NCLEX: Pulmonary Embolism (PE), HF, DVT, CVD, HTN, CAD & Angina Pectoris,

Troponin blood test

a family of proteins found in skeletal and heart (cardiac) muscle fibers that produce muscular contraction. tests measure the level of cardiac-specific troponin in the blood to help detect heart injury. Normally, troponin is present in very small to undetectable quantities in the blood. When there is damage to heart muscle cells, troponin is released into the blood. The more damage there is, the greater the concentration in the blood. tests are used to help determine if an individual has suffered a heart attack. They may also be helpful in evaluating someone for other forms of heart injury. When a person has a heart attack, levels of cardiac-specific troponins I and T can become elevated in the blood within 3 or 4 hours after injury and may remain elevated for 10 to 14 days.

ventilation-perfusion scan (V/Q) scan

a scan that tests whether a problem in the lungs is caused by airflow (ventilation) or blood flow (perfusion) nuclear scan that measures air & blood flow in the lungs helps identify blood clots or PE *PT will breath in a special slightly radioactive gas and receive a small injection of radioactivity IV into blood. Pt placed in scanner focusing on chest. Multiple pictures of chest will be taken at different angles to measure the flow of radioactivity & blood in lungs. painless, takes about 1 hr. Risk of small exposure to radiation, and possible reaction to INJ https://www.youtube.com/watch?v=EDYW5v9IczU

NSTEMI & STEMI *Signs & Symptoms*

Unrelenting pain- severe & crushing character in the pericardial or substernal chest ares may radiate to arms, jaw neck, or thorax Atypical symptoms: dyspnea fatigue lethargy indigestion tachycardia cool, clammy skin ventricular dysrhythmias Nausea/vomiting lung sounds: crackles (with cardiogenic shock or papillary muscle dysfunction) Murmurs or S4 heart sounds Altered LOC Anxiety *Diagnostics* 12 lead ECG - no definitive diagnostic changes might see non-specific alteration in T waves Labs: Cardiac enzymes only way to diagnose NSTEMI Echocardiography: to determine the EF & wall motion disturbances Chest X-ray: detects presence of HF Cardiac catheterization -primary coronary re-perfusion therapy to open coronary artery blockages once MI ruled in *Nursing Implications* Physical assessment Comorbidities Anticipate complications based on area of myocardium affected Continuous monitoring: Rhythm, HR, urinary output, respiratory & oxygenation Oxygen/drug/advanced therapies: monitor effectiveness Alternate rest-activity periods Emergent Surgical revascularization if re-perfusion strategy fails Cardiac Rehab

NSTEMI

Unstable, complicated lesion of CAD *PARTIALLY OCCLUDES* the vessel/ lumen of the affected coronary artery causing injury & infarction of myocardium (necrosis) ST depression T wave inversion on ECG Elevated Cardiac enzymes Lethal response to unrelieved myocardial ischemia. Often dose not get early, aggressive therapy done Treatment for UA and NSTEMI Trending biomarkers Echocardiogram Monitoring and r/o other causes Stress testing Treadmill or chemical stress testing with EKG and BP monitoring *Troponin Lab: detects damage to the heart (cardiac biomarkers)* *Medical Management* In addition to UA drugs Anticoagulants Morhphine IV Vasodilators IV Positive inotropes IV Antidysrhythmics

STEMI

Unstable, complicated lesion of CAD *TOTALLY OCCLUDES* the vessel/lumen of the affected coronary artery causing injury & infarction of myocardium (necrosis) ST elevations on ECG Elevated cardiac enzymes More severe symptoms *Jaw pain, fatigue, back pain* *Need 2 leads out of 3 to be elevated* tx Interventions to re-establish blood flow via Coronary Angiography - Percutaneous coronary intervention (PCI) - If STEMI and no immediate access to Cath Lab, Fibrinolytic therapy with tPA is given *Drug therapy* - antiplatelets-clopidogrel (Plavix) or prasugrel (Effient) - IIb/IIIa glycoprotein inhibitors (Integrilin)-given in cath lab - nitroglycerin - low molecular weight heparin (Lovenox) or unfractionated heparin Coronary artery bypass surgery (CABG)- if indicated *Medical Management* In addition to UA & NSTEMI drugs Fibrinolytic Therapy (TPA) Intra-Aortic Ballon Pump

Anti-platelets

ASA, clopidogrel first line (or prasugrel or ticgrelor)

dysrhythmia

Abnormal heart rhythm

Intra-aortic balloon pump (IABP)

An intra-aortic counterpulsation device - used as an invasive intervention to improve myocardial perfusion, reduce preload & afterload, & facilitate left ventricular ejection. - used when patients do not respond to drug therapy

Aortic Aneurysm

Aortic Aneurysm Pathophysiology When the aorta is under extreme high pressure from hypertension, the wall of the vessel can weaken, causing a dilation or outpouching of the vessel that is extremely weak, causes turbulent flow, and is at high-risk for rupture. Aortic aneurysms are classified by location: Thoracic and Abdominal. There are four types of aneurysms that can be seen on diagnostic imaging: Fusiform: dilation that involves the entire circumference Saccular: localized outpouching Dissecting: pressure tears lining of vessel away from outer layer, blood gets trapped between the layers - often decreases distal blood flow False: clot forms outside the vessel wall Etiology Most commonly caused by chronic hypertension. Can also be caused by any other weakening of the vessel walls, such as in connective tissue disorders, Marfan Syndrome, or Elers-Danlos Syndrome. Desired Outcome Subjective Data Chest pain Burning / tearing Radiates to back, shoulder, abdomen, flank, or groin s/s Low CO Weakness Fatigue Shortness of breath Objective Data Abdominal Assessment Visible and palpable pulsatile mass Systolic bruit s/s ↓ CO ↓ BP ↑ HR ↓ pulses Slow cap refill Skin - cool, pale, diaphoretic ↓ LOC ↓ UOP Hematoma on flank Nursing Interventions Full Pain Assessment (PQRST or OLDCARTS) RATIONALE Need to determine how quickly the pain came on - sudden onset may indicate rupture. Need to determine if the pain radiates - aneurysms tend to radiate to the back and abdomen. Severe pain may indicate worsening aneurysm or even rupture. Full Abdominal Assessment RATIONALE AAA's can be seen and felt pulsating in the abdomen and a bruit can be heard. A detailed abdominal assessment can help to identify a AAA. Inspection - visible pulsation Auscultation - systolic bruit Palpation - pulsation and tenderness Assess VS and hemodynamics RATIONALE Since cardiac output can be compromised, it's important to monitor hemodynamics and vital signs to monitor for deterioration. Assess peripheral perfusion RATIONALE Since cardiac output can be compromised, peripheral perfusion may be decreased. Monitor for diminished pulses, cool, pale, clammy skin, and slow cap refill. Manage Pain Administer analgesics Position of comfort RATIONALE Aortic aneurysms are often accompanied by pain that radiate to the back. It can even be burning or tearing pain. We need to manage this with analgesics as well as encouraging the patient to be in their position of comfort. For some, this might be side-lying, while others may prefer to be on their backs. Administer antihypertensives RATIONALE Controlling blood pressure is a top priority with an aortic aneurysm. The goal is to decrease the pressure on the walls of the aorta while still maintaining a MAP sufficient enough to perfuse the rest of the body. Usually this means a MAP > 65 mmHg. Monitor for evidence of rupture RATIONALE Larger aortic aneurysms are at high risk for rupture. This would be evidenced by sudden, severe pain that radiates to the back, flank, or groin, a hematoma on the flank (retroperitoneal bleed), and signs of shock (↓ BP, ↑ HR, ↓ pulses, slow cap refill, cool, pale, clammy skin) Prepare patient for emergency surgery if needed RATIONALE Ruptured aneurysms need to go to the OR emergently for repair to prevent death from hemorrhage. Other patients may need their aneurysm repaired in the OR or in the cath lab (EVAR) to prevent complications.

Pulmonary artery vs vein

Artery: branches off the right ventricle & carries deoxygenated blood from the heart to the lungs where it is oxygenated Vein: brings blood back to heart into the left atrium

Antiplatelets

Aspirin Clopidogrel (Plavix) *Inhibit platelet aggregation*

Core Measures *Acute MI (AMI)*

Aspirin at arrival Assessment of left ventricular function: patients with EF < 40% receive ACE-1 or ARB Adult smoking cessation advice/counseling, if a current smoker, during hospital stay Beta-blocker prescribed at discharge

Bacterial Endocarditis - Symptoms

BE JOAN OF ARC B-Blood culture positive E-Echo evidence of vegetation J-Janeway lesion O-Oslers node A-Aneurysm (mycotic); Abuse(substance) N-Nephritis O-Other predisposing heart condition F-Fever A-Arterial emboli R-Roth's spot; Rheumatoid factor C-Culture positive not meeting major criteria

pulmonary embolism (PE)

Blockage of pulmonary arteries by thrombus, fat or air embolus, or tumor tissue. - Obstructs alveolar perfusion (Clot from leg broke free & obstructed vein in lungs: most commonly affects lower lobes) Risk Factors - Deep Vein Thrombosis (DVT) 90% - Immobility (Surgery, Obesity) - Malignancy - Oral Contraceptives/Hormones* - Pregnancy/Delivery - Smoking - HF, Clotting Disorders - Atrial Fibrillation - Central Venous Catheters - Fractured Long Bones s/s - *Hypoxemia* w/ a low CO2 (abnormally low o2 in blood) = Change in LOC"Chronically Hypoxic" - *Dyspnea* (difficult or labored breathing) *Most Common* - Tachypnea (rapid breathing) - Cough, CP, Hemoptysis (cough up blood), Crackles, Wheezing - *Tachycardia* (increased HR) - Fever - Syncope (Dependent on size & extent of emboli - Right Ventricular Hypertrophy (Secondary due to Pulmonary HTN) complications Pulmonary Infarction Pulmonary Hypertension Diagnostic Studies of PE *D-Dimer (Gold standard)* *Spiral (Helical) CT Scan (Gold standard)* Ventilation-perfusion (V/Q) scan Pulmonary Angiography (Most sensitive but invasive) - Arterial Blood Gases (ABGs) - Serum Troponin Levels & b - type natriuretic peptide (BNP) levels are frequently elevated

*Mixed Systolic and Diastolic (Biventricular)* pathophysiology

Both ventricles - right & left - are dilated and have poor filling & emptying capacity

Intra-aortic balloon pump (IABP)

