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nur 141 > 2.2 Cardiovascular Cardiac/Hypertension > Flashcards

2.2 Cardiovascular Cardiac/Hypertension Flashcards

1
Q

Understanding Hypertension

what is it?

A

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

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2
Q

Understanding Hypertension

what is high BP

A

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

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3
Q

Understanding Hypertension

what do the numbers measure

A

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

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4
Q

How the body controls BP

A

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

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5
Q 
Primary Hypertension (essential)
Major contributing factors: subjective & objective data
A 
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
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6
Q 
Primary Hypertension (essential)
Assessment
A

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

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7
Q

Primary HTN

A

Primary: much more common, gradual onset

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8
Q

Secondary HTN

A

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

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9
Q

Diagnostic tests for HTN

A 
Urinalysis
CBC
BUN, Creat., Creat clearance, Glomerular filtration rate (GFR)
Electrolytes (K+ for hyperaldosteronism)
Glucose & Hgb A1C (diabetes)
Lipid profile
ECG
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10
Q

Complications (Target Organ Damage)

Heart disease

A

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

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11
Q

Complications (Target Organ Damage)

Cerebrovascular disease

A

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

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12
Q

Complications (Target Organ Damage)

Peripheral Vascular Disease (PVD)

A

Peripheral Vascular Disease (PVD)

Speeds up peripheral atherosclerosis → PVD, aortic aneurysm, dissection

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13
Q

Complications (Target Organ Damage)

Nephrosclerosis

A

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

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14
Q

Collaborative Care for HTN

A

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

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15
Q

Antihypertensive medication types

A

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

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16
Q

Understanding CAD(CHD):

A

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

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17
Q 
Understanding CAD(CHD):
what causes it
A

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

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18
Q 
Understanding CAD(CHD)
NONMODIFIABLE risk
A 
NONMODIFIABLE risk factors- 
Age
Gender
Ethnicity
Family history/Genetic inheritance
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19
Q 
Understanding CAD(CHD)
MAJOR MODIFIABLE risk
A

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

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20
Q

Angina

A

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

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21
Q

Chronic stable angin

A

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

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22
Q

Silent ischemia

A

Silent ischemia: more common in DM

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

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23
Q

Prinzmetal’s angina:

A

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

24
Q

Unstable angina

A

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

25
Q

When doe angina occur?

A 
Angina occurs when oxygen demand exceeds oxygen supply to cardiac tissue.
 This can be RT (or a combination of):
 	↑WORKLOAD
	↓PERFUSION
	↓ O2 CONTENT
26
Q

Heart attack, MI: caused by

A

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

27
Q

Assessing angin

A 
Assessing angina:
P: precipitating events
Q: quality of pain
R: radiation of pain
S: severity of pain
T: timing
28
Q

Diagnostic tests CAD & angina

A

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)

29
Q

Checking the heart pump’s function:

A

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,

30
Q

Nitroglycerin

A

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
31
Q

Nitroglycerin Contraindicate

A

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

32
Q

Medications for CAD

A

Goals: ↓oxygen demand and/or ↑oxygen supply

  • Nitrates- short and long acting
  • Beta-adrenergic blockers
  • Calcium Channel Blockers
  • Angiotensin-converting Enzyme Inhibitors
33
Q

Medications for CAD

Cholesterol-lowering

A

Cholesterol-lowering therapy

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

Antiplatelet agents

34
Q

Understanding heart failure

A

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
35
Q

heart failure

Characterized by

A

Characterized by:

  • Ventricular dysfunction
  • Reduced exercise tolerance
  • Diminished quality of life
  • Shortened life expectancy
36
Q

Compensatory mechanisms

Sympathetic nervous system

A

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

37
Q

Compensatory mechanisms

Neurohormonal

A

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

38
Q

Compensatory mechanisms

Dilation

A

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

39
Q

Compensatory mechanisms

Hypertrophy

A

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

40
Q

Causes of HF

PRIMARY

A 
PRIMARY:
CAD, MI
HTN
Rheumatic heart disease
Congenital defects
Pulmonary hypertension
Cardiomyopathy
Hyperthyroidism
Valve disorders
Myocarditis
41
Q

Causes of HF

PRECIPITATING

A 
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
42
Q

Classifying Types of Heart Failure

A

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
43
Q

Acute HF

A

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

44
Q

Chronic HF
S/S
FACES

A 
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)
45
Q

Systolic vs. Diastolic failure

Systolic failure

A

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

46
Q

Systolic vs. Diastolic failure

Diastolic failure

A

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
47
Q

LEFT VS RIGHT FAILURE

LEFT

A

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)

48
Q

LEFT VS RIGHT FAILURE

RIGHT

A

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)

49
Q

S/S HF

A
  • 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)
50
Q

Diagnostic tests for HF

A 
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
51
Q

B-type Natriuretic Peptide (BNP)

A

Protective mechanism

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

52
Q

B-type Natriuretic Peptide (BNP)

Work by?

A

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
53
Q

Echocardiogram

A
  • 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)
54
Q

Medications for HF

A

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

55
Q

Patient/Family Teaching

A

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

56
Q

Decreased oxygen supply:
Noncardiac
Cardiac

A 
Noncardiac:
anemia
asthma
COPD
hypovolemia
hypoxemia
pneumonia
Cardiac:
coronary artery spasms
thrombosis
dysrhythmias
heart failure
valve disorder
57
Q

Increased oxygen demand:
Noncardiac
Cardiac

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

nur 141 (48 decks)

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