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nurs pathophysiology > rrd 7 > Flashcards

rrd 7 Flashcards

cardiovascular diseases pt 2

1
Q

HR and rhythm changes that may pathologically affect CO

A
  • tachycardia
  • bradycardia
  • rhythm pattern irregular
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2
Q

tachycardia

A

HR faster than normal (>100 bpm)

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3
Q

causes of tachycardia

A
  • SNS neurohormonal influences
  • certain electrolyte changes (EX: hyperkalemia - hypopolarization)
  • glitches in SA node and AV node regulation (genetic, idiopathic, chronic disease-related)
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4
Q

neurohormonal influences of SNS causing tachycardia

A
  • SNS governs fight or flight
  • kicks in during activity, stress, need to compensate in situations such as shock, heart attack, etc.
  • secretes epinephrine -> bind with beta receptors of heart -> increases HR
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5
Q

bradycardia

A

HR slower than normal (<60 bpm)

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6
Q

causes of bradycardia

A
  • ParaNS neurohormonal influences
  • certain electrolyte changes (EX: hypokalemia -> hyperpolarization)
  • ischemia from right coronary artery (RCA) narrowing/blockage (RCA feeds SA + AV node)
  • glitches in SA node and AV node regulation (genetic, idiopathic, chronic disease-related)
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7
Q

neurohormonal influences of ParaNS causing bradycardia

A
  • ParaNS governs slower processes (digestion, urination)
  • related to heart, vagus nerve secretes ACh -> decreases HR
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8
Q

rhythm pattern that can affect cardiac fxn

A
  • dysrhythmia (or arrhythmia) like:
  • atrial fibrillation (Afib)
  • ventricular fibrillation (Vfib)
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9
Q

dysrhythmia (arrhythmia) causes include

A
  • ischemic/infarcted tissue interferes w/ normal impulse conduction
  • electrolyte imbalances (esp related to K+, hypo + hyper)
  • age-related wear & tear of conduction system
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10
Q

atrial fibrillation - Afib

A

a chaotic series of electrical impulses in the atria that cause them to quiver ineffectively instead of contracting smoothly

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11
Q

afib is fairly common amongst _____, due to heart disease or simple _____ - 3% of ______ population has chronic afib

A
  • elderly
  • aging
  • adult
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12
Q

afib can occur during ______ but most often begins when myocardium has to endure ______ stain or a chronic problem such as _____.

A
  • acutely ischemic situations
  • long-term hypoxic
  • heart failure
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13
Q

categories of possible sequelae of afib

A
  • small but sometimes significant decrease in CO
  • pooling of blood in atria
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14
Q

small/significant decrease in CO as sequelae of afib

A
  • atria have small coordinated contraction @ end of diastole (atrial kick)
  • helps propel more blood into ventricles before they contract
  • when atria quiver instead of contracting effectively -> diminish CO to varying degrees bc no atrial kick
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15
Q

pooling of blood in atria as sequelae of afib

A
  • if atria muscles quiver instead of delivering blood to ventricles = blood remain in atria
  • form static pools = thrombi + emboli formation
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16
Q

atrial thrombi/emboli formation bc pooling of blood in atria as sequalae of afib

A
  1. atrial thrombi in LA
  2. thrombi gets loose -> become emboli to brain arteries
  3. stroke (S/S weak on one side, confusion, etc. bc brain ischemia)
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17
Q

venous thrombi/emboli formation bc of blood pool in atria as sequalae of afib

A
  1. venous thrombi in RA
  2. thrombi gets loose -> emboli to lungs
  3. PE (S/S SOB, chest pain, hemoptysis, shock/decreased BP & perfusion)
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18
Q

T/F people with afib will most likely have fatal outcomes

A

FALSE: people can often live fine with stable afib as long as they are on meds to help prevent thrombi (clots) and keep HR from being too fast

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19
Q

ventricular fibrillation - Vfib

A

chaotic series of electrical impulses in the ventricles that cause them to quiver ineffectively instead of contracting smoothly

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20
Q

Vfib is the _____ dysrhythmia because?

