Related Circulatory Stressors/Test 2 Flashcards
Hypertension defined as
- sustained elevation of b/p
- diagnosis requires that increased readings be present on more than one occasion during several weeks
- HTN makes the heart work harder, putting both the heart and vessels under strain, and contributing to other disorders
- considered a “silent” disease
A HTN heart is _____ and has _____ ventricles
bigger and thickening
Optimal b/p is
<80
Normal b/p is
<85
High normal b/p is
130-139 and 85-89
HTN Stage I b/p is
140-159 and 90-99
HTN Stage II b/p is
160-179 and 100-109
HTN Stage III b/p is
> 180 or >110
Hypertension etiology- Primary (essential) hypertension
no identifiable cause; accounts for 90%-95% of all cases
Hypertension etiology- Secondary hypertension
a specific cause can be identified and corrected, like:
*Renal disease *sleep apnea
*Endocrine disorders *Aorta narrowing
*Brain tumors *Pregnancy-induced
*SNS stimulants
(cocaine, MAO inhibitors, oral contraceptives, NSAIDS, estrogen replacemen therapy)
Manifestations of hypertension
What are it’s early symptoms?
Second symptoms may include:
No early symptoms Second symptom: *Fatigue *decreased activity intolerance *Dizziness *palpitations *Angina *Dspnea If extremely high- HA, blurred vision, nosebleeds
Modifiable HTN risk factors
- Excessive alcohol ETOH intake
- Smoking
- Uncontrolled DM
- increased serum lipids
- Excess dietary Na+
- Obesity
- Sedentary lifestyle
- Stress
Non-modifiable risk factors HTN
- Socioeconomic status
- Family history
- Ethnicity
- Gender
- Age
Controls of Blood Pressure
- SNS- sympathetic nervous system
- RAAS- renin angiotensin aldosterone system
- CO and SVR
Order of controls of b/p
Heart+increased salt intake= High b/p
Heart-renin, angiotensinogen I,(andgiotensin converting enzyme), angiotensinogen II, = high b/p or from angiotensinogen II back to heart to aldosterone to high b/p
Treatment of HTN
- weight reduction
- DASH eating plan
- Na++ reduction
- ETOH
- Exercise
- Smoking
- Stress
Treatment of HTN 2 main actions:
- decrease circulating voluem- thiazide diuretics and loop diuretics
- Reduce SVR (stroke volume rate)- adrenergic SNS inhibitors, andiotensin inhibitors, direct vasodilators
Treatment of HTN, stepped are approach
Go low and slow
- diuretics 1st med to be used- usually thiazide
- Beta blockers
- Calcium channel blockers
If b/p goes up stay on
diuretics and change to ace inhibitors
- angiotensin II receptors antagonists
- alpha blockers, central
- alpha blockers, peripheral
- alpha, adrenergic blockers
- vasodilators
Pharmacological approach
- diuretics- thiazides-HCTZ, potassium sparing-triamterene, loops-lasix, aldosterone receptor blockers-aldactone, combination-dyazide-HCTZ/triamterene
- Beta blockers- metoprolol (lopressor) or atenolol (Tenormin)
- Calcium channel blockers- cardiazem
- ace inhibitors-zestril
- ace receptor blockers- valsartan
- non-nitrate vasodilators-hydralazine, hyperstat
- central blockers- clonidine, catapress
- combination-lisinopril+HCTZ-Zestoretic
Side effects of medications
- impotence
- syncope
- dizziness
- orthostatic hypotension (sit on side of bed)
NSG Interventions for meds
avoid standing in hot showers, rise slowly from sitting or laying. avoid long standing
Symptoms and interventions
- Synergistic effects of medications
- Symptoms of syncope, fatigue- leading to falls
- Self-checks
- Diuresis
- Lo Na diet
- Hypokalemia
- K+ replacements
Diet- teach the benefits of DASH (Dietary approaches to stop HTN)
- Low sodium foods
- Potassium rich foods
- 3 servings of fish/week
Evaluations of complications
- End organ damage
1. renal failure
2. retinal damage
3. CVA
4. MI, CHF - Hypertension crisis
1. Definition
2. Treatment
Definition of CHF
Not a disease but a group of responses r/t inadequate pump performance. Pump failure leads to hypoperfusion of tissue with pulmonary and venous congestion. The supply of oxygen will not equal demand due to pump failure
CHF Pathophysiology
- CHF may be caused by any interference with the normal mechanisms regulating cardiac output
- CO depends on: preload, afterload, myocardial contractility, and heart rate
- Any alteration in any of these can lead to decreased ventricular function and the resulting manifestations of CHF
- Remember, supply must equal demand!
