Hypertension
Normal Range: 90-100
Risk Factors
sitting or standing in one position for long periods of time
obesity
pregnancy
thrombophlebitis (a blood clot in a vein causing inflammation and pain)
What is atherosclerosis?
- most often caused by high cholesterol
- initiating factor is endothelial cell injury. Injury can be caused by smoking, elevated LDL, HTN.
Monocytes attach to endothelium, travel to tunica intima, and turn into macrophages. There they engulf lipids and turn into foam cells.
Foam cells and smooth muscle cells begin the formation of the plaque. Foam cell macrophages die, leaving deposits of necrotic debris and lipids in the vessel wall forming a "fibrous cap".
The fibrous cap formation is composed of smooth muscle cells, macrophages, leukocytes, elastin, and collagen. All of which forms the plaque.
Left Sided Heart Failure (causes, clinical manifestations)
-caused by hypertension, CAD, MI
-decreased cardiac output due to pulmonary congestion
-Clinical manifestations: fatigue, S3 heart sound, blood tinged frothy sputum, oliguria, pulmonary edema, orthopnea, paroxysmal nocturnal dyspnea
Lisinopril
"ACE inhibitor"
-prevents conversion of angiotensin 1 to angiotensin 2
-prevents vasoconstriction and sodium/water retention.
-used to treat hypertension
Risk Factors
(Modifiable & Non-Modifiable)
Non-Modifiable: Age, Gender, Family History, Genetics, Ethnicity
Modifiable: Diet, smoking, alcohol use, sedentary lifestyle, stress, contraceptives, chronic disease(CKD,DM)
Causes of Chronic Venous Insufficiency
Increased hydrostatic pressure (prolonged standing)
incompetent valves
DVT's
Decreased function of skeletal muscle pumps
Inflammatory process
Risk Factors for PAD
Hypertension
Hyperlipidemia (high cholesterol)
Diabetes
Sedentary Lifestyle
Males, post menopausal females, older adults (increased risk)
Right Sided Heart Failure (causes and clinical manifestations)
caused by left side heart failure, COPD, pulmonary fibrosis, pulmonary HTN
Congestion of peripheral tissues
Clinical Manifestations: JVD, dependent edema, ascites, hepatomegaly, fatigue and weakness, weight gain
Lasix
"Loop Diuretic" (furosemide)
used to treat HTN - inhibit sodium and chloride reabsorption from loop of Henle, increases urine flow
used to treat HF - reduces preload, and promotes excretion of fluid
Hypertension Classifications
Normal: <120/<80 (both)
Elevated: 120-129/<80 (both)
Stage 1: 130-139/80-89 (either)
Stage 2: >140/>90 (either)
Hypertension Crisis: >180/>120 (both, either)
Clinical Manifestations for CVI
Edema (worse with long periods of standing)
Stasis Ulcers (medial malleolus, lower leg, brawny discoloration)
Dull leg discomfort (worse with standing)
Weeping (fluid seeping out)
Clinical Manifestations
Intermittent Claudication (pain in calves occurring with walking)
Changes in appearance of leg (ulcers on bottoms of feet and toes, skin is shiny and thin, hair loss, cold, pulses weak or absent)
Cardiac Output
amount of blood heart pumps each minute
Factors of Stroke Volume: Preload, afterload, contractility
Factors of Cardiac Output: same as stroke volume PLUS heart rate
Hydrochlorothiazide
"Thiazide Diuretic"
prevents tubular reabsorption of sodium
promotes excretion of sodium and water
reduces blood volume
Primary vs. Secondary Hypertension
Primary: presence of hypertension without evidence of specific cause. This is the primary risk factor for cardiovascular disease.
Secondary: elevation of blood pressure due to another disease/condition. Commonly caused by kidney disease, adrenal cortical hormone disorders (Cushing's disease), contraceptives, illicit drug use, diet pills, pregnancy, hypothyroidism.
a vein where blood has pooled producing distended, tortuous, palpable vessels.
More common in women
More common in people 30+ years old
Acute Arterial Occlusion
Two main causes:
1) Embolus
2) Thrombus
Clinical Manifestations -7 P's:
1)Pistol shot
2)Pain
3)Polar
4)Paresthesia
5)Paralysis
6)Pulselessness
7)Pallor
Ejection Fraction
Percent of end diastolic volume ejected during systole.
normal range: 55%-70%
relation to heart failure: low EF indicates heart muscle is not contracting properly (indicative of systolic HF)
most common cause is a congenital or structural defect, or a genetic/inherited disorder
first symptom is respiratory distress
first systemic clinical manifestation is hepatomegaly
What is Renin Angiotensin Aldosterone System? How does it affect blood pressure?
When blood pressure is decreased kidneys release renin.
Renin converts angiotensinogen to angiotensin 1.
ACE converts angiotensin 1 to angiotensin 2.
Angiotensin 2 increase peripheral vascular resistance, which increases blood pressure. Also causes decrease in sodium excretion, which increases salt and water retention in kidneys, and increases the blood pressure.
Testing and Treatment for CVI
Testing:
Doppler
Treatment:
Compression stockings, elevation, avoid crossing legs
Testing and Treatment for PAD
Testing:
ABI (ankle brachial index): systolic blood pressure of ankle should be greater than systolic blood pressure in arm
Treatment:
Anti-Coagulants: heparin
Statins: lowers cholesterol
Smoking Cessation
Testing and Treatment for Heart Failure
Testing:
BNP - Brain Natriuretic Peptide;
Normal Range: less than 100pg/mL
Echocardiogram - gold standard test
Treatment:
Diuretics and ACE inhibitors
Nitric Oxide (function)
Causes relaxation of vascular smooth muscles - vasodilates
inhibits platelet aggregation (clot formation)
Produced by the endothelium