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Patho > Exam 4 pt. 2 > Flashcards

Exam 4 pt. 2 Flashcards

1
Q

heart failure

A

(pump failure)

-inability of heart to maintain sufficient cardiac output to optimally meet the metabolic demands of tissues and organs

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2
Q

heart failure does not mean

A

cardiac arrest

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3
Q

heart failure involves

A

-multiple systems

-progressive

-fluid volume overload (CHF)

-causes pulmonary congestion

-high mortality

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4
Q

cardiac output

A

volume of blood left ventricle pumps per min

-CO=HR x SV

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5
Q

stroke volume (SV)

A

mL of blood ejected per contraction

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6
Q

heart rate (HR)

A

number of ventricular contractions per min

-not enough volume causes increased HR

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7
Q

ejection fraction (EF)

A

% of blood ejected from left ventricle during systole

-normal is 60-70%

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8
Q

contractility

A

how forceful the chambers squeeze blood

-ability to stretch and contract

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9
Q

preload

A

VOLUME! the heart chambers have to pump

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10
Q

afterload

A

RESISTANCE! the chambers have to push against to eject blood

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11
Q

high afterload

A

hypertension, atherosclerosis

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12
Q

cardiovascular regulation of renin-angiotensin aldosterone system (RAAS)

A

raises BP (vasoconstricts) and increases blood volume

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13
Q

in heart failure RAAS

A

continually cycles and weakens the heart

-increases resistance (afterload)

-increases workload

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14
Q

cardiovascular regulation of natriuretic peptides

A

-respond to increased water and sodium retention and raised blood volume and induce natriuresis which increases EXCRETION of sodium and water

-decreases blood volume

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15
Q

natriuretic peptides induce natriuresis which

A

Increases excretion of sodium and water by BLOCKING release of renin and aldosterone, and OPPOSES vasoconstrictive effects angiotensin II

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16
Q

diagnostic of heart failure

A

elevated B-type natriuretic peptide (BNP)!

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17
Q

cardiovascular regulation of antidiuretic hormone (ADH)

A

responds to decreased tissue perfusion

-release ADH from posterior pituitary

-reabsorbs water into bloodstream

-vasoconstrictor effects

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18
Q

cardiovascular regulation of autonomic nervous system - PNS

A

-cholinergic receptors

-slow HR!

-decrease force of contraction!

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19
Q

cardiovascular regulation of autonomic nervous system - SNS

A

-alpha adrenergic receptors: vasoconstrict

-beta 1 adrenergic receptors: increase HR! strengthen force of contraction!

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20
Q

heart failure etiology

A

-ischemic heart disease: MI

-hypertension: COPD, pulmonary hypertension

-dysrhythmias

-cardiac infections

-PE

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21
Q

heart failure risk factors

A

-age

-ethnicity

-family history and genetics

-diabetes

-obesity

-lifestyle

-meds

-sleep apnea

-congenital heart defects

-viruses

-alcohol abuse

-kidney conditions

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22
Q

acute heart failure

A

-rapid

-sudden development

-massive MI

-severe shock: cardiogenic

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23
Q

chronic heart failure

A

-most common

-heart gradually weakens over time

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24
Q

systolic dysfunction heart failure

A

-difficulty ejecting blood! (low EF <40%)

-reduced contractility/pumping

-inadequate ventricular emptying: blood accumulates, pressure increases, backup hydrostatic pressure in chamber and lungs

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25
Q

diastolic dysfunction heart failure

A

-ventricles cant relax

-poor filling!

-pumps out insufficient volume

-low CO!

-low SV!

-normal or almost normal EF (>50%)

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26
Q

SNS Compensatory Mechanism for HF

A

-increase HR and contractility

-vasoconstriction increases afterload which increases BP

-kidneys release renin

-RAAS conserves salt and water

-increased HR, after load, workload, decreased SV

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27
Q

RAAS compensatory mechanism for HF

A

-elevates blood volume by sodium and water retention, potassium excretion, increases preload (volume)!

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28
Q

what to give patient with HF

A

diuretics! beta blockers! ACEIs or ARBS!

-already have too much volume

-want to lower preload

-beta blockers inhibit effects of SNS

-ACEIs or ARBS inhibit vasoconstriction

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29
Q

arterial vasoconstriction increases

A

afterload and workload

-give ACEI or ARBS to inhibit vasoconstriction!

