8.1 Cardiovascular Part 1 Flashcards
Atherosclerosis
- The major cause of cardiovascular disease
Lipids
- Organic fat, oils, hormones, and elements of certain membranes
- Does not interact significantly with water
- High levels of lipids is strongly related to atherosclerosis
Triglycerides
- Fat in adipose tissue
- Serves as energy storage and provides thermal regulation
- Used as energy during metabolism
Phospholipids
- They make up biological membranes
- They are part of lipoproteins, blood clotting components, myelin sheath, and cell membranes.
Cholesterol
- Synthesized in body and taken in via diet
- The steroid nucleus of cholesterol is made up of fatty acids
- Hypercholesteremia correlates with atherosclerosis and increases risk of MI and CVA (strokes)
Lipoproteins
- Fat carrying proteins that carry plasma transport and encapsulate cholesterol and triglycerides
- Categorized by density
TYPES OF LIPOPROTEINS
Chylomicrons (Least dense)
- Made in the small intestines wall
- Transport dietary triglycerides and cholesterol that have been absorbed in the GI tract to muscle and fat cells.
Very Low-Density Lipoproteins (VLDL)
- Synthesized in liver
- Primary pathway of transport for endogenous triglycerides to muscle and fat cells produced in the liver.
Intermediate Density Lipoproteins (IDL)
- Formed when triglycerides are removed from VLDL
- In the liver they are converted back to VLDL
- In the vascular compartment they are converted to LDL
Low Density Lipoproteins (LDL)
- “Bad cholesterol”
- It is the main carrier of cholesterol
- The main target when patients are treated for cholesterol
High-Density Lipoproteins (HDL)
- Made in the liver
- Transports cholesterol from the tissue back to the liver
- “Good cholesterol”
Hyperlipidemia/Hypercholesterolemia/Hyperlipoproteinemia
- Increased lipids in the blood
- Caused by increase in lipoprotein
- Causes include nutrition, genetics, metabolic disease
Primary Hyperlipidemia
- Genetic/Familial
- Extremely high LDL levels
- Xanthomas - Skin lesions containing cholesterol and fat
- Significant risk of MI before age 40
Secondary Hyperlipedemia
- Associated with underlying health problems such as obesity, DM, hypothyroidism.
LDL Lab Values
Ideal - <100 Good - 100-120 Borderline - 130-159 High - 160-189 Very High - 190+
HDL Lab values
Low risk - >60 Men (average risk) - 40-50 Women (average risk) - 50-59 Men (increased risk) - <40 Women (increased risk) - <50
Triglyceride Values
Best - <150
Borderline - 150-199
High - 200-499
Very High - >500
Statistics
- Total cholesterol greater than 240 doubles risk of HD
- Low HDL is a risk for HD
- LDL goal is less than 160 if there is no history of DM or CHD (Coronary Heart Disease)
- With 2 or more risk factors LDL goal is 130
- With CHD or DM - Goal is less than 100
- High triglycerides can speed up atherosclerosis which increases risk of MI and CVA
Atherosclerosis
- Presence of intra-arterial fibrofatty lesions in a vessel wall that hardens over time
- Leading cause of coronary artery disease and cardiovascular disease
- 1% increase in cholesterol leads to 3% increase risk for atherosclerosis
- Clinical manifestations can take 20-40 years to appear
Modifiable Risk Factors (CAD and Atherosclerosis)
- Nicotine and Diet
- Hypercholesterolemia
- Hypertension
- Diabetes
- Obesity
- Stress
- Sedentary lifestyle
- C-Reactive Protein (marker of inflammation for atherosclerosis lesions)
- Hyperhomocysteinemia - Protein breaks down into homocysteine. Causes enhanced blood clotting and thrombus formation. Can be managed by assessing nutrition, smoking, alcohol, DM
Nonmodifiable Risk Factors
- Age, Male, Family history of CAD
- Postmenopausal women
- Family pre-disposition
- Genetic disorders of lipid metabolism
Pathophysiology
- Inflammation plays a major role in everything to do with atherogenesis
STEPS OF LESION DEVELOPMENT - Injury to endothelial cells
- Migration of inflammatory cells
- Accumulation of smooth muscle cell proliferation
- Development of plaque with lipid core
Atherosclerosis Patho
- Lipid plaque form in arteries (arteriosclerosis)
- Lipid plaque causes arteries to narrow and harden
- Affects the coronary arteries that supply oxygen and nutrients to the heart. Blockage can cause MI
STEPS - Endothelial calls of arteries get damaged (HTN, Smoking, Hyperglycemia, Hypercholesterolemia)
- Damage increases permeability of walls allowing LDL to enter
- Monocytes also get stuck due to adhesion molecules released by damaged endothelial cells
- Monocyte (WBC) produces free radicals which oxidize with the LDL that is stuck inside the artery. Once WBC consume these oxidized LDL, more WBC comes and LDLs come in a continued cycle.