Cardiac assist device that reduces afterload & enhances coronary artery perfusion care planning Cardiac pump effectiveness Pain control Activity Tolerance Knowledge deficit: cardiac disease Process Anxiety Self-Control

cardiomyopathy

Cardiomyopathy Pathophysiology Cardiomyopathy is an abnormality of the cardiac muscle that leads to functional changes or impairment. There are three types: Dilated, Hypertrophic, and Restrictive. Etiology Cardiomyopathy is typically caused by prolonged, uncontrolled hypertension, congestive heart failure, or congenital diseases. In each case the heart is having to work extra hard - the ventricles begin to change shape (or remodel) in response to the extra work. Desired Outcome Subjective Data Symptoms of Heart Failure Fatigue Chest Pain Shortness of Breath Dyspnea on exertion Objective Data Signs of Heart Failure Extra Heart Sounds (S3, S4) Poor peripheral perfusion Dysrhythmias JVD Crackles in lungs Enlarged heart on imaging ↓ Stroke volume ↓ CVP (preload) Nursing Interventions Monitor CV status & VS RATIONALE Cardiomyopathy can mimic heart failure and is often caused by hypertension. It's important to monitor the patient's cardiovascular status and vital signs to be alert to any evidence of decompensation. Assess Oxygenation, Apply O2 as needed RATIONALE Because cardiac output is compromised, oxygenation may be compromised as well due to poor perfusion and fluid backing up in the lungs. Assess SpO2 and give supplemental oxygen Administer antihypertensives RATIONALE Controlling hypertension is important to control symptoms as well as to prevent any further damage to the heart muscle. Beta Blockers ↓ workload of heart ACE Inhibitors ↓ afterload ARBs ↓ afterload Diuretics ↓ preload Encourage rest and minimize stress RATIONALE Because of the poor cardiac output, patients will be short of breath and easily fatigued. Encourage frequent rest periods and clustered activities. Minimizing stress can decrease blood pressure and workload on the heart, as well as decrease inflammatory chemicals within the heart muscle (↓ cortisol). Monitor for s/s heart failure RATIONALE Cardiomyopathy can mimic heart failure. The patient may experience signs of poor perfusion such as weakness, pale, clammy skin, and diaphoresis, as well as shortness of breath and pink frothy sputum due to pulmonary edema. Educate patient on low-sodium diet (DASH diet) RATIONALE A low sodium diet should be followed to help decrease hypertension and water retention (volume overload). This involves avoiding processed or canned foods, not adding salt to food, and avoiding sodas.

Other drugs: central-acting agents, central adrenergic inhibitors, & central alpha agonists.

Clonidine (Catapres), Guanabenz (Wytensin), Guanfacine (Tenex), Methyldopa (Aldomet) work by preventing your brain from sending signals to your nervous system to speed up your heart rate and narrow your blood vessels. As a result, your heart doesn't pump as hard and your blood flows more easily through your blood vessels. used to treat or improve symptoms in conditions: High blood pressure Attention-deficit/hyperactivity disorder (ADHD) Hot flashes Drug withdrawal Tourette syndrome

Anticoagulants

Coumadin, heparins prevents new clots from forming or current ones from getting bigger

Patho of Idiopathic Pulmonary Arterial HTN

Vascular scarring (Narrower & stiffer) - Inflammation & Cell proliferation Endothelial Dysfunction - Vasoconstriction (Imbalance between normal vasodilators and vasoconstrictors) Intimal & Medial Proliferation (Hypertrophy from smooth muscle proliferation *CANNOT BE FIXED* but can try to prevent wall from getting thicker = more prone in young women! Diagnostic Studies of IPA HTN - Chest X-Ray (Cardiomegaly, enlarged Pulmonary vasculature) - CT Chest - Echocardiogram (Right Ventricular Enlargement) - Right Heart Catheterization (Elevated mean pulmonary arterial pressure, Most definitive for diagnosis) Medication Management of IPA HTN *Calcium Channel Blockers* "-pine" Act on smooth muscle to dilate & lower PA pressure *Phosphodiesterase Enzyme Inhibitors* - selective smooth muscle relaxation in vasculature *Vasodilators* - Prostacyclin analog dilate systemic & pulmonary vasculature *Endothelin (1) Receptor Antagonists* - Binds to endothelin 1 receptors reducing PA pressure, MAP & Pulmonary Vascular resistance Inter-professional care of IPA HTN *no cure* - Symptomatic Relief - Low flow O2 Drugs to promote (Vasodilation, Reduce RV overload, reverse remodeling) Diuretics (Manage peripheral edema) Decrease venous return = everything is backing up into legs (Think R & L heart married, lungs is counselor)

Nursing interventions: priorities STEMI/NSTEMI

DECREASE WORKLOAD OF HEART! *Preload reduction*: nitrates, diuretics *Afterload reduction*: vasodilators *HR reduction*: β-adrenergic blockers *Pain relief* - oxygen, morphine - Treat symptomatic dysrhythmias: anti-arrhythmics - Stop further clots from forming: anti- platelets, heparin - Decrease oxygen consumption - Avoid large meals, straining during BM - Progressive activity: cardiac rehab - Diversional activities: reduce stress *Fluid status* - Monitor for signs of fluid overload - *STRICT I&Os/Intake & Output important *Emotional support* - Patient and Family Explain procedures/technology *Education/Prevention* Assess needs early - referrals to cardiac rehab Risk factor management Psychological adjustment

Hypertension - *Diuretics*

DIURETIC • Daily Weight • Intake and Output (I & O) • Urine Output • Response of BP • Electrolytes • Take Pulses • Ischemic Episodes (TIA) • Complications: 4C's

Coronary Artery Disease (CAD)

Damage or disease in the heart's major blood vessels (Atherosclerosis) Caused by: - deposits of lipids (atheromas) and cholesterol within the intimal wall of coronary arteries (plaque) - inflammation Also known as ASHD, CVHD, IHD, CHD

(SNS) Sympathetic Nervous System Stimulation

Decreased CO --> Decreased BP --> Baroreceptors & vasomotor regulatory centers (Medulla) Increased circulating catecholamines --> a & b receptors --> Increased HR, contractility, & peripheral vasoconstriction --> Increased CO *NEGATIVE EFFECT: Increased O2 demand --> ischemia, arrhythmias*

*Acute & Chronic* Nutritional/Other

Diet education: - fluid & sodium restriction Weight monitoring & management Tobacco cessation

Arterial Disorders

Disorders of the arteries, which are the vessels that are responsible for delivering oxygenated blood to the body. This includes Peripheral Arterial Disease, which is chronic occlusion of the arteries in the lower extremities leading to decreased oxygen supply. Another form is Raynaud's disease, which occurs when small arterioles in the hands vasospasm and prevent blood flow. The third is Buerger's disease which is an inflammatory disease of the medium to small arteries and veins of the arms and legs. In this condition, microthrombi form which can lead to vasospasm and occlusions. Etiology The most common cause of peripheral arterial disease is atherosclerosis. Raynaud's can be secondary to atherosclerosis, lupus, or rheumatoid arthritis and can be triggered by cold or stress. The cause Buerger's disease isn't exactly known, but there is a link to genetics as well as tobacco use s/s Intermittent Claudication Pain at rest - awaken from sleep Numbness and tingling in extremities Hair loss on lower extremities Cool, pale skin on extremities Triphasic color changes (Raynaud's) - Rubor (red) - Cyanosis (blue) - Pallor (white) Swelling Diminished pulses Ulceration in extremities Nursing Interventions for Arterial Disorders Assess peripheral circulation May need to use a doppler to locate peripheral pulses RATIONALE Arterial disorders affect the arteries that bring oxygenated blood to the tissues. This most often affects the extremities where the vessels are smaller. You may see cool, pale skin, or feel diminished pulses - it's imperative to monitor peripheral perfusion to prevent necrosis of tissue or the need for amputation. Educate patient on smoking cessation RATIONALE Smoking causes vasoconstriction and is the #1 cause of complications in a patient with arterial disease. Quitting smoking can improve the risk of complications dramatically. Educate patient on appropriate levels of activity Exercise to the point of claudication, then rest RATIONALE Intermittent claudication is muscle pain that occurs with a predictable amount of activity and goes away with rest. It is indicative of ischemia to the muscle tissue. The patient should be taught not to exercise past the claudication. They should stop when it occurs and rest until it dissipates. Educate patient on avoiding triggers for Raynaud's RATIONALE Raynaud's can be triggered by cold, stress,caffeine, etc. Patients should be taught how to identify those triggers and avoid them whenever possible. Assess pain and administer analgesics RATIONALE Arterial disorders can be very painful because of the ischemia to the tissues. Pain control is important Administer medications as ordered Vasodilators Calcium Channel Blockers RATIONALE Vasodilators are given to open up the vessels in the periphery to improve the flow of oxygenated blood. Calcium channel blockers are given because they act on vascular smooth muscle to prevent vasospasm. Prepare patient for surgical intervention Bypass grafting Angioplasty Endarterectomy Sympathectomy RATIONALE Bypass grafting - a graft is placed to bypass the occluded arterial structure Angioplasty - a balloon is inserted into the occlusion and inflated to compress plaque and open the narrowed area. Endarterectomy - the plaque is surgically removed from the inside of the artery Sympathectomy - nerve endings are dissected to decrease pain sensation in the affected area

Fibrinolytic Therapy (TPA)

