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EMER 110 CARDIAC AND RESPIRATORY THEORY > LO1 Cardiovascular Disorders > Flashcards

LO1 Cardiovascular Disorders 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 pills
Malignancy 
Coagulopathies 
Smoking
Varicose 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 strengthen

End 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
causes of pericarditis
Trauma Heart attacks
26
Acute Coronary Syndrome (ACS)
refers to distinct conditions caused by a similar sequence of pathologic events involving abruptly reduced coronary blood flow
27
Acute Coronary Syndrome (ACS) conditions
Unstable Angina (UA ``` Non-ST-segment elevation myocardial infarction (NSTEMI), ``` ST-segment elevation myocardial infarction (STEMI)
28
Ischemia
Lack of oxygen to the tissues ST depression or T inversion
29
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
30
Clinical Features of Ischemic Heart Disease
``` retrosternal chest pain, pressure, heaviness squeezing lasting 10 minutes or longer that usually occurs at rest or with minimal exertion ``` Can be accompanied by angina equivalents such as unexplained new-onset or increased exertional dyspnea, unexplained fatigue, diaphoresis, nausea/vomiting, or syncope
31
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
32
what does schema lead to
Injury prolonged ischemia ST elevation
33
infarct
death of tissue may or may not show in Q wave
34
angina Three types:
Stable Angina (Exertional Angina) Unstable Angina (Preinfarction Angina) Prinzmetal’s Angina
35
Prinzmetal’s Angina
Vasospastic angina: no blockage or clot just spasm of segment of coronary artery Cause: cocaine Treatment: nitro
36
Angina
Imbalance between myocardial O2 supply and demand ``` choking pain in the chest” Burning Tightness Pressure Crushing heavy ```
37
The coronary arteries can spasm as a result of :
``` Exposure to cold weather Stress Medicines- Anti-migraines, Chemo, Antibiotics Smoking Cocaine use ```
38
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.
39
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.
40
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
41
ACS CALL vs NON ACS CALL
ACS CALL Heavy, burning tight NON ACS CALL Sharp pain Increases with palpation Increase with inspiration
42
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
43
UNSTABLE angina signs and symptoms
Lasts longer than 20mins Can occur at rest
44
MI: STEMI, NSTEMI signs and symptoms
At rest Doesn’t get better Shock symptoms - -Nausea vomiting - -Pale cool clammy
45
Cardiomyopathies
Diverse group of diseases that affect the myocardium Most result from underlying disorders In response to injury, the heart may undergo dilation or hypertrophy Cardiomyopathies are incurable diseases and the only hope is heart transplantation
46
Cardiomyopathies are divided into three forms:
Dilated Cardiomyopathy Hypertrophic cardiomyopathy Restrictive cardiomyopathy
47
cardiac output stroke volume Formula
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
48
Factors that affect CO
1. Heart rate 2. Preload: 3. afterload: 4. Contractility:
49
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
50
Pulmonary Edema
Swelling within the lungs Sign of left sided CHF Decrease of output to left side of heart
51
One of the most common causes of pulmonary oedema is
left ventricular failure from an acute MI Other cause are inhaled toxins, infections, and sometimes trauma and altitude changes
52
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
53
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.
54
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.
55
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
56
Right sided CHF
Pumps blood to lungs JVD Pedal edema Pitting edema SOB
57
Right-Sided heart failure Signs and Symptoms
Jugular vein distention Pedal/pitting edema
58
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
59
Pulmonary edema treatment
Crackles: nitro CPAP Wheezing: Ventolin and Atrovent --Call ALS if Combivent doesn’t work
60
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
61
Causes for pulmonary edema
Cardiogenic | Noncardiogenic
62
Cardiogenic Noncardiogenic
Cardiogenic 1. Left sided failure 2. Systemic hypertension Noncardiogenic - Toxins - Lung infections - Sepsis
63
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 ```
64
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
65
Signs and symptoms of cardiogenic shock brain
Altered LOC Coma Lethargy Possible stroke
66
Signs and symptoms of cardiogenic shock lungs
SOB Accessory muscle use Stats less than 90 Tachnyepia
67
Signs and symptoms of cardiogenic shock heart
Increase HR Decrease BP Arythmias MI
68
Signs and symptoms of cardiogenic shock skin
Cool Clammy Delayed cap refill
69
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
70
Frank-starling mechanism
One characteristic of cardiac muscle is that when it’s stretched a contract with greater force
71
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
72
- Changes in contractility may be induced by
medication’s that have a positive or negative inotropic effect
73
- Nervous system controls regulate the
contractility of the heart from beat to beat
74
- Positive chronotropic effect
how hard can increase its cardio output by increasing the number of contractions per minute (HR)
75
- Pacemaker
the area of conduction tissue in which the electrical activity arises at any given time
76
- AV node
is gatekeeper to the ventricles o In 85-90% of humans blood supply comes from the branch of the RCA o 10-15% of ppl it comes from the left circumflex artery
77
- Electric impulses from SA node take how may secs to read AV node
o.o8secs
78
- The conduction is delayed in the AV node for approximately how many secs
0.12sec
79
- It takes approx. how many sec for an electrical impulse to spread across the ventricles
0.08
80
what happens with ions during depolarization
depolarization sodium and calcium ions rush into cell causing inside of cell to be positive
81
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
82
- Refectory period
period when the cell is depolarized or in the process of repolarizing
83
- Absolute refractory period
the cell is still highly depolarized and a new action protentional cannot be initialed
84
- Relative refractory period
the heart is partially depolarized and a new action potential will be inhibited but not impossible
85
The parasympathetic nervous system
- Sends messages mainly through vagus nerve | - Atropine blocks actions of PNS and vagus nerve causing HR to increase
86
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
87
- Alpha 1 receptors
``` are primarily located on peripheral blood vessels and stimulation results in: o Peripheral vasoconstriction o Mild bronchoconstriction o Increased metabolism o Stimulation of sweat glands ```
88
- Alpha 2 receptors
are primarily located on nerve endings and stimulation results in: o Control release of neurotransmitters
89
- 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)
90
- Beta 2 receptors
are primarily located on bronchial smooth muscle and stimulation results in: o Bronchodilation o Peripheral vasodilation
91
Causes of dysrhythmias
- Acid base disturbance - ANS imbalance - CNS damage - Certain poisons - Drugs - Endocrine disorders - Hypothermia - Hypoxemia - Ischemia o infarction - trauma
92
- disrhythmias happen after an AMI for 2 reasons
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

EMER 110 CARDIAC AND RESPIRATORY THEORY (8 decks)

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