Exam 3- Hypertension Flashcards
Symptoms of hypertension
NONE
Or if severe HTN=
Headache
Bounding pulse
Late physiologic changes with hypertension
Sclerosis Tortorous:twisted arteries Narrow lumen Decreased blood flow Occlusion and hemorrhage Target organ damage
Nursing diagnosis for patients with hypertension
Ineffective management of therapeutic regimen.
Knowledge deficit.
Ineffective coping
Anxiety
Imbalanced nutrition: > body requirements
Altered health maintenance
Risk for impaired tissue perfusion
General features of metabolic syndrome
Abdominal obesity Atherogenic dyslipidemia Elevated triglycerides Small LDL particles Low HDL cholesterol Raised blood pressure Insulin resistance ( glucose intolerance) Prothrombotic state Proinflammatory state
Arterial Compliance
Ability of the vessel to stretch
stretchability = compliance
Athersclerosis
Decrease in compliance leads to a decrease in pulse pressure.
Preload
Venous return from the upper body to the right atrium - Controlled By:
- Blood Volume: Diuretics, ACE Inhibitors
- Venouse Dilation: Nitrates, Antagonists, Ca block
Afterload
Work required to open the aortic valve, eject volume of loaded blood, resistance to flow in arteries. Peripheral Vascular Resistance (PFR) Affected by:
Vasoldialtors, ACE inhibit, Ca block
What is hypertension
Chronically increased BP that damages arteries and impacts blood flow to end organs.
Two types of Hypertension
Primary HTN (idiopathic): No known cause = 90-95% Secondary HTN - Definable Cause; sleep apnea, drugs, kidney disease, coarctation of the aorta, thyroid disease, shronic steroid Rx
Risk Factors of Hypertension
Genetics, ethnicity, age gender, geography
Stress, obesity, diet, smoke, alcohol, blood glucose control, phys activity
Hypertension Patho
- Stretch & chemoreceptors may become desensitized.
- Na reabsorption threshold changes; Na retention over time.
- Overproduction of Na retaining hormones
- Increased SNS effect
- increased renin
- insulin resistance and hyperinsulinemia
- Endothelial cell dysfunction
Pharmacologic Mgmt of Hypertension
- Diuretics:
- Beta Blockers:
- ACE inhibitors:
- Calcium Channel Blockers:
- ARBs Angiotensin II Antagonists
Diuretics
Act on kidneys to increase urine output.
Thiazide: Promotes renal excretion of water, Na, K, H - Hydrodiuril (hydrochlorathiazide)
Loop: Inhibits absorption of Na and Cl from ascending loop of Henle; Lasix (furosemide)
Potassium Sparing: Competes with aldosterone for receptor sites in distal renal tubes: Spironaldactone.
Beta Blockers
Block action at beta receptor sites to slow heart rate, decrease BP and decrease contractility
**Do NOT give diabetic- it masks S&S of Hypoglycemia
Lopressor (metoprolol)
Tenormin (atenolol)
ACE inhibitors
Block conversion of angiotensin I to angiotensin II. Helps blood vessels relax, helps decrease pressure on heart.
- Captopril, enalapril, fosinopril, lisinopril
- reduces periph vas resistance w/o changing CO. Leads to vasodil and helps prevent target organ damage.
- Good for diabetics: does not raise sugar AND protects kidneys.
- Side effect: Cough
Calcium Channel Blockers
Blocks entry of calcium ions into smooth muscle channels in arterials causing smooth muscle relaxation
- Decrease BP and Slows HR
- Used for cardio protective effects with angina, a-fib, diabetes. Can control irregular heartbeat.
- Cardizem (diltiazem); Procardia (nifedipine)
ARBs Angiotensin II Antagonists
Block action of Ang II from all pathways from which its formed. Inhibits constriction of vessels and increases release of H2O and Na.
- Good for Type 2 Diabetics
- Cozaar (Iosartan)
- Diovan (valsartan)
Vasodilators
2nd line therapy Relaxes arterioles, lowers peripheral vascular resistance and BP - Can increase HR, can cause Hypotension - Hydralazine (apresoline) - Minolxidil - Isordil (isosorbide)
Contractility
Forcefulness of contraction. Affected by:
B antagonists
Ca block
Heart Rate Affected by?
B antagonists
Ca channel blockers
