2.2 Cardiovascular Cardiac/Hypertension Flashcards
Understanding Hypertension
what is it?
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 do 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
How the body controls BP
Its all about perfusion
Systemic and local effects
- Cardiac output: How much blood does the heart put out? (volume)
- SVR (systemic vascular resistance): What is the heart pushing against (peripheral resistance)
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) Major contributing factors: subjective & objective data
Age: stiffness of myocardium r/t collagen Alcohol Cigarette smoking: vasoconstrictor DM, Insulin resistance, Hyperinsulinemia Elevated serum lipids Excess dietary Na; low K, Mg, Ca Gender, family history, ethnicity Obesity Sedentary lifestyle Socioeconomic Status Stress
Primary Hypertension (essential) Assessment
Clinical S/S:
“silent killer”- asymptomatic until target organ damage occurs, HA
Secondary symptoms due to effects of HTN on vessels in organs & tissues or the ↑workload of the heart
fatigue, ↓activity tolerance, dizziness, palpitations, angina & SOB
with HTN crisis: nosebleeds, HA, dizziness,
dyspnea, anxiety
Measuring BP accurately
Primary HTN
Primary: much more common, gradual onset
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
Heart disease
Coronary artery disease (CAD)- atherosclerosis
Left ventricular hypertrophy
Heart failure & dysrhythmia
Complications (Target Organ Damage)
Cerebrovascular disease
Cerebrovascular disease
Cerebral atherosclerosis & stroke
Carotid atherosclerosis = TIA and stroke
Complications (Target Organ Damage)
Peripheral Vascular Disease (PVD)
Peripheral Vascular Disease (PVD)
Speeds up peripheral atherosclerosis → PVD, aortic aneurysm, dissection
Complications (Target Organ Damage)
Nephrosclerosis
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 medication types
2 main actions: decrease CO or reduce SVR (Systemic vascular resistance) 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?
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
coronary Artery Disease: What causes it?
Atherosclerosis: deposits lipoproteins & fibrous tissue on arterial wall; RT abnormal lipid metabolism, inflammation & endothelial injury
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) NONMODIFIABLE risk
NONMODIFIABLE risk factors- Age Gender Ethnicity Family history/Genetic inheritance
Understanding CAD(CHD) MAJOR MODIFIABLE risk
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 (high fat) 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: more common in DM
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
When doe angina occur?
Angina occurs when oxygen demand exceeds oxygen supply to cardiac tissue. This can be RT (or a combination of): ↑WORKLOAD ↓PERFUSION ↓ O2 CONTENT
Heart attack, MI: caused by
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
Assessing angin
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)
Checking the heart pump’s function:
Electrical function – EKG, Telemetry
Plumbing- cardiac catheterization, angiography, nuclear perfusion studies (MUGA scan), stress testing
Mechanical function-looking at valves & pumping function
of chambers = echocardiogram, cardiac catheterization,
Nitroglycerin
Works by dilating blood vessels & ↑oxygen supply
- How to use SL nitro: (Lemone p.1006 & 1007)
- Side Effects: HA, burning & tingling uner tongue, dizziness, N/V, Orthostatic hypotension
- Teaching: Keep Nitro in dark bottle and replace q 6 mo, repeat Q 5min, GET HELP if unrelieved pain
Nitroglycerin Contraindicate
Contraindicated: Sildenafil, tadalafil and vardenafil increase risk of serious and potentially fatal hypotension
Sildenafil- Viagra half life 3-4 hours
Tadalafil- Cialis-half life 17.5 hrs
Vardenafil- Levitra half life 4.7 hrs
Medications for CAD
Goals: ↓oxygen demand and/or ↑oxygen supply
- Nitrates- short and long acting
- Beta-adrenergic blockers
- Calcium Channel Blockers
- Angiotensin-converting Enzyme Inhibitors
Medications for CAD
Cholesterol-lowering
Cholesterol-lowering therapy
- Statins
- Fibric-acid derivatives
- Bile-acid squestrants
- Cholesterol Absorption Inhibitors
- Complementary lipid lowering agents
Antiplatelet agents
Understanding heart failure
Heart failure is a chronic, progressive clinical syndrome resulting from any structural or functional disorder that impairs the ability of the to fill with or eject blood. The heart fails to pump blood adequately to meet the body’s metabolic needs.
