Exam 2 Flashcards
the most common type of cardiovascular disease and accounts for the majority of cardiovascular deaths.
CAD
- Begins as soft deposits of fat that harden with age
- Referred to as “hardening of arteries”
- Can occur in any artery in the body
Atherosclerosis
Atheromas
(fatty deposits)
Preference for the coronary arteries
CAD Non-modifiable risk factors
- Age
- Gender
- Ethnicity
- Family history
- Genetic predisposition
Modifiable risk factors
- Elevated serum lipids (*LDL)
- Hypertension
- Tobacco use
- Physical inactivity
- Obesity
- Diabetes
highest incidence of CAD & MI are in?
white middle aged men
Two risk factors for coronary artery disease that increase the workload of the heart and increase myocardial oxygen demand are:
A) Obesity and smokeless tobacco use.
B) Hypertension and cigarette smoking.
C) Elevated serum lipids and diabetes mellitus.
D) Physical inactivity and elevated homocysteine levels.
Answer: B
Rationale: An elevated blood pressure and cigarette smoking (causes vasoconstriction) increase the rate of atherosclerosis. Atherosclerosis increases the workload of the heart and increases myocardial oxygen demand.
Diagnostic Tests for CAD
- Cardiac catheterization
- H& P
- Chest X-ray
- ECG
- Lipid Profile
- Percutaneous Cardiac Intervention
- Angioplasty
- Stenting - must be on antiplatelet therapy for as
long as the stent is place - CT (Electronic Beam)
- Calcium and plaque deposits
- Stress Test: shows of blood flow through coronary artery
- ECG
- Echocardiogram: shows chambers an EF
Most definitive diagnostic test for CAD
- Cardiac catheterization
Patient teaching for CAD
- Health promoting behaviors
- 30 minutes of physical activity >5 days/week
- Weight training 2 days/week
- Regular physical activity contributes to
- Weight reduction
- Reduction of >10% in systolic BP
- Increase in HDL cholesterol
- smoking cessation
- stress reduction
Nutrition/Diet
- Low fat
- 30% of kcal
- most from mono/polysaturated fats
- low cholesterol
- low sodium diet
- increase complex carbs
- whole grains
- fruits/veggies
- fiber
Sources of mono-unsaturated fats
- fish oil
- Oils (canol, peanut, olive)
- Avocado
- Nuts (almonds, peanuts, pecans)
- Olives
Sources of poly-unsaturated fats
- vegetable oils
- nuts
- seeds
- margarine
Drugs that restrict lipoprotein production
Statins, niacin
Drugs that increase lipoprotein removal:
Questran (Cholestyramine)
Drugs that decrease cholesterol absorption:
Ezetimibe (Zetia)
Drugs that decrease triglycerides:
Omega-3 fatty acids
Why would a patient with CAD need antiplatelet therapy?
- decrease risk factors
- prevent clotting
Unless contraindicated, this medication is recommended for most people at risk for CAD.
low-dose aspirin
Medication of choice or patients with a stent and why?
- Clopidogrel (Plavix)
- keeps platelets “slippery” to prevent sticking to the stent
β-Adrenergic Blockers actions
- Decrease
- myocardial contractility
- HR
- CO
- BP
Calcium Channel Blocker actions
- Vasodilation
- decreases
- myocardial contractility
- blood pressure
Ace Inhibitors actions
- decreases blood pressure by causing vasodilation
- decrease risk for cardiac events (MI)
Demand for myocardial O2 exceeds the ability of the coronary arteries to supply
Myocardial Ischemia
Chest pain caused by reversible myocardial ischemia
Angina
chest pain that occurs intermittently over a long period of time with the same pattern of onset, duration, and intensity of symptoms
Chronic Stable Angina
diagnostics for Chronic Stable Angina
- H&P
- Chest Xray
- ECG
- Cardiac markers: myocardial injuries
- Lipid Panel
- Cardiac catheterization-Most Specific
- Stress Test
- Visualize blockage (diagnostic)
- Open blockages (interventional)
- Echocardiogram
Nitrate action
- vasodilation
- decreases pre & afterload
- decreases cardio O2 demand
Tx for chronic stable angin
- nitrate
- β-Adrenergic blockers
- Calcium channel blockers
- Ace Inhibitors (patients with an EF of <40%)
Nitrate A/E
- orthostatic hypo-tension
- dizziness
- HA
ischemic discomfort resulting from plaque accumulation and/or rupture leading to thrombus formation
Acute Coronary Syndrome (ACS)
Types of Acute Coronary Syndrome (ACS)
- Unstable angina (UA)
- Non-ST segment elevation myocardial infarction (NSTEMI)
- ST segment elevation myocardial infarction (STEMI)
- chest pain that is new in onset
- occurs at rest or with increasing frequency, duration, or with less effort.