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30
Q

hypertrophy compensatory mechanism for HF

A

-chronic myocardial wall tension

-from high preload, hypertension or MI

-initial boosts contractility

-RAAS

-remodeling: eventually detrimental with fibrous stiffening and worsens HF

-treat with ACEIs or ARBs

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31
Q

left ventricular heart failure etiology

A

-hypertension: increased afterload

-hypertrophy: decreased filling

-insufficient CO

-diminished O2 to tissues and organs

-vasoconstriction

-RAAS

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32
Q

left ventricular heart failure pathophysiology

A

fluid accumulation from congestion of blood behind failing left ventricle!

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33
Q

left ventricular heart failure backward effects

A

due to congestion behind pumping chamber!

-increased hydrostatic pressure

-pulmonary dysfunction: backs to left atrium and lungs !

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34
Q

left ventricular heart failure forwards effects

A

decreased perfusion! to brain, kidneys and lungs (hypoxemia)

-due to decreased CO!

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35
Q

orthopnea

A

to breathe comfortably patient requires head elevation with specific number of pillows because blood flow is best at base of lungs

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36
Q

left ventricular heart failure backward effect signs and symptoms

A

-pink sputum!

-DOE

-orthopnea

-cough

-paroxysmal nocturnal dyspnea

-cyanosis

-basilar crackles

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37
Q

left ventricular heart failure forward effects signs and symptoms (same as right forward effects)

A

-fatigue

-oliguria (decreased UOP)

-increase HR

-faint pulses

-restlessness

-confusion

-anxiety

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38
Q

right ventricular (cor pulmonale) heart failure etiology

A

-caused by left side HF or lung disorders

-RV difficulty pumping blood forward to pulmonary artery

-increased hydrostatic pressure

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39
Q

right ventricular heart failure backward effects

A

congestion of blood behind failing right ventricle

-systemic venous circulation (systemic congestion)!

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40
Q

right ventricular heart failure forward effects

A

decreased CO!

-same as left

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41
Q

right ventricular heart failure backwards effects signs and symptoms

A

-edema!

-ascites: fluid in stomach

-hepatomegaly and splenomegaly!

-JVD

-anorexia from not feeling like eating with fluid backup

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42
Q

right ventricular heart failure forward effects signs and symptoms

A

-fatigue

-oliguria (decreased UOP)

-increase HR

-faint pulses

-restlessness

-confusion

-anxiety

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43
Q

diagnosis of heart failure

A

-no universal diagnostic test

-FACES: Fatigue, Activity limitation, Congestion, Edema, SOB

-echocardiogram gold standard: shows EF

-labs: electrolyte

-B type natriuretic peptide: >500

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44
Q

treatment of lifestyle modifications for heart failure

A

-limit fluid: daily weights

-limit salt: salt increases preload

-limit cholesterol

-limit alcohol

-daily walking regimen

45
Q

treatment of medications for heart failure-diuretics:

A

-diuretics: decrease preload

46
Q

treatment of medications for heart failure-angiotensin converting enzyme inhibitors (ACEI):

A

decrease afterload and inhibit RAAS

-beta adrenergic blockers: decrease HR and vasoconstriction (inhibit SNS)

47
Q

treatment of medications for heart failure-beta adrenergic blockers:

A

decrease HR and vasoconstriction (inhibit SNS)

48
Q

treatment of medications for heart failure- inotropic agents:

A

increase contractility

-before administering digitalis: check apical pulse for 1 min!

49
Q

treatment of medications for heart failure-synthetic natriuretics:

A

decrease pulmonary edema

50
Q

treatment of medications for heart failure- nitrates:

A

-dilators

-decrease workload

-decrease BP

-be careful on viagra!

51
Q

treatment of medications for heart failure-arterial vasodilators:

A

decrease workload and afterload

52
Q

treatment of interventional cardiology for heart failure

A

-cardiac resynchronization

-aortic balloon pump

-cardiac assist devices

-cardiac transplant

53
Q

what is valvular function

A

unidirectional flow

54
Q

valvular structures may be damaged by

A

-MI

-trauma

-infection

-calcification

-congenital defects

-rheumatic fever

55
Q

valvular stenosis

A

failure of valve to open completely

-increased work from blood being forced through high resistance

-hypertrophy

56
Q

valvular regurgitation (insufficiency)

A

failure of valves to close completely

-backflow of blood into previous chamber

-increased workload and hypertrophy

57
Q

valvular prolapse

A

valve balloons backwards into supplying chamber

58
Q

clinical manifestations of mitral stenosis

A

due to pulmonary congestion and increased left atria pressure, then to lungs (can’t get blood to left ventricle)

-DOE

-cough

-orthopnea

-PND

-murmur at apex

59
Q

mitral stenosis diagnosis and treatment

A

-diagnosis: transthoracic, TEE

-treatment: preventative antibiotics, prosthetic valve

60
Q

mitral regurgitation clinical manifestations

A

due to backflow of blood from left ventricle to the left atrium

-orthopnea

-cough

-DOE

-chest pain

-chronic weakness and fatigue! (From decreased forward pumping of blood to aorta)

