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155 > unit 2/exam2 > Flashcards

unit 2/exam2 Flashcards

1
Q

CHAMBERS of the Heart

4 hollow chambers – 2 upper atria & 2 lower ventricles – separated longitudinally by the interventricular septum

A

Right side: The Rt. Atrium receives deoxygenated blood from the veins (superior and inferior vena cava) of the body and coronary sinus (blood from the heart). The Rt. Ventricle receives deoxygenated blood from the Rt. Atrium through the triscupid valve and pumps it through the pulmonary artery to the pulmonary capillary bed for oxygenation.
Left side: This newly oxygenated blood travels through the pulmonary veins to the Lt. Atrium. Blood enters the Lt. Atrium and crosses the Mitral (bicuspid) valve into the Lt. Ventricle. This oxygenated Blood is then pumped out of the aorta to the arterial circulation.

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2
Q

D. HEART SOUNDS

A
  1. First heart sound = (S1) = Systole (contraction)
    characterized by what syllable: “Lub”
    produced by closure of Atrioventricular valves
    1. Second heart sound (S2) = Diastole (relaxation)
      characterized by what syllable: “Dub”
      produced by closure of Semilunar valves
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3
Q

SYESTEMIC & CORONARY CIRCULATION

1. Define systemic circulation:

A

Consists of the left side of the heart, the aorta and its branches, the capillaries that supply the brain and peripheral tissues, the systemic venous system, and the vena cava. The systemic system, which must move blood to peripheral areas of the body, is a HIGH pressure system.

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4
Q

SYESTEMIC & CORONARY CIRCULATION

. Define coronary circulation:

A

The heart muscle itself is supplied by its own network of vessels through the coronary circulation.

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5
Q

CORONARY ARTERIES Defined

A

Originate from the base of the aorta and branch out to encircle the myocardium supplying blood, oxygen and nutrients to the myocardium.

Blood flow to coronary arteries occurs during diastole, when the muscle is relaxed.

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6
Q

Left coronary artery

2 branches

A
  1. Anterior Descending Artery-supplies the anterior interventricular septum and the left ventricle.
  2. Circumflex Artery-supplies the left lateral wall of the left ventricle
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7
Q

Right coronary artery:

A

Supplies the right ventricle and forms the posterior descending artery.

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8
Q

Physiology of the Cardiac Cycle and Cardiac Output
Cardiac Cycle
Definition:

A

The contraction and relaxation of the heart constitutes one heart beat and is called the cardiac cycle. Normally the complete cardiac cycle occurs about 70-80 times per minute, measured as the heart rate.

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9
Q

Physiology of the Cardiac Cycle and Cardiac Output
Cardiac Cycle
Ventricular Systole
Definition:

A

A phase during which the ventricles contract and eject blood into the pulmonary and systemic circuits.

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10
Q

Physiology of the Cardiac Cycle and Cardiac Output
Cardiac Cycle
Diastole Definition:

A

Follows systole: Phase during which the ventricles refill, the atria contract, and the myocardium is perfused.

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11
Q

Physiology of the Cardiac Cycle and Cardiac Output
Cardiac Cycle
Stroke Volume Definition:

A

The difference between the end-diastolic volume and the end-systolic volume. Stroke volume ranges from 60-100 ml/beat and averages about 70 ml/beat in adults.

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12
Q

Physiology of the Cardiac Cycle and Cardiac Output
Cardiac Cycle
Cardiac Output Definition:

A

The amount of blood pumped by the ventricles into the pulmonary and systemic circulations in one minute. Indicator of how well the heart is functioning as a pump. Average adult cardiac output: 4-8 L/minute

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13
Q

Physiology of the Cardiac Cycle and Cardiac Output
Cardiac Cycle
Ejection Fraction Definition:

A

The stroke volume divided by the end-systolic volume and represents the fraction or percent of the diastolic volume that is ejected from the heart during the systole. Normal EF: 50 – 70%