A
  • deadliest
  • results in no CO at all -> no perfusion to brain -> unconsciousness & death
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21
Q

stroke volume (SV) changes that may pathologically affect CO

A
  • contractility changes (negative inotropic changes)
  • preload changes
  • afterload changes
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22
Q

pathologic contractility changes

A
  • ischemia: something blocking coronary arteries -> ischemia to heart muscle distal to plaque -> decreased contract
  • neurohormonal and electrolyte effects can also influence inotropic status - similar to what they do to HR
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23
Q

preload changes that can be pathologic

A
  • increased preload -> increased blood volume = fluid volume overload -> increase workload on sick heart
  • decreased preload -> decreased blood volume = fluid volume deficient -> decrease CO + BP
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24
Q

afterload changes that are pathologic

A
  • pathologically increased afterload makes it harder for the ventricles to eject blood into the receiving arteries
  • decreased afterload for the LV related to massive peripheral arterial vasodilation -> shock state
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25
Q

increased afterload for RV

A

lung disorders (chronic bronchitis) cause pulmonary artery vasoconstriction -> increased pulm vasc resis

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26
Q

increased afterload for LV

A

atherosclerosis of aorta and systemic arteries
- peripheral arterial vasocon; HTN -> increased syst vasc resis

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27
Q

anaphylaxis from allergic rxn example of massive vasodilation related to decreased afterload

A
  1. over-release of inflamm mediators over-dilates blood vessels
  2. blood pools in periphery
  3. less volume centrally
  4. decreased BP
  5. shock
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28
Q

shock example of massive vasodilation related to decreased afterload

A

septic shock - same principle but the inflammatory mediator release is caused by toxins of bacteria

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29
Q

coronary artery disease (CAD)

A

a disorder in which the coronary arteries are narrowed and/or occluded

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30
Q

risk of getting CAD

A
  • increased w/ elevated serum levels of homocysteine
  • correlated with an elevated serum C-reactive protein (CRP)
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31
Q

homocysteine

A

amino acid that can contribute to atherosclerosis via oxidative damage
- some people more prone to having higher homocysteine levels than others

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32
Q

c-reactive protein (CRP)

A

linked to inflammatory process of plaque formation in the coronary arteries

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33
Q

T/F infarction can happen to any tissue in the body

A

TRUE

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34
Q

____ is the primary problem in CAD - coronary vessels are ____ and occluded by _____ due to the atherosclerotic/inflammatory processes

A
  • ischemia
  • narrowed
  • plaques
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35
Q

ischemia to cardiac cells is a _____ influence on the heart and can lead to?

A
  • negative inotropic
  • decreased cardiac output
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36
Q

if not revered, ischemia leads to cellular death (_______); tissue _____ in the heart caused by ischemia is known as _____ which is an even worse _________.

A
  • necrosis, necrosis
  • myocardial infarction
  • negative inotropic influence
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37
Q

various cells in the cardiac tissue can be affected to ______ and may all be in?

A
  • different degrees
  • different stages of O2 deprivation
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38
Q

spectrum of ischemia

A
  • mild ischemia to maximal ischemia
  • mild: effect on cells mini and can be reversed by restore O2
  • max: infarction (irreversible)
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39
Q

there is a great _____ in patient presentation and sometimes S/S is?

A
  • variety
  • mild + vague and/or patient might just have nausea, back pain, etc.
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40
Q

most common symptom of CAD is?

A

angina

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41
Q

angina

A
  • painful constriction or tightness
  • short for angina pectoris (chest pain)
  • refers to ischemic pain in heart muscle
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42
Q

characteristics of classic angina

A
  • tightness, heaviness (elephant sitting on me); burning, indigestion-like
  • pain radiates into areas like left arm, jaw, back
  • clenched fist over sternum
  • intensity varies
  • duration of 3-5 mins and may go away on own (nitroglycerin needed to relieve it sometimes)
  • exacerbated by exercise and lessened by rest
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43
Q

CAD status of a person is based on?

A

degree of coronary occlusion and ischemia - usually reflected in severity of S/S

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44
Q

a person w/ CAD can be?