- Accumulation of cells and lipids form a plaque. The endothelial cells cover the plaque which can block the artery (atherosclerosis)
Damaged Endothelium
- Injured endothelial cells become inflamed which causes macrophages to bind and release oxygen radicals that further injure the vessel wall
Foam Cells
- Macrophages that have absorbed LDL’s that have penetrated the lining of the vessel.
Fatty Streak
- This is when foam cells produce more vessel damage
Fibrous plaque (basic lesion)
- Smooth muscle proliferate and rebuild over the fatty streak covering it in collagen.
- This causes necrosis in underlying tissue and narrowing of vessel lumen.
- ## This is what causes atherosclerosis
Complicated Lesion
- Fibrous plaque that ulcerates causing platelets to adhere and initiate the coagulation cascade. This can cause total occlusion, ischemia, and infarction
Clinical Manifestations Artherosclerosis
- Does not cause symptoms until 60%+ occlusion occurs
- Effects of narrowing of vessels produces ischemia, vessel obstruction, thrombus formation, emboli, aneurysms over weakened artery walls.
Major Organs Affected by Decreased Perfusion
- Heart Vessels (myocardial ischemia and MI)
- Brain Vessels (CVA/Stroke and TIA)
- Kidney Vessels (Ischemia/Nephritis/Renal Failure)
- Lower Extremities (Peripheral Arterial Disease - PAD)
- Small Intestines (Ischemia and Infarction)
Coronary Atherosclerosis and Coronary Artery Disease (CAD)
- Narrowing of coronary arteries reduces blood flow to myocardium
- ## Leading cause of death in US (CVD)
Coronary Artery Atherosclerotic Plaque Disruption
- Disruption of plaque leads in coronary arteries leads to MI and Sudden Cardiac Death
Coronary Arteries - RCA - Right Coronary Artery
- LAD - Left Anterior Descending
- Left Circumflex
- Left artery feeds the LAD and the circumflex
- Disruption of LCA is called “widow maker”
Risk of CAD
- Same as atherosclerosis
- Elevated LDL is primary target for cholesterol lowering medications
Metabolic Syndrome
Having 3+ of the following below
- Waist size 40+ (men) 35+ (women)
- BP over 130/85
- Fasting Triglycerides (TG) over 150 mg/dL
- Fasting HDL Cholesterol less than 40 mg/dL (men) 50 mg/dL (women)
- Fasting glucose over 100 mg/dL
Clinical Manifestations of CAD
- Symptoms caused by myocardial ischemia
- Related to the location of the obstruction
- Angina pectoris (chest pain due to ischemia) is the most common manifestation
- Epigastric distress
- Pain that radiates to jaw or left arm
- SOB
- MI, Heart Failure, Sudden Cardiac Death
Prevention of CAD
- Control High Cholesterol
- Diet
- Physical Activity
- Medications
- Smoking Cessation
- Manage Hypertension
- Control Diabetes
HMG-CoA Reductase Inhibitors (Statins)
- Atorvastatin (Lipitor)
- Simvastatin (Zocor)
- Fluvastatin (Lescol)
- Pravastatin (Pravachol)
- Lovastatin (Mevacor)
- Rosuvastatin (Crestor)
- Lovastatin (Prototype)
Statin Pharmacodynamics
- Inhibits HMG-CoA Reductase which helps synthesize cholesterol
- Lowers LDL, Raises HDL, Lowers Triglycerides
- They also promote plaque stability, improve abnormal endothelial function, decrease inflammation at plaque sites, enhance dilation in blood vessels (decreasing risk of thrombosis), slows calcification of coronary arteries, decreases risk of A-Fib
Statins Contraindications/Side Effects
Contraindications
- Active liver disease
- Drugs that inhibit CYP3A4 Hepatic Pathways
- Category X
Side Effects
- Myopathy (disorder that effects voluntary muscle movement)
- Hepatotoxicity (Liver function test every 6 months)
- GI disturbances
- Muscle/Joint aches
- Weakness/Tingling in Hands and Feet/Difficulty walking
Statins How to Administer
- Most effective when administered at night
- Immediate release taken after food
- Extended release before bed
- Monitor AST and ALT before therapy and 6 months after (liver function)
- Very important to monitor muscle pain for CK (creatine kinase)
- Lipid profiles should be monitored every 6 months to measure effectiveness
- Liver Function and CK periodically during therapy
- Eye exams annually
Fibric Acid Derivatives (Fibrates)
- Gemifibrozil (Lopid), Fenofibrate (Lipidil, Tricor)
- Treats high triglyceride levels