-high pitch blowing murmur at apex

61
Q

mitral regurgitation diagnosis and treatment

A

-diagnosis: echocardiogram

-treatment: preventative antibiotics, surgery

62
Q

mitral valve prolapse clinical manifestations

A

females 14-30yrs

  • degeneration valve tissue causing loose valve leaflets

-most asymptomatic and no know cause

-fatigue, dyspnea, chest pain, murmur, palpitations, dysrhythmias, dizziness

63
Q

mitral valve prolapse diagnosis and treatment

A

-diagnosis: echo

-treatment: none, meds, oxygen

64
Q

aortic stenosis clinical manifestations

A

from calcium deposits (aortic sclerosis) on aortic cusps (narrowing so left ventricular outflow of blood is obstructed)

-may lead to L side HF

-syncope

-chest pain

-dyspnea

-low systolic BP

-faint pulses

-systolic murmur

65
Q

aortic stenosis diagnosis and treatment

A

-diagnosis: echo

-treatment: meds or surgery

66
Q

aortic regurgitation clinical manifestations

A

from blood leaking from aorta back to left ventricle (can’t remain closed due to deformity)

-may lead to left side HF

-throbbing or pounding because of large left ventricle stroke volume

-bounding pulse!

-chest pain

-fatigue

-dyspnea

-peripheral edema

67
Q

aortic regurgitation diagnosis and treatment

A

-diagnosis: echo

-treatment: meds or surgery

68
Q

what is shock

A

life threatening imbalance between metabolic and oxygen supply requirements of peripheral tissues

-cell doesnt have adequate O2 and nutrients

69
Q

initial stage of shock

A

-sudden drop in tissue perfusion

-systolic BP <90

-increased HR

-increased blood volume and vasoconstriction

-patient is anxious, pale, cold, clammy

70
Q

progressive stage of shock

A

-decreased perfusion to lungs, kidneys, gut, pancreas, liver

-requires active therapeutic intervention

-signs of MODS

71
Q

refractory-irreversible stage of shock

A

-brain and heart have decreased perfusion

-widespread cellular hypoxia and extensive anaerobic metabolism

-patient unresponsive to therapeutic interventions

-death

72
Q

inflammatory response from shock

A

influx of neutrophils, macrophages, T cells

-increased demand for oxygen cannot be met

-accumulation of interstitial edema

73
Q

lactic acidosis shock response

A

-anaerobic metabolism: lactic acid production

-liver: cant detoxify lactic acid

-kidneys: decreased removal of lactic acid

-adversely affects heart, lungs, brain, neurological function

74
Q

gastrointestinal shock response

A

-pancreas cant make enough insulin causing hyperglycemia which increased risk for infection from hormonal release of epinephrine and cortisol!

-normal GI bacteria enter circulation

-endothelium of abdominal organs become permeable

75
Q

coagulation system shock response

A

blood susceptible to clotting: lodge in capillaries, block blood flow, tissue ischemia

76
Q

shock response prevention

A

hand hygiene!

77
Q

systemic inflammatory response (SIRS)

A

overwhelming inflammatory response with all systems attempting to compensate

-increased HR, CO, RR

-decreased GI, UOP

-sepsis often follows SIRS

78
Q

septic shock etiology

A

-severe sepsis!

-infection: bacterial, viral, fungal, parasitic

-vasodilation

-hypotension: vessels hugely dilated!

-tissue hypoxia

79
Q

most vulnerable to septic shock

A

-immunocompromised

-invasive technology

-very young or old

-malnourished

-chemo

-chronic health issues

80
Q

Septic Shock Pathophysiology

A

-widespread vasodilation!

-initiated coagulation pathway: micro thrombi

-increased capillary permeability with edema

-reduced insulin

-impaired WBCs

81
Q

septic shock clinical manifestations

A

-initial phase: pink warm phase “warm shock”!

-low BP

-fever

-chills

-fatigue

-fatigue

-dysuria

-altered mental status

-HR >90

-RR >20

-patient may look bloated

82
Q

septic shock treatment

A

-multiple specialists

-isotonic fluid!

-antibiotics

-vasoconstrictor meds

-respiratory support

-IV insulin

-inotropes

-increased CO and O2 delivery

83
Q

cardiogenic shock etiology

A

-MI most common cause

-ventricle dysfunction

-cardiac tamponade

-cardiomyopathy

-wall rupture

-heart defects

-tachy and brady arrhythmias

84
Q

cardiogenic shock pathophysiology

A

-low CO

-severe hypotension from heart not pumping!

