Class 2 CV Flashcards
Coagulation modifiers
-Anticoagulants
-Antiplatelets
Coagulation modifiers: General overview
-Anticoagulants, antiplatelet & thrombolytic drugs
-Hemorheological drugs→ alter platelet function (don’t block)
-Antifibrinolytic drugs→ promote coagulation and manage conditions with excessive bleeding
Anticoagulant drugs and functions (SCDHg)
-Heparin & glycosaminoglycans; inhibit clotting factors IIa (thrombin) and Xa
-Direct thrombin (IIa) inhibitors
-Selective factor Xa inhibitor
-Coumadins; inhibit vitamin K clotting factors II, VII, IX & X
Heparin drugs
-“parins”
Coumadin drugs
Warfarin Na+
Glycosaminoglycan drugs
Danaparoid Na+
Direct thrombin inhibitor drugs (BDHA)
-Human antithrombin III
-Argatroban
-Bivalirudin
-Dabigatran etexilate mesylate
Selective factor Xa inhibitor drugs (FAR)
-Fondaparinux
-“abans”
Antiplatelet drugs (MGAP)
-P2Y12 inhibitors
-Aggregation inhibitors/vasodilators
-Glycoprotein IIb/IIIa inhibitors
-Miscellaneous
Aggregation inhibitors/vasodilators
Treprostinil
P2Y12 inhibitors
-“grel”
Glycoprotein IIb/IIIa inhibitors (TEA)
-Abciximab
-“fib”: Eptifibatide,Tirofiban
Miscellaneous antiplatelet drugs
-Anagrelide hydrochloride
-Dipyridamole
Coagulation modifiers
-Lyse clots
-Thrombolytics
-Promote clot formation
-Antifibrinolytics
-Reversal drugs
Thrombolytic functions
-Dissolve thrombi
-Activate plasminogen
-“plase”
Antifibronolytics
-Prevent lysis of fibrin
-Reduce blood viscosity
Prevent lysis of fibrin
-Systemic hemostats
-Tranexamic acid, aprotinin
Reduce blood viscosity (HP)
-Hemorheological
-Pentoxifyline
Reversal drugs
-Heparin Na+ antagonist; protamine sulphate
-Warfarin Na+ antagonist; vitamin K
Anticoagulants: General overview
-Prevent formation of a clot
-Remember, they cannot lyse any clot that has already been formed (as in the case of a stroke or pulmonary embolism)
Common anticoagulants
-“parins”, “abans”
-Warfarin (Coumadin)
-Argatroban, Bivalirudin, Dabigatran
-Fondaparinux
Low molecular weight heparin (LMWH); enoxaparin, dalteparin, tinzaparin: Indications for use
-AMI, UA, stroke
-Immobility, DVT, PE
-Indwelling devices such as heart valves
-Pre-op to prevent pooling of blood
Warfarin, rivaroxaban, or apixaban indications for use
Atrial fibrillation
Dabigatran indications for use
Prevention of strokes and thrombosis in patients with nonvalvular atrial fibrillation
Argatroban indications for use
Treatment of active or risk for HIT and PCI operation
About heparin (half-life, onset, peak, duration)
-1-2 hour half-life
-Onset:
-SC: 20-60 minutes
-IV: Immediate
-Peak
-SC: 2-4 hours
-Duration: Dose-dependent
Heparin (Hepalean, Heparin LEO, Hep LOK)
-Prevents
-“heparin” refers to “unfractionated heparin”
-Q6H measurement of PTT until anticoagulant effect is reached
Heparin (Hepalean, Heparin LEO, Hep LOK): SC & IV therapy indications for use
-S.C., dosing used post-op or with decreased mobility
-I.V. therapy: DVT, PE, AMI, A fib
Heparin (Hepalean, Heparin LEO, Hep LOK) toxicity symptoms
-hematuria, melena, petechiae, ecchymoses, and gum or mucous membrane bleeding
Heparin induced thrombocytopenia (HIT)
-Thrombocytopenia- low platelet count
-Allergic reaction mediated by the production of IgG antibodies
-Immune complexes bind to platelets, resulting in platelet activation and thrombin generation
Heparin induced thrombocytopenia (HIT) types of increased
-HIT I→ gradual reduction in platelets (heparin is usually continued)
-HIT II→ >50% acute drop in platelet level
Treatment of heparin induced thrombocytopenia (HIT)
thrombin inhibitors bivalirudin and argatroban
Nursing considerations of heparin induced thrombocytopenia (HIT)
-Thrombosis in the presence of HIT can be fatal
Low molecular weight heparin (LMWH) (form, function, why its better than heparin)
-Enoxaparin, dalteparin, tinzaparin
-Synthetic SC injection
-Greater affinity for factor Xa
-Higher bioavailability and longer half-life than unfractionated Heparin
-More predictable anticoagulant response than heparin
-Frequent lab monitoring not required
-Patients can be “bridged” with Coumadin therapy (warfarin)
Low molecular weight heparin reversal
Protamine, same as heparin reversal
About Warfarin (Coumadin) (half-life, onset, peak, duration, form, use, monitoring)
-Half-life: 0.5-3 days
-Onset: 12-24 hours
-Peak: 3-4 days
-Duration: 2-5 days
-PO, long-term anticoagulation
-Monitor PTT/INR
-A ‘normal’ INR is 1, for someone receiving Coumadin a therapeutic INR is usually 2-3 OR 2.5-3.5 for a mechanical valve
Warfarin (Coumadin) antidote (when to discontinue, how it works & how long to resynthisize, drug reversal, resistance time)
-Discontinued if INR is high