- pain typically lasts 10 minutes or more.
- must be treated immediately
Unstable Angina
occurs because of abrupt stoppage of blood flow through a coronary artery from a thrombus caused by platelet aggregation.
Myocardial Infarction
Types of MI
- ST elevation (STEMI)
- Non-ST elevation (NSTEMI)
In order to limit the infarct size during a STEMI, the artery must be opened……..
- within 90 minutes of presentation.
- By:
- PCI (preffered)
- thrombolytic or fibrinolytic therapy
The acute MI process evolves over time. The earliest tissue to become ischemic is?
the subendocardium (the innermost layer of tissue in the heart muscle).
If ischemia persists during an MI, it takes approximately how long for the entire thickness of the heart muscle to become necrosed.
4 to 6 hours
an inferior wall and/or posterior wall MI results from?
Blockage of the right coronary artery
an anterior wall infarction results from?
blockages in the left anterior descending artery
LV wall MIs result from?
blockages in the left circumflex artery
Why would a younger person have a more serious first MI than an older person with the same degree of blockage?
the older person may have good COLLATERAL CIRCULATION, resulting from a long hx of CAD
MI clinical manifestations (typical)
Chest Pain that is
- Severe
- not relieved by rest, position change, or nitrate administration
- described as heaviness, pressure, tightness, burning, constriction, crushing
- located substernal or epigastric
- May radiate to neck, lower jaw, arms, back
- Often occurs in early morning
- usually lasts > 20 min
- Atypical in women, elderly
- No pain if cardiac neuropathy (diabetes)
MI clinical manifestations (atypical)
- discomfort instead of pain
- weakness
- nausea
- indigestion
- shortness of breath.
MI symptoms, some women may experience?
- Fatigue/weakness
- sleep disturbances
- SOB
- nausea
- anxiety
- dizziness
- cold sweats
MI symptoms in patients with diabetes?
- may experience silent (asymptomatic) MIs because of cardiac neuropathy
- SOB
- fatigue/weakness, -
- abdominal pain (instead of chest pain)
- n/v
- diaphoresis
MI symptoms in older patients?
- may experience a change in mental status (e.g., confusion)
- fatigue/weakness
- abd pain
- diaphoresis
- shortness of breath
- pulmonary edema
- dizziness
- dysrrhythmia
early warning signs of a heart attack?
- pressure in center of chest
- pain in shoulder, neck or arms
- chest discomfort with fainting, sweating, or nausea
diagnostic testing for an MI?
- H&P
- Characteristics of CP
- Serum cardiac markers (troponin, myoglobin)
- Released into the blood from necrotic heart muscle
- ECG
- Stress test (ONLY if cardiac markers are negative)
- Cardiac Catheterization
Initial Tx for Acute Coronary Syndrome (ACS)
- Assess ABC’s
- Position upright, -
- administer O2
- Vitals and pox
- Listen to heart and lungs
- 12 lead ECG-continuous monitoring
- Establish IV (2)
- Assess pain
- Medicate for pain (nitro, morphine)
- Sublingual NTG q 5min X 3 (hold SBP <90)
- Baseline blood work
- Chest Xray
- Assess for CI for antiplatelet, anticoagulation, or thrombolytic therapy-PCI
- Administer ASA
- Administer antidysrhythmics
Ongoing Tx: Angina wiith negative cardiac markers
- Antiplatelet/anticoag
- ASA and/or Heparin
- Coronary angiography
- PCI (percutaneous Intervention)
- angioplasty/stenting
Ongoing Tx: STEMI or NON-STEMI with positive cardiac markers
- Thrombolytic therapy
- PCI
- Surgical revascularization
- CABG
Nursing assessments post PCI
- Frequent vitals
- Evaluation of puncture site for bleeding
- Maintain bed rest
Scar tissue replaces necrotic tissue how long after MI?