What happens in CHF
Blood overflows to back into lungs. Heart overfills with blood. Limited ventricular squeezing capacity. Damaged heart muscle is weakened and stiff.
Stages of CHF
Compensation and decompensation
Compensatory Mechanisms:
- Ventricular dilation
- Ventricular hypertrophy
- increased SNS stimulation
- Neurohormonal responses
Types of CHF
- left sided failure
* right sided failure
Manifestations of CHF- Left sided
- pulmonary edema *Dyspnea
- orthopnea *PND
- Fatigue *increased HR
- Crackles (pulm edema) *S3, S4 heart sounds
- Cheyne stokes respiration increased
Manifestations of CHF- Right sided
- Dependent and peripheral edema
- JVD
- More noticeable wt. gain
- fatigue
- increased HR
- Ascites/hepatomegaly (fluid backs up into liver, abdomen, and spleen)
- Rt sided pleural effusions
CHF…you can get
JVD
Diagnostics for CHF
Brain natriuretic peptide- also called B-type natriuretic peptide. BNP is a hormone that promotes vasodilation, is produced by the ventricles and it’s release is triggered by increased pressure there ( when they’re stretched).
The BNP assay is a blood test that has a very quick turn around time. (only 15 minutes)
Brain natriuretic Peptide (BNP)
- Normal level is 0-100; above 100 indicates CHF, but levels <400 mean difficult treatment.
- Positive results can diagnose acute decompensated CHF
- Often used to differentiate dyspnea caused by CHF as compared to dyspnea caused by pulmonary disease
Other CHF diagnostics
The primary goal is diagnosis is to determine the underlying etiology of the heart failure and assess it, so treatment can begin.
- Chest xray
- 12 lead ECG
- Echocardiogram or TEE
- ABG’s
- Serum studies
- Nuclear imaging
- Cardiac catherterization
- Hemodynamic monitoring
CHF collaborative care
- Treatment of the underlying cause
- High fowlers position
- O2 by mask or nasal canula
- Telemetry and pulse oximetry
- Rest
- Diet- low Na+, maybe fluid restriction
- daily weights
- I&O’s
- Remember general rule of thumb is that for every 1000cc in excess fluid (imbalance between I&O) you can expect a weight gain of 1K (2.2 lbs)
- So 1 L = 2.2 lbs
- Drug therapy; overall goal is to increase CO
CHF drug therapy
- Diuretics: lasix, bumex, demadex
- Inotropics: digoxin, dopamine, dobutrex (ventrical more effiecient
- Vasodilators: Nipride, NTG
- Anti-anxietals: Ativan, maybe morphine
CHF Drug Therapy…goal of medication is to
reduce workload of the heart
Diuretics
reduce volume
Inotropes
Improves contractility
Vasodilators
reduce preload and oxygen demand
Anti-Anxietals
reduce oxygen demand
Name Loop Diuretics:
- furosemide (Lasix)
- torsemide (Demadex)
- bumetanide (Bumex)
Name Thiazides
- metolazone (Zaroxolyn) (30 b/f lasix sometimes) empty foley before giving lasix
- hydrochlorathiazide (HCTZ)
Name Potassium Sparing
*triamterene (Dyrenium)
Name Aldosterone Receptor Blockers
spironolactone (Aldactone)
Name Vasodilators
- nitroprusside (Nipride)
- nitrates (Nitroglycerin)(Imdur)
- nesiritide (Natrecor)
Natrecor (nesiritide) IV
- Dump a lot of fluid quickly,,,monitor b/p
- Recombinant form of BNP
- Dilates veins and arteries
- Used to dramatically unload fluid