- Associated with HTN, CAD, MI
- High morbidity & mortality rates & frequent hospitalizations
heart failure
Characterized by
Characterized by:
- Ventricular dysfunction
- Reduced exercise tolerance
- Diminished quality of life
- Shortened life expectancy
Compensatory mechanisms
Sympathetic nervous system
Sympathetic nervous system: heart works faster & harder to ↑CO (↑HR & contractility)
Danger: vasoconstricts, ↑myocardial 02 demand, ↑venous return
Compensatory mechanisms
Neurohormonal
Neurohormonal: RAAS system, ADH, endothelin, inflammatory
Danger: vasoconstriction & Na + H20 retention = ↑blood volume, remodeling (bigger is not better for heart muscle)
Compensatory mechanisms
Dilation
Dilation: chambers enlarge RT ↑internal pressure, overstretch
Danger: elasticity of cardiac muscle is lost & contraction impaired
Compensatory mechanisms
Hypertrophy
Hypertrophy: gradual ↑heart muscle mass
Danger: contractility, O2 demands, poor circulatory supply, prone to dysrhythmias
Causes of HF
PRIMARY
PRIMARY: CAD, MI HTN Rheumatic heart disease Congenital defects Pulmonary hypertension Cardiomyopathy Hyperthyroidism Valve disorders Myocarditis
Causes of HF
PRECIPITATING
PRECIPITATING: acute (often ↑ workload) Anemia: decreased 02 capacity of blood causes increased CO to compensate Infection Hypothyroid: predisposes to CAB (coronary artery bypass) Dysrhythmias Bacterial endocarditis Pulmonary disease Nutritional deficiencies Hypervolemia
Classifying Types of Heart Failure
Acute vs chronic
Systolic vs diastolic (pumping vs filling problem)
Left ventricular vs right ventricular
***Classification/stages; (table 31-1, 31-2, p 1055)
Classification stages are based on activity tolerance, symptoms: Severity: 1: no limit 2: with strenuous 3: with mild strenuous 4: at rest
Acute HF
Pulmonary edema
-Lung alveoli filled with ISF
Interstitial edema
-RT ↑ intravascular pressure
S/S: tachypnea ≥30 RR; anxious; pale, clammy, & cold skin; dyspnea, respiratory distress; frothy blood-tinged sputum, rales/rhonchi/wheeze
Often fluid overload
Chronic HF
S/S
FACES
S/S depend on pt age & extent of underlying CV disease FACES F- fatigue A- activity limitation C- cough/chest congestion E- edema S- SOB ***See page 1060 for multisystem effects of HF (acute & chronic)
Systolic vs. Diastolic failure
Systolic failure
Systolic failure: decreased pumping function
Caused by:
-Damage to cardiac muscle: ischemia/infarct, inflammation (cardiomyopathy)
-Increased afterload (force the heart works against) eg: HTN, CAD
-abnormalities eg valve dysfunction
Ventricle doesn’t generate enough pressure to eject blood forward
Ejection fraction (EF) is decreased, S/S RT ↓output
Systolic vs. Diastolic failure
Diastolic failure
Diastolic failure: inability of ventricles to relax & fill;
- Caused by stiff ventricles →High filling pressures that cause venous engorgement in pulmonary & peripheral vessels
- S/S RT congestion behind ventricle & ↑pressure
- Dx.- pulmonary congestion, pulmonary HTN, ventricular hypertrophy with a normal EF
LEFT VS RIGHT FAILURE
LEFT
More useful concept in acute failure, chronic often both
LEFT HF
Causes: CAD, HTN
S/S
pulmonary congestion (SOB, cough, orthopnea, crackles, murmur)
↓output (fatigue, dizziness, syncope)
LEFT VS RIGHT FAILURE
RIGHT
More useful concept in acute failure, chronic often both
RIGHT HF
Causes: pulmonary disease, LHF
S/S RT venous pressure in systemic circulation= edema, ascites, JVD (jugular vein distention)
S/S HF
- Fatigue-earliest symptom due to decreased cardiac output
- Dyspnea-caused by interstitial and alveolar edema, PND (paroxysmal nocturnal dyspnea).
- Orthopnea-how many pillows for sleep?
- Tachycardia-Early sign of HF. Compensation for failing ventricular function.
- Edema- dependent, liver, ascites, lungs, grade pitting
- Nocturia-6-7 times per night (increased renal blood flow)
- Skin changes-dusky, cool and damp
- Behavioral changes-cerebral circulation impaired
- Chest pain-decreased coronary perfusion
- Weight changes-fluid retention (3 lbs in 2 days)
Diagnostic tests for HF
ABGs if acute distress B-type Natriuretic Peptide (BNP) Liver function tests Chest x-ray 12-lead EKG Nuclear imaging studies: Thallium scan Echocardiography Exercise Stress test Cardiac catheterization
B-type Natriuretic Peptide (BNP)
Protective mechanism
Released by the myocytes of the ventricles in response to excess stretch created by volume overload
B-type Natriuretic Peptide (BNP)
Work by?
Work by:
- SHIFT FLUID TO EXTRAVASCULAR COMPARTMENT BY INCREASING PERMEABILTY
- ACT ON KIDNEY = diuresis (loss of water) & natriuresis (loss of Na)
- DILATE ARTERIOLES & VEINS
- PREVENT PROLIFERATION OF MYOCYTES IN EARLY HF
- BNP levels correlate with the degree of left ventricular dysfunction
- Very useful in differentiating cardiac and respiratory causes of dyspnea
Echocardiogram
- Several types of echos (TTE 2D, 3D, duplex, stress, TEE)
- Sometimes combined with dopplers to measure flow
- All are ultrasounds – use sound waves to evaluate the structure and function of the heart (heart size, wall motion, valve abnormalities, vegetation)
Medications for HF
Diuretics – for volume excess
RAAS inhibitors – ↓workload, remodeling, Aldosterone
- ACE /ARB *
- Aldosterone antagonists –reduce remodeling/fibrosis
- Direct renin inhibitors
Vasodilators
Beta adrenergic blockers
Neprilysin inhibitors – Entresto (sacubitril/valsartan)
Positive inotropes - digoxin
Antidysrhythmics
Anticoagulants if afib
*guideline-directed medical therapy
Patient/Family Teaching
Daily weights:
-notify Dr, if gain of 2-4 lbs in 1-3 days or 3-5 lbs in a week. Symptoms of SOB, swelling and fatigue
Report S/S exacerbation;
Edema, swelling, SOB, or fatigue
Weight management
Sodium-restricted low fat diet
Activity plan
Medication Education
Decreased oxygen supply:
Noncardiac
Cardiac
Noncardiac: anemia asthma COPD hypovolemia hypoxemia pneumonia
Cardiac: coronary artery spasms thrombosis dysrhythmias heart failure valve disorder
Increased oxygen demand:
Noncardiac
Cardiac
Noncardiac: anxiety HTN hyperthermia hyperthyroid physical exertion substance abuse
Cardiac: aortic stenosis cardiomyopathy dysrhythmias tachycardia
