2.2 Cardiovascular, cardiac Flashcards
(45 cards)
Understanding Hypertension
Why the fuss?
Why the fuss?
Direct relationship with HTN and CVD
↑ risk of CAD, MI, HF (3x), CVA (4x), renal disease
Elevated SBP greater risk than DBP
Understanding Hypertension
What is “high” BP?
What is “high” BP?
Persistent SBP ≥ 140 mmHg or DBP ≥ 90 mmHg
Current use of antihypertensives
“Prehypertension” = 120 - 139 SBP or 80 – 89 DBP
2017 guidelines = 130/80
Understanding Hypertension
What the numbers measure
What the numbers measure:
BP is the force exerted by the blood on walls of vessels
SBP= max pressure on walls of the arteries while heart pumping
DBP=minimum pressure between beats while heart is filling
What is MAP
MAP= average pressure in arterial circulation, calculated value = SBP+2(DBP)/3
Isolated systolic HTN
Isolated systolic HTN
more common in older adults due to changes in BP patterns
SBP & DBP rises with age until about 55 yr old then DBP begins to decline
How the body controls BP
Cardiac output
SVR
Its all about perfusion
Systemic and local effects
Cardiac output: How much blood does the heart put out? (volume)
SVR: What is the heart pushing against? (peripheral resistance)
ST and LT mechanisms – usually multiple causes
ST and LT mechanisms – usually multiple causes
Sympathetic nervous system :
↑HR, contractility, vasoconstriction, renin release baroreceptors in carotids & aorta communicate w/ brainstem =↑↓BP maintains: normal tone, flow with postural change or exercise
Vascular endothelium: produce vasoactive substances - constrict/dilate
Renal system: controls Na+ excretion and ECF volume, RAAS
Natriuretic peptides: promotes Na and water excretion & vasodilator
Endocrine: adrenal hormones epi and nor epi same as SNS stimulation, pituitary: vasopressin (ADH) raises BP by ↑volume & constriction
ASHD – impacts vessel compliance
Primary Hypertension (essential) Without an identified cause; 90 – 95% of all cases Major contributing factors: subjective & objective data
Age Alcohol Cigarette smoking DM, Insulin resistance, Hyperinsulinemia Elevated serum lipids Excess dietary Na; low K, Mg, Ca Gender, family history, ethnicity Obesity Sedentary lifestyle Socioeconomic Status Stress
Secondary HTN
Secondary Hypertension:
-5 – 10% all cases
-Elevated BP with a specific, identifiable cause
-Suddenly develop high BP, can be severe (crisis)
-Causes: renal disease, cirrhosis, narrowing of aorta, endocrine disorders, meds, neurologic disorders, PIH, sleep apnea, medications
-Clinical findings depend on cause
Unexplained hypokalemia
Abdominal bruit
Variable BP with hx of tachycardia, sweating, & tremor
Renal diseases
Treatment aimed at the underlying cause
Diagnostic tests for HTN
Urinalysis CBC BUN, Creat., Creat clearance, Glomerular filtration rate (GFR) Electrolytes (K+ for hyperaldosteronism) Glucose & Hgb A1C (diabetes) Lipid profile ECG
Complications (Target Organ Damage)
Heart disease
Coronary artery disease (CAD)- atherosclerosis
Left ventricular hypertrophy
Heart failure & dysrhythmia
Cerebrovascular disease
Cerebral atherosclerosis & stroke
Carotid atherosclerosis = TIA and stroke
Peripheral Vascular Disease (PVD)
Speeds up peripheral atherosclerosis → PVD, aortic aneurysm, dissection
Nephrosclerosis (leading cause of ESRD)
Ischemic damage RT ↓lumen of intrarenal blood vessels = tubular atrophy, glomerular destruction, nephron death
Retinal damage
Collaborative Care for HTN
Lifestyle modification
-Reducing overall CV risk & target organ disease
-BP control
Weight reduction: improvements with moderate weight loss
Diet modification
Reduce calories
Reduce sodium (≤2300mg healthy, ≤1500mg if HTN, CKD, DM)
Maintain K and calcium intake
Reduce fat to slow progress of CAD & ↓CVD risk
DASH plan: emphasizes fruits, veggies, low fat dairy, whole grains, fish, beans, seeds, and nuts (box 32-3)
-Moderation of ETOH
-Physical activity - regular exercise
-Avoid tobacco products
-Management of psychosocial risk factors
-Goal BPs (<120/80 if CV risk) guidelines are changing
Antihypertensive medications
2 main actions: decrease CO or reduce SVR or both
Diuretics: Thiazide, loop diuretics, K+-sparing diuretics
Beta-andrenergic blockers
Centrally acting sympatholytics
Vasodilators
Angiotensin-converting enzyme (ACE) inhibitors
Angiotensin II receptors blockers (ARBs)
Calcium channel blockers
Understanding CAD(CHD) Why the fuss?