A
  • asymptomatic
  • symptomatic: stable angina or acute coronary syndrome (ACS)
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45
Q

stable angina

A
  • pain pattern predictable and well-controlled by lifestyle changes, meds, etc.
  • “tightness in chest center when I walk too long, always goes away when take one NTG”
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46
Q

patho of stable angina

A
  1. blockage/plaque causes angina develop slowly w/ no dramatic changes
  2. steady, small, subtle ischemia to tissues stimulate arteriogenesis
  3. establishment of collateral circulation - new branches of coronaries develop + feed tissue beyond occluded or nearly-occluded vessel
  4. the better the collateral circulation, the more stable the CAD
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47
Q

treatment of stable angina is focused on?

A
  • maximizing coronary patency -> increase perfusion to myocardium
  • decreased workload of heart
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48
Q

treatment of stable angina includes?

A
  • NTG under tongue prn and/or daily as patch or extended release pill -> dilates coronary arteries so artery can bring more oxygen to myocardium
  • aspirin as anti-inflamm and decrease platelet adhesion (less clotting = less chance of worse plaque)
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49
Q

acute coronary syndrome (ACS) occurs when

A
  • sudden clot development
  • an arterial embolus flows into a narrowed coronary artery
  • an existing plaque ruptures and its contents fill up the lumen
50
Q

AVS is manifested as?

A
  • unstable angina
  • myocardial infarction (MI)
51
Q

unstable angina

A

when someone w/ stable angina develops a change for the worse (usually sudden) in their pattern of S/S

52
Q

unstable angina usually indicated ______ or ______ in existing coronary plaques that leads to worsening of ischemia

A

worsening, change

53
Q

S/S unstable angina

A
  • substantial change in pain (patient who usually gets rid of pain w/ one NTG suddenly can only make better w/ 3)
  • EKG shows acute ischemic changes
54
Q

w/ unstable angina: patient usually ends up admitted to hospital where treatment is geared towards?

A
  • maximizing coronary patency
  • decreasing workload of the heart
55
Q

acute interventions for unstable angina

A
  • IV NTG
  • IV morphine
  • possible angioplasty
  • heart surgery
56
Q

myocardial infarction

A

myocardial cells are starting to undergo necrosis

57
Q

in MI: though some cells have become necrosed, which is ____, if the patient is very early into infracting process + interventions successful = tissue damage can be?

A
  • irreversible
  • minimized by preventing more cells from undergoing necrosis
58
Q

S/S of MI

A
  • severe, unrelenting pain
  • S/S of blocked artery
  • EKG changes reflecting ischemia + certain degree of necrosis
59
Q

MI dx based on hist + S/Ss and include certain lab test finding that shows increase in?

A
  • non-specific enzymes that are released by most injured/dying cells (CK - creatine kinase)
  • troponin: only related by injured and dying myocardial cells (higher the serum titer, more extensive the damage)
60
Q

treatment of MI

A
  • similar to unstable angina but more emergent
  • may also need clot-busting drugs
61
Q

S/S of ACS

A
  • chest pain more severe, prolonged, and/or unpredictable
  • CNS rxn to pain: N&V, large amt of sweating (diaphoresis)
  • variations in HR + rhythm
  • worse the ischemia, worse the S/S above + worse effect on contractility and CO and perfusion
62
Q

S/S low CO and perfusion

A
  • fatigue, weakness
  • mental status change, deterioration of responsiveness
  • hypotension
  • dyspnea
  • prolonged capillary refill (>2 secs)
  • low urine output
63
Q

depending on severity of CAD, can have?

A
  • rapid deterioration - ACS, valve problems, shock
    and/or
  • have CAD for long time w/ manageable S/S
64
Q

can have CAD for ____ time w/ ____ S/S depending on how well the heart compensates w/ techniques such as?

A
  • long, manageable
  • angiogenesis
  • hypertrophy leading to cardiomegaly
65
Q

angiogenesis

A

development of collateral circulation around blocked artery

66
Q

hypertrophy leading to cardiomegaly: ____ in size of cells over time due to cells ____ to compensate for less oxygen.

A

increase, working harder

67
Q

hypertrophy is an effective compensatory mech ______. if ischemic stressors and O2 delivery cannot keep up with O2 demand of big muscle, what happens?

A
  • up to a point
  • decompensatory process may occcur, like heart failure
68
Q

normally, valves open/shut ____, which accomplishes what 2 fxns?

A
  • crisply
  • full open: blood pass thru from one chamber to next
  • full close: blood doesn’t back up into previous chamber
69
Q

disease processes that can cause valve malfxn include?

