• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/46

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

46 Cards in this Set

  • Front
  • Back
Perfusion
Adequate blood flow to organs
Adequately functioning cardiovascular system
Mean Arterial Pressure (MAP)
Average Pressure throughout the cardiac cycle
Diastole is longer than systole
Need a MAP of 90 to perfuse vital organs
MAP=DBP + 1/3 pulse pressure
Pulse Pressure
Difference between SBP & DBP
Increased pulse pressure - exercise or people with atherosclerosis of larger arteries (increased SBP)
Decreased pulse pressure - cardiac failure or hypovolemia (decreased SBP)
Perfusion Disorders
Impediment to blood flow
Lack of adequate O2 and nutrients
Heart, blood vessels (CV disease)
Hypertension
Peripheral Vascular Disease
Aneurysm
Anemia, Leukemia, Lymphoma
Cardiovascular Disease
Most common cause of death in older adults in North America
Most common is CAD secondary to atherosclerosis
Difficult to separate normal aging changes from pathophysiologic changes of atherosclerosis
Some of normal changes of aging promote atherosclerosis, HTN, and cardiac failure
Age Related Changes in CV System
Heart-increased collagen/scarring, decreased elastin
Calcification/sclerosis/fibrosis of valves and conduction system
Blood vessels-arterial stiffening secondary to decreased elastin in walls, thickening of intima, and fibrosis of media
Table 31-12
PERFUSION DISORDERS: Assessment
CVD risk factors (HTN & CVA)
Physical Assessment
Vital Signs
Palpation
Inspection
Auscultation
Physical Assessment
Vital Signs-B/P, HR, RR, Sats, EKG
Palpation-pulses, temperature of extremities, liver enlargement, displaced PMI (point of maximal intensity)
Inspection-dyspnea, edema, distended neck veins(sign of right-sided heart failure), cyanosis, color changes to extremities, stasis ulcers, cap refill, varicose veins
Auscultation-lung, heart, arterial bruit(turbulent blood flow)
Alteration in Perfusion: Hypertension
Definition-B/P
The force exerted by the blood against the walls of the blood vessel
Must be adequate to maintain tissue perfusion during activity and rest
A function of cardiac output and systemic vascular resistance
Arterial BP=CO x SVR
Normal regulation of BP
Sympathetic Nervous System
-Increases BP by increasing CO and SVR (alpha and B-adrenergic receptors)
-Baroreceptors - aortic arch and carotid sinus- sensitive to stretch and pressure-info to vasomotor centers in the brain to stimulate sympathetic or parasympathetic
Chemoreceptors - aortic arch and carotid body - initiate changes in HR and arterial pressure in response to decreased PaO2, increased PCO2, and decreased arterial pH, also stimulates vasomotor center to increase cardiac activity
Release of epinephrine and norepinephrine stimulate alpha and beta adrenergic receptors (increase heart rate and vasoconstriction)
Normal regulation of BP
Vascular Endothelium
-has ability to produce vasoactive substances and growth factor (vasodilatory effects & inhibit platelet aggregation)
Alpha-adrenergic receptors in vascular smooth muscle-Increased stimulation leads to vasoconstriction, Decreased stimulation leads to vasodilation
Normal regulation of BP
Endocrine System
-Stim of SNS = release of epi & norepi by the Adrenal Medulla
Release of aldosterone by adrenal cortex (kidneys retain NA and water - B/P increases)
ADH released from posterior pituitary in response to increased sodium osmolarity level - reabsorption of H2O in distal renal tubules
Normal Regulation of BP - Renal System
*Fluid volume & NA regulation
Renin-angiotensin system-renin is secreted by juxtaglomerular apparatus in the kidney
Renin converts angiotensinogen to angiotensin I
Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II
Angiotensin II is a potent vasoconstrictor (increases B/P)
Angiotensin II stimulates the adrenal cortex to secrete aldosterone, which leads to NA and water retention by the kidneys (increasing B/P)
**ACE inhibitors block enzyme which in turn lowers B/P**
Hypertension (HTN)
Sustained elevation of BP
-Elevated readings on at least three occasions during several weeks
-Exists when:
SBP is equal to or greater than 140 mm Hg
DBP is equal to or greater than 90 mm Hg
Classifications of Blood Pressure: Normal
Systolic <120
Diastolic <80
Classifications of Blood Pressure: Pre HTN
Systolic 120-139
Diastolic 80-89
Classifications of Blood Pressure: Stage 1 HTN
Systolic 140-159
Diastolic 90-99
Classifications of Blood Pressure: Stage 2 HTN
Systolic greater than or = 160
Diastolic greater than or = 100
Classification of HTN
Primary HTN
Onset between 30-50 years old
Accounts for 95% of all HTN
Contributing factors:
*Increased SNS activity
*Increased Na retaining hormones and vasoconstrictors
*Increased Na intake
*Weight gain
*DM
*ETOH use
Classification of HTN
Secondary HTN
-Elevated B/P due to a specific cause that can be detected and treated
-Accounts for less than 5% of all HTN
-Contributing factors:
*congenital
*renal disease
*endocrine disorders
*neurologic disorders
*sleep apnea
*medications/drugs
*pregnancy
Risk Factors: Primary HTN
Age
Sex
Race
Family History
