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Consequences of High BP
stroke
HF
sexual dysfunction
heart attack
vision loss
kidney disease/failure
Stages of HTN
Normal: <120 / <80
Elevated: 120-129 / <80
Stage 1: 120-139 / 80-89
Stage 2: 140 / 90
2 Main Factors in HTN
cardiac output
peripheral resistance
Determinants of BP
cardiac output (systolic)
systemic vascular resistance (diastolic)
Cardiac Output Formula
HR x SV
(heart rate times stroke volume)
Cardiac Output
total amount of blood ejected by one of the ventricles in L/min
Cardiac Output Normal Value
4 - 6 L
Stroke Volume
amount of blood ejected from one of the ventricles per beat
impacted by preload, afterload, contractility
Stroke Volume Normal Value
60 to 130 L
Preload
amount of blood in the left ventricle at the end of diastole
Afterload
resistance to ejection of blood from the ventricle
Systemic Vascular Resistance
the resistance of the systemic BP to left ventricular ejection
Contractility
force generated by the myocardium
enhancers: sympathetic activity + some meds (digoxin, dopamine or dobutamine)
depressors: hypoxemia, acidosis + certain meds (beta blockers)
Kidney BP Regulation
control of fluid volume
RAAS
BV BP Regulation
vasoconstriction
vasodilation
injury to endothelial lining
Beta 1 Receptors
in cardiac tissue, stimulate increased cardiac activity & HR
Beta 2 Receptors
in smooth vessels in muscle in blood cells, in bronchi, periphery and uterine muscle
Beta 3
in kidneys to help stimulate RAAS
Renin-Angiotensin System
Decreased pressure causes renin secretions from kidney
Liver produces angiotensinogen
Angiotensinogen to angiotensin I then angiotensin 2
Angiotensin 2 triggered aldosterone
Aldosterone causes increase NA and K reabsorption
Final cause: higher BV, sodium and water
Hypotension Response
SNS stimulation
secretion of adrenal medulla by epinephrine and norepinephrien
formation of angiotensin II and aldosterone
kidneys retain fluid
increase BP
Hypertension Response
increase in renal secretion causing fluid loss
depleted circulatory volume
decrease CO, BP and ABP
First Line B/P Controls
lifestyle changes
stress reduction
reduction of weight
exercise
decrease sodium intake
decrease alcohol intake
no smoking
Antihypertensive Meds and Prototypes
Captopril (ACE Inhibitors)
Losartan (ARBs)
Amlodipine (CCB)
Propranolol (BB)
Furosemide/Nitro (Diuretics)
Hydralazine (Direct Vasodilators)
ACE Inhibitors
works in lung
prevents ACE from conversion of angiotensin II (vasoconstrictor)
decrease BP
slight potassium increase
loss of NA and fluid
cause little change in CO and rate, decreases peripheral resistance
ACE Inhibitor Uses
hypertension
heart failure
MI
ACE Inhibitor Adverse Effects
angioedema (sudden swelling or welts under skin, common in areas of eyes, lips and swelling of tongue)
neutropenia (serious complication of captopril)
persistent irritating cough
insomnia, hyperkalemia, teachycardia
nausea, vomiting
ACE Inhibitor Contraindications
potassium-sparing direutics such as spiralactone
salt substitutes that contain potassium risk for hyperkalemia
black box: pregnancy
Angiotensin II Receptor Blockers (ARB)
ARBs are one of the recommended classes as first-line agents for controlling hypertension
blocks vasoconstricing and aldosterone secreting effects of angiotensin II at receptors
increases renal flow
decrease systemic vascular resistance
less likely to cause hyperkalemia, angioedema, cough
Angiotensin II Receptor Blockers (ARB) Uses
first line agent to control HTN
diabetic nephropathy
patients who can not take ACE inhibitor
less likely to produce dry cough
Angiotensin II Receptor Blockers (ARB) Uses
dizziness
muscle cramps
heartburn
diarrhea
decreased sensation to touch
angioedema
hyperkalemia
caution with herbs/food
black box: pregnancy
Calcium Channel Blocker
block calcium vessels
lead to vasodilation of vascular smooth muscle
decrease contraction force, oxygen consumption and HR
slow AV node conduction
Calcium Channel Blocker Uses
HTN
CAD
Angina
Calcium Channel Blocker Contraindications
hypersensitivity
Calcium Channel Blocker Adverse Reactions
edema of feet and hands
pulmonary edema
hypotension
headache
drowsiness
fatigue
dizziness
flushing
palpations
nausea
abdominal pain
Beta-Adrenergic Blockers (Beta Blockers)
inhibits SNS activity
beta 1 in heart
decrease HR (neg chrono)
decrease myo contractility (neg ino)
decrease rate of conduction (neg dromo)
alpha block adds vasodilation in meds like labetalol - (reduces renin release which decreases angiotensin II, causes vasodilation and promotes excretion of NA and water)
dilates BP
decreases vascular resistance
Beta-Adrenergic Blockers (Beta Blockers) Usage
decrease HR
decrease force of myocardial contraction
decrease CO
decrease renin
Beta-Adrenic Blockers (Beta Blockers) Contraindications
extensive hepatic first pass
first dose phenomenon
black box warning: abrupt withdrawal for CAD
Vasodilators
used in severe hypertension not responding to other medications
acts directly on smooth muscle to cause vasodilation —> decrease BP
most potent = nitroprusside
Vasodilator Use
acts on arterioles to decrease B/P
limited effect on HTN when used alone