A

autoimmune processes like rheumatic fever (post-strep autoantibod invade/inflame heart valves, joints, and/or kidneys)

70
Q

sequela of valve problems depend on __ but generally negatively affect?

A
  • severity and which valves involved
  • CO
71
Q

categories of valvular problems

A
  • stenosis
  • incompetence
72
Q

stenosis

A
  • narrowing, stiffening
  • adversely affects full opening
73
Q

in stenosis: valve orifice is?

A

constricted + narrowed so blood cannot easily flow forward through it

74
Q

blood flowing thru smaller opening generates _____, the rumbling sound is known as?

A
  • more turbulence
  • murmur
75
Q

incompetent valve

A
  • floppiness, prolapse, insufficiency, regurgitation
  • adversely affects full closing
76
Q

incompetent valve results in?

A
  • regurgitation of blood back into chambe it came from
77
Q

backflow of regurgitation can also cause?

A

turbulence -> murmur

78
Q

murmur is applied when referring to?

A
  • sound of blood not flowing smoothly thru heart valves
79
Q

basic causes of heart failure (HF)

A
  • heart can’t pump
    and/or
  • heart can’t overcome high afterload
    and/or
  • heart is being overwhelmed by high preload
80
Q

HF is ____ in the UF due mostly to ______ population

A

epidemic, aging

81
Q

HF is a general term used to describe?

A

several types of cardiac dysfunction secondary to the failure of the heart to eject/propel blood forward effectively

82
Q

congestive HF refers to?

A

HF almost always involves fluid overload

83
Q

HF occurs because of what pathologic precipitants?

A
  • pump problem: heart contractility has been weakened
    and/or
  • increased resistance: increased afterload to forward flow
    and/or
  • increased preload: fluid volume overload increased workload
84
Q

general sequelae to pathologic precipitants of HF

A
  • diminished CO, inadequate perfusion of tissues (lack of O2 + nutrients)
  • problems related to back-up of fluid + gen problems of fluid overload
85
Q

as CO diminishes, the ____ kicks in to compensate for what it perceives to be a ____. this process is ____ to the body and combines with increased ______ make the heart work even harder.

A
  • RAAS
  • low blood volume problem
  • harmful
  • preload and afterload
86
Q

see notability for chart on HF PATHO

A

OKAY

87
Q

categories of LHF S/S

A
  • gen S/S of decreased CO
  • S/S/ of fluid backup into lungs (lung congestion, ie, lung edema)
88
Q

categories of RHF S/S

A
  • S/S of decreased CO bc RV failing to move blood forward into left side of heart to be ejected to body
  • S/S of fluid backup into periphery (i.e, peripheral edema)
89
Q

general S/S of decreased CO

A
  • fatigue, weakness
  • mental status change, deterioration of responsiveness
  • hypotension
  • dyspnea
  • prolonged capillary refill (>2 secs)
  • low urine output
90
Q

S/S of fluid backup into lungs (pulm edema)

A
  • crackles upon auscultation of lungs
  • hemoptysis
  • orthopnea
  • increased resp rate
  • decrease SO2 (saturated o2)
91
Q

patho of fluid backup into lungs bc LHF

A
  • LV contractility decreases, preload + afterload increase
  • LV cannot keep blood flowing forward -> back pressure
    1. LV
    2. LA
    3. pulm veins
    4. pulm capillaries
    5. back pressure forces fluid out into alveolar tissue
    6. cardiogenic pulm edema
92
Q

hemoptysis

A
  • cough w/ frothy blood-tinged sputum
  • froth due to air + fluid
  • blood-tinges/pink color due to back pressure pushing fluid + some RBCs into alveoli
93
Q

orthopnea

A
  • SOB upon lying down
  • supine position increases backflow into lungs -> more lungs edema
94
Q

S/S fluid backup into periphery veins (peripheral venous congestion)

A
  • jugular venous distention (JVD)
  • liver congestion - enlarged liver
  • ascites
  • edema of legs and feet
95
Q

ascites

A
  • state of extra fluid in abdominal cavity due to fluid being pushed out engorged abdominal veins
  • edema of abdominal cavity
96
Q

patho for S/S fluid backup into periphery

A
  • RV contractility decreases, preload + afterload increase
  • RV cannot keep all blood flowing forward and back pressure
    1. RV
    2. RA
    3.1. superior vena cava
    3.2 inferior vena cava
    4.1 jugular veins
    4.2 portal veins, leg and feet veins
97
Q

RHF causes

A
  • ischemia and MI cause reduced contractility
  • pathologically increased PVR (pulm vascular resistance)
98
Q

if RHF caused by pulm vascular resistance, it is called?