6 weeks
Normal myocardium will hypertrophy and dilate in an attempt to compensate for infarcted muscle
Ventricular remodeling
MI Complications
- dysrhytmias (80% of pt)
- HF
- Cardiogenic shock
S/S of Cardiogenic shock
- Occurs when there is decreased CO
- S/S similar to HF
- Tachycardic,
- hypotensive,
- tachypneic
- crackles
- S/S of hypo-perfusion
S/S of hypo-perfusion
- Cyanosis
- pallor
- diaphoresis
- weak peripheral pulses
- cool
- clammy skin
- delayed Cap Refill
- decreased renal blood flow = decreased urine output
indications for Coronary Surgical Revascularization
- Failed medical management
- Presence of left main coronary artery or three-vessel disease
- Not a candidate for PCI (e.g., lesions are long or difficult to access)
- Failed PCI with ongoing chest pain
- Diabetes
- Long term benefits
How long do CABG pts stay in the ICU?
24-36 hrs
Risk factors for Sudden Cardiac Death
- LV hypertrophy
- myocarditis
- hypertrophic cardiomyopathy
the total blood flow through the systemic or pulmonary circulation per minute
cardiac output
amount of blood pumped out of the left ventricle =____mL
70
Pre-HTN values
- Systolic BP: 120 - 139
OR - Diastolic BP: 80 - 89
Subtypes of HTN
- Isolated systolic hypertension (ISH)
- Pseudo hypertension
Isolated systolic hypertension (ISH)
- Average SBP > 140 & DBP < 90 mm Hg
- due to loss of elasticity from atherosclerosis
- more common in older pts
Pseudo hypertension
- occurs with advanced atherosclerosis
- sclerotic arteries do not collapse when the cuff is fully inflated, cause higher cuff pressures than are actually present within the vessels.
- Suspect if arteries feel rigid, or when few retinal or cardiac signs are found relative to the pressures obtained by cuff.
Risk factors or Primary HTN
- Age
- Alcohol
- Cigarette smoking
- Diabetes mellitus
- Elevated serum lipids
- Excess dietary sodium
- Gender (more in men)
- Family history
- Obesity
- Ethnicity (more in AA men)
- Sedentary lifestyle
- Socioeconomic status
- Stress
action of nitric oxide
causes vaso-relaxation/dilation
BP is highest during which part of the day?
early morning
How long should pts be seat prior to a BP reading?
5 min
Hypertension Diagnostic Studies
- Urinalysis
- creatinine clearance
- Serum electrolytes -
- glucose
- BUN
- serum creatinine
- Serum lipid profile
- ECG
- Echocardiogram
Hypertension Complications
- speeds up atherosclorosis development
- Coronary artery disease
- LV hypertrophy
- HF
- Peripheral Artery Disease
- aortic aneurysm
- aortic dissection
- Cerebro Vascular Disease (stroke risk x4 higher)
- Nephrosclorosis
- ESRD (leading cause)
- Retinal damage
- blurred vision
- hemorrhage
- loss of vision
Lifestyle modifications needed for patients with HTN?
- Weight reduction
- DASH eating plan
- Dietary sodium reduction: Normal is <2300 mg of sodium/day
- AA, DB, CKD <1500mg of sodium/day
- Physical activity
- Moderation of alcohol consumption:
- Men: 2 drinks/day
- Women: < 1 drink/day
AVG sodium intake should be?
< 2300 mg/day
Effects of weight loss on HTN?
- Weight loss of 10 kg (22 lb) may decrease SBP by approx. 5-20 mm Hg
DASH diet?
- Dietary Approaches to Stop HTN
- emphasizes:
- fruits/veggies
- fat free or low fat dairy
- whole grains
- fish/poultry
- beans, nuts, seeds
Physical activity recommendations for pts with HTN?
- Regular physical (aerobic) activity, at least 30 minutes, most days of the week
- Vigorous aerobic activity at least 20 minutes x3 days/week
- Muscle strengthening x2 days/week
- Flexibility and balance exercises x2 days/week
Physchosocial Risk Factors for HTN?