Why the fuss?
CV disease is the leading cause of death in the US
Can lead to MI & contributes to heart failure
Multiple sites of impact: cardiac, peripheral, carotid
Understanding CAD(CHD)
What causes it?
Atherosclerosis: deposits lipoproteins & fibrous tissue on arterial wall; RT abnormal lipid metabolism, inflammation & endothelial injury
http://www.webmd.com/heart-disease/video/atherosclerosis
- Progressive disease
- Advanced disease by the time its symptomatic
- ↑Calcification = ↑CAD severity
- Collateral circulation
- Framingham study: study of risk since 1949
AKA: CAD, ASHD, ischemic HD
Understanding CAD(CHD) Major contributing factors: subjective& objective data
NONMODIFIABLE risk factors-
Age
Gender
Ethnicity
Family history/Genetic inheritance
MAJOR MODIFIABLE risk factors-
-Elevated serum lipids
Cholesterol ≥200 mg/dl, triglycerides ≥150mg/dl, LDL ≥160mg/dl, or ≤HDL 40 ♂ ( 50♀)
Elevated BP: ≥ 140/90 (≥ 120/80 if DM or CKD)
-Behavioral :Tobacco use, Physical inactivity, Atherogenic diet
-Obesity: waist circumference
-DM – (HTN, obesity)endothelial effects, inflammation, ↑insulin /BS levels
-HTN – damages endothelium & increases atherosclerosis
-Metabolic syndrome
-Emerging risk factors: : ↑homocysteine levels , inflammation (CRP,
♀ risks: early menopause, BCP, HRT
Angina
Angina: clinical manifestation of cardiac ischemia RT ↑ oxygen demand and/or ↓ oxygen supply. Demand for myocardial oxygen exceeds the ability of coronary arteries to deliver it.
Commonly caused by coronary atherosclerosis that narrows arteries
Inadequate oxygen and glucose to cells in myocardium
Pain is related to anaerobic metabolism & lactic acid buildup
C/O pain, pressure, heavy, squeezing, epigastric burning, can radiate
Chronic stable angin
Chronic stable angina: intermittent, predictable pain/pressure, relieved when precipitating factor removed, med controlled
“pain” “pressure” “ache” “constrictive” “squeezing” “heavy” rarely sharp or stabbing, “epigastric burning”
Generally substernal, but can radiate to neck, jaw, shoulders, arms, shoulder blades
Pain lasts 5 to 15 min and often goes away when precipitating factor goes away
Rare rest pain
Can schedule meds due to predictable nature of pain
Early am most common
Silent ischemia
Silent ischemia: periods of ischemia that occur without sensation of pain or pressure, common in DM, equal prognosis
Prinzmetal’s angina
Prinzmetal’s angina: at rest, pain RT coronary artery spasm
Pain caused by spasm of coronary artery, not always have CAD. Can occur in pts with Raynaud’s or migraines
Unstable angina
Unstable angina: emergency, new or worse pain, pain at rest, or with minimal exertion, can indicate impending MI
new or worse, can occur in those with hx of unstable angina or can be the first clinical manifestation of CAD; rapid progression
Heart attack, MI
Heart attack, MI: caused by prolonged, irreversible ischemia caused by plaque rupture → intima exposure→ platelet aggregation → vasoconstriction & thrombus formation
Ischemia leads to cell death and necrosis = loss of contractile function
Degree of damage depends on
location and size of infarct
Heart attack, MI
Assessing angina
Assessing angina: P: precipitating events Q: quality of pain R: radiation of pain S: severity of pain T: timing
Diagnostic tests CAD & angina
Labs:
Serum lipids
Cardiac enzymes
Chest xray (CXR)
Cardiac contours, heart size, fluids around heart
Electrocardiogram (EKG)
12 lead; assess the heart’s electrical function/conduction, rhythm, local ischemia or damage, med effectiveness
Telemetry
Stress test (radionuclide testing)
Cardiac catheterization (coronary angiography)