A

cor pulmonale

99
Q

people w/ chronic bronchitis often have lungs filled with ______, causing decreased _______.

A
  • mucous and congestion
  • blood oxygen levels (hypoxemia)
100
Q

low oxygen levels cause the ______ and _____ to vasoconstrict.

A

pulmonary artery and pulmonary vessels

101
Q

the constriction of pulmonary vasculature in people with chronic bronchitis creates _____ pressure, making it _______ difficult for the RV to pump blood into _________.

A
  • higher
  • more
  • pulm artery and rest of lungs’ vascular system
102
Q

difficulty of the RV to pump blood into pulm artery and rest of lungs’ vascular system causes what?

A
  1. RV fails
  2. fluid backs up
  3. RV
  4. RA
  5. SVC and IVC
  6. JVD, liver congestion, ascites, leg edema
103
Q

lung congestion (pulm edema) is caused by?

A

LHF and its retrograde (back-up) flow

104
Q

lung congestion (chronic bronchitis) causes?

A

RHF and retrograde venous flow

105
Q

treatment of HF focuses on

A
  • increasing strength of pump, which increasing forward blood flow
  • decrease HR if too high to lessen workload
  • decreasing resistance to forward flow (afterload - SVR & PVR)
  • inhibiting RAAS
  • decreasing preload
106
Q

HF treatments

A
  • positive inotropic drugs (digoxin) to increase pump
  • vasodilator drugs (NTG) to decrease afterload
  • ACE inhibitors to inhibit RAAS
  • diuretics to decrease preload
107
Q

____ to fluid and ___ of fluid that give HF congestive label - HF almost always have ____ as main component, which is why ___ is key part of treatment.

A
  • hanging on
  • back-up
  • fluid overload
  • diuresis
108
Q

the ____ system is body’s compensatory mech when we have fluid overload

A

natriuretic

109
Q

the natriuretic system causes more ____ to be excreted into the urine -> ____ follows. this makes natriuretic peptides ____ when we need to get rid of fluid.

A
  • sodium
  • water
  • natural diuretics
110
Q

what substances are part of the natriuretic system and are secreted by the heart in varying amts into blood daily as part of natural reg system?

A
  • atrial natriuretic peptide, ANP (secreted by atria)
  • b-type natriuretic peptide, BNP (secreted by ventricles)
111
Q

ANP + BNP help to increase ____ of sodium and water from kidneys when we need to ____ of water.

A

secretion, get rid

112
Q

high BNP means

A

heart is frantically and usually unsuccessfully trying to compensate for the fluid overload that is always part of HF

113
Q

when patients present S/S of HF, gold standard for confirmation and quantification of HF is a blood test that measures?

A

BNP (if abnormally elevated, HF occuring0

114
Q

patient in RHF or LHF or both, circulating blood volume (____) is ____.

A

preload, increasing

115
Q

heart notices a _______ volume of blood returning to the _____. ANP + BNP is secreted by the ______, respectively, and these hormones circulate to the ____ to get them to ____ some volume.

A
  • larger than normal
  • right atrium
  • RA and LV
  • kidneys
  • diurese
116
Q

kidneys already involved with misguided overdrive of ____ as part of original HF, so what happens with ANP + BNP?

A
  • RAAS
  • kidneys don’t respond appropriately to ANP + BNP
117
Q

as preload continues to be high, heart _____ keeps ____ its hormones, so serum ____ goes ___, which helps with diagnosis. the ___ the BNP, the ____ the HF.

A
  • frantically
  • increasing
  • BNP
  • up
  • higher, worse
118
Q

healthy man BNP level

A

50 pg/mL

119
Q

BNP of man in mild HF

A

130 pg/mL

120
Q

BNP of man in severe HF

A

1000 pg/mL

nurs pathophysiology (13 decks)

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