- IV loading Bolus, then IV drip
- Isolate the line
- Used 24-48 hrs
- Monitor B/P, hold if b/p below 90 systolic
Name Ace Inhibitors
- lisinopril (Zestril)
- captopril (Capoten)
- enalapril (Vasotec)
Name ARB’s
- losartan (Cozaar)
- valsartan (Diovan)
- ibesartan (Avapro)
Name Beta-Blockers
- metoprolol (Lopressor)
- atenolol (Tenormin)
- nadolol (Corgard)
Name a & b Blockers
- carvedilol (Coreg)
* labetalol (Normodyne)
Name Positive Inotropes
- Digoxin
- Dobutamine
- Dopamine
Action of Digoxin is
digitalization
Digitalis Effects:
beta blocker slow HR
- therapeutic level 0.8-2.0 ng/ml
- s/s of toxicity
- -anorexia
- -n/v
- -decreased HR (bradycardia) dysrhythmias
- -visual disturbances (halos)
- -possible decrease in potassium
Nursing diagnosis of CHF
*decreased cardiac output
*excess fluid volume
*impaired gas exchange
*anxiety
*activity intolerance
*PC: pulmonary edema
Pt. teaching is essential
Overall goals of CHF
- determine cause and effects- echos, EF
- Improve LV function, cardiac function
- Decrease intravascular volume
- Decrease venous return
- Decrease afterload
- Improve oxygenation
- Improve perfusion
- Decrease anxiety
Outcomes of CHF
- Improved CO= HR, BP, UO
- Balanced I&O, decreased edema, no crackles, wt. stable
- Improved gas exchange
- Able to do ADL’s without dyspnea
- Feeling less fatigued, increasing activity
- Compliant with Na restricted diet
- knowledgeable about
- s/s to report
- measures for prevention
Nursing Interventions: respiratory management
- Assess breath sounds
- Trend breath sounds
- Assess cough
- Trend pulse ox
Nursing Interventions: fluid management
- I&O compare, trend
- Foley
- Daily weights, compare, trend
- Fluid restriction: 1000 ml, 1200, 1500, 2000
- low sodium diet
- oral care for dry mouth
- Skin care for edematous tissues
Nursing Interventions: nutrition
- low sodium diet
- List inappropriate foods
- K+ sparing diuretics- avoid
- K+ wasting diuretics- Eat
Nursing Interventions: circulation
- Cardiac- telemetry assess for S3 and S4
* Peripheral- TEDS, Heparin SC
Nursing Interventions: anxiety
- Rest
- Environment
- Positioning
- Room placement
- Medications- ativan, morphine
Nursing Interventions: in general
- Environment: cool with fan
- Positioning
- Relief of anxiety
- Emotional support
- Skin care
- Elimination
Patient Home teaching tips:
- Management/self monitoring
- Wt. gain of >2 lb
- shortness of breath with activity
- Increased orthopnea
- Medication usage
- ADL
- Na restricted diet
- Lifestyle
- Other chronic conditions as DM
Heart failure complication:
Pulmonary edema
- precipitating causes:
- afib
- pneumonia or any physical stressor
- volume overload
- missed medications
- MI
- Severe valve disease
Complications of CHF: Manifestations
- sudden, acute dyspnea
- Wet, moist lungs
- Wet crackles throughout
- Frothy sputum to pink tinged
- Cyanosis, restlessness
- hypoxia, O2 decreased
- Cardiac rhythm?
Complications of CHF: Immediate actions
- Position upright
- stop the cause, if possible
- give oxygen
- assess, report
Collaborative Interventions for Pulmonary Edema
Medications:
- Morphine
- Diuretics
- Vasodilators
- Digoxin
- Dopamine