Dissolves fibrin clots; used when there is no immediate access to cath lab

IV Positive Inotropes

Dopamine, dobutamine *increase contractility*

Complications of STEMI

Dysrhythmias most common cause of death in the first hour - common with: excessive caffeine, ETOH, nicotine, digoxin toxicity, electrolyte imbalances - especially potassium and magnesium, and stress; - common in diseases such as: CAD, MI, cardiomyopathy, and HF (Delayed) *Pericarditis* - 2-3 days post-MI - Inflammation of pericardium - very painful (Dressler's syndrome": 4-6 weeks post-MI; pericarditis with effusion and fever) - Pain aggravated by position changes or breathing/coughing - Heart sounds - pericardial friction rub *Treatment - anti-inflammatory, analgesics IF UNTREATED: Heart failure - LV pump failure Papillary muscle dysfunction or rupture Both of the above can lead to: Cardiogenic shock

endocarditis

Endocarditis Pathophysiology Endocarditis is inflammation of the lining and valves of the heart. It is often from an infectious source and can cause disorders of the valves and life threatening arrhythmias. Vegetations can form because of bacteria adhering to valves, which can then become embolic - causing heart attacks or strokes. Etiology The two most common causes are IV drug use (because of the introduction of bacteria into the vascular system) and artificial valve replacement (because the bacteria tend to adhere to the artificial device). Desired Outcome Subjective Data Chest Pain Symptoms of Heart Failure Objective Data Temperature ↑ WBC Signs of Heart Failure Heart murmurs ↓ SpO2 Embolic complications Splinter hemorrhages in nail beds Janeway lesions on fingers, toes, nose Clubbing of fingers Nursing Interventions Assess Heart Sounds RATIONALE Patients with endocarditis may develop valve disorders - listen for heart murmurs or extra sounds. Assess and Address Oral Hygiene RATIONALE There is a significant connection between oral health and pericarditis. Bacteria can travel to the heart easily from the oral cavity. Patients should brush their teeth twice daily to prevent complications. Administer IV Antibiotics RATIONALE Endocarditis is almost always a bacterial source, therefore, IV antibiotics will be required to treat the infection. Be sure to obtain blood cultures prior to initiating antibiotics. Administer and Monitor Anticoagulant Therapy RATIONALE The provider may order anticoagulant therapy to prevent further collection of platelets or clots around the valves and to prevent major complications from emboli. Depending on the medication, the therapy may require monitoring. For example IV Heparin requires PTT monitoring. Apply SCDs or TED hose RATIONALE Patients are at risk for embolic complications. SCD's or TED hose can help prevent DVT's from developing. This can help to prevent pulmonary embolism. Assess for s/s emboli RATIONALE The vegetation on the valves is at risk for breaking off and becoming lodged in smaller vessels. This includes risk for Stroke, MI, Pulmonary Embolism, but also damage to the smaller vessels in the extremities, hands, and feet. Educate patient on s/s infection RATIONALE Endocarditis is an infectious process, therefore infection control is imperative. They need to be taught hand hygiene as well as other infection precautions. They should also be taught s/s of infection to report to their provider. Educate patient to inform other providers before procedures May need prophylactic antibiotics No dental procedures for at least 6 months RATIONALE Because the patient is at high risk for recurrence and complications, it's important that they notify other providers of their history of endocarditis. They may require prophylactic antibiotics prior to any invasive procedures and they should avoid dental procedures for at least 6 months after their hospitalization.

Oral anticoagulant *(DOAC) Direct Oral Anticoagulants*

Factor Xa inhibitors/direct thrombin inhibitors -Produces *rapid* anti-coagulation *No blood monitoring needed* (Cannot be measured with INR) - Baseline creatinine before initiation of therapy - Does require periodic *monitoring of renal function* (bc filtered through kidneys) - *Dabigatran* direct thrombin inhibitor - Rivaro*xa*ban, Api*xa*ban= factor *Xa* inhibitors Pt considered anticoagulated after 1 dose (Ex: Xarelto)

Thrombolytic/Fibrinolysis & Surgical Intervention

Fibrinolysis - Catheter directed administration of clot lysing agents - *Urokinase, tPA* - Direct dissolution of clot Surgical thrombectomy - Indications: used when Pt has massive swelling, "Phelegmasia cerulean dolens" (Blue leg), or when fibrinolysis is unsuccessful in reducing the volume of thrombus

Heart valve closure sequence

Heart valve closure sequence: *Try Pulling My Aorta* *T*ricuspid *P*ulmonic *M*itral *A*ortic Other memory tools: TRI before you BI (Blood flows through the TRIcuspid before BIcuspid) - always "tri" to do the "right" thing (Tricuspid valve in the Right Heart)

Natriuretic Peptides

Hormones secreted by myocytes - plasma levels increase in HF - Atrial NP: produced in atria - Brain NP: produced in ventricles in response to stretching/pressure *Positive effects*: - Promote vasodilation & decrease preload & afterload - Reduce Na+ & water retention & inhibits cardiac hypertrophy

IV Vasodilators

IV NTG, Nipride venodilators reduce preload; arterial vasodilators reduce preload & afterload

Collaborative Care: Percutaneous Transluminal Coronary Angioplasty (PTCA)

Important to implement life-style changes after intervention such as no smoking, exercise, diet (low fat), and stress management. *"Door to balloon"* means the second they enter the hospital door from the ambulance to the balloon tx less than 90 min (for pt safety and a certification for hospitals. Hospitals want this for certification/accreditation) - A balloon is placed next to the plaque, blocking the artery-balloon is inflated crushing the plaque. - May be performed as the first line of treatment Stent-a small, expandable wire-mesh stent is permanently inserted into the artery during angioplasty. The balloon is placed inside the stent and inflated, which opens the stent and pushes it into place against the artery wall to keep the narrowed artery open. Because the stent is meshlike, the cells lining the blood vessel grow through and around the stent to help secure it. TPA most potent blood thinner can also be given (Tissue plasminogen activator is a protein involved in the breakdown of blood clots).

ACE-inhibitors or ARBs

Improve ventricular remodeling

Rapid Ventricular Response

In some cases of AFib, the fibrillation of the atria causes the ventricles, or lower chambers of the heart, to beat too fast.

Coronary Artery Disease *Unmodifiable Risk Factors*

Increased age - CAD begins early and develops gradually Gender - Highest incidence for middle-aged male - Males more than females until 65 years of age Race - Caucasian males highest risk - African-Americans earlier age of onset of CAD Genetic - Inherited tendencies for atherosclerosis *Modifiable* *#1 Hyperlipedemia* - elevated serum lipids *#2 Hypertension* - salt intake a factor Diabetes - glucose intolerance & abnormal lipid metabolism Tobacco use - second hand smoke a factor Obesity - BMI > 30 kg/m2 Physical Inactivity Stress

Sympathetic Nervous System (SNS) Stimulation

Increased heart rate & contractility increase cardiac workload in the failing heart

Cardiac hypertrophy

Increased muscle mass leads to less contractility resulting in decreased cardiac output and dysrhythmias.

CAD/Stable Angina *Non-modifiable* Risk factors

Increasing Age Gender (males > females until 65 yrs) Ethnicity (Whites) Family History & Genetics *Major Modifiable* Risk Factors Major: Elevated Serum Lipids HTN Tobacco Use Physical Inactivity Obesity Contributing: Diabetes Metabolic Psychological (Depression; Chronic Stress) High Homocysteine Levels ID of high risk individuals is key so that modifable risk factors can be addressed and client education provided

Angina Collaborative Care

Interventions to re-establish blood flow - Coronary angiography - angioplasty/stent Surgery (if stent doesn't work = reroute blood with new construction)

renin-angiotensin-aldosterone system (RAAS)

Kidney response to decrease CO due to decreased perfusion Stimulates release of angiotensin II & aldosterone --> increase Na+ & water retention --> increased CO *Negative Effect: increase blood volume increased mycardial O2 demand on an already compromised heart*

Diagram of the heart

Know the movement of blood

Venous Thrombi

Low shear force Rich in Fibrin (around valves/lower extremities) NO plaque. If breaks= becomes PE

Antilipemics

Lowers cholesterol or lipids

Cardiac dilation

Myocardium loses elasticity eventually leading to decreased cardiac output

Classification Systems

NY association Functional Assessment - Class I - IV American Heart Association System - Stage A - D

cardiac troponin I (cTnI)

Negative: < 0.5 ng/mL Indeterminate: 0.5 - 2.3 ng/mL Positive: > 2.3 ng/mL Rises in 4 - 6 hrs Peaks in 10 - 24 hours Remains elevated for 10 to 14 days

CPK-MB

Normal range: 0 to 4-6% of total CK > 6% positive Rises in 6 hrs Peaks in 18 hrs Remains elevated for 24 - 36 hours - enzymes are fractionated into bands - band is specific to heart muscle cells & help to quantify myocardial damage.

cardiogenic shock

Not enough oxygen is delivered to the tissues of the body, caused by low output of blood from the heart (pump failure)

β-adrenergic blockers

Offsets effects of SNS activation

Silent/Atypical Angina

Often seen in women and diabetics Silent (Atypical): NO CHEST PAIN - *#1 Fatigue* - Shortness of breath - Epigastric burning: "heart burn heart burn" - Anxiety

Pharmacologic Tx of DVT

Parenteral Anticoagulants (IV/Subcut) - Thrombin inhibitors - Selective for FactorXa Oral Anticoagulants (clot busters: dissolve clots/fibrin) Thrombolytic/Fibrinolysis Surgical Intervention

Pericarditis

Pathophysiology Pericarditis is inflammation of the pericardium - the outer layer of the heart and pericardial sac. Fluid and inflammation build up around the heart inside the pericardial sac, putting pressure on the heart and making it harder for the heart to fully relax and contract. It can cause heart failure or cardiac tamponade. Etiology Pericarditis is caused by an infectious source, either viral, bacterial, or fungal. Fungal is the least common, while the Coxsackie virus is a common source. Desired Outcome Subjective Data Chest Pain Aggravated by breathing, coughing, swallowing Worse when supine Symptoms of Heart Failure Objective Data ↑ Temperature ↑ WBC Signs of Heart Failure ST Elevation possible ↓ SpO2 S/S Cardiac Tamponade Muffled heart sounds Narrow Pulse Pressure Pulsus Paradoxus JVD with clear lungs ↓ Cardiac Output Nursing Interventions Assess Heart and Lung Sounds RATIONALE May hear a pericardial friction rub, muffled heart sounds, or extra sounds because of the pressure being placed on the heart. It's possible, but unlikely that you will hear fluid in the lungs - in cardiac tamponade the lungs will be clear. Assess and Address Oral Hygiene RATIONALE There is a significant connection between oral health and pericarditis. Bacteria can travel to the heart easily from the oral cavity. Patients should brush their teeth twice daily to prevent complications. Administer IV Antibiotics RATIONALE If the source is bacterial, IV antibiotics will be required to treat the infection. Be sure to obtain blood cultures prior to initiating antibiotics. If the source is viral - providers may order anti-inflammatory medication since antibiotics aren't effective. If the virus is known and susceptible, an antiviral medication could be used. Perform 3-5 lead ECG monitoring and/or 12-lead ECG RATIONALE Pericarditis could cause arrhythmias or ST elevation as the fluid puts pressure on the heart. Cardiac tamponade is a risk - in which case we'll see the QRS amplitude decrease with inspiration. Assess and Manage Pain RATIONALE Patients will have significant chest pain that is worse with breathing or when supine. Perform OLDCARTS pain assessment and administer pain medication as ordered. Positioning the patient in High-Fowler's position can also relieve pressure on the heart and be more comfortable for the patient. Assess for s/s Cardiac Tamponade RATIONALE Assess for Beck's Triad - JVD, ↓ BP, muffled heart sounds. May also see Pulsus Paradoxus and narrowing pulse pressures. This is a medical emergency and needs to be treated as such. Prepare patient for emergent pericardiocentesis RATIONALE A physician will insert a large, long needle into the pericardial sac, using ultrasound as a guide, to drain off the fluid that is collecting around the heart. This will allow the heart to beat more freely and should improve cardiac output rapidly. Educate patient on s/s infection RATIONALE Pericarditis is an infectious process, therefore infection control is imperative. They need to be taught hand hygiene as well as other infection precautions. They should also be taught s/s of infection to report to their provider. Educate patient to inform other providers before procedures May need prophylactic antibiotics No dental procedures for at least 6 months RATIONALE Because the patient is at high risk for recurrence and complications, it's important that they notify other providers of their history of pericarditis. They may require prophylactic antibiotics prior to any invasive procedures and they should avoid dental procedures for at least 6 months after their hospitalization.