Contraindications - Do not use in patients with kidney/liver disease, biliary cirrhosis, gallstones
- Use with caution in patients with peptic ulcers, and pregnancy (Category C)
Adverse Effects - GI Upset, nausea, diarrhea
- Headache, fatigue
- Cholelithiasis/Liver damage/Myopathy
Interactions - Increases anticoagulation of Warfarin
- Increases myopathy in statins
Cholesterol Absorbing Inhibitor
- Ezetimibe (Zetia)
- Inhibits absorption of dietary cholesterol causing it to be secreted into bile
- Used in adjunction with dietary modifications for hypercholesterolemia
ADVERSE EFFECTS - Myopathy (Effects muscles that control voluntary movement)
- Rhabdomyolysis (damaged muscle releases damaged protein into blood damaging heart and kidneys)
- Hepatitis, Pancreatitis, Thrombocytopenia
CONTRAINDICATIONS - Liver damage or Pregnancy (Category C)
INTERACTIONS - Increased risk of myopathy and liver damage with Statins
- Fibrates increases risk of gallstones and myopathy
- Cyclosporine increases level of Ezetimibe (used to lower cholesterol)
- Bile-Acid Sequestrants decreases absorption of Ezetimibe (administer 2-4 hours after)
Nicotinic Acid (Niaspan, Niacor)
- Lowers LDL and TG (triglycerides) and raises HDL
- Drug of choice for lowering TG in patients at risk for pancreatitis
- Causes adverse effects in all patients so use is limited
- Causes flushing of face which can be counteracted by providing aspirin 30 min prior
- Can cause liver injury, especially with sustained release
Bile Acid Sequestrants
- Colestipol, Cholestyramine, Colesevelam
- Increases secretion of LDL and prevents reabsorption
- Contraindicated in patients with bile obstruction
- Can cause bloating, pruritis, prolonged prothrombin time
- Decreases absorption of fat soluble vitamins (A,D,E,K)
- MONITOR SERUM LIPID LEVELS
- Colesevelam has less adverse effects
Other Medications
Lovaza - Medically pure fish oil that can lower high levels of triglycerides
Fish Oil - Can help with CVD, Cancer, Asthma, RA
Phytosterols - Similar in structure to cholesterol so it competes for absorption with cholesterol. Results in cholesterol not being absorbed as much
Estrogen - Raises HDL and keeps LDL in check
Cholestin - Chinese remedy of red yeast rice. Inhibits cholesterol synthesis and secretion in hepatic cells.
Coronary Heart Disease (CHD) and Coronary Artery Disease (CAD)
- Heart muscles are deprived of oxygen and nutrients which causes heart pumping impairment
Chronic Ischemia Heart Disease
- Chronic, relatively stable angina
- Controlled with medications and lifestyle management
- Stable/Variant/Silent Myocardial Ischemia
Acute Coronary Syndrome
- Medical Emergency
- Unstable angina
Angina Pectoris
- Causes paroxysmal pain (pressure in anterior chest)
- Caused by insufficient coronary blood flow
Stable Angina
- Predictable and consistent chest pain. Happens during exertion, stress/temperature extremes, large meals, relieved by stress and nitroglycerine (NTG)
Unstable Angina (crescendo angina) - Not relieved by stress or NTG, or a new onset in patients with no history of angina. Increase in frequency and severity
Intractable/Refractory Angina
- Ongoing severe incapacitating chest pain
Variant Angina (Prinzmetal's Angina or Vasospastic) - Chest pain that occurs during rest (caused by coronary artery vasospasm)
Silent Ischemia Angina
- No pain but can be seen
Angina Clinical Manifestations
- Tightness/Choking/Heaviness in substernal area which can radiate to neck/jaw/shoulders/back/arms (left side) Other Manifestations - Dyspnea/SOB - Nausea/Dizziness - Vomiting - Anxiety
Angina in Geriatrics
- Diminished pain transition alters symptoms
- More likely to have Silent CAD
- Important to teach how to recognize chest pain like symptoms such as weakness
- Medications should be used cautiously
Treatment of Angina
- Decrease myocardia oxygen demand and increase oxygen supply
- Supplemental Oxygen
- NTG (Nitroglycerin)
- Beta adrenergic Blockers
- Calcium Channel Blockers
- Antiplatelet/Anticoagulation
- Aspirin
- Clopidogrel
- Reperfusion Therapy
Antianginal Drugs
- Organic Nitrates (Nitroglycerin)
- Beta Blockers (Propranolol)
- Calcium Channel Blockers (Verapamil)
- Therapeutic agents can be supplemental oxygen, NTG, IV morphine
- ACE inhibitors, beta blockers, antiplatelets, anticoagulants
Nitroglycerine (NTG)
- Relaxes smooth muscles and dilates arterial/venous vessels (decreases BP)
- Reduces systemic vascular resistance and arterial pressure and afterload
- Overall these decrease myocardial oxygen consumption and improve circulation to ischemic areas
- THERE IS EXTENSIVE FIRST PASS METABOLISM by mouth so other ways of entering the blood stream is preferred (sublingual, transmucosal, translingual spray, IV, transdermal)
CONTRAINDICATIONS - Hypotension, head trauma, cerebral hemorrhage, increased intracranial pressure
PRECUATIONS - Hepatic/Renal impairment, and it is Category C
ADVERSE EFFECTS - Orthostatic hypotension, headaches, lightheaded, dizziness, reflex tachycardia
INTERACTIONS - DO NOT GIVE WITH PDE5 INHIBITORS (Intensifies vasodilation causing life threatening hypotension)
- These include drugs like viagra, beta-blockers, verapamil, diltiazem
ENVIRONMENTAL FACTORS - Loses potency with light exposure, humidity, heat, and plastic IV bags. It is hung with a glass bottle Most forms last around 24 months
INTERVENTIONS - Monitor BP and pulse prior to administration
- Patient should sit/lie before taking it
- If pain is not relieved, patient may have a MI
Beta Blockers (propranolol and metoprolol)
- Used in stable angina by protecting against exertion angina pain. This increases exercise tolerance and frequency of angina attacks. Decreases risk of death in MI
- Slows HR, Decreases CO, Reduces BP (decreases oxygen demand)
- Decreased HR ultimately leads to increased oxygen supply (increased diastole time, increased time blood flows through coronary arteries)
ADVERSE EFFECTS - Decreased HR, AV conduction, myocardial contractility
- Bronchoconstriction
- Hypoglycemia can be masked (use cautiously in DM)
- Insomnia, depression, bizarre dreams
CONTRAINDICATIONS - Sick Sinus Syndrome
- HF
- 2nd and 3rd degree AV block
- Asthma (except metoprolol)
Ranolazine (Ranexa)
- Works better in men than women
- Only modest effects
- Decreases anginal attacks and increases exercise tolerance
- NOT A FIRST LINE DRUG
- Used when other drugs do not work and used adjunctly with BB and CCB’s (calcium channel blockers)
CONTRAINDICATIONS - Pre-existing prolonged QT interval
- ECG
- Hepatic Impairment
ADVERSE EFFECTS - Prolonged QT Interval (increased risk of ventricular dysrhythmias)
- Hypertension in patients with renal failure
- Constipation/Nausea/Dizziness/Headache
Calcium Channel Blockers (Verapamil, Diltiazem, Nifedipine)
- Used in chronic stable angina where BB and Nitrates cannot be used.
- Drug of choice for Prinzmetal’s Angina
- Inhibits calcium from moving across cell membranes
- Slows HR, impulse formation, velocity of conduction (decreases o2 demand)
- Decreases peripheral resistance
- Only verapamil and diltiazem block channels in the heart (decreased HR, contractility, AV conduction, coronary vasospasm)
ADVERSE EFFECTS - Reflex Tachycardia (due to decreased BP) and Worse with Nifedipine
- Patients on BB must be monitored for bradycardia, HF, and AV Block
Adjunct Medications
- Slows CAD (does not decrease oxygen demand)
Aspirin - Suppresses platelet thromboxane synthesis to prevent arterial thrombosis
Clopidogrel - Inhibits platelet aggregation
Abciximab - Inhibits platelet aggregation
Eptifibatide - Antiplatelet
Nursing Process for Angina
- Collect information on what preceded the angina attack and what may have caused it
- Assess distress, skin color, moisture, VS, pulse, associated symptoms
Diagnosis for Angina
- Risk for decreased cardiac perfusion
- Anxiety related to cardiac symptoms and possible death
- Deficient knowledge about underlying disease and methods for avoiding complications
Collaborative Problems and Complications
- Acute Coronary Syndrome (ACS)
- MI
- Dysrhythmias
- Cardiac Arrest
- HF
- Cardiogenic Shock
Goals of Angina
- Prevention
- Reduce anxiety
- Understand disease process and prescribed care
- Adherence
Treating Angina
- Stop activity. Sit and rest in semi-fowler
- 2 L/min o2 via nasal cannula
- Assess VS, respiratory distress, pain, ECG
- Administer NTG and re-assess pain (up to 3 doses)
Preventing Angina Pain
- Identify level of activity that causes pain and plan activities accordingly
- Alternate activities with rest periods
Angina Education
- Balance activity with rest
- Follow prescribed exercise regime
- Avoid exercise in extreme temperatures
- Emotional support resources
- Stop tobacco
- Medications (carry NTG at all times)
- Avoid OTC products that increase HR/BP
- Maintain normal BP and glucose levels
- Low Fat High Fiber Diet
Acute Coronary Syndrome (ACS) and MI
- Acute coronary syndrome includes unstable angina and MI
- Caused by unstable plaque or risk of plaque rupture and thrombosis
- Characterized by acute onset of myocardial ischemia which results in myocardial necrosis (MI)
Unstable Angina (UA)
- Chest discomfort that occurs at rest or with exertion causing extreme activity limitations
- Increasing frequency/intensity of episodes
- Pain lasts longer than 15 minutes and is not relieved by NTG or rest
- New onset less than a month is unstable
UA vs MI
UA
- Reversible Ischemia. No serum biomarkers
MI
- Ischemia that leads to death of cells with release of serum biomarkers
Diagnosis
- Based on clinical history, ECG findings, Serum Biomarkers
Effects of Ischemia/Injury/Infarction on ECG
- MI causes aerobic metabolism to turn into anerobic metabolism (causes lack of energy for proper heart function)
- Lactic acid buildup causes chest pain
- Lack of blood flow for 20 minutes causes cell death
Subendocardial MI
- Only myocardium directly below endocardium is involved
Transmural MI
- Entire myocardium from endocardium to epicardium are involved
- Q Wave appears (indicates cell death and permanent loss of function)
ACS Assessment
- Chest pain despite rest and medication
- SOB, Cool Pale Skin, Increased HR and RR
- ECG elevation in ST segment in 2 contiguous leads is the key diagnostic for MI
Biomarkers
- Troponin, Creatine Kinase, Myoglobin (cardiac enzymes)
- Released when myocardial cells die
- Used to diagnose acute MI
Collaborative Problems with ACS
- Pulmonary Edema
- HF
- Cardiogenic Shock
- Pericardial Effusion (buildup of fluid in pericardium)
- Cardiac Tamponade (compression of heart cause by fluid buildup)
- Dysrhythmias/Cardiac Arrest
Goals of ACS
- Pain relief
- Prevention of Myocardial damage with PCI (percutaneous coronary interventions) - Gold Standard
- Fibrinolytic Administration if PCI unavailable
- Maintenance of respiratory function and tissue perfusion
- Reduced anxiety
Nursing Interventions ACS
- Pain relief and s/s of Ischemia is top priority
- Improve respiratory function/adequate tissue perfusion
- Oxygen/Medication therapy
- Frequent VS
- Rest with bed elevated
- Frequent position changes
PCI
- Invasive procedure to treat CAD by improving coronary blood flow
- Puncture not surgical incision
- Involves stent placement or PTCA
- Gold Standard for MI, and UA
Angioplasty - balloon catheter to open blocked vessel
Stent - Small wire mesh tube that props arteries open decreasing chances of narrowing.
(Used in conjunction)
Stents can be covered in medication (drug-eluting stents) that prevent thrombi or scar tissue from forming.
- Antiplatelets are given immediately after a PCI. Patient should continue to take clopidogrel for a year and aspirin indefinitely
Complications after PCI
- MI
- Bleeding/Hematoma during IV anti-coagulation therapy
- Arterial occlusion from plaque
- Pseudoaneurysm from weakened area of vessel where access was used
- AV fistula from trauma
- AKI
Patient Care
- Observe Surgical Site
- VS
- Maintain patient flat in bed with legs straight for 4 hours
- Manage discomfort
- Resume activity as ordered
Coronary Artery Bypass Grafts (CABG)
- Replacement blood vessel grafted to occluded artery
- Preferred vessel is internal mammary artery whenever possible
- Combination of Venous and Arterial Grafts (arterial preferred over venous)
CABG
- Alleviate angina where medication and PCI do not work
Nursing Management CABG
- Maintain CO
- Promote adequate gas exchange
- Maintain fluid/electrolytes
- Maintain adequate tissue perfusion
- Maintain body temperature
- Relieve pain/fear/anxiety
