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Cardiovascular - TCC Internal DX
Terms in this set (35)
The amount of blood the heart pumps through the circulatory system in one minute.
Positive chronotrope: any medicine that increases heart rate.
Negative chronotrope: Any medicine that decreases heart rate
Shortness of breath
A method of studying the heart's structure and function by analyzing sound waves bounced off the heart and recorded by an electronic sensor placed on the chest. A computer processes the information to produce a one-, two- or three-dimensional moving picture that shows how the heart and heart valves are functioning.
A measurement of blood that is pumped out of a filled ventricle.
Electrocardiogram (ECG or EKG)
A test in which several electronic sensors are placed on the body to monitor electrical activity associated with the heartbeat.
Rapid, uncoordinated contractions of individual heart muscle fibers. The heart chamber involved can't contract all at once and pumps blood ineffectively, if at all.
The rapid, ineffective contractions of any heart chamber. A flutter is considered to be more coordinated than fibrillation.
General term for conditions in which the electrical impulse that activates the heart muscle cells is delayed or interrupted somewhere along its path.
An amino acid normally found in small amounts in the blood. Too much homocysteine in the blood may promote the buildup of fatty plaque in the arteries. For some people, high homocysteine levels are genetic. For others, it is because they do not get enough of certain B vitamins in their diet (B-12, B-6, and folic acid). Most people can keep their homocysteine levels in check by eating foods rich in B vitamins.
Positive inotropes: Any medicine that increases the strength of the heart's contraction. Negative inotropes: Any medicine that decreases the strength of the heart's contraction and the blood pressure in the vessels.
An uncomfortable feeling within the chest caused by an irregular heartbeat.
Pansystolic = holosystolic
murmur starts at S1 and continues to S2
Percutaneous coronary intervention (PCI)
Any of the noninvasive procedures usually performed in the cardiac catheterization laboratory. Angioplasty with stenting is an example of a percutaneous coronary intervention
Paroxysmal Nocturnal Dyspnea
attacks of severe shortness of breath and coughing that generally occur at night, often seen in patients with CHF
It is a long-term, ongoing cardiovascular cohort study on residents of the town of Framingham, Massachusetts. The study began in 1948 with 5,209 adult subjects from Framingham, and is now on its third generation of participants. Prior to it almost nothing was known about the "epidemiology of hypertensive or arteriosclerotic cardiovascular disease". Much of the now-common knowledge concerning heart disease, such as the effects of diet, exercise, and common medications such as aspirin, is based on this longitudinal study.
Known as the "Silent Killer"
Known as the "Widow Maker"
Left Coronary Artery
African-americans >Hispanics >Caucasian >Chinese
45yo +, prevalence increases w/age
Approx. 75 million Americans (29% of pop) & only 54% of them have it controlled
Hypertension 5 Pathologies
1. Sympathetic Nervous System Activation
2. Dysfunction of Renin-angiotension-aldosterone system (RAAS)
3. Endothelial dysfunction
5. Defect in Natriuresis (sodium excretion)
Sympathetic Nervous System (SNS) activation
Increased HR and peripheral resistance > HTN
Increase in insulin resistance > Endothelial dysfunction > narrowing of BV & vasospasm > HTN
Vascular remodeling > narrowing of BV & vasospasm > HTN
Dysfunction of Renin-angiotension-aldosterone system (RAAS)
Important role in regulating blood volume and systemic vascular resistance, which together influence cardiac output and arterial pressure.
Renal blood flow reduced, juxtaglomerular cells convert prorenin into renin and secrete it directly into the circulation. Plasma renin converts angiotensinogen (by the liver) to angiotensin I. Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE) found in the lungs. Angiotensin II is a potent vasoconstrictor resulting in increased blood pressure. Angiotensin II also stimulates the secretion of the hormone aldosterone from the adrenal cortex. Aldosterone causes the renal tubules to increase the reabsorption of sodium and water into the blood, while at the same time causing the excretion of potassium (to maintain electrolyte balance). This increases the volume of extracellular fluid in the body, which also increases blood pressure.
