Exam 4 pt. 2 Flashcards
(108 cards)
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
2
Q
heart failure does not mean
A
cardiac arrest
3
Q
heart failure involves
A
-multiple systems
-progressive
-fluid volume overload (CHF)
-causes pulmonary congestion
-high mortality
4
Q
cardiac output
A
volume of blood left ventricle pumps per min
-CO=HR x SV
5
Q
stroke volume (SV)
A
mL of blood ejected per contraction
6
Q
heart rate (HR)
A
number of ventricular contractions per min
-not enough volume causes increased HR
7
Q
ejection fraction (EF)
A
% of blood ejected from left ventricle during systole
-normal is 60-70%
8
Q
contractility
A
how forceful the chambers squeeze blood
-ability to stretch and contract
9
Q
preload
A
VOLUME! the heart chambers have to pump
10
Q
afterload
A
RESISTANCE! the chambers have to push against to eject blood
11
Q
high afterload
A
hypertension, atherosclerosis
12
Q
cardiovascular regulation of renin-angiotensin aldosterone system (RAAS)
A
raises BP (vasoconstricts) and increases blood volume
13
Q
in heart failure RAAS
A
continually cycles and weakens the heart
-increases resistance (afterload)
-increases workload
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
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
16
Q
diagnostic of heart failure
A
elevated B-type natriuretic peptide (BNP)!
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
18
Q
cardiovascular regulation of autonomic nervous system - PNS
A
-cholinergic receptors
-slow HR!
-decrease force of contraction!
19
Q
cardiovascular regulation of autonomic nervous system - SNS
A
-alpha adrenergic receptors: vasoconstrict
-beta 1 adrenergic receptors: increase HR! strengthen force of contraction!
20
Q
heart failure etiology
A
-ischemic heart disease: MI
-hypertension: COPD, pulmonary hypertension
-dysrhythmias
-cardiac infections
-PE
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
22
Q
acute heart failure
A
-rapid
-sudden development
-massive MI
-severe shock: cardiogenic
23
Q
chronic heart failure
A
-most common
-heart gradually weakens over time
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
25
diastolic dysfunction heart failure
-ventricles cant relax
-poor filling!
-pumps out insufficient volume
-low CO!
-low SV!
-normal or almost normal EF (>50%)
26
SNS Compensatory Mechanism for HF
-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
27
RAAS compensatory mechanism for HF
-elevates blood volume by sodium and water retention, potassium excretion, increases preload (volume)!
28
what to give patient with HF
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
29
arterial vasoconstriction increases
afterload and workload
-give ACEI or ARBS to inhibit vasoconstriction!
30
hypertrophy compensatory mechanism for HF
-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
31
left ventricular heart failure etiology
-hypertension: increased afterload
-hypertrophy: decreased filling
-insufficient CO
-diminished O2 to tissues and organs
-vasoconstriction
-RAAS
32
left ventricular heart failure pathophysiology
fluid accumulation from congestion of blood behind failing left ventricle!
33
left ventricular heart failure backward effects
due to congestion behind pumping chamber!
-increased hydrostatic pressure
-pulmonary dysfunction: backs to left atrium and lungs !
34
left ventricular heart failure forwards effects
decreased perfusion! to brain, kidneys and lungs (hypoxemia)
-due to decreased CO!
35
orthopnea
to breathe comfortably patient requires head elevation with specific number of pillows because blood flow is best at base of lungs
36
left ventricular heart failure backward effect signs and symptoms
-pink sputum!
-DOE
-orthopnea
-cough
-paroxysmal nocturnal dyspnea
-cyanosis
-basilar crackles
37
left ventricular heart failure forward effects signs and symptoms (same as right forward effects)
-fatigue
-oliguria (decreased UOP)
-increase HR
-faint pulses
-restlessness
-confusion
-anxiety
38
right ventricular (cor pulmonale) heart failure etiology
-caused by left side HF or lung disorders
-RV difficulty pumping blood forward to pulmonary artery
-increased hydrostatic pressure
39
right ventricular heart failure backward effects
congestion of blood behind failing right ventricle
-systemic venous circulation (systemic congestion)!
40
right ventricular heart failure forward effects
decreased CO!
-same as left
41
right ventricular heart failure backwards effects signs and symptoms
-edema!
-ascites: fluid in stomach
-hepatomegaly and splenomegaly!
-JVD
-anorexia from not feeling like eating with fluid backup
42
right ventricular heart failure forward effects signs and symptoms
-fatigue
-oliguria (decreased UOP)
-increase HR
-faint pulses
-restlessness
-confusion
-anxiety
43
diagnosis of heart failure
-no universal diagnostic test
-FACES: Fatigue, Activity limitation, Congestion, Edema, SOB
-echocardiogram gold standard: shows EF
-labs: electrolyte
-B type natriuretic peptide: >500
44
treatment of lifestyle modifications for heart failure
-limit fluid: daily weights
-limit salt: salt increases preload
-limit cholesterol
-limit alcohol
-daily walking regimen
45
treatment of medications for heart failure-diuretics:
-diuretics: decrease preload
46
treatment of medications for heart failure-angiotensin converting enzyme inhibitors (ACEI):
decrease afterload and inhibit RAAS
-beta adrenergic blockers: decrease HR and vasoconstriction (inhibit SNS)
47
treatment of medications for heart failure-beta adrenergic blockers:
decrease HR and vasoconstriction (inhibit SNS)
48
treatment of medications for heart failure- inotropic agents:
increase contractility
-before administering digitalis: check apical pulse for 1 min!
49
treatment of medications for heart failure-synthetic natriuretics:
decrease pulmonary edema
50
treatment of medications for heart failure- nitrates:
-dilators
-decrease workload
-decrease BP
-be careful on viagra!
51
treatment of medications for heart failure-arterial vasodilators:
decrease workload and afterload
52
treatment of interventional cardiology for heart failure
-cardiac resynchronization
-aortic balloon pump
-cardiac assist devices
-cardiac transplant
53
what is valvular function
unidirectional flow
54
valvular structures may be damaged by
-MI
-trauma
-infection
-calcification
-congenital defects
-rheumatic fever
55
valvular stenosis
failure of valve to open completely
-increased work from blood being forced through high resistance
-hypertrophy
56
valvular regurgitation (insufficiency)
failure of valves to close completely
-backflow of blood into previous chamber
-increased workload and hypertrophy
57
valvular prolapse
valve balloons backwards into supplying chamber
58
clinical manifestations of mitral stenosis
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
mitral stenosis diagnosis and treatment
-diagnosis: transthoracic, TEE
-treatment: preventative antibiotics, prosthetic valve
60
mitral regurgitation clinical manifestations
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
mitral regurgitation diagnosis and treatment
-diagnosis: echocardiogram
-treatment: preventative antibiotics, surgery
62
mitral valve prolapse clinical manifestations
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
mitral valve prolapse diagnosis and treatment
-diagnosis: echo
-treatment: none, meds, oxygen
64
aortic stenosis clinical manifestations
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
aortic stenosis diagnosis and treatment
-diagnosis: echo
-treatment: meds or surgery
66
aortic regurgitation clinical manifestations
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
aortic regurgitation diagnosis and treatment
-diagnosis: echo
-treatment: meds or surgery
68
what is shock
life threatening imbalance between metabolic and oxygen supply requirements of peripheral tissues
-cell doesnt have adequate O2 and nutrients
69
initial stage of shock
-sudden drop in tissue perfusion
-systolic BP <90
-increased HR
-increased blood volume and vasoconstriction
-patient is anxious, pale, cold, clammy
70
progressive stage of shock
-decreased perfusion to lungs, kidneys, gut, pancreas, liver
-requires active therapeutic intervention
-signs of MODS
71
refractory-irreversible stage of shock
-brain and heart have decreased perfusion
-widespread cellular hypoxia and extensive anaerobic metabolism
-patient unresponsive to therapeutic interventions
-death
72
inflammatory response from shock
influx of neutrophils, macrophages, T cells
-increased demand for oxygen cannot be met
-accumulation of interstitial edema
73
lactic acidosis shock response
-anaerobic metabolism: lactic acid production
-liver: cant detoxify lactic acid
-kidneys: decreased removal of lactic acid
-adversely affects heart, lungs, brain, neurological function
74
gastrointestinal shock response
-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
coagulation system shock response
blood susceptible to clotting: lodge in capillaries, block blood flow, tissue ischemia
76
shock response prevention
hand hygiene!
77
systemic inflammatory response (SIRS)
overwhelming inflammatory response with all systems attempting to compensate
-increased HR, CO, RR
-decreased GI, UOP
-sepsis often follows SIRS
78
septic shock etiology
-severe sepsis!
-infection: bacterial, viral, fungal, parasitic
-vasodilation
-hypotension: vessels hugely dilated!
-tissue hypoxia
79
most vulnerable to septic shock
-immunocompromised
-invasive technology
-very young or old
-malnourished
-chemo
-chronic health issues
80
Septic Shock Pathophysiology
-widespread vasodilation!
-initiated coagulation pathway: micro thrombi
-increased capillary permeability with edema
-reduced insulin
-impaired WBCs
81
septic shock clinical manifestations
-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
septic shock treatment
-multiple specialists
-isotonic fluid!
-antibiotics
-vasoconstrictor meds
-respiratory support
-IV insulin
-inotropes
-increased CO and O2 delivery
83
cardiogenic shock etiology
-MI most common cause
-ventricle dysfunction
-cardiac tamponade
-cardiomyopathy
-wall rupture
-heart defects
-tachy and brady arrhythmias
84
cardiogenic shock pathophysiology
-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
cardiogenic shock clinical manifestations
-increased HR
-vascular resistance (maintains BP)
-S3 gallop
-crackles
-cool, clammy skin
-pericardial friction rub: tension pneumothorax
86
cardiogenic shock treatment
-myocardial damage is irreversible
-decrease myocardial O2 demand
-increased myocardial O2 delivery
-positive inotropes: dopamine/dobutamine
-intraaortic balloon counter pulsation
-vasodilators: nitroglycerin
87
obstructive shock etiology/pathophysiology
-heart is prevented from pumping effectively
-impaired ventricle filling
-decreased CO
-pulmonary embolism or tension pneumothorax
88
obstructive shock clinical manifestations and treatment
-right side heart failure
-tension pneumothorax: deviated trachea, absent breath sounds
-pulmonary embolism: sudden severe dyspnea, abnormal ABG
-treatment: correct above causes
89
hypovolemic shock etiology
inadequate circulating blood volume and perfusion of tissues
-hemorrhage most common!
-burns
-severe vomiting/diarrhea
-fluid leaks into interstitial spaces
90
hypovolemic shock clinical manifestations
-decrease: CO, preload, pulmonary artery pressure, oxygen delivery
-increased: systemic vascular resistance, compensatory mechanisms to maintain perfusion
91
hypovolemic shock treatment
-stop bleeding!
-give fluids: NS or lactate ringers
-normalize BP, CO and perfusion
-PRBCs: blood
92
distributive shock
abnormally expanded vascular space causes by excessive vasodilation!
93
anaphylactic shock etiology/pathophysiology
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
anaphylactic shock clinical manifestations
-initial: anxiety, increased HR and RR
-followed by: hypotension, urticaria and pruritus, impending doom, angioedema, wheezing, cyanosis, stridor
95
anaphylactic shock treatment
-epinephrine, antihistamine, glucocorticoids
-IV saline
-carry epipen
96
anaphylactic shock common triggers
-peanuts
-shellfish
-penicillin
-wasps
-red ants
-animals
97
neurogenic shock etiology/pathophysiology
-widespread vasodilation: pooling of blood
-medulla or spinal cord depression
-loss of sympathetic tone in vasculature
98
neurogenic shock clinical manifestations
-hypotension
-syncope with standing
-bradycardia
-decreased CO
99
neurogenic shock treatment
-elevate legs
-slow position changes
-vasoconstrictive drugs
-fluid
-atropine
-treat underlying injury
100
astute assessment for shock
prevent, detect, manage
101
monitoring for shock
-CO
-volume status
-oxygen delivery
-oxygen consumption
102
hemodynamic monitoring for shock
-critical care setting
-subclavian vein into heart
-pulmonary artery catheter: intracardiac pressures, SVO2
103
complications of shock- ARDS (acute respiratory distress syndrome)
-whiteout
-respiratory failure
-most common with septic shock
-refractory hypoxemia
-tissue ischemia
-inflammatory response: exudate in interstitial space, alveolar collapse
104
complications of shock- DIC (disseminated intravascular coagulopathy)
-abnormal clotting
-platelets and clotting factors consumed
-risk for bleeding
-hemorrhage
105
complications of shock- abdominal compartment syndrome
-fluid escaped into bowel and peritoneal cavity: syncope, decreased UOP
-abdomen distended with gas
106
complications of shock- acute kidney injury
-acute renal failure
-kidneys undergo prolonged hypoperfusion
-increased blood urea nitrogen (BUN) and creatinine
107
complications of shock- MODS (multiple organ dysfunction)
-two or more systems
-sepsis and septic shock most common
-cant maintain homeostasis
-ongoing inflammatory response: tissue and organ dysfunction, death
108
complications of shock - hepatic failure
decreased blood supply to liver. Ischemia and liver dysfunction. Impairs ability to eliminate waste: jaundice, decreased LOC, abdominal distension