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14
Q

Four Aspects of Cardiac Function and Their Relationships

FOUR ASPECTS OF CARDIAC FUNCTION

A
  1. Circulation of blood through the heart chambers
  2. Coronary circulation
  3. Electrical activity in the heart
  4. Heart sounds
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15
Q

Four Aspects of Cardiac Function and Their Relationships
FOUR ASPECTS OF CARDIAC FUNCTION
1. Circulation of blood through the heart chambers

A

– as it comes in and exits out;

  • Pump function
  • Cardiac output – volume that gets pumped
  • Blood pumped out of the heart
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16
Q

Four Aspects of Cardiac Function and Their Relationships
FOUR ASPECTS OF CARDIAC FUNCTION
2. Coronary circulation

A
  • Blood supply to heart muscle
  • Oxygen and nutrients to heart muscle – so the muscles of the ht. can function
  • Coronary arteries
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17
Q

Four Aspects of Cardiac Function and Their Relationships
FOUR ASPECTS OF CARDIAC FUNCTION
3. Electrical activity in the heart

A

-Rhythm
-Rate
-Conduction system – electrical path that it follows until the ventricles receive that impulse and the muscles respond and contract – that is what causes the pump action. Heart starts as an electrical activity and ends with a muscular activity.
EKG

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18
Q

Four Aspects of Cardiac Function and Their Relationships
FOUR ASPECTS OF CARDIAC FUNCTION
4. Heart sounds

A

– can tell how well valves are functioning

  • Valve closure - (2) AV Valves, (1) Aortic, (1) Pulmonic
  • Lubb/dub-
  • Murmurs - abnormal sound – abnormal flow of blood across valve – valve may not close completely or is too stiff and won’t open well enough
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19
Q

Four Aspects of Cardiac Function and Their Relationships

Circulation to the body is affected if decreased oxygenation to heart muscle D/T impaired coronary circulation (pump not as effective) #__ & #__; if coronary arteries (which are supplying the heart) are blocked, you have a decreased circulation to the heart, so the circulation to the body is affected because the heart isn’t getting the oxygen it needs and cannot pump effectively.

A
  1. Circulation of blood through the heart chambers–
    as it comes in and exits out;
    -Pump function
    -Cardiac output – volume that gets pumped
    -Blood pumped out of the heart
  2. Coronary circulation
    - Blood supply to heart muscle
    - Oxygen and nutrients to heart muscle – so the muscles of the ht. can function
    - Coronary arteries
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20
Q

Four Aspects of Cardiac Function and Their Relationships

Electrical system is affected if decreased oxygenation to heart muscle D/T impaired coronary circulation (arrhythmias) #__ & #__; could cause a dysrhythmia; in order for electrical system to function, it needs oxygen and nutrients

A
  1. Coronary circulation
    - Blood supply to heart muscle
    - Oxygen and nutrients to heart muscle – so the muscles of the ht. can function
    - Coronary arteries
  2. Electrical activity in the heartRhythm
    - Rate
    - Conduction system – electrical path that it follows until the ventricles receive that impulse and the muscles respond and contract – that is what causes the pump action. Heart starts as an electrical activity and ends with a muscular activity.
    - EKG
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21
Q

Four Aspects of Cardiac Function and Their Relationships

is affected if valves inadequate #__ & #__; if valve damaged by some disease for example

A
  1. Circulation of blood through the heart chambers–
    - as it comes in and exits out;
    - Pump function
    - Cardiac output – volume that gets pumped
    - Blood pumped out of the heart
  2. Heart sounds
    - can tell how well valves are functioning
    - Valve closure - (2) AV Valves, (1) Aortic, (1) Pulmonic
    - Lubb/dub-
    - Murmurs - abnormal sound – abnormal flow of blood across valve – valve may not close completely or is too stiff and won’t open well enough
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22
Q

Four Aspects of Cardiac Function and Their Relationships

is affected if rhythm irregular #__ & #__; lubb, dub, lubb, dub is good; irregular beat will affect circulation

