2.2 Cardiovascular Cardiac/Hypertension

Question 1

Understanding Hypertension

what is it?

Answer 1

Direct relationship with HTN and CVD
↑ risk of CAD, MI, HF (3x), CVA (4x), renal disease
Elevated SBP greater risk than DBP

Question 2

Understanding Hypertension

what is high BP

Answer 2

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

Question 3

Understanding Hypertension

what do the numbers measure

Answer 3

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

Question 4

How the body controls BP

Answer 4

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

Question 5

Primary Hypertension (essential)
Major contributing factors: subjective & objective data

Answer 5

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

Question 6

Primary Hypertension (essential)
Assessment

Answer 6

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

Question 7

Primary HTN

Answer 7

Primary: much more common, gradual onset

Question 8

Secondary HTN

Answer 8

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

Question 9

Diagnostic tests for HTN

Answer 9

Urinalysis
CBC
BUN, Creat., Creat clearance, Glomerular filtration rate (GFR)
Electrolytes (K+ for hyperaldosteronism)
Glucose & Hgb A1C (diabetes)
Lipid profile
ECG

Question 10

Complications (Target Organ Damage)

Heart disease

Answer 10

Heart disease
Coronary artery disease (CAD)- atherosclerosis
Left ventricular hypertrophy
Heart failure & dysrhythmia

Question 11

Complications (Target Organ Damage)

Cerebrovascular disease

Answer 11

Cerebrovascular disease
Cerebral atherosclerosis & stroke
Carotid atherosclerosis = TIA and stroke

Question 12

Complications (Target Organ Damage)

Peripheral Vascular Disease (PVD)

Answer 12

Peripheral Vascular Disease (PVD)

Speeds up peripheral atherosclerosis → PVD, aortic aneurysm, dissection

Question 13

Complications (Target Organ Damage)

Nephrosclerosis

Answer 13

Nephrosclerosis (leading cause of ESRD)
Ischemic damage RT ↓lumen of intrarenal blood vessels = tubular atrophy, glomerular destruction, nephron death
Retinal damage

Question 14

Collaborative Care for HTN

Answer 14

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

Question 15

Antihypertensive medication types

Answer 15

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

Question 16

Understanding CAD(CHD):

Answer 16

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

Question 17

Understanding CAD(CHD):
what causes it

Answer 17

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

Question 18

Understanding CAD(CHD)
NONMODIFIABLE risk

Answer 18

NONMODIFIABLE risk factors- 
Age
Gender
Ethnicity
Family history/Genetic inheritance

Question 19

Understanding CAD(CHD)
MAJOR MODIFIABLE risk

Answer 19

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

Question 20

Angina

Answer 20

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

Question 21

Chronic stable angin

Answer 21

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

Question 22

Silent ischemia

Answer 22

Silent ischemia: more common in DM

periods of ischemia that occur without sensation of pain or pressure, common in DM, equal prognosis

Question 23

Prinzmetal’s angina:

Answer 23

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

Question 24

Unstable angina

Answer 24

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

Question 25

When doe angina occur?

Answer 25

``` Angina occurs when oxygen demand exceeds oxygen supply to cardiac tissue. This can be RT (or a combination of): ↑WORKLOAD ↓PERFUSION ↓ O2 CONTENT ```

Question 26

Heart attack, MI: caused by

Answer 26

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

Question 27

Assessing angin

Answer 27

``` Assessing angina: P: precipitating events Q: quality of pain R: radiation of pain S: severity of pain T: timing ```

Question 28

Diagnostic tests CAD & angina

Answer 28

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)

Question 29

Checking the heart pump’s function:

Answer 29

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,

Question 30

Nitroglycerin

Answer 30

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

Question 31

Nitroglycerin Contraindicate

Answer 31

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

Question 32

Medications for CAD

Answer 32

Goals: ↓oxygen demand and/or ↑oxygen supply - Nitrates- short and long acting - Beta-adrenergic blockers - Calcium Channel Blockers - Angiotensin-converting Enzyme Inhibitors

Question 33

Medications for CAD | Cholesterol-lowering

Answer 33

Cholesterol-lowering therapy - Statins - Fibric-acid derivatives - Bile-acid squestrants - Cholesterol Absorption Inhibitors - Complementary lipid lowering agents Antiplatelet agents

Question 34

Understanding heart failure

Answer 34

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

Question 35

heart failure | Characterized by

Answer 35

Characterized by: - Ventricular dysfunction - Reduced exercise tolerance - Diminished quality of life - Shortened life expectancy

Question 36

Compensatory mechanisms | Sympathetic nervous system

Answer 36

Sympathetic nervous system: heart works faster & harder to ↑CO (↑HR & contractility) Danger: vasoconstricts, ↑myocardial 02 demand, ↑venous return

Question 37

Compensatory mechanisms | Neurohormonal

Answer 37

Neurohormonal: RAAS system, ADH, endothelin, inflammatory Danger: vasoconstriction & Na + H20 retention = ↑blood volume, remodeling (bigger is not better for heart muscle)

Question 38

Compensatory mechanisms | Dilation

Answer 38

Dilation: chambers enlarge RT ↑internal pressure, overstretch Danger: elasticity of cardiac muscle is lost & contraction impaired

Question 39

Compensatory mechanisms | Hypertrophy

Answer 39

Hypertrophy: gradual ↑heart muscle mass Danger: contractility, O2 demands, poor circulatory supply, prone to dysrhythmias

Question 40

Causes of HF | PRIMARY

Answer 40

``` PRIMARY: CAD, MI HTN Rheumatic heart disease Congenital defects Pulmonary hypertension Cardiomyopathy Hyperthyroidism Valve disorders Myocarditis ```

Question 41

Causes of HF | PRECIPITATING

Answer 41

``` 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 ```

Question 42

Classifying Types of Heart Failure

Answer 42

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 ```

Question 43

Acute HF

Answer 43

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

Question 44

Chronic HF S/S FACES

Answer 44

``` 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) ```

Question 45

Systolic vs. Diastolic failure | Systolic failure

Answer 45

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

Question 46

Systolic vs. Diastolic failure | Diastolic failure

Answer 46

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

Question 47

LEFT VS RIGHT FAILURE | LEFT

Answer 47

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)

Question 48

LEFT VS RIGHT FAILURE | RIGHT

Answer 48

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)

Question 49

S/S HF

Answer 49

- 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)

Question 50

Diagnostic tests for HF

Answer 50

``` 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 ```

Question 51

B-type Natriuretic Peptide (BNP)

Answer 51

Protective mechanism | Released by the myocytes of the ventricles in response to excess stretch created by volume overload

Question 52

B-type Natriuretic Peptide (BNP) | Work by?

Answer 52

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

Question 53

Echocardiogram

Answer 53

- 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)

Question 54

Medications for HF

Answer 54

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

Question 55

Patient/Family Teaching

Answer 55

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

Question 56

Decreased oxygen supply: Noncardiac Cardiac

Answer 56

``` Noncardiac: anemia asthma COPD hypovolemia hypoxemia pneumonia ``` ``` Cardiac: coronary artery spasms thrombosis dysrhythmias heart failure valve disorder ```

Question 57

Increased oxygen demand: Noncardiac Cardiac

Answer 57

``` Noncardiac: anxiety HTN hyperthermia hyperthyroid physical exertion substance abuse ``` ``` Cardiac: aortic stenosis cardiomyopathy dysrhythmias tachycardia ```