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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
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 (UA

Non-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, 
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

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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 artery

Cause: 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
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.

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.

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

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

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

43
Q

UNSTABLE angina signs and symptoms

A

Lasts longer than 20mins

Can occur at rest

44
Q

MI: STEMI, NSTEMI signs and symptoms

A

At rest

Doesn’t get better

Shock symptoms

  • -Nausea vomiting
  • -Pale cool clammy
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 hypertrophy

Cardiomyopathies are incurable diseases and the only hope is heart transplantation

46
Q

Cardiomyopathies are divided into three forms:

A

Dilated Cardiomyopathy

Hypertrophic cardiomyopathy

Restrictive cardiomyopathy

47
Q

cardiac output

stroke volume

Formula

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

48
Q

Factors that affect CO

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

50
Q

Pulmonary Edema

A

Swelling within the lungs

Sign of left sided CHF

Decrease of output to left side of heart

51
Q

One of the most common causes of pulmonary oedema is

A

left ventricular failure from an acute MI

Other cause are inhaled toxins, infections, and sometimes trauma and altitude changes

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
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
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

systematic vascular resistance leads to

A

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

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 RCA
o 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 vasoconstriction
o	Mild bronchoconstriction
o	Increased metabolism
o	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 Bronchodilation
o 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

EMER 110 CARDIAC AND RESPIRATORY THEORY (8 decks)

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