management of HTN

Patients are usually *asymptomatic* *Blurry Vision, headache, chest pain* (TOP 3). Also see nose bleeds/dizzy, ringing in the ears Need to Assess, Educate, and Evaluate! - measure BP (both arms, 5 min in-between, family hx, look for sensory changes (bc high bp can hurt blood vessels to eyes and other areas), BMI, report increased BP to MD, med compliance (make sure meds are being taking regularly) Educate: *Limiting Na+, ETOH, & Caffeine* - also smoking cessation, encourage exercising (cardio), teach how to measure BP, & keep a record *Pharmacology management* Typically non-pharm methods used first for 1 - 3 months while monitoring before meds are used = start low & add on as needed Thiazide Diuretics ACE Inhibitors ARBS CCBs

Provoking Factors of Angina

Physical exertion Temperature extremes Strong emotions Heavy meal Tobacco use Sexual activity Stimulants

Compensatory mechanisms of heart failure

Possible abrupt onset & rapid atrial fibrillation - heart tries to compensate to maintain CO with: 1. Increased (SNS) sympathetic nervous system activation 2. (RAAS) Renin-angiotensin-aldosterone System activation 3.ventricular hypertrophy & dilation (Remodeling) 4. Natriuretic Peptides B-type (BNP)

Pre HTN BP Range

Pre HTN BP Range SBP: 120 - 139 / DBP: 80 - 89 Stage 1 SBP: 140 - 159 / DBP: 90 - 99 Stage 2 SBP: >160 / DBP > 100

Unstable Angina (UA) Risks Factors

Risks Factors associated w/worsening CAD due to increased cardiac workload from myocardial ischemia *Signs & Symptoms* Worsening pain pattern - constricting or squeezing character in the pericardial or substernal chest areas may radiate to arms, jaw, neck or thorax Typically relieved with rest and/or (NTG) Nitroglycerine *Diagnostics* 12-lead ECG ST segment depression or T wave inversion Stress testing Labs: Cardiac enzymes & proteins to rule out MI Cardiac catheterization: to detect presence & extent of coronary artery blockages *Nursing Considerations* Physical assessment Comorbidities Health promotion (physical activity) Nutritional therapy Drug therapy (cholesterol/lipid-lowering, anti-platelets, nitrates, beta-blockers) Education on how to reduce energy demands & importance of medication therapy

Normal BP Range

SBP <120 - 90 / DBP <80 - 60

Nitrates

SL for immediate use PO for maintenance & spasm control *Reduce preload/afterload & dilates coronary arteries

Hypertension, Primary—Risk Factors

SOSAD IC •Sodium and fat intake •Obesity •Stress •Alcohol •D vitamin deficiency •Inactivity •Caffeine

PE Prevention (Collaborative Care) & Supportive Care

Sequential Compression Devices (SCDs) Early ambulation Prophylactic Anticoagulation (Anticoagulants) Support: Oxygen: mechanical ventilation pulmonary hygiene Fluids, Diuretics, analgesics Drug Therapy for PE *anticoagulants* (keep the embolus from enlarging & prevent formation of new clots. DO NOT destroy current clots) - Low Molecular Weight Heparin (LHWH) - Unfractionated IV Heparin - Warfarin (Coumadin) - Xarelto *Fibrinolytic agents* - altepase (Activase): INJ: dissolves blood clots - Tissue Plasminogen Activator (tPA) (plasminogens enzyme that destroyes fibrin "clots") Surgical Therapy of PE - Pulmonary embolectomy for massive PE - Inferior Vena Cava (IVC) Filter (used if anticoagulation doesnt work) Prevents migration of clots in pulmonary system Nursing Management of PE Semi- Fowler's Position IV access Oxygen therapy Frequent assessments Monitor Laboratory results Emotional support & Reassurance

Serum Cardiac Biomarkers After MI

Serum cardiac biomarkers are proteins released into the blood from necrotic heart muscle after an MI AND helps to differentiate between a diagnosis of UA (negative biomarkers) & NSTEMI (positive biomarkers). *TROPONIN elevates sooner & last longer* - biomarkers are important in the diagnosis of MI. *Cardiac-specific troponin has two subtypes*: - cardiac-specific troponin T (cTnT) - cardiac-specific troponin I (cTnI) (biomarkers are highly specific indicators of MI, have greater sensitivity and specificity for myocardial injury than creatine kinase (CK-MB)) Serum levels of cTnI and cTnT - increase 4 to 6 hours after onset of MI - peak at 10 to 24 hours - return to baseline over 10 to 14 days.

superior vs inferior vena cava

Superior:Returns deoxygenated blood *from the upper portion of the body* in the RA Inferior: returns deoxygenated blood *from lower portion of the body*

Sacral Edema

Swelling around the low back in bedridden patients

Blood flow order

T- tricuspid P-pulmonic M- mitral A- aortic

Heart valve blood flow sequence:

TRIPS BIAS Tricuspid Pulmonary Semilunar Bicuspid Aortic Semilunar

Stroke Volume

The amount of blood (mL) ejected from the ventricle with one contraction.

Shock—Stages

"CPR" *Compensatory Stage* - Confusion Decreased urinary output BP systolic < 100 when decrease in blood volume significantly reduces the hearts cardiac output decrease in CO sympathetic nervous system to release adrenalin to increase CO, BP, ADH (kidney's hold onto h20) vasoconstriction *Progressive Stage* Weak thready pulse Excessively low BP Edema Dysrhythmia vasodilation d/t lactic acidosis decrease in CO and BP, hypotension when compensatory mechanisms fail. organ functions begin to deteriorate *Refractory Stage* This stage of shock is irreversible. Severe acidosis and organ failure occur. Cell death and tissue damage occurs from too little O2 reaching the tissues. There is no response to fluids or vasopressors, and multiple organ failure results.

Spiral (Helical) CT Scan (Gold Standard)

"Computerized Tomography" (AKA CAT scan) *confirms diagnosis* *Requires IV contrast Media* *more detailed than conventional x-ray* - Combines many x ray images with aid of a computer to generate cross sectional images of bones, soft tissue, and organs. - 2 or 3 dimensional images are created through the computer to define normal and abnormal structures in the body and/or assist in procedures by helping to accurately guide the placement of instruments or treatments.abnormal structures* https://www.youtube.com/watch?v=l9swbAtRRbg

Shock—Causes

"HAVANA" • Hypovolemia • Adrenal Crisis • Vascular Stasis • Acute Respiratory Obstruction • Neurogenic • Anaphylaxis

(MI) myocardial infarction *Women experience*

"Heart attack" - throat, neck, & jaw pain, Fatigue, SOB Difficult to spot

LDL cholesterol (Low Density Lipoprotein)

(bad cholesterol) <130 desirable *< 100 mg/dL optimal* "want low) -once it attaches to the wall, HDL CANT move it*

HDL cholesterol (High Density Lipoprotein)

(good) *>30 desirable* "want high" more HDL = lower the risk for CAD >50 mg/dL (females); >40 mg/dL (males) optimal - grabs free floating LDL & removes them from blood stream

ß-Adrenergic Blockers/Beta Blockers

*"-lol"* reduce your blood pressure by blocking effects of hormone epinephrine. Allows heart to beat more slowly & with less force

Angiotensin II Receptor Blockers (ARBs)

*"-sartan"* - Block angiotensin II, a vasoconstrictor, so helps widen blood vessels to allow blood to flow more easily & lowers blood pressure. Usually prescribed for pt who cannot tolerate ACE inhibitors

Angiotension Receptor Blockers (ARBs)

*"-sartan";* Losartan, Olmesartan (Benicar) - *used if patient cant tolerate ACE's* - Blocks aldosterone & angiotension receptors lowering BP - same side effects as ACE's except Dry cough - Watch renal function & H+ level

ACE inhibitors (Anti-hypertensive)

*"PRIL"* Blocks ACE in lungs from converting angiotensin I to angiotensin II (powerful vasoconstrictor) - Decreases BP, Aldosterone secretions, Sodium and fluid loss. Check BP before giving (hypotension) *Orthostatic Hypotension*

*Right-Sided* HF

*"Warm & Dry"* - Elevated hydrostatic pressures force more blood into the venous systemic circulation *often follows Left-sided failure; or secondary to COPD, Pulmonary HTN, Right Ventricle (RV) infarction* *SIGNS/SYMPTOMS* (*Based on R sided HF*) "SWELLING" Swelling of leg, hands, liver Weight gain Edema (pitting) Large neck vein (JVD) Lethargic Irregular HR (afib) Nocturia (lying down allow fluid to go to kidneys) Girth (abdomen increase size: breathing issues, anorexia, nausea) *ASSESSMENT/SYMPTOMS* Dependent edema (*Early Sign*) - Symmetric pitting edema - Bedrest (Sacral edema) - Anasarca (*Late Sign*) Ascities - Fatigue - Anxious/Frightened/Depressed - Right upper quadrant pain - Anorexia/Nausea & GI bloating - Cyanosis of Nail Beds - Dysrhythmias - Accentuated (more noticeable) JVD - Weight Gain > 2lbs daily

*Left- Sided* Heart Failure

*"Warm & Wet"* - Hydrostatic forces cause intracellular fluid to accumulate in the pulmonary vascular bed causing congestion (CHF) *majority of HF patients secondary to HTN, MI, Cardiomyopathy, CAD* *SIGNS/SYMPTOMS* increase retention of sodium & water due to lowered glomerular filtration -->> EDEMA - Crackles (pulmonary edema)/Pleural effusion - Orthopnea/Dry-hacking cough - Hypoxemia/Dyspnea/Shallow breathing - *Pink-tinged/frothy sputum* - Fulminant (severe/sudden onset) pulmonary edema - paroxysmal nocturnal dyspnea (PND) - nocturia "DROWNING: Dyspnea Rales (Crackles) Orthopnea Weakness Nocturnal Paroxysmal Dyspnea Increased HR Nagging cough (frothy/blood tinged sputum) Gaining weight (2-3lbs in day or 5 lbs in a wk) Tachycardia/Tachypnea - (CP) Chest Pain/Dysrhythmia - PMI (point of maximal impulse) displaced downward & posteriorly; - S3 or S4 heart sounds Exercise intolerance/Fatigue/muscular weakness - Restlessness/Anxiety - Altered LOC/Confusion