-Coumadin inactivates the vitamin K-dependent clotting factors which are synthesized in the liver; discontinuing therapy may take 36-42hrs before it can be resynthesized
-10-15 mg vitamin K IV can reverse anticoagulation effects within 6 hrs; risk of anaphylaxis
-Fresh Frozen Plasma to reverse the anticoagulation effects during an acute bleed
-Redraw INR
-After administration of vitamin K, warfarin resistance will occur for up to 7 days
Dibagatran: Thromboprophylaxis after elective hip or knee replacement
-150-220mg daily
-14 days for knees and 30 days for hips
Dabigatran dosing: Non-valvular atrial fibrillation
-110 or 150mg BID
-CR Cl>30mL/min
Rivaroxaban: Thromboprophylaxis after elective hip or knee replacement
-10mg daily
-14 days for knees, 30 days for hips
Rivaroxaban dosing: Non-valvular atrial fibrillation
-15 or 20mg daily
-CR Cl 30-49mL/min
Rivaroxaban dosing: Venous thromboembolism
-15mg BID for 21 days then 20mg daily
Anticoagulant contraindications
-Thrombocytopenia
-Pregnancy
-LMWHs cannot be administered to patients with indwelling epidural catheter; epidural hematomas
Anticoagulant adverse events
-Bleeding, no IM injections, be cognizant of surgery
-Use of aspirin or other drugs that impair platelet function
-N/V, abdominal cramps, thrombocytopenia
-Warfarin (Coumadin); bleeding, lethargy, muscle pain, necrosis, and “purple toes” syndrome
Warfarin: Drug to drug interactions: Acetaminophen, amiodarone, bumetanide
-Displacement from inactive protein-binding sites
-Increased anticoagulant effect
Warfarin: Drug to drug interactions: Furosemide, ASA/NSAIDs, broad spectrum anitbiotics
-Decreased platelet activity
Warfarin: Drug to drug interactions: Barbiturates, carbamazepine, rifampin, phenytoin
-Enzyme induction
-Decreased anticoagulant effect
Warfarin: Drug to drug interactions: Amiodarone, cimetidine, ciprofloxacin, erythromycin, ketoconazole, metronidazole, omeprazole, sulfonamides, macrolides
-Enzyme inhibition
-Increased anticoagulant effect
Warfarin: Drug to drug interactions: HMG-CoA reductase inhibitors (statins), cholestyramine, sucralfate
-Impaired warfarin, Na+ absorption
-Decreased anticoagulant effect
Warfarin: Drug to drug interactions: Natural Health Products: dong quai, garlic, ginkgo biloba
-Increased INR
-Increased bleeding risk
Warfarin drug to food interactions: St. John’s Wort, ginseng (alone & in cold-FX)
-Decreases INR
-Increased risk for clotting
Heparin Na+ drug to drug interactions: Aspirin & other NSAIDs
-Decreased platelet activity
-Increased bleeding risk
Heparin Na+ drug to drug interactions: Oral anticoagulants & thrombolytics
-Additive
-Increased anticoagulant effect
Antiplatelet drug to drug interactions: Aspirin & other NSAIDs
-Decreased platelet activity
-Increased bleeding risk
Antiplatelet drug to drug interactions: Warfarin, heparin Na+. thrombolytics, rifampin
-Additive
-Increased bleeding risk
Antiplatelet drug to drug interactions: Natural health products; garlic, ginkgo, kava
-Increased effects
-Increased bleeding risk
Antipatelet drug to food interactions
-Foods high in vitamin K increase risk of clotting
Anticoagulant nursing considerations
-Will administration increase or decrease bleeding or clotting, what conditions do I need to monitor for in this patient post administration, are there any procedures that warrant holding the medication
-Monitor labs daily when on anticoagulants; know what is important to follow for trends and why INR vs PTT
-Understand what bridging patient therapy means for management of conditions
-Monitor for treatment outcomes
Anticoagulant patient teaching
-Regular lab testing
-Avoid foods high in vitamin K
-Consume with 1 cup of water
Antiplatelet therapy: General overview
-Prevent clot formation by inhibiting platelet aggregation at the site of injury
-Each drug has unique mechanism of action properties
Antiplatelet common medications
-Acetylsalicylic acid (ASA/aspirin)
-Dipyridamole, pentoxyfylline
-“grels”
-GP IIb/IIIa Inhibitors
Aspirin MOA
-Used for antiplatelet & analgesic, anti-inflammatory and antipyretic properties
-Effects last lifespan of platelet which is 7 days
-Prevents the formation of thromboxane A2 from leading to dilation of blood vessels and platelet aggregation
Dipyridamole MOA
-Prevent release of substances that stimulate platelet aggregation
Clopidogrel MOA
-ADP inhibitors
-Inhibits platelet aggregation by altering the platelet membrane so that it doesn’t receive signals to form a clot
Pentoxifylline MOA
-Reduces blood viscosity by increasing flexibility of red blood cells and reduces the aggregation of platelets
-Inhibits ADP, serotonin, and platelet factor IV
GP IIb/IIