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valves that clinically have the most problems
aortic and mitral valves
stenosis
narrowing or tighterning of valve → obstruct forward blood flow
regurgitation
insufficiency or leaking of valve → allow backward blood flow
mitral valve stenosis
causes
pathophysiology
presentation
monitoring
treatment
causes
due to rheumatic HD
pathophysiology
mitral valve narrow → increased pressure in LA → LA enlargement → high risk of AF and thromboembolic events
presentation
symptomatic when 50 - 60 years old
pulmonary/systemic edema, fatigue
monitoring
echo (every 1 - 5 years)
treatment
meds (symptom control) = diuretics, BBs, non-DHP CCBs
mehanical intervention or valve replacement
balloon valvuloplasty
mitral valve regurgitation
causes
pathophysiology
presentation
monitoring
treatment
causes
mitral valve prolapse
dilation of LV
pathophysiology
blood flow back to LA → decreased CO → LV enlarges to increase CO → HF
presentation
asymptomatic
mild → pulmonary congestation
severe → pulmonary HTN, HF symptoms
monitoring
echo annually
treatment
reduce preload → diuretics
LV dysfunction → HF therapy
valve replacement
aortic valve stenosis
causes
pathophysiology
presentation
monitoring
treatment
causes
most common valvular disorder
calcification of aortic valve
pathophysiology
narrowed aortic valve → LV pumps against higher pressure → LV hypertrophy
presentation
present at 60 - 90 years
mild → chest pain during exertion
severe → chest pain, SOB, syncope, HF
monitoring
echo (every 1 - 5 years)
treatment
valve replacement
balloon valvuloplasty
aortic valve regurgitation
causes
pathophysiology
presentation
monitoring
treatment
causes
abnormal valve leaflets, dilated aortic root
pathophysiology
aorta dilated → LV enlarges and thickens
presentation
asymptomatic due to cardiac compensation
pulmonary congestion, peripheral edema, chest pain
monitoring
echo (every 0.5 - 3 years)
treatment
afterload-reducing agents
valve replacement
valve repair
fix and preserves patient’s valve
preferred over replacement
no anticoagulation needed
valve replacement
open heart surgery
transcatheter aortic valve implantation (TAVI)
less invasive
mechanical valves vs bioprosthetic valves
mechanical
high durability
highly thrombogenic → lifelong anticoagulation
preferred if risk factors for bleeding, refuses/CI to anticoagulation
bioprosthetic
porcine or bovine
less thrombogenic
low durability
preferred if pt is young
antithrombotic therapy for valve replacement: bioprosthetic
aortic
mitral
aortic
aspirin 50 - 100 mg/day indefinitely
opt. add clopidogrel 75 mg daily for 3 - 6months if TAVI
mitral
warfarin w/ INR 2 - 3 for 3 months, then aspirin 50 - 100 mg/day indefinitely
antithrombotic therapy for valve replacement: mechanical
aortic
mitral
bridging
additional aspirin
aortic
warfarin w/ INR 2 - 3 indefinitely
mitral
warfarin w/ INR 2.5 - 3.5 indefinitely
bridging
w/ IV UFH or SC LMWH if INR subtherapeutic
additional aspirin
add 50 - 100 mg/day if add. risk factors for thromboembolism
Afib, low EF, older age, history of TE)
ODACs in valvular disease
dabigatran, rivaroxaban, apixaban, edoxaban
CI in mechanical heart valves
increased risk of thromboembolism and bleeding compared to waefarin
which valve preferred if women wish to have children in future
bioprosthetic
which drug increases risk of congenital fetus abnormalities, fetal loss, hemorrhagic complications
warfarin
if willing, warfarin can be continued in —- trimester if daily dose —-
1st trimester; < 5 mg
which med is chosen instead of warfarin due to congenital effects
LMWH
which is last line option
which is added for high risk pts
UFH IV
low dose aspirin
shock
acute, generalized state of inadequate perfusion of critical organs
SBP < 90 mmHg OR reduction of at least 40 mmHg from bseline
perfusion triangle
inadequate perfusion due to problems w. heart, blood vessels, blood
goal and monitoring of shock
achieve/maintain MAP > 65 mmHg
assess perfusion and oxygenation of body
assess organ specific O2 delivery and utilization
cardiogenic shock
description
etiologies
treatment
description
heart fails to pump out blood
etiologies
HF
valve dysfunction
treatment
increase CO
inotropes
obstructive shock
description
etiologies
treatment
description
heart pumps well
outflow obstructed
etiologies
PE
tamponade
treatment
treat obstruction
hypovolemic shock
description
etiologies
treatment
description
heart pumps well
not enough blood volume to pump
etiologies
blood loss
fluid loss
treatment
IV fluids
distributive shock
description
etiologies
treatment
description
heart pumps well
peripheral vasodilation
etiologies
anaphylaxis
sepsis
treatment
IV fluids
vasopressors
receptor actions
alpha 1
beta 1
beta 2
D
V
alpha 1
vasoconstriction, increased chronotropy
beta 1
increased ionotropy, chronotropy
beta 2
vasodilation (blood vessels), bronvhodilatioin, vasodilation (kidneys)
D
vasodilation in kidneys
V
v1 = vasoconstriciton
v2 = reabsorption of water in kidneys
vasopressor agents
epinephrine
norepinephrine
dopamine
phenylephrine
vasopressin
epinephrine
dose
receptors
effects
use
dose
IV push or titratable infusion
receptors
alpha 1, beta 1, beta 2
effects
vasoconstriction, increased inotropic/chronotropic activity
use
most common in life-threatening situations (cardiac arrest)
3rd or 4th line vasopressor in shock
Norepinhrine (Levophed)
dose
receptors
effects
use
dose
IV as titratable infusion
receptors
alpha 1 > > beta 1
effects
vasoconstriction
increased inotropic/chronotropic activity
use
preffered in sepsis
most common in ICU
dopamine
dose
receptors
effects
use
dose
IV as titratable infusion
receptors
dopamine, beta 1, alpha 1 - dose dependent
effects
low dose = increased renal blood flow (D)
medium dose = increased inotropic/chronotropic activity (beta 1)
high dose = vasoconstriction (alpha 1
use
cardiogenic shock
phenylephrine (Neo-synephrine)
dose
receptors
effects
use
dose
IV as titratable infusion
receptors
alpha 1
effects
vasoconstriction
use
alt if tachyarrhythmias from NE or D are concern
vasopressin
dose
receptors
effects
use
dose
IV as titratable infusion
receptors
V1 and V2
effects
vasoconstriction (V1)
reabsorption of water in kidneys (V2)
use
adjunct to NE in sepsis
used for diabetes insipidus
not affected by acidosis
general ADE of vasopressors
arrhythmias
tachcardia
tissue ischemia