Obesity
Cigarette smoking
Increased homocysteine (homecysteine damages endothelium of vessels)
Increased C-reactive Protein
Excessive dietary Na
Elevated serum lipids
ETOH
Sedentary lifestyle
DM
Socioeconomic status
Stress
Pathophysiology
In order for HTN to occur there must be an increase in CO or SVR
Hemodynamic hallmark is a persistent increased SVR
Incidence
More than 50% of US over 60 years old have HTN
Most common cardiovascular disorder in the US
More common among men up to age 55
More common among women after age 55
Highest in African-American population
Primary Prevention: Lifestyle modifications
Activity
ETOH
Smoking
Stress reduction
Primary Prevention: Dietary modifications
Sodium and fat intake
Weight loss
Higher intake of potassium and calcium & magnesium
Clinical Manifestations: Primary symptoms
-Asymptomatic
-"Silent Killer"
Clinical Manifestations: Secondary symptoms
-Fatigue
-Reduced activity tolerance
-Dizziness
-Palpitations
-Angina
-Dyspnea
-H/A
Complications/Target Organ Disease
Heart can no longer pump enough blood to meet the metabolic demands of the body
Complications/Target Organ Disease
Hypertensive Heart Disease
-CAD
-LVH
-Heart Failure
Cerebrovascular Disease
Peripheral Vascular Disease
Nephrosclerois
Retinal Damage (Look at changes in vessels in retina and determine HTN)
Manifestations on Major Organs
Cardiac
-Aneurysm, hemorrhage, CHF, MI
Cerebrovascular
-TIA, CVA
Peripheral Vascular
-PVD
Renal
-Renal Failure
Retinopathy
-Blindness, Retinal Hemorrhage, Blurred Vision
Diagnosis
History and Physical
Blood Pressure
CXR
EKG
UA
Complete Blood Work-Up
Management
Lifestyle modifications
DASH diet
Drug theraphy
Goal-reduce overall cardiovascular risk factors and control BP by the least intrusive means
Lifestyle Modifications
Weight reduction
Increase physical activity
Limit ETOH, sodium, and fat intake (DASH diet)
Maintain adequate potassium, calcium and magnesium intake
Smoking cessation/chewing
Stress reduction
DASH diet (Dietary Approaches to Stop Hypertension)
Lower saturated fat, total fat, and cholesterol and increase fruits and vegetables
Includes 4-5 servings per week of nuts, seeds, and beans
Several servings of fish each week
Increase water intake
Restrict Na in diet to <6 grams/day
**Read food labels, OTC drugs, baking soda toothpaste
Drug Therapy: Goals
B/P of <131/85 in young adult with mild HTN
<130/80 if client has DM, CV disease, renal disease
Older adults <140/90
Two Main Actions to lower B/P
1. Decrease SVR
2. Decrease volume of circulating blood
Drug Therapy
Diuretics
Adrenergic Blockers (sympathetic)
Vasodilators
Angiotensin Inhibitors (ACE, ARBS)
Calcium Channel Blockers
Drug Therapy
Initial therapy - Usually diuretics (thiazide) or beta blockers (Stage I)
ACE inhibitors, ARBS, and CA Channel Blockers may be used as 1st line drugs
Direct acting vasodilators, x-adrenergic blockers, & peripheral acting adrenergic blockers are not recommended for single drug therapy secondary to side effects
Drug Therapy
Initial monotherapy (Stage I)
If B/P is not controlled in a few months
1. The first drug can be increased
2. The first drug can be substituted with a different drug from a different class.
3. A second drug from a different class can be added to the first drug.
*Stage 2 - initial therapy - thiazide plus a beta blocker or ACE, ARB, or CCB
Diuretics
Thiazide Diuretics - promote Na and H20 excretion
Loop Diuretics - reduce plasma volume
Potassium-Sparing Diuretics - reduces vascular response to catecholamines
Thiazide Diuretics
Diuril
Hydrochlorothiazide (HCTZ)
Side Effects - decreased K+, dizziness, decreased B/P, increased blood sugar, hyperuricemia, vertigo, impotence
Loop Diuretics
Bumex
Lasix
Side Effects - decreased potassium, increased BS, dizziness, decreased B/P, ototoxicity (IV Push too fast)
Loop diuretics can be given to patients with renal disease
K+ Sparing Diuretics
Aldactone
**NSAIDS** - can decrease the diuretic and B/P effect of ALL diuretics
Side Effects - hyperkalemia, headache, leg cramps, dizziness
*AVOID with renal disease
Adrenergic Blockers
Beta Blockers
Alpha(x) Adrenergic Blockers
Central Acting
Adrenergic Neuron blockers
Suppresses the influence of the SNS on the heart, blood vessels and other structures
Produces vasodilation
Reduces SVR
Decreases HR
Beta Adrenergic Blockers
Lopressor, Inderal, Atenolol
Action: blocks beta adrenergic effect - leads to decreased CO (decreased HR) and decreased renin release from the kidneys (vasodilation)
Side Effects: bronchospasm, depression, weakness, heart block, bradycardia
*Lopressor is B1 selective & is the drug of choice with a client with asthma
Alpha Adrenergic Blockers
Cardura, Minipress, Hytrin
Action: blocks alpha adrenergic effect on vessels, leads to peripheral vasodilation and decreased SVR
Side Effects: postural hypotension, Na/H20 retention, reflex tachycardia
Alpha/Beta Blockers
Carvedilol, Labetalol
Action: blocks alpha effect which leads to dilation of arterioles, blocks beta effect which leads to decreased heart rate and contractility
Side Effects: Bradycardia, heart block, exacerbation of asthma & postural hypotension