Types of Hypertension
Essential (Benign, Primary or Idiopathic) (85% of Cases) - Ace Inhibitors and Diuretics given here
Secondary - CKD (5%); Drug-induced (5%) (NSAIDs, steroids, decongestants, alcohol, MAOIs); Endocrine (<2%) thyroid disease, aldosteronism, cushings, etc; CVD, sleep apnea, etc
Malignant (only 1% of pts with HTN develop it) - extremely high bp (180/120) that develops quickly should be considered emergent because pt is probably experiencing end-organ damage encephalopathy
- Due to: existing HTN, missing anti-hypertensive dose, kidney disease, spinal cord injuries, medications, illegal drug use (cocaine)
- African-american males with low socioeconomic status are at greatest risk
Joint National Committee (JNC)-8 Classification (2014) - Most Common
• Normal: <120/<80
• Prehypertension: 120-139/80-89
• Stage 1: 140-159/90-99
• Stage 2: 160+/100+
Am College of Cardiology 2017 Guidelines
• Normal: <120/<80
• Elevated: 120-129/<80
• Stage 1: 130-139/80-89
• Stage 2: >140/>90
#1 Clinical Manifestation of Hypertension
Signs/symptoms usually result from: end-organ damage, malignant hypertension (hypertensive crisis), or 2nd causes for HTN
Clinical Manifestations of Hypertension
• Regular nosebleeds
• Headache - pulsating
• Chest pain - sharp or pulsing
• Fatigue - foggy or confused
• Blurry or distorted vision or visible blood spots on sclera
• Difficulty sleeping - sleep apnea
• Sexual dysfunction - decrease perfusion
• Dull pounding or throbbing sensation in chest, upper back, neck, head, ears
• Flushed face
• Difficulty breathing/SOB
• Funduscopic exam reveals: papilledema (optic disc swelling), retinal exudates (opacities that result from the escape of plasma and white blood cells from defective blood vessels), hemorrhages, AV nicking (a small artery (arteriole) is seen crossing a small vein (venule), which results in the compression of the vein with bulging on either side of the crossing)
• Possible JVD or carotid bruits
• Possible enlarged thyroid
• Laterally displaced PMI
• S3, S4, &/or murmurs
• Bruit over aorta or renal arteries
• Truncal obesity (cushings)
• Pedal edema (HF)
Diagnostic Studies for Hypertension
• Creatinine & BUN (Renal Function Tests to see if it is primary or secondary)
• UA (CBC) > proteinuria, microalbuminuria
• FPG or A1C
• Electrolyte panel > Sodium, Potassium, Chloride, Carbon dioxide
• Calcium levels > hyperparathyroidisim
• Glucose is secondary cause of HTN
• Aldosterone, cortisol, renin levels
• Renovascular hypertension - Doppler US
• Imaging as needed depending on lab results
*First identify the cause of HTN > Benign or secondary
*Most times order CBC, Metabolic Panel, and Glucose
BP Goal with individuals with known CVD (chronic vascular disease), CKD (chronic kidney disease)
Non-Pharmacologic Management of Hypertension
Weight loss for overweight or obese patients with a heart healthy diet
Dietary Approaches to Stop Hypertension (DASH) - Standard DASH up to 2300mg of Na/d, Low Na+ DSH < 1500mg/d, NA should be less than 1200mg/day
Potassium supplementation within the diet (need to check K+ levels first) >3500mg/d
Increased physical activity with a structured exercise program (at least 30min/d on most days of week).
Men < 2 & women < 1 standard alcohol drink(s) per day.
Stress reduction: occupation, socioeconomic, lifestyle
The usual impact of each lifestyle change is a 4-5 mm Hg decrease in SBP and 2-4 mm Hg decrease in DBP; but diet low in sodium, saturated fat, and total fat and increase in fruits, vegetables, and grains may decrease SBP by approximately 11 mm Hg.
Pharmacologic Management of Hypertension
ACE inhibitors - stop the conversion of Angiotension I into angiotension II, stopping vasoconstriction of arteries therefore decreasing BP
- DO NOT GIVE AFRICAN AMERICANS ACE INHIBITORS BECAUSE IT CAUSES SWELLING AND THROAT CLOSES UP (ANGIODEMIA (is the rapid swelling (edema) of the dermis, subcutaneous tissue, mucosa and submucosal tissues. It is very similar to urticaria, but urticaria, commonly known as hives, occurs in the upper dermis.)
Diuretics - causes increase in frequency of urination, decrease fluid in the system so decrease in BP
Beta-blocker - blocks or interferes with the action of epinephrine (decrease heart rate)
Calcium channel blocker (or calcium blocker) - A medicine that lowers blood pressure by regulating calcium-related electrical activity in the cardiovascular system
1st line: diuretics, ACEI/ARBs, or CCBs (No ACEI/ARBS with African-american)
2nd line: multiple possibilities
What group of people do you NOT give ACE Inhibitors and why?
DO NOT GIVE AFRICAN AMERICANS ACE INHIBITORS BECAUSE IT CAUSES SWELLING AND THROAT CLOSES UP (ANGIODEMIA (is the rapid swelling (edema) of the dermis, subcutaneous tissue, mucosa and submucosal tissues. It is very similar to urticaria, but urticaria, commonly known as hives, occurs in the upper dermis.)
DASH Diet Na Limits
<1500mg/day is the low Na DASH Diet
Standard DASH diet is <2300mg/day
Hypertension Diagnosis Consists of:
Prior to labeling a person with hypertension, it is important to use an average based on ≥2 readings obtained on ≥2 occasions to estimate the individual's level of BP. If BP on initial is >180/110mm Hg a dx can be made on one visit or if there are symptoms/signs of end organ damage
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