carries out the following steps (C-A-B): Assess for cardiac arrest Start chest compressions. Assess rhythm and need for defibrillation. Ensure a clear airway, suction if required, and provide ventilation. Sequence for Manual Defibrillation

123
Q

Treatment for VF or pulseless VT

A
  • Follow the “C-A-B” approach to CPR. - Interpret the rhythm with a simultaneous - pulse check for a maximum of 10 seconds Confirm VF or Pulseless VT on the monitor-defibrillator. - Verify patient is unresponsive, has no palpable pulse, and you have good lead connections. - If shockable rhythm, clear the patient and then defibrillate. - Attach the adhesive defibrillation pads to the chest as instructed on the package. - Turn the power switch on. - Charge the defibrillator to appropriate joule setting. - Remove nitroglycerin patch if present. - Clear the area and press the Shock button. - Resume CPR immediately. - An implanted artificial pacemaker is not a contraindication to defibrillation.
124
Q

Transcutaneous Pacing (TCP)

A
  • Also called external cardiac pacing- Included in the treatment algorithms for symptomatic bradycardia for ACP• Electrode attachment for external pacing: • preferred anterior-posterior placement
125
Q

Synchronized Cardioversion

A
  • Used for SVTo Adenosine is used first but if it doesn’t work then synchronized cardioversion- Used to terminate tachy dysrhythmias other than VF and pulseless VT - Designed to deliver the shock about 10 milliseconds after the peak of the QRS complex, avoiding the “vulnerable” relative refractory periodMay reduce the energy required to end the dysrhythmia - May decrease the potential for development of secondary complicating dysrhythmias
126
Q

Extracorporeal life support

A
  • Cannulating large blood vessels and diverting blood to a machine that oxygenates the blood before returning it to the body - Allows physcians extra time to reverse the life threatening effects of reversible causes
127
Q

Intra-aortic pump

A
  • Helium filled balloons placed in the proximal descending aorta- These balloons are synchronized to an ECG waveform of a beating heart to inflate during diastole and deflate during systole
128
Q

Impella heart pump

A
  • Percutaneous LVAD- It has an inlet and outlet and is capable of pumping 5 L of blood in a minute through the left ventricle
129
Q

LVAD

A
  • are implemented mechanical devices that support circulation in patients with severe left-sided heart failure- Do not generate a pulse but rather a continuous pressure equivalent to the map- Often respond well to small fluid boluses if have hypertension

PRIMARY CARE PARAMEDIC 2021/22 (12 decks)

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