- Socioeconomic status
- social isolation
- lack of support
- stress at work and family life
- depression
Smoking cessation reduces risk factors for HTN within?
1 yr
Metoprolol mechanism of action, class and generic name?
- Selective B1-Adrenergic inhibitor
- Anti HTN/anginal
- Loressor
Metoprolol therapeutic affects?
- slows hr
- decrease CO
- decreases BP
Clonidine mechanism of actions and class?
- adrenergic antagonist
- antihypertensive
Clonidine therapeutic affects?
- vasodilation
- decreases BP
- decrease HR
- produces analgesia in epidural
Furosemide mechanism of action, class and generic name?
- increases excretion of Na, Cl, K at the ascending loop of henle
- Diuretics
- Lasix
Furosemide uses?
- edema associate with HF and renal/liver disease
- acute pulmonary edema
- HTN
Lisinopril mechanism of action and class?
- prevents conversion of angiotensin I into angiotensin II (dilation)
- ACE Inhibitor/anti HTN
Valsartan mechanism of action & class?
- Angiotensin II Receptor Blocker (ARB)
- Anti HTN
Valsartan Therepeutic affects?
- vasodilation
- decrease peripheral resistance
- decrease BP
Amlodipine mechanism of action & class?
- inhibits movement of calcium across cardiac and smooth muscle cell membranes
- Anti anginal/HTN
Amlodipine therapeutic affects?
- vasodilation of the coronary arteries and peripheral arteries/arterioles
- decreases BP by reducing peripheral resistance
Most common AEs with cardiac meds?
- Orthostatic hypotension
- Sexual dysfunction
- Dry mouth
- Frequent urination
- Electrolyte imbalance (K, Mg)
- Some side effects may decrease over time
ausculatory gap
- a wide gap between the first Korotkoff sound and subsequent beats.
- caused by under inflation of the BP cuff, use 2 step method
How to assess for orthostatic hypotension?
- BP and HR supine, sitting, and standing
- Measure within 1 to 2 minutes of position change
- Positive if:
- ↓ of 20 mm Hg or more in SBP
- ↓10 mm Hg or more in DBP,
- ↑ 20 beats/minute or more in heart rate
Contributing factors to secondary HTN?
- Coarctation of aorta (narrowing)
- Renal disease (artery stenosis)
- Endocrine disorders
- Neurologic disorders (brain tumors)
- Cirrhosis
- Sleep apnea
- Cocaine
Tx of secondary HTN?
tx is aimed at the cause
2 types of hypertensive crisis?
- Hypertensive emergency
- Hypertensive urgency
Hypertensive emergency
- develops over hrs to days
- Severe increase in BP (>220/140mm Hg)
- Evidence of acute organ damage
- Usually hospitalized
- secondary HTN is a contributing cause
Hypertensive urgency
- develops over days to weeks
- Severely elevated BP
- NO evidence of organ damage
- May NOT require hospitalization
hypertensive encephalopathy
- a syndrome in which a sudden rise in BP is associated with:
- severe headache,
- N/V
- seizures
- confusion
- coma.
A hypertensive emergency is often manifested as?
hypertensive encephalopathy
Evidence of acute organ damage in pts in hypertensive emergency?
- Hypertensive encephalopathy cerebral hemorrhage - Acute renal failure - Myocardial infarction - Heart failure with pulmonary edema
S/S of Hypertensive Encephalopathy?
- Severe headache
- N/V
- Seizures
- confusion
- Coma
- Renal failure
- MI
- Pulmonary edema
Nursing Interventions for Hypertensive Emergency
- Requires Hospitalization
- IV drug therapy: Titrated to decrease no more than 25% of the MAP in first hour
- If stable, the goal is 160/100 to 110 mm Hg over the next 2 to 6 hours.
- Monitor cardiac and renal function
- Neurologic checks
- Determine cause
- Education to avoid future crises
Nursing Interventions for Hypertensive Urgency?
- May or may not require hospitalization
- Managed with oral medications
- Requires frequent follow up until BP is controlled
Normal Mean Arterial Pressure (MAP) range?
- 70-110
- need > 60 for normal cardiac function