A
  1. Circulation of blood through the heart chambers–
    as it comes in and exits out;
    -Pump function
    -Cardiac output – volume that gets pumped
    -Blood pumped out of the heart
  2. Electrical activity in the heartRhythm
    - Rate
    - Conduction system – electrical path that it follows until the ventricles receive that impulse and the muscles respond and contract – that is what causes the pump action. Heart starts as an electrical activity and ends with a muscular activity.
    - EKG
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23
Q

Cardiac Function

Conduction system –

A

electrical path that it follows until the ventricles receive that impulse and the muscles respond and contract – that is what causes the pump action. Heart starts as an electrical activity and ends with a muscular activity.

24
Q

Coronary Artery Disease (CAD) or arteriosclerotic heart disease (ASHD)
Pathophysiology

Atherosclerosis or arteriosclerosis
Definition:

A
  • referred to as fatty deposits, atherosclerotic lesions, atheroma, plaque
  • Lipids build up on artery wall and block blood flow
  • Can occur in ANY artery, not just coronary arteries
  • If it occurs in carotid artery it’s called a “stroke”
  • If it occurs in legs it’s called “peripheral vascular disease”
25
Q

Coronary Artery Disease (CAD) or arteriosclerotic heart disease (ASHD)

Atherosclerosis or arteriosclerosis: Process

A

lipids accumulate on artery wall, fibroblasts respond by producing collagen, smooth muscle proliferates (enlarge) which forms plaque = impaired blood flow in that vessel

26
Q

Coronary Artery Disease (CAD) or arteriosclerotic heart disease (ASHD)

Angina pectoris
Definition:

A
  • Chest Pain resulting form reduced blood flow to the heart muscle;
  • Lack of O2 to muscle = pain
  • Temporary instability in oxygen supply and demand causing reversible myocardial ischemia
  • Not permanent damage yet = just chest pain
27
Q

Coronary Artery Disease (CAD) or arteriosclerotic heart disease (ASHD)

Angina pectoris
Cause of pain

A
  • Narrowing of /Or spasm of artery
  • Pain occurs when O2 supply is compromised; metabolism ends up changing from aerobic metabolism (cells functioning with O2) to anaerobic metabolism (cells functioning without O2).
  • Whenever the body changes from aerobic to anaerobic metabolism, it builds up lactic acid.
  • When lactic acid builds up, histamines and kinins are released.
  • Histamines and kinins stimulate nerve fibers which cause pain.
  • When the occlusion is relieved (by meds or the spasm stops), O2 gets in and circulation is restored and the waste products (lactic acid) are cleared which makes the pain go away.
28
Q

3 Types of angina

A
  1. Stable angina
  2. Unstable angina
  3. Prinzmetal’s angina
29
Q
  1. Stable angina
A
  • Chest pain with EXERTION or STRESS doesn’t occur until pt stresses self)
  • Most common type of angina
  • Most predictable angina
  • Common manifestation of CAD/CHD (coronary artery disease/coronary heart disease)
  • Relieved by rest (once pt stops stressful activity the pain stops)
  • Can be relieved with Nitrates (nitroglycerine)
30
Q
  1. Unstable angina
A
  • Angina of NEW ONSET that OCCURS AT RESTor with MINIMAL exertion
  • Pt can WAKE UP in the middle of the night (resting) with chest pain
  • Occurs with INCREASE FREQUENCY AND DURATION
  • Pain is UNPREDICTABLE (pt doesn’t know what will trigger it)
  • Puts pt at risk for heart attack
31
Q
  1. Prinzmetal’s angina
A
  • ATYPICAL angina that is caused by coronary artery SPASM with or without an atherosclerotic lesion (not caused by plaque buildup)
  • Don’t know the cause
  • RARE
  • Can be associated with cocaine use
32
Q

Acute Myocardial Infarction (MI, AMI, heart attack, {ACS}acute coronary syndrome)
– encompasses the angina and the blockage
Definition:

A

-NECROSIS or DEATH of cardiac cells when the heart muscle is SEVERELY deprived of O2 by COMPLETE occlusion of a coronary artery.
(circulation to the heart is cut off; the area of the heart that the blocked artery supplied will die – the heart won’t pump when part of it is damaged)

  • Cellular injury occurs by lack of O2 and nutrients
  • The longer the occlusion, the more damage to the heart muscle
  • Infarct is the area of muscle death
  • When cardiac muscle dies, it is not an efficient pump anymore
33
Q

Acute Myocardial Infarction

Process:

A
  • atherosclerotic plaque present in the arteries can have single or multiple lesions
  • some plaque may be stable, some may be unstable
34
Q

Acute Myocardial Infarction

Process: Stable Plaque/ collateral circulation

A

-progresses and grows by occluding vessels
-when vessel gets occluded, the circulatory system develops COLLATERAL CIRCULATION (builds a new vessel to go around the damaged area – builds a new highway)
usually occludes 90% or more of the vessel eventually
-NOT as dangerous as unstable plaque because it DOESN’T form a clot, it just occludes.

35
Q

Acute Myocardial Infarction

Process: Unstable Plaque

A
  • Tends to rupture and crack
  • As body tries to heal a clot forms
  • The clot will occlude the vessel COMPLETELY which interrupts the blood flow to myocardium
  • Unstable is WORSE than stable because the whole artery is blocked by the clot
  • Plaque usually blocks 70% or less of the vessel
  • The SMALLER plaques are the more unstable ones; the smaller ones tend to rupture
36
Q

Acute Myocardial Infarction

Clinical Manifestations

A
  • Chest Pain – this is not just angina, this is an ACS (acute coronary syndrome)
  • unrelieved by nitroglycerin or rest
  • pain not always excruciating (varies person to person)
  • it’s not the intensity that distinguishes it from angina, it’s the duration and continuous nature
  • Sudden onset, not associated with activity – classic sign but DM don’t always notice r/t neuropathy
  • Severe and crushing – classic sign but DM don’t always feel it r/t neuropathy
  • Pressure
  • Tightness
  • Heaviness
  • Burning
  • Squeezing
  • Usually substernal
  • Radiation to jaw, shoulder, back, left arm or both arms
  • Diaphoresis
  • Changes in B/P (up or down depending on what stage of the MI the pt is in; syncope = lower B/P)
  • weak pulse r/t heart damage
  • Gray facial color or pallor
  • Anxiety, sense of impending doom; pt knows something is wrong
  • Temperature elevation; low grade and not immediate; r/t inflammation of cardiac muscle
  • Indigestion, N&V – most common mix up of MI
  • SOB – sometimes the only symptom the pt has
  • Tachycardia or Bradycardia
  • Cool, clammy skin
  • Tachypnea – rapid respiration
  • Sudden death- no symptoms, just collapse and die
37
Q

Acute Myocardial Infarction

Risk Factors-Uncontrollable – un-modifiable

A
  • Age
    • Risk increase with age
    • Over 50% of MI sufferers are >65 years old
    • Men get them earlier (45 years old) than women (55 years old)
    • Women may be protected in their earlier years by hormones
  • Family Hx - increase risk if parent had MI
  • Ethnic background – greater risk in Caucasians
  • Gender – most previous studies were done on men
  • Men are 3-4 times more likely to have an MI
  • Occur at younger age of men than women
    • # 1 leading cause in death in men and women
38
Q

Women in heart disease

-Unique risk factors

A
  • Premature menopause
    • HDL drops
    • ADL rises
  • Oral contraceptive use
    • Causes higher risk in clots, especially if a smoker
  • Hormone replacement therapy
39
Q

Women in heart disease

symptoms in women

A
  • more likely than men to die from the dz
  • Less likely to have classic chest pain
  • More likely to have back pain (atypical areas)-most common sx
  • Chief complaint is usually indigestion, fatigue, lightheadedness, N&V, anxious and unsure why
40
Q