*Atherosclerosis* & the steps that cause it

*Atherosclerosis*: build-up of fats, cholesterol on artery walls. 1. Irritants (too many Lipids -> LDL/Cholesterol/Toxins [Cigarettes]/HTN) 2. Damage to the Endothelium 3. LDL - C deposits into endothelium 4. Monocytes -> macrophages -> Foam Cells on top 5. Plaque forms https://www.youtube.com/watch?v=EWTxRgIKIqw

(Meds Angina) *Calcium Channel Blockers* "-pine"

*Block the influx of Ca+ ions into cells* (smooth muscle* - *Dihydropines* (Does not increase HR) (think di= die = no hr/no increase) - *Nondihydropines* (Increases HR)* *s/s*: Hypotension, peripheral edema, bradycardia

Bile acid sequestrants

*Blocks cholesterol re-absorption in the ileum* = increase excretion of Cholesterol in stool *s/s: abd pain, bloating, steatorrhea (fatty/foamy stool bc cholesterol/fat)

"Cant have your *CAKE* and eat it too" Systems affected by High BP

*C*ardiovascular System: continuous High BP causes CHF (overworking heart muscle, causes ventricle to become enlarged = doesnt pump very well) Br*a*in: stroke (increased pressure causes arteries to weaken & narrow, or rupture causing clots or strokes) *K*idneys: renal failure (blood moving to kidneys at fast/hard rate weakens arteries to kidneys = decrease perfusion) *E*yes: visual changes (hard blood flow to eye wears out & damages blood vessels to retina = blurred vision/cant focus on objects)

Unstable Angina (UA)

*Chest Pain with rest* - change in the usual pattern or worsening of symptoms - Increasing in frequency or easily provoked *Unstable, complicated lesion of CAD partially occludes the lumen of the affected coronary artery causing spasms & Ischemia* Signals worsening of chronic angina/CAD that can lead to acute myocardial infarction - Rupture of a stable plaque leading to vasoconstriction and thrombus formation S/S *Chest Pain* - Unrelenting, varying location, intensity & quality - No improvement with rest, oxygen, position change, or nitrates *SNS Stimulation* (release of catecholamines) - Elevated blood glucose, HR & BP - Peripheral vasoconstriction: cool, ashen, clammy skin Appearance: - Anxious, restless, pallor, diaphoresis - Evident jugular venous distention (JVD) - Orthopnea, dyspnea Auscultation - Heart sounds: S3 or S4 - Lung sounds: clear or with crackles Diagnostics 12 Lead EKG Chest X-Ray Assessment of cardiac size and pulmonary congestion Serum Cardiac Biomarkers /enzymes Medical Managment Nitrates Antiplatelets Beta-blockers Calcium channel blockers ACEs/Arbs Antilipemics

Heart Failure Diagnostics

*Chest X-ray* - Cardiac enlargement/Vascular Markings - Cardiac Catheterization *12-Lead ECG/EKG* - Dysrhythmias (Afib/PACs) *Echocardiography* - Assess ejection fraction *Labs*: - BNP levels Increase - Liver enzymes (AST/ALT) - Increase creatinine/Decreased GFR - Cardiac Enzymes - Serum Chemistries - Thyroid Function

*Stable* Angina

*Chest pain w/exertion due to decreased BF to the heart* - usually stable plaque that is about 70% occlusive - subsides w/*rest* or *Nitroglycerin*: (directly dilates coronary artery to increase BF) - *Reversible:* if perfusion restored quickly so no permanent damage *Can not accommodate*

Diagnostic Assessments (Angina)

*Diagnostic Angiography* (*Gold standard*) (take pictures/view arteries & blood vessels) - but can increase risk bc of numerous steps & *INVASIVE* - Contrast material can cause renal failure (CHECK creatinine level prior to exam) *Echocardiogram* (Ultrasound pictures of the heart) *Non invasive* -Identify wall motion abnormalities & Evaluate LV function *Stress testing* -Treadmill, Nuclear scan (w or w/o a contrast medium)

Thiazide Diuretics *usually used first*

*End in "-iazide"* Hydrochlorothiazide (HCTZ), Chlorothiazide - remove H20 & Na+ via kidneys - not for pt with renal issues - watch closely for pt on Lithium (increased toxicity of lithium bc of Na) Educate: consuming enough K+ (diet/supplements) bc drug wastes K - Protect skin due to photo-sensitivity

*Diastolic Failure* Pathophysiololgy

*Heart CAN'T FILL* - Failure of ventricle to relax & fill during diastole - Ventricular filling is slow because the ventricle is not able to stretch (its stiff or not pliable; "dead meat don't beat/stretch") - Results: decrease stroke volume & cardiac output - *1/3* HF population Hallmark: signs of HF but *EF is normal or elevated*

*Systolic Failure* Pathophysiology

*Heart CAN'T PUMP w/reduced Ejection Fraction"* Ventricle loses ability to generate pressures to eject blood forward & unable to pump blood out effectively - Poor contractility - Impaired ventricular wall motion & ejection - Ventricle becomes dilated & hypertrophied - *2/3* of the HF population Hallmark: *LV Ejection Fraction (EF) <40%*

*Silent* Angina

*Heart attack w/no subjective symptoms (no chest pain). Silent killer *Diabetics* - Fatigue, SOB, Anxiety - Epigastric burning: "Heartburn" (But no chest pain!) Often seen in diabetics ECG changes are seen - *Decreased BF & Do not feel it*

heart failure (HF) or congestive heart failure (CHF)

*Heart is unable to pump enough sufficient blood to the tissues of the body* (nutrients/oxygen) - "Chordae Tendineae": tendons that contract to open tricuspid & mitral valves (best heard @ 5th intercostal space) - Results from any structural or functional cardiac disorder impairing the ability of the ventricle to either fill or eject - Develops over time; progressive - Ventricular remodeling (hypertrophy) due to prolonged myocardial stress (becomes more spherical) *Risk factors* of HF *#1 Hypertension (HTN)* *#2 Diabetes (DM)* - Coronary Artery Disease (CAD) - Diabetes/Metabolic Syndrome - Cardiomyopathy - Advanced Age - Tobacco Use - Obesity - Hypercholesterolemia - African-American Gender (Male) *Primary Causes* of HF - Coronary Artery Disease (CAD): MI/Unstable Angina - Hypertension - Rheumatic Heart Disease - Congenital Heart Defects (e.g. VSD) - Pulmonary HTN - Cardiomyopathy - Hyperthyroidism - Valvular Heart Disorders (eg. MS, AS) - Myocarditis *Precipitating Causes* of HF *these conditions can put patient in HF, can cause permanent damage, & trigger exacerbation due to increased cardiac workload* - Anemia - Infection: Sepsis (Bacterial/Viral) - Thyrotoxicosis - Hypothyroidism - Dysrhythmias (Atrial Fib w/RVR) - Pulmonary Embolism - Hypervolemia - Alchohol abuse

*MI Areas of Damage* (TEST)

*Inferior Wall MI* - iNCLUSION OCCURING IN Right Coronary Artery - Leads that look at inferior wall: Leads II, III, AVF *Anterior Wall MI* - Left Anterior Descending - Leads V1-V4 (go under the breast) *Lateral Wall MI* - Circumflex artery - Leads I, AVL, V5, V6

Internal Mammary Artery and Saphenous Vein Grafts

*Internal mammary artery (IMA)* most common artery used for bypass graft - It is left attached to its origin (the subclavian artery) but then dissected from the chest wall. Next is the anastomosed (connected with sutures) to the coronary artery distal to the blockage. Saphenous veins are also used for bypass grafts. - The surgeon endoscopically removes the saphenous vein from one or both legs. A section is sutured into the ascending aorta near the native coronary artery opening and then sutured to the coronary artery distal to the blockage. The use of antiplatelet and statin therapy after surgery improves vein graft patency.

Cardiac Output (CO)

*It's how much blood your heart pumps in 1 minute* HR (bpm) x SV (mL) = CO (L/min) Factors influencing Cardiac Output (CO) preload, afterload, Myocardial Contractility, HR

Medications PAD

*Lipid lowering* - Statins - PCSK9 inhibitors - Niacin - Bile acid sequestrants - Cholesterol Absorption inhibitor - Fibric Acid derivatives *Liver needs cholesterol to make bile but too much rests in the arteries (excess) Double check ALT & AST labs to check liver statis & LDLs

ACUTE pulmonary edema *Severe Decompensation*

*Medical Emergency! Leads to Asphyxia!* Elevated pulmonary capillary hydrostatic pressure -->> fluid pushed from circulating blood to interstitial tissues -->> alveoli, bronchioles, & bronchi

Risk factors for (CAD)

*Non-modifiable* *Age*: Increased age - CAD begins: early fatty streaks are evident by age 15 - Fibrous plaque can be evident by age 30 *Gender*: common middle-aged males & Menopausal women *Race*: Caucasian (white) males common - African Americans develop CAD earlier *Genetic*/family Hx: Inherited tendencies for atherosclerosis & heart disease *Major Modifiable* risk factors of CAD *Hyperlipidemia*: (elevated lipids) - hx: (DM) diabetes mellitus, (CKD) chronic kidney disease - Drugs: corticosteriods, (HRT) Hormone replacement therapy *Hypertension* (Increased salt intake) - Shearing stress injuries endothellum = increase inflammation - increases atherosclerosis => narrowed vessel walls *Tobacco use (smoking)* - Nicotine causes catecholamine release (H&H always high in smoker) *Physical inactivity*: associated with decrease HDL -Obesity (BMI>30KG/m2) Other *Contributing Modifiable* Risk factors for CAD *Diabetes*: glucose intolerance & abnormal lipid metabolism *Metabolic syndrome* *Psychological states*: depression; stress *Homocysteine*: elevated levels associated w/ inflammation & endothelial injury *Substance abuse*