-adequate fluid status!

-pulmonary and alveolar edema

-pink frothy sputum

-RAAS makes more difficult for heart to pump

85
Q

cardiogenic shock clinical manifestations

A

-increased HR

-vascular resistance (maintains BP)

-S3 gallop

-crackles

-cool, clammy skin

-pericardial friction rub: tension pneumothorax

86
Q

cardiogenic shock treatment

A

-myocardial damage is irreversible

-decrease myocardial O2 demand

-increased myocardial O2 delivery

-positive inotropes: dopamine/dobutamine

-intraaortic balloon counter pulsation

-vasodilators: nitroglycerin

87
Q

obstructive shock etiology/pathophysiology

A

-heart is prevented from pumping effectively

-impaired ventricle filling

-decreased CO

-pulmonary embolism or tension pneumothorax

88
Q

obstructive shock clinical manifestations and treatment

A

-right side heart failure

-tension pneumothorax: deviated trachea, absent breath sounds

-pulmonary embolism: sudden severe dyspnea, abnormal ABG

-treatment: correct above causes

89
Q

hypovolemic shock etiology

A

inadequate circulating blood volume and perfusion of tissues

-hemorrhage most common!

-burns

-severe vomiting/diarrhea

-fluid leaks into interstitial spaces

90
Q

hypovolemic shock clinical manifestations

A

-decrease: CO, preload, pulmonary artery pressure, oxygen delivery

-increased: systemic vascular resistance, compensatory mechanisms to maintain perfusion

91
Q

hypovolemic shock treatment

A

-stop bleeding!

-give fluids: NS or lactate ringers

-normalize BP, CO and perfusion

-PRBCs: blood

92
Q

distributive shock

A

abnormally expanded vascular space causes by excessive vasodilation!

93
Q

anaphylactic shock etiology/pathophysiology

A

extreme allergic reaction, antigen/IGE antibody reaction

-released histamines and bradykinins

-shock occurs when peripheral dilation is massive

-“pseudo” hypovolemic shock: volumes there but dilated out

94
Q

anaphylactic shock clinical manifestations

A

-initial: anxiety, increased HR and RR

-followed by: hypotension, urticaria and pruritus, impending doom, angioedema, wheezing, cyanosis, stridor

95
Q

anaphylactic shock treatment

A

-epinephrine, antihistamine, glucocorticoids

-IV saline

-carry epipen

96
Q

anaphylactic shock common triggers

A

-peanuts

-shellfish

-penicillin

-wasps

-red ants

-animals

97
Q

neurogenic shock etiology/pathophysiology

A

-widespread vasodilation: pooling of blood

-medulla or spinal cord depression

-loss of sympathetic tone in vasculature

98
Q

neurogenic shock clinical manifestations

A

-hypotension

-syncope with standing

-bradycardia

-decreased CO

99
Q

neurogenic shock treatment

A

-elevate legs

-slow position changes

-vasoconstrictive drugs

-fluid

-atropine

-treat underlying injury

100
Q

astute assessment for shock

A

prevent, detect, manage

101
Q

monitoring for shock

A

-CO

-volume status

-oxygen delivery

-oxygen consumption

102
Q

hemodynamic monitoring for shock

A

-critical care setting

-subclavian vein into heart

-pulmonary artery catheter: intracardiac pressures, SVO2

103
Q

complications of shock- ARDS (acute respiratory distress syndrome)

A

-whiteout

-respiratory failure

-most common with septic shock

-refractory hypoxemia

-tissue ischemia

-inflammatory response: exudate in interstitial space, alveolar collapse

104
Q

complications of shock- DIC (disseminated intravascular coagulopathy)

A

-abnormal clotting

-platelets and clotting factors consumed

-risk for bleeding

-hemorrhage

105
Q

complications of shock- abdominal compartment syndrome

A

-fluid escaped into bowel and peritoneal cavity: syncope, decreased UOP

-abdomen distended with gas

106
Q

complications of shock- acute kidney injury

A

-acute renal failure

-kidneys undergo prolonged hypoperfusion

-increased blood urea nitrogen (BUN) and creatinine

107
Q

complications of shock- MODS (multiple organ dysfunction)

A

-two or more systems

-sepsis and septic shock most common

-cant maintain homeostasis

-ongoing inflammatory response: tissue and organ dysfunction, death

108
Q

complications of shock - hepatic failure

A

decreased blood supply to liver. Ischemia and liver dysfunction. Impairs ability to eliminate waste: jaundice, decreased LOC, abdominal distension

Patho (10 decks)

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