Acute Myocardial Infarction

Risk Factors- Modifiable – factors that pts can change

A
  • Hypertension – increases risk for MI; can take meds, exercise, diet to lower B/P
  • Diabetes – 80% of deaths in DM are linked to CAD; can control diabetes- pre DM are also at risk.
  • Metabolic syndrome (AKA Syndrome X) – abdominal (central) obesity (apple shaped); high B/P, high triglycerides, and high insulin resistance; low HDL; at risk for MI
  • Hyperlipidemia – high cholesterol
  • Obesity – is associated with HTN, DM, hyperlipidemia; can lose weight
  • Inactivity – today’s normal routines don’t include exercise; allowing children to grow up with inactivity
  • Diet – in US is high in saturated fats, fast foods
  • Smoking – hasten the onset of heart disease by a decade; can quit smoking. Nicotine is a vasoconstrictor and formes plaque
41
Q

Smoking – hasten the onset of heart disease by a decade; can quit smoking
Physiological effects

A

Carbon monoxide damage vascular endothelium which promotes fat deposits (if vessel is damaged or cracked on the inside it tends to collect fat deposits)
Nicotine stimulate catecholamine release which  blood pressure, heart rate and myocardial O2 use – hard work for the heart
Nicotine constricts arteries, limiting tissue perfusion (if vessel is already constricted with fat this will constrict it even more)
Nicotine reduces HDL (the good cholesterol)
Nicotine  platelet aggregation leading to clotting
Tar has carcinogenic and pathologic affects on the lungs
Smoking is addictive

42
Q

Smoking – hasten the onset of heart disease by a decade; can quit smoking
-Diseases caused by smoking

A 
Lung cancer
COPD
Heart disease
Hypertension
Peptic ulcer disease and GERD
Polycythemia
Birth defects
43
Q

Smoking – hasten the onset of heart disease by a decade; can quit smoking
-Results of quitting

A

Can cut risk of CAD in half by first year
Lung function is improved immediately
Chance of developing lung cancer or lung disease is reduced

44
Q

Smoking – hasten the onset of heart disease by a decade; can quit smoking
-Smoking cessation

A

Nicotine replacement therapy
Chantix (varenicline)
-lessens pleasurable effects of nicotine start one week before quit date
- works in the brain

45
Q

Interventions/Medical Management
Medications
-Nitrates (vessel dilators – especially veins)

A
  • Nitroglycerin (NTG) – relieves chest pain
  • Isosorbide mononitrate
  • Isosorbide dinitrate
46
Q

Interventions/Medical Management

Medications- Nitrates (vessel dilators – especially veins) (NTG) -Nitroglycerin (NTG)

A

– relieves chest pain

  • sublingual: Nitrostat, Nitroquick
  • transdermal patch: Nitro-dur, Transderm-Nitro
  • topical ointment: Nitro-bid
  • intravenous – Nitro-bid IV
47
Q

Interventions/Medical Management
Medications -Nitrates (vessel dilators – especially veins) (NTG)
Actions –

A
  • Overall action of nitrates is dilation of coronary arteries and VEINS
  • Acts on vascular smooth muscle to produce vasodilation
  • Acts primarily on VEINS
  • Decreases pain in CAD by decreasing cardiac oxygen demand
  • Dilate veins which slows down the amount of blood coming back to the heart
  • effects are from work on peripheral vessels and not dilation of narrowed coronary arteries
48
Q

Interventions/Medical Management
Medications- Nitrates (vessel dilators – especially veins) (NTG) -
-Isosorbide mononitrate

A
  • oral tablets, IR (immediate release): ISMO, Monoket

- oral tablets, ER (extended release): Imdur

49
Q

Interventions/Medical Management
Medications- Nitrates (vessel dilators – especially veins) (NTG) -
-Isosorbide dinitrate

A
  • sublingual: Isordil, Sorbitrate
    • chewable tablets: Sorbitrate
    • oral tablets, IR (immediate release): Isordil titradose, Sorbitrate
    • oral tablets, SR (sustained release): Isordil Tembids
50
Q