Acute Left Failure: Pulmonary Edema Management

*O2 tx* (Nasal cannula; BiPAP; mechanical ventilation) *Drug tx* - Diuretics (Lasix/furosemide) - Vasodilators- NTG (Venodilator at <10mcg/kg/min) - Morphine - Digoxin or other positive inotrope (Dobutamine; Milrinone) - Human BNP = Natrecor (Nesiritide) IV infusion (for severe cases) *Positioning* - Semi to high Fowlers *Frequent Focused heart/lung assessments* *I&O's* *Report to MD immediately* -persistent productive cough;dyspnea; pedal edema; restlessness; frothy pink tinged sputum

Collaborative care CAD

*Prevention & early tx is key* - Healthy weight: 5-10 lb weight loss beneficial - Reduce Na+ intake - Increase physical activity (30 min of moderate activity most days of the week) - Avoid use/exposure to tobacco - Limit alcohol intake to small-to-moderate amount - Diet: Low cholesterol, Low saturated fats, High fruits/veggies, lean meats/poultry/fish - Drug therapy: restrict lipoprotein production, removal or absorption Diet Saturated (Use sparingly) - Animal fat (bacon, lard, egg yolk, dairy fat) - Oils (coconut, palm oil) - Butter, cream cheese, Sour cream Monounsaturated - Fish oil - Oils (canola, peanut, olive) - Avocado - Nuts (almonds, peanuts, pecans) - Olives (Green, black) Polyunsaturated (Use primarily) - Vegetable oils (safflower, corn, soybean, cottonseed, flaxseed) - Some fish oil, shellfish - Nuts (walnuts) - Seeds (pumpkin, sunflower) - Margarine

arterial fibrillation (AFib)

*Quivering/Irregular Heartbeat* (Cardiac Arrhythmia) - Chaotic, rapid electrical impulses in the atria - can lead to blood clots, stroke, heart failure and other heart-related complications

ADHF drug therapy:

*REDUCE PRELOAD* *Diuretics*: reduce preload & intravascular volume - Lasix/Furosemide *Venous Dilators*: - Nitroglycerin (NTG) - Morphine (reduces preload/afterload & controls anxiety *REDUCE AFTERLOAD* *arterial vasodilators* - Nitroprusside - High-dose NTG intra-aortic balloon Pump *INCREASE CONTRACTILITY* *Positive Inotropes* - Dobutamine - Milrinone - Digoxin *OXYGENATE* - Oxygen delivery - Airway Management (CPAP/BIPAP mask) Advanced Therapeutic modalities (Circulatory Assist) *Airway management* - 100% FiO2 Non-rebreather Mask or Noninvasive positive pressure ventilation (CPAP/BiPAP mask) *Artifical airway* (endotracheal tube) *mechanical ventilation* (if respiratory failure occurs) (IABCs) Intra- Aortic Ballon Counterpulsation (VADs) Ventricular assist devices: to bridge end-stage patients to heart transplant Ultrafiltration: slow excess volume removal

Stable Angina (Classic)

*REVERSABLE* - intermittent w/same pattern/duration/intensity of symptoms - if perfusion restored no permanent damage *Chest Pain with exertion* - subsides with rest or nitroglycerin Usually stable plaque that is about 75% occlusive TX *Top three: Clopidogrel, Prasugrel, & Ticagrelor* Drug therapy - antiplatelets, nitroglycerin, lipid-lowering agents, β-adrenergic blockers, Ca-channel blockers Manage the modifiable risk factors Interventions to re-establish blood flow - Stress testing to monitor progression of CAD - Coronary angiography (cath lab) - angioplasty/stent or refer for surgery if disease progressing

Diastole

*Relaxation* of the heart - Muscle fibers lengthen, heart dilates, & cavities fill w/blood

Lipodermatosclerosis

*Scarred, leathery skin = increased pigmentation (redness)* - tapered "inverted bottle" appearance changes in the skin of lower legs. a form of panniculitis (inflammation of the layer of fat under the skin). *S/S: pain, hardening of skin, change in skin color (redness), swelling, and a tapering of the legs above the ankles.*

*Prinzmetal (Variant)* Angina

*Spasm (sudden closing)* of the coronary artery that can lead to heart attack "think fake out!" - Same S/S of Myocardial Infarction but symptoms will relieve when spasm stops - *not always associated Coronary Artery Disease* or stress w/exercise - sudden ST elevation but occlusion (blocked blood vessel) don't show later on scan (bc spasm stopped/fake out) - *a sudden increase in myocardial O2 demand* due to: Nicotine/Histamine release Tx: Calcium-channel blockers

*Microvascular* Angina (aka MVD or Syndrome *X*)

*Spasms of very small arterial blood vessels (distal)* Occurs in the absence of significant CAD & Coronary spasm *Primarily women* (think "x" chromosome for women) - Postmenopausal women - Can be caused by physical exertion - Can diffuse (spread) evenly distributed plaque

CAD/Stable Angina STAGES

*Stage 1* *Fatty Streaks* - fatty streaks develop within smooth muscle cells *Stage 2* *Fibrous Plaques* - accumulation of fatty streaks & other factors from platelets promote smooth muscle proliferation and arterial wall thickening leading to endothelial injury - Collagen covers fatty streaks and forms fibrous plaques that decrease arterial blood flow *Stage 3* *Complicated Lesions* - as fibrous plaques grow the ongoing inflammation leading to plaque instability; ulceration and rupture results which cause platelets to aggregate and develop into a thrombus (clot)

NSTEMI & STEMI Stages

*Stage 1* Death of myocardial cells following prolonged oxygen deprivation & ischemia The injured & dying cells are no longer able to effectively contract or conduct and electrical impulse *Stage 2* Pain or other atypical symptoms, is unrelenting and not relieved by rest, position changes, or nitrates *Stage 3* Time is muscle! Sustained ischemia leads to irreversible cell death (necrosis) and complications: - Dysrhythmias - Heart failure - Cardiogenic shock - papillary muscle dysfunction - Ventricular aneurysm - Pericarditis - Death

Unstable Angina (UA) Stages

*Stage 1* In patient with chronic, stable angina the pattern of chest pain often changes *Stage 2* Pain becomes unpredictable or has a worsening pattern Increasing in frequency, severity, and duration *OCCURRING AT REST* or with decreasing levels of activity or stress *Stage 3* *Medical Emergency* due to unpredicatable nature and the fact that the spasm prone thrombus leads to insufficient oxygen to meet metabolic myocardial demands. condition is reversible does not lead to cell death

Statins

*Stops production of cholesterol* by blocking HMG-CoA reductase enzyme that creates it & forces body to *reabsorb existing cholesterol* bc it cant produce it. *S/S*: Myopathy (disease of muscle tissue)/ Liver impairment

Inotropy (contractility)

*Strength of contraction* the tension & Velocity developed of shortening of myocardial fibers at a given preload & afterload.

Phlegmasia cerulea dolens

*Sudden massive swelling w/ deep pain & intense cyanosis* (RARE) - so much (venous congestion) *venous thrombus pressure pushes on artery & cuts off BF* Pt will lose leg if nothing done (can get gangrene) Cerulea (swelling & cyanosis) "Think Cerulea = blue crayon"

Thrombosis

*The Clot* - local coagulation or clotting of the blood in a part of the circulatory system

Parenteral Anticoagulants (IV/Subcut) *Heparin/Lovenox/Fondaparinux*

*Thrombin inhibitors* (Indirect) activates antithrombin III which inhibits thrombin (heparin/lovenox) (Direct) bind *reversibly* to thrombin preventing formation of fibrin - Pregnancy ok (heparin) *Selective for Factor Xa* - selectively inhibits factor Xa (Fondaparinux subcut) Continuous IV infusion of *heparin requires PTT* monitoring - *Reversed w/protamine sulfate* (takes time to reverse) *Lovenox* (#1 choice over Heparin) DONT HAVE TO MONITOR LABS - More selective to factor Xa inhibition w/superior bio-availability -- *No lab monitoring/10x less likely to cause thrombocytopenia

A*T*ropine

*Treats Bradycardia* causes *T*achycardia

a*D*edonsine

*Treats Tachycardia* Causes a drop in HR

ACEs and ARBs

*Vasodilators; reduce afterload & BP* - especially effective if EF < 40%

rapid ventricular response (RVR)

*Ventricles of the heart beat too fast* - common problem seen with atrial fibrillation.

PO anticoagulant *Warfarin (Coumadin)*

*Warfarin (Coumadin)* PO = Monitor w/*INR* (Therapeutic range 2-3) - *Reversal: Vitamin K* (frozen plasma) - NO PREGNANCIES - Inhibits 2 enzymes involved in the formation of Vit K Delayed onset & offset of action PO dose 2 - 10 mg/day Patients w/protein C or S deficiency are at risk of developing skin necrosis *Need 24 hr of crossover from heparin to coumadin before turning off heparin completely to be safe

States of HF: *Warm & Dry*

*Warm & Dry* - Normal perfusion - No pulmonary congestion *Warm & Wet* *Most common ADHF* - Normal perfusion - Pulmonary congestion (Dyspnea, edema) *Cold & Dry* *Chronic Lt-Sided HF* - Low perfusion (decrease CO): Cool extremities - Some pulmonary congestion *Cold & Wet* *ADHF into Cardiogenic Shock* - Low perfusion (decreased CO) - Pulmonary Congestion

Acute Decompensated HF (ADHF)

*a sudden worsening of the signs & symptoms of heart failure/common acute respiratory distress* - Fluid overload life threatening (pulmonary edema develops) - Compensatory mechanisms have failed - Vasoactive IV's required: Venodilators; inotropes - Advanced therapeutic modalities required

(Meds Angina) *ACE-inhibitors* "-pril"

*block angiotensin I conversion to Angiotensin II (causes vasoconstriction = increases BP)* - No angiotension II no vasoconstriction = no increase BP *s/s*: cough, hypotension, hyperkalemia

Cholesterol Absorption Inhibitor

*blocks absorption of cholesterol in the jejunum* Example: - *Ezetimibe*: blocks absorption in small intestine *s/s*: (URI) Upper respiratory infection, nasopharyngitis (common cold), diarrhea -Do not give w/bile acids sequestrants!