Vasodilator Adverse Effects
sodium retention
H20 retention
Diuretics
first line for mild HTN
helps the kidneys get rid of excess water and salt
reduces blood vol —> decrease BP
categorized by where they function
combination used when more than one variety is used together
used with antihypertensive due to fluid retention
Heart Failure
complex clinical syndrome resulting in insufficient oxygen supply to tissues and organs
decreased CO —> decreased tissue perfusion
EF is amount of blood pumped out of LV
occurs when reduced EF of the LV
occurs with defect in filling
associated with CV disease
sometimes reversible
chronic, progressive
Heart Failure Risk Factors
hypertension
CAD
certain comorbities
genetic risk cardiomyopathy
Stages of Heart Failure
stage A - high risk, no symptoms
stage B - structural, no syptoms
stage C - structural, previous or current symptoms
stage D - refractory symptoms needing interventions
Classes of HF
class 1 - no limit in activity, ordinary activity doesn’t cause undue symptoms
class 2 - slightly limited, fatigue, SOB, palpitation during activity
class 3 - marked limitation, fatigue, SOB, palpation at less than norm activity
class 4 - struggle at rest, worsens with activit
Types of HF
left sided systolic (HF with reduced EF)
left sided diastolic (HF with same EF)
right sided
biventricular
Blood Flow in Heart
superior vena cava / inferior vena cava
right atrium
tricuspid valve
right ventricle
pulmonary valve
pulmonary artery
pulmonary vein
left atrium
mitral valve
left ventricle
aortic valve
Left Sided HF
most common form of HF
results from inability of LV to:
fill during diastole
empty during systole
blood backup into LA
pulmonary hydrostatic pressure causes fluid leakage —> pulmonary edema
observations:
pulmonary congestion/edema
S3/gallop
DOE
low O2
oliguria
Pulmonary Edema
can cause severe hypoxemia
monitor lung sounds for changes
frothy blood tinged sputum, restless, cyanosis, confusion, tachypnea, tachycardia
actions: O2, diuretics, vasodilators
HF with reduced EF
systolic failure
can’t pump effectively because:
low contraction
increased afterload
mechanical abnormalities
decreased LV ejection fraction (LVEF)
Ejection Fraction Percentage
amount of blood pumped out of ventricle / total amount of blood in ventricle
HF with preserved EF
diastolic HF
inability of ventricles to relax and fill during diastole
decreased SV and CO
primary cause is HTN
same end result as systolic failure
Right Sided HF
RV doesn’t pump effectively
fluid backs up in venous system
fluid moves into tissues and organs
left-sided HF is most common cause
other causes: stenosis, regurgs, valve disease, etc.
Biventricular Failure
both right and left
inability of both ventricles to pump effectively
fluid build-up
venous engorgement
decreased perfusion to vital organs
compensatory mechanisms
BNP Levels
100 - Good!
101-299 - Mild Increase
300+ - Mild HF
600+ - Moderate HF
900+ - Severe HF
Natriuretic Peptides
ANP, BNP
released in response to increased BV and ventricular wall stretch
high BNP = fluid retention
causes diuresis, vasodilation and lowered BP
Complications of Heart Failure
pleural effusion
dysrythmias and dysyncronous contraction
hepatomegaly
cardiorenal syndrome
anemia
Management of Heart Failure
vary according to severity/cause of condition
oral/IV meds
lifestyle modifictaions
supplemental O2
surgical interventions
Heart Failure Patient Education
nutrition
low sodium diet
fluid restriction
daily weights
Heart Failure Meds and Prototypes
Enalapril (ACE Inhibitors)
Digoxin (Cardiac glycosides)
Sacubitril/Valsartan (ARNi)
Metoprolol (Beta Blocker)
Furosemide (Diuretics)
Milrinone (CIA)
ACE Inhibitors
improve morbidity and mortality in HF with reduced EF
block conversion of angiotensin I to II
promotes vasodilation (lowers BP, LV afterload and aldosterone)
treats hypertension, acute + chronic HF & asymptomatic LV dysfunction
ACE Inhibitor Adverse Effects
angioedema
neutropenia
increased cough
hyperkalemia
ACE Inhibitor Contraindications
taking NSAIDS
pregnancy
allergies
ACE Inhibitor Nursing Implications
assess BP before and after
check electrolytes
Cardiac Glycosides
positive ino, neg chrono, neg dromo
(increases contract, decreases rate, decreases conduction)
increases CO, kidney function, SV
decreases preload
used to manage mild to moderate HF
used to control ventricular response in adults with AFIB
Digoxin Adverse Effects
life threatening:
AV block
cardiac dysrhythmias
PVCs
nausea
vomiting
dizziness
loss of appetite
abdominal discomfort
visual disturbances
mental changes
Digoxin Antidote
digibind
ARN Inhibitors
blocks vasoconstriction effects of RAAS
stimulates vasodilation
inhibits neprilysin and angiotensin II dependent release
used to manage chronic HF with reduced EF
Adverse Effects of ARN Inhibitors
hypotension
hyperkalemia
cough
dizziness
renal impairment
angioedema
ARN Inhibitor Contraindications
pregnancy
allergy
use with ARB/ACE
hx of angioedema
ARN Inhibitor Nursing Implications & Education
interaction with lithium, grapefruit, St. John Wart
birth control, take as directed, move slowly, stay hydrated, signs and symptoms of angioedema