Interventions/Medical Management
Medications -Nitrates (vessel dilators – especially veins) (NTG)
-Adverse affects

A

-Headache – very common especially with IV r/t dilating the veins in the head

  • Orthostatic hypotension - decrease in B/P with position change’s; when vessels are dilated the blood pools in the legs and doesn’t return to the heart as fast (decreased venous return)
    • B/P is all about vessel SIZE and VOLUME (ex. if we increase the size of our garden hose it will decrease the pressure of water coming thru the hose)

-Reflex tachycardia – is a compensatory mechanism; r/t decrease in B/P so body speeds up pulse to try to compensate

51
Q

Interventions/Medical Management
Medications -Nitrates (vessel dilators – especially veins) (NTG)
-Uses – for chest pain

A
  • Angina treatment
  • Angina prophylaxis - to prevent angina
  • Acute MI and perioperative hypertension - IVroute
52
Q

Interventions/Medical Management

Medications -Nitrates (vessel dilators – especially veins) (NTG) -Angina treatment

A
  • Sublingual form – no swallowing; let it melt
  • Used at onset of pain
  • Absorbed from oral mucosa into bloodstream; fast because it by passes the liver
  • Onset of action: 1-3 minutes; pt should sit down while it works r/t dizziness
  • 3 doses 5 minutes apart; if not working call 911; NO DRIVING for pt or family member (family cannot administer CPR if needed while driving)
  • Store in tinted (brown) bottle to protect from sunlight, with tight seal and away from heat
  • Discard after expiration date; loses potency
53
Q

Interventions/Medical Management

Medications -Nitrates (vessel dilators – especially veins) (NTG) -Angina prophylaxis

A
  • to prevent angina
    -Sustained release tablets and capsules
    -Transdermal patches – applied daily to hairless area, remove old patch; rotate sites
    -Topical ointment – caution: can be absorbed thru nse’s skin
    Onset is 20-60 min
    Duration 12 hours
54
Q

Interventions/Medical Management

Medications -Nitrates (vessel dilators – especially veins) (NTG)

A

Acute MI and perioperative hypertension

  • IVroute
  • NTG used in IV continuous drip
  • Bottle must glass because NTG will adhere to plastic bags
  • Tubing is special so it won’t absorb the NTG; regular IV tubing absorbs NTG
  • Close monitoring of B/P and pulse
55
Q

The client with CAD- Assessment

-Pain – PQRST

A

P – what PRECIPITATES the discomfort (was pt running, resting?)
Q – the QUALITY of the discomfort (sharp, dull, pressure, aching? Don’t give pt the words-let them describe)
R – whether the pain RADIATES to other areas of the body (up to jaw, down arm?)
S – the SEVERITY of the pain (scale 0-10, where, what makes it worse/better, etc)
T – the TIMING of onset (how long has current episode been going on?)

56
Q

The client with CAD- Assessment -Cardiovascular

A

-Pulse rate and rhythm (was it regular yesterday, but irregular today?)
-Blood pressure – compare to baseline
Peripheral pulses (strong, weak?)

  • 12-lead EKG – can tell which areas of heart are damaged
  • Arrhythmias – can pick up abnormal rhythm
  • ST- and T- Wave changes’s – reflect ischemia (lack of O2) and injury to myocardial cells
    • T-Wave inversion can occur as a result of decreased O2
    • ST segment elevation is specific to MI – S is supposed to come back to baseline; pretty conclusive that an MI has occurred

-Pathologic Q-Wave
– indicator of tissue death
-Q goes way below baseline before it shoots up to R
Permanent change on EKG
Doesn’t show up until days later
Pt could have an MI without symptoms if have nerve damage (the DM pt)

57
Q

The client with CAD- Assessment- Psychosocial

A
  • Denial – put off treatment, “can’t be happening to me”
  • Fear – of death
  • Anxiety – of pain, SOB, pt feels like he/she is dying

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