(Meds Angina) *Angiotensin Receptor Blockers* "-sartan"

*blocks angiotensin II receptor* (Angiotension II cannot attach & cause vasoconstriction) *s/s*: hypotension, dizziness, hyperkalemia

Arterial Thrombi

*blood clot in the artery* - Arteries are blood vessels that carry blood from the heart to the rest of the body *Rich in platelets* & mobilize quickly/rupture under *high shear force* (Need to have damaged endothelium) Arteries have a natural high pressure bc of heart constriction of blood to the rest of the body

Cardiomyopathy (CMP)

*causes heart muscle to become enlarged, thick or rigid* - disease of the heart muscle which causes generalized deterioration of the muscle & its pumping ability

collateral circulation

*circulation formed by smaller blood vessels branching off from or near larger, occluded blood vessels* BYPASS blockage! (sacrifice few to save many; collateral damage) Body's defense mechanism to prevent ischemia* - Develop over time, most common in older pts. Slowly blocking over time always slow alteration of heart muscle to stay alive "Sacrifice the one for the greater good" - add more routes for blood to flow bc current route is dying

Venous thrombi

*clot in a vein* *Rich in fibrin & low shear force* - from body back to heart (Endothelium not necessarily damaged)

(Meds Angina) *B-adrenergic blockers* (aka beta-blockers)

*competes w/catcholamine's (epinephrine/adrenaline) at adrenergic receptor sites* (blocking the effects of epinephrine (adrenaline) decreases HR & force = decrease BP - usually used to protect heart from 2nd heart attack *s/s*: N/V, Hypotension, bradycardia, fatigue

Systole

*contraction* of the heart - Mycardial fibers are tightening & shortening, blood pushed out of cavities

Infarction

*death of tissue* - resulting from obstruction of the blood supply to an organ or region of tissue & lack of oxygen from RBC's

Niacin (Vitamin B)

*decreases VLDL. triglycerides & LDL levels/increases HDL* -*Dilates blood vessels* (improve circulation) "flushing occurs" - improves blood sugar which can damage arterial walls *s/s: severe flushing/itching common

acute coronary syndrome (ACS)

*develops when CAD is not well controlled and causes persistent & prolonged myocardial ischemia from rupture of a once stable atherosclerotic plaque* sudden symptoms of insufficient blood supply to the heart indicating unstable angina or acute myocardial infarction - Prolonged ischemia - Not readily reversible *spectrum of three entities* - Unstable angina (UA) - Non ST-segment elevation myocardial infarction (NSTEMI) - ST-segment elevation myocardial infarction (STEMI)

Beta Blockers

*end in "-olol"*; Labetalol, Metoprolol (Lopressor) - Blocks epinephrine which blocks sympathetic system of the heart (fight or flight response) = decreases BP & dilates vessels NOT FOR ASTHMA or COPD patients bc blocks beta receptors which are found in lungs. Beta receptors cause bronchodilation, so if blocked patient experiences bronchoconstriction. Diabetics: need to watch glucose levels bc medication masks symptoms of HYPOglycemia like tachycardia. watch patients for Bradycardia & Orthostatic Hypotension

ACE Inhibitors

*end in "-pril"; Lisinopril* - Prevents vasoconstriction by blocking Angiotension 1 & 2 receptors Educate: *Dry cough* - avoid K+ substitutes/supplements (bc med causes body to retain K+) - compliance. (Never stop abruptly bc can cause rebound HTN) - Best to take 1 hour before meal (esp. w/Captopril & Moexipril bc it increases absorption)

*BNP* (Brain Natriuretic Peptide) Levels

*helps detect and evaluate heart failure* *GOLD STANDARD LAB* - A hormone: helps regulate blood pressure (Vasodilation), decrease preload & afterload, and body's salt & water content. Tries to counteract RAAS Are substances produced in the heart (primarily Left Ventricle) & *released when the heart is stretched* (working too hard to pump blood) *healthy Level: below 100 pg/ml* - Increased levels indicate the heart is working too hard & having more trouble meeting the body's demands.

Troponin test

*helps detect heart attack or heart injury* - are proteins that regulate muscle contraction. They are released when the heart muscle has been damaged (myocardial cell death) *More damage = Greater concentration in blood* - Increased concentration also increases risk of future heart events - labs will be elevated within 3 - 4 hours after injury and may remain elevated for 10 to 14 days

Right Ventricular Hypertrophy

*increase in thickness of the myocardium of the Right ventricle* If conditions occur which decrease pulmonary circulation, meaning blood does not flow well from the heart to the lungs, extra stress can be placed on the right ventricle

PCSK9 inhibitors

*inhibits PCSK9 from binding to LDL receptors & degrading them. This allows an increase in LDL receptors & clearance* (So more LDL can be used and removed) - used in pts w/familial hypercholesterolemia & heart disease - INJ *s/s: Fatigue/muscle pain*

(Meds Angina) *Anti-platelets*

*interfere w/plt aggregation (clumping)* - *Aspirin*: inhibits the formation of thromoxane A2 (stimulates platelet activation & increases platelet aggregation) - *Plavix*: ADP blocker (prevent plt aggregation & prevent clots) *s/s*: Bleeding, abd pain, dyspepsia (indigestion/impaired digestion)

thrombogenic

*material to make clot/formation of clot* (genic= genesis) Tendency of a material in contact w/the blood to produce a thrombus (or clot)

*primary & secondary causes* of HTN

*primary/essential* causes* UNKNOWN CAUSE: "RISK FACTORS" *R*ace (black males) *I*creased intake of Na+/ETOH *S*moking/Stress *K* & vitamin D levels decreased *F*amily hx *A*dvanced Age *C*holesterol increased *T*oo much caffeine *O*bese (BMI) *R*estricting Activity *S*leep Apnea *Secondary Causes* of HTN PRE-EXISTING CAUSING ISSUE Pregnancy Cushing syndrome CRF Diabetes Hypo/Hyperthyroidism

Angina Pectoris

*reduced blood flow to the heart* (not receiving enough oxygenated blood) - Atherosclerotic stenosis (narrowing) - Coronary artery spasm (constriction) - Coronary thrombosis (clot) results in mycardial ischemia (damaged cells/cell death) - Anaerobic metabolism causes pain as lactic acid builds in the cells

(Meds Angina) Organic *Nitroglycerin*

*relaxes/dilates arterial & venous smooth muscle to increase BF (reduce preload)* - Short acting & long acting (nitrate free intervals) *s/s*: Headache, hypotension, relfex tachycardia, tolerance *take pt off @ night to avoid tolerance & makes med less effective if always on. Body gets used to it

Embolism

*sudden blocking of an artery* - Thrombus mobilized & blocked artery

Pulmonary hypertension

*type of high blood pressure that affects the arteries in your lungs and the right side of your heart* In one form of pulmonary hypertension, tiny arteries in your lungs, called pulmonary arterioles, and capillaries become narrowed, blocked or destroyed. This makes it harder for blood to flow through your lungs, and raises pressure within your lungs' arteries. As the pressure builds, your heart's lower right chamber (right ventricle) must work harder to pump blood through your lungs, eventually causing your heart muscle to weaken and fail Right ventricle= heart to lungs Left Ventricle = heart to body

Cholesterol

*types of fats (lipids)* - *Building blocks in certain hormones, cell membranes, & bile acids* Circulates in blood w/triglycerides, encapsulated by fat carrying lipoproteins - <200 mg/dL desirable for total cholesterol level

Pathophysiology of DVT

- *Platelets & fibrin aggregate at site & form initial clot* (where damage has occurred or at the cusp of the valve) - *Thrombus enlarges* producing a large clot with a "tail" blocking the lumen (RBC are trapped in the fibrin meshwork) - *Thrombus propagates (spreads) in the direction of the BF* - *Inflammation is triggered* (cause tenderness, swelling, & *erythema*(skin redness)) - *Fibroblasts invade thrombus* (scarring vein wall & destroying valves, patency (open/expanded/unobstructed) may be restored but valve damage is permanent, affecting directional flow) - *Pieces of thrombus may break loose & travel* through circulation (become emboli) *STENTS are not put in veins (only ARTERIES). FILTERS are placed in VEINS instead* s/s -*Proximal DVT's* (above popliteal/thigh) are *more dangerous* than distal DVT's (below popliteal/calf) S/S: - Calf pain or tenderness - Swelling & Edema - *Erythema* (skin redness), *Paresthesia* (burning/prickling/tingling/numbing sensation), *Fever* (redness, warmth, systemic) - Superficial venous dilatation Diagnostics (*D*VT = *D*-*d*imer blood test & *D*uplex ultrasound ) Blood tests (1st) *D Dimer (Gold standard)*: products of clot degradation. If d-dimer is +, then ultrasound needed to locate clot (ultrasound second) - when body breaks down a clot, D-dimer (a protein) is leftover floating in the blood. Too much D-dimer in your blood is a sign for DVT (body continuously trying to break it down) Imaging Studies - (2nd) *Duplex Ultrasound (Gold standard)* Invasive Venous Studies - CT or MRI venography Other labs - coagulation studies - H & H - Platelet Count

*Chronic* HF *Circulatory Assist*

- Biventricular Pacing: Resynchronize the ventricles - Implantable cardioverter (defibrillator) - Cardiac Transplant

(HF) Heart Failure/Chronic Heart Failure (CHF) Treatment

- Dietary & lifestyle changes: recognition of symptom worsening; tobacco cessation: follow up with MD - Lasix, Beta-blockers, Nitrates, Oxygen, Positioning, ACE-Is, or ARBs - Rescynchronization therapy w/biventricular pacing - planned Rest periods;Cardiac Rehab - Daily Weights - Cardiac transplant ultimately with temporary left ventricular assist device

Heart Failure Care Planning

- Fluid Balance - Respiratory Status: Gas Exchange - Activity Tolerance - Cardiac Pump Effectiveness - Knowledge Deficit: Disease Process - Support End-of-Life decisions/Palliative Care *Core Measures* - HF Discharge instructions include: - Prognosis of heart failure; Activity level; discharge meds; follow-up appointment; weight monitoring; what to do if symptoms worsen - Assessment of left ventricular function - Patients with known systolic dysfunction (EF <40%) receive an ACE-I or ARB - Smoking cessation advice or counseling, if a current smoker, during hospital stay

*Chronic* Heart Failure *Drug Therapy*

- PO Vasodilators - ACE-Inhibitors - Angiotensin II Receptor Blockers (ARBs) - ß-adrenergic blockers - Nitrates

Nursing Implications of Heart Failure

- Physical assessment - Co-morbidities - Treat underlying cause as prescribed (Base on staging of disease) - Daily weights - Diet modification (sodium/fluid) - Patient positioning - Continuous monitoring (rhythm, HR, urinary output, respiratory, & oxygenation) - Oxygen/Drug/Advanced therapies (monitor effectiveness) - Alternate rest-activity periods - Cardiac rehab

DVT Prevention & Prophylaxis

- Pts on bedrest need to change positions q 2 hr, flex & extend feet/ankles/knees/hips - Ambulatory patients need to sit in a chair for all meals & walk @ least 4-6 x per day - Elastic compression (anti-embolism) stockings; measure for correct size - Sequential Compression Devices (SCD's) *Not w/active DVT* (bc it will loosen clot) - Pharmacologic Prophylaxis: Low Molecular Weight Heparin in low dose BID Benefits of VTE prophylaxis (taking action to prevent) - Improved pt outcomes - Reduced costs

