HTN Flashcards
what is HTN (high blood pressure)
classification of BP in adults
normal <120/<80
elevated 120-129/<80
stage I HTN 130-139/80-89
Stage II HTN >140/>90
AHA defines HTN as
sustained SBP > 130 mmHg and DBP > 80 mmHg
HTN leads to an age related assocatiation to
ischemic heart disease, stroke, renal failure, retinopathy, PVD, and overall mortality
common risk for perioperative M&M shows ___ as a common risk factor if left untreated
HTN
in addition to SBP and DBP elevation, a widened pulse pressure is a risk factor for
CV remodeling as it correlates with vascular remodeling and stiffness
cause of primary HTN
SNS activity, dysregulation of RAAS, and deficency in endogenous vasodilators
genetic and lifestyle risk factors for HTN
obestity, alcholism and tobacco
secondary HTN causes in adults
hyperaldosteronism, thyroid dysfunction, OSA, Cushings, and pheochromocytoma
drugs that increase BP
secondary HTN causes for children birth to 12 years
coarction of aorta
renal parynchymal disease
secondary HTN in adolescence (12-18 years old)
coarction of aorta
secondary HTN causes of young adults
thyroid dysfunction
fibromuscular dyplasia
renal parychema
secondary causes of HTN in middle age adults (40-64)
hyperaldosteronism
cushing
pheo
OSA
thyroid dysfunction
secondary causes of HTN in older aldults >65 years
artherosclerotic renal artery stenosis
renal failure
hypothryoidism
chronic HTN leads to remodeling of
small and large arteries, endothelial dysfunction, and potentially irreversible end-organ damage
what can diagnose early vasculopathy
US of the common carotid intimal to medial thickness and arterial pulse wave velocity
cerebrovascular damage secondary to HTN
acute hypertensive encephalopathy
stroke
ICH
lacunar infarct
vascular dementia
retinopathy
heart disease secondary to HTN
LV hypertrophy
afib
coronary microangiopathy
CAD - MI
heart failure
neprhopathy secondary to HTN
albuminuria
proteinuria
chronic renal insufficency
renal failure
vasculopathy secondary to HTN
endothelial damage
remodeling
generalized atherosclerosis
arteriosclerotic stenosis
aortic aneursym
what is resistant HTN
above goal BP despite3+ antihypertensive drugs at max dose
usually increases a CCB, ACE-I or ARB, and diuretic
controlled resistant HTN
controlled BP requiring 4+ medications
refractory HTN
uncontrolled BP on 5+ drugs
psuedo-resistant HTN
intolerance to drugs can result from BP inaccuracies (white coat syndrome) and or medication noncompliance
lifestyle modifications to help manage HTN
weight loss, decrease ETOH, exercise, smoking cessation
T/F there is a continuous relationship between increased BMI and HTN
true! weight loss is an effective nonpharm intervention through direct BP reduction and syngergistic enhancement of drug efficacy
for every 1kg of weight loss what decrease in BP would there be
1 mmHg
excessive ETOH is associated with what and BP
increased HTN and resistance to antihypertensives
T/F dietary K+ and Ca++ intake are inversely related to HTN and cerebrovascualr disease
true
T/F salt restriction is not assocaited with small but consistent BP drops
false
According to ACC/AHA Guidelines
evidence supports treating which patients with BP meds if SBP > 130 mmHg
hint: theres 4
ischemic heart disease
cerebrovascular disease
CKD
artherosclerotic disease
According to ACC/AHA Guidelines
evidence supports treating which patients with nonpharm therapy if SBP > 130 mmHg or DBP>80
patients without CV or cerebrovascular disease
According to ACC/AHA Guidelines
effective antihypertensive medications for nonblack HTN patients
ACE-Is, ARBs, CCBS, thiazide diuretics
According to ACC/AHA Guidelines
in black patients with HTN without HF or CKD but including those with DM.. what is the initial therapy for HTN
CCB or thiazide diuretic
According to ACC/AHA Guidelines
antihypertensive therapy in those with CKD
ACE-Is, ARBs improve kidney outcomes
Beta blocker therapy is reserved for
patients with CAD or tachydysrhtymias
or multidrug treatment in resistant HTN
treatment for secondary HTN
surgical correction of renal stenosis, adrenal adenoma, pheochromocytoma
is renal artery repair is not possible BP management is through
ACE-Is alone or with a diuretic
when are ACE-I, ARBs, and direct renin inhibitors not recommended for renal artery stenosis
bilateral renal artery stenosis
as they accelerate renal failure
primary hyperaldosteronism is treated with
aldosterone antagonist such as spironolactone
current guidelines state the diagnosis of HTN needs
multiple elevated BP readings over time
if BP elevated
check the other arm (contralateral arm)
T/F elevated BP is a direct prompt to delay surgery asymptomatic patients without risk factors
false
elevated BP is not a direct prompt
when can a surgey be delayed due to transient HTN
extreme HTN (>180/110) or end organ injury that could be reversed with BP control
name the secondary cause based on symtpoms
flushing, sweating, palpitations
pheochromocytoma
name the secondary cause based on symtpoms
renal bruit
renal artery stenosis
name the secondary cause based on symtpoms
name the secondary cause based on symtpoms
hypokalemia
hyperaldosteronism
stopping BB or clonidine can be assocaited with
rebound effects
which BP meds are held prior to surgery
ACE-Is, ARBs
stopping CCB preop are assocaited with
increased perioperative CV events
perioperative HTN increases _____ _____ as well as what M&M event
blood loss and incidence of MI and CVA
brief moments of HypoTN with chronic HTN patients are assocaited with
AKI, myocardial injury, and death
HTN patients are hemodynamically vulnerable to induction of GA bc…
induction drugs produce HypoTN; DL and intubation elicit HTN and tachycardia
pre-induction considerations of the HTN patient
Aline
multimodal induction including a Short acting BB (esmolol)
poorly controlled HTN is often accompanied by
volume depletion; especially if the patient is on a diuretic
when might modest volume loading prior to induction be counterproductive
LVH and diastolic dysfunction patients
hypertensive crisis is categorized as either urgent or emergent based on
presence of progressive organ damage (MI/stroke/AKI)
women with PIH (pregnancy induced HTN) may show evidence of end-organ dysfunction with what DBP
encephlopathy
DBP>100
peripartum HTN recommends immediate intervention for
SBP>160
DBP > 110
1 drug for peripartum HTN
labetolol
for rapid arterial dilation _____ infusion is gold standard due to fast onset and easy titration
sodium nitroprusside
Clevidipine, a 3rd gen dihyropyridine CCB, can be used for
selective arteriolar vasodilating properities
*short Duration of Action - 1 min 1/2 life
expensive
what is nicardipine
2nd gen dihydropyridine CCB
half life 30 min
less titratable than clevidipine
primary agents for encepholapathy and ICH
clevidipine, nitroprusside, labetalol, nicardipine
primary agents for aortic dissection
clevidipine, esmolol, labetalol, nicardipine
primary agents for AKI
clevidipine, nicardipine, labetolol
primary agents for preeclampsia and eclampsia
labetolol, nicardipine
primary agents for pheochromocytoma
phentolamine, phenoxybenzamine, propanolol. labetalol
primary agents for cocaine intoxication
labetalol, dexmedetomidine, clevipine
pulmonary HTN is defined as a MPAP
> 20 mmHg
symptoms of pulmonary HTN
accenuated S2&S4 “gallop”, LE swelling
precapillary PH
PVR > 3 wood units without elevated LAP or PAWP
PAWP < 15 mmHg = normal
isolated postcapillary PH
result from incerased pulmonary venous pressure usually due to elevated LAP from LV dysfuntion
PAWP>15 mmHg with normal PVR
combined pre and postcapillary PH
chronic pulmonary venous HTN with secondary pulmonary arterial vasoconstriction and remodeling
PAWP > 15 mmHg and PVR >3.0 WU
high flow PH
occurs without elevation in PAWP or PVR and results in increased pulmonary blood flow caused by a systemic to pulmonary shunt or high cardiac output
pulmonary artery HTN requires what for a diagnosis
right heart cath
mPAP can be increased by what 4 mechanism
- elevated resistance to blood flow within arterial circulation
- increased pulmonary venous pressure from LV heart disease
- chronically increased pulmonary blood flow
- combo of these processes
with pulmonary artery HTN; what will a TEE show
enlarged RV/RA and peaked tricuspid regurgitation velocity
severity of PH through right heart cath
mild PH (mPAP = 20-30 mmHg)
moderate PH (mPAP = 31-40 mmHg)
severe PH ( mPAP > 40 mmHg)
normal pulm circulation can accomodate a ________ increase in cardiac output without a marked change in mPAP
4-fold
1 out of 8 PAH patients show improvements with which drug
CCBs
prostanoids
mimic prostacyclin to produce vasdilation while inhibiting platelet aggregation. they also have anti-inflammatory effects and may reduce proliferation of vascular smooth muscles
prostanoid examples
eprostenol (IV)
iloprost (inhaled)
treprostinil (SQ, IV, INH, PO)
peraprost (PO)
all provide improvement; eprostenol reduces mortality
endothilin receptor antagonists (ERAs)
vascular endothelial dysfunction assocaited with PAH involves an imbalance bertwen nitric oxide (dilator) and endothelin (constrictor) substances
ERAs improve hemodynamics and exercise capacity
nitric oxide/guanylate cyclase
vasodilation by guanyl cyclase and cGMP formation in smooth muscle cells
transient bc nitric oxide binds to Hgb and degraded by PDE type 5
PAH symptoms
nonspecific - fatigue, dyspnea, cough
more advanced include angina and syncope with can occur with exercise if coronary blood flow cannot meet demand due to RV hypertrophy
physical exam findings of PAH
parasternal lift, accentuated S2,S3 and or S4 gallop, JVD, peripheral edema, hepatomegaly and ascites
PAH preop consideration due to potential
venous embolism, elevations in venous and or airway pressue, hypoxic pulmonary vasoconstriction, reduction in pulmonary vascular volume, systemic inflammation
rarely, dilated pulmoanry artery may leads to
recurrent laryngeal nerve damage and hoarseness
history of PH should prompt what preop test/assessment
functional status, cardiac performance, PFTs
pts with moderate or severe PH prior to moderate-high risk surgery need a
right heart cath
perioperative complexities that can potentially serious consequences in PH patient
transient HypoTN
mechanical vent
modest hypercarbia
small bubbles inIV
trendelenburg
pneumoperitoneum
single lung ventilation
any intervention that affect RV preload, inotropy, afterload, oxygen supply/demand relationship
what vent settings can effect RV afterload
addition of PEEP
hypoventilation
hypercarbia
acidosis
atelactasis
t/f in contrast to LV, the RV is thin walled and is subject to greater wall tension for the same degree of increase in EDV - increasing RV myocardial O2 demand
true
with PAH, the elevated RV pressure leads to
increased coronary flow during diastole - making the RV more vulnerable to systemic Hypotension
worsening O2 supply/demand can potentially case MI
systemic HypoTN + RV ischemia + high afterload can result in
lethal combo of RV dilation, insufficient LV filling, reduced stroke volume, and further systemic hypotension
CO2 pneumoperitoneum has an impact on
biventricular load and pump function
-both pneumoperitnoeum, head down increase inspiratory pressure affecting RV pressures and afterload
there is an increase periop M&M in patients with PH undergoing which ortho surgery
hip and knee replacement
3 features of lung collapse
some centers transiently pressurize the chest to induce atelectasis
potential for systemic hypoxia
HPV will further increase RV afterload
what is recommended for PAH patients for single lung ventilation
inhaled pulmonary vasodilators