Diagnostics: Cardiac enzymes

- Troponin levels (I and T) are used in conjunction with CK-MB findings - have high specificity for myocardial infarction Combined elevation of Troponin and CK-MB indicate that coronary artery blood flow has been sufficiently obstructed to cause myocardial necrosis

Calcium Channel Blockers

-dipine *Peripheral & Coronary vasodilator; reduces HR, impulse conduction velocity, contractility & BP*

Beta-Blockers

-olol *Inhibits sympathetic response; reduces HR, contractility, & blood pressure*

INR Range NOTE

0.8-1.1 normally you want INR range to be negligible HOWEVER if drugs are needed like warfarin you want the range of INR to stay between 2-3

Complications of DVT

1. *Post-thromotic Syndrome* (PTS) - redness, swelling, ulcers, and chronic leg pain. affects mobility and is expensive to treat, preventative measures best - occurs 20-50% of pts - manifests as chronic venous HTN from valve destruction - Causing painful congestion (heaviness) & edema of leg, w/lymphangitis

Virchow's triad

1. Venous Stasis, 2. hypercoagulability, 3. endothelial damage Venous Stasis *"Blood sitting in vein"* - prolonged immobility - obesity -pregnancy - HF/A-fib - Orthopedic surgery - prolonged surgical procedures - Extended travel in a seated position Hypercoagulability *increase clotting of blood* - Severe anemias - Malignancy - Estrogen based oral contraceptives (increase DVT & Stroke risk) - Smoking - Inherited disorder of coagulation - Acquired disorders of coagulation - Sepsis - Dehydration Endothelial Injury *Damage to the endothelium stimulates platelet activation* (Platelets stick and are released when body is injured) *Direct* (Physical) - Trauma, surgery, invasive procedure, iatrogenic causes (Central venous catheters, subclavian, internal jugular lines: can cause upper extremity DVT) *Indirect* (Illness/Disease) -Chemotherapy, Diabetes, Sepsis

STEMI *Diagnostics*

12 lead ECG - ST segment elevation with T wave inversions pathologic Q waves Echocardiography: to determine the EF & wall motion disturbances Chest xray: detects presence of HF Cardiac catheterization: primary coronary re-perfusion therapy to open coronary artery blockages Cardiac enzymes: confirms MI diagnosis (but does not delay need to go to cath lab)

Hypertension—Causes

ABCDE Aldosterone/Apnea Bad kidney/Bruits Catecholamines/Cushings syndrome Drugs/Diet Endocrine

coronary artery disease (CAD) "Stable Angina"

a blood vessel disorder resulting from atherosclerosis STABLE ANGINA *Progressive atherosclerotic development* Caused by deposition of cholesterol and lipids within the intimal walls of the arteries S/S Chest Pain Interscapular pain (jaw/neck pain) intermittent pain that is relieved with rest or Nitroglycerine (NTG) *Diagnostics* 12-Lead ECG ST segment depression or T wave inversion Stress Testing *Nursing Implications* Physical assessment Co-morbidities Health promotion (Physical Activity) Nutritional therapy Drug therapy (cholesterol/lipid-lowering, antiplatelets, nitrates, beta blockers) Education on how to reduce energy demands importance of medication therapy

Triglycerides

a combination of glycerol w/3 fatty acids: "Transportable fuel (energy source)" -Strongly influenced by diet *<150mg/dL* optimal

cardiovascular disease (CVD)

a disease of the heart and blood vessels. *a major cause of death* - 1.1 million deaths per year - decreased mortality in the last 10 years defined by several disease processes - Coronary artery disease - Chronic stable/Unstable angina - Silent/Variant angina - Acute coronary syndrome - Non-ST segment-elevation myocardial infarction - ST segment-elevation myocardial infarction

Embolectomy

surgical removal of an embolus

Syncope

temporary loss of consciousness caused by a fall in blood pressure

DVT

the formation of a blood clot in one of the deep veins of the body, usually in the leg *Low shear force & Rich in Fibrin* etiology Starts in lower extremity (calf veins) -> progressing proximally to involve -> Popliteal, Femoral, Iliac System Risk Factors - Lung Disease - Family or Patient has history of VTE - Older Age - *African Americans* greater than white; Hispanic lowest - *Men* greater than women

JVD (jugular vein distention)

this is bulging of the external jugular vein which indicates increased blood volume and usually congestive heart failure (CHF)

Echo cardiogram

ultrasound of the heart

coronary angiography

used to determine the degree of stenosis or obstruction of the arteries that supply blood to the heart

Collaborative Care: Fibrinolytic Therapy

uses medications that act to dissolve blood clots.(Door-to-Drug < 30 min)

Preload

volume of blood in ventricles at end of diastole - venous blood return to atria - filling pressure of the right & Left side of the heart

ascites

abnormal accumulation of fluid in the abdomen

Hypercholesteremia

abnormal condition of excessive cholesterol in the blood

Arrhythmias

abnormal heart rhythms

Tachypnea

abnormally rapid breathing

IV Antidysrhythmics

amiodarone only for sustained ventricular rhythms *treats wide complex Tachycardia*

Ejection Fraction (EF)

amount of blood pumped out of the ventricle with each heart beat divided by amount of blood present in the ventricle just prior to systole *Normal: 55 - 60%* - Measured by echo-cardiogram or directly via cardiac catheterization

Hypertension (HTN)

amount of resistance of blood pumping through the body/arteries - narrowing of arteries causes increase BP & resistance effecting major organ systems *Silent Killer* (Does not present with Symptoms until it is bad)

thyrotoxicosis (thyroid storm)

an acute and potentially deadly condition caused by an overactive thyroid

Morhpine

analgesic & sedative

pulmonary infarction

area of necrosis (*death of lung tissue*) - Alveolar necrosis can result in: hemorrhage, Abscess development, Pleural Effusion death of a section of lung tissue caused by vascular obstruction — is a fairly common in PE

Neurohormonal response - Antidiuretic hormone (ADH)

causes volume overload by promoting re-absorption of water in the kidneys

Hemoptysis

coughing/spitting up blood

asphyxia

deprivation of oxygen for tissue use; suffocation

Dyspnea

difficult or labored breathing

orthopnea

difficulty breathing when lying down

echocardiography (ECHO)

echoes generated by high-frequency sound waves produce images of the heart - Determines the Ejection Fraction (EF) & wall motion disturbances

Idiopathic Pulmonary Arterial Hypertension (IPAH)

elevated pulmonary artery pressure resulting from an increase in resistance to BF through the pulmonary circulation (right ventricle thickens) - *Inability of cardiac output to increase in response to O2 demand* "Idiopathic" = dont know why - Mean pulmonary artery pressure > 25 mm/Hg @ rest - Mean pulmonary artery pressure > 30 mm/Hg w/exertion Causes form of pulmonary hypertension w/ - Cause Unknown - Possible associated w: drugs, toxins, heart disease, HTN - Affect females more than males - If untreated: rapidly progresses to the right sided HF & death

Calcium Channel Blockers (CCBs)

end in "-dipine"; Diltiazem (Cardizem) & Verapamil - lowers HR & causes vasodilation = decreases workload on the heart - *watch for bradycardia* (bc affects HR) - caution w/patients of CHF & AV Heart blocks

Hypertrophy/Dilation

enlargements of the heart - Ventricles dilate in attempt to adapt to increase in circulating volume -->> increased contractility & CO - Can get overstretched - Muscle mass & cardiac wall thickness increase in response to increase cardiac workload w/chronic dilation *Negative effect: heart works harder = increase myocardial O2 demand*

EPinephrine

every pulseless individual

diaphoresis

excessive sweating

Atheroma

fatty material that forms plaques in the arteries

Afterload

force or resistance that the ventricle must generate to open pulmonary or aortic valves - Correlates w/Diastolic BP

Atherosclerosis

hardening of the arteries Begins as soft deposits of fat that harden with age

Hypervolemia

increased blood volume

myocarditis

inflammation of the heart muscle

endocarditis

inflammation of the inner lining of the heart s/s signs FROM JANE • Fever • Roth's spots • Osler's nodes • Murmur • Janeway lesions • Anemia • Nail hemorrhage (splinter hemorrhages) • Emboli

D-Dimer Test (Gold Standard)

is a global marker of coagulation activation and measures *fibrin degradation products* produced from fibrinolysis (clot breakdown) (clots made of fibrin) - used for the diagnosis of DVT - sensitive test but has a poor specificity, it should only be used to rule out deep vein thrombosis (DVT), not to confirm a diagnosis (CT used to confirm)

Ischemia

lack of blood flow (supply)

myocardial infarction (MI)

leading cause of death of all cardiovascular diseases (56%) *Sustained ischemia leading to irreversible cell injury and death (necrosis) bc a STEMI or NSTEMI* - Perfusion distal to occlusion halted - Loss of contractile function

Nitrates/Nitrites

nitroglycerin relax arteries so blood can flow more easily to heart.

cardiac catheterization (CC)

passage of a catheter into the heart through a vein or artery to provide a comprehensive evaluation of the heart - Helps to rule out presence of coronary artery blockages

Collaborative Care: stent placement

placement of a mesh tube inserted into a natural passage or conduit in the body to prevent or counteract a disease-induced, localized flow constriction

atheromas

plaques in blood vessel walls

Cardiopulmonary Bypass

procedure that temporarily circulates and oxygenates a patient's blood during the portion of heart surgery where the heart is stopped - blood is diverted from the patient's heart to a machine where it is oxygenated and returned (via a pump) to the patient. - allows surgeon to operate on a quiet, non beating, bloodless heart while perfusion to vital organs is maintained.

Coronary Artery Bypass Graft (CABG)

recommended for patients with unstable angina who demonstrate poor response to traditional Rx. - Grafts use: saphenous vein or internal mammary artery. - Provides the patient with improved outcomes, quality of life and survival. Nursing Role: Teaching Pre-Op-location/purpose of post-op tubes (chest tubes) and when they will be removed. Encourage support groups to help quit smoking, manage stress etc; low fat diet, exercise at every opportunity. - Take Aspirin regularly to reduce chances of having an MI. MD Role: Risks/Complications of symptoms; modifying regimen; nature and procedures of symptoms.

Anasarca

severe generalized edema

Paroxysmal nocturnal dyspnea (PND)

shortness of breath that occurs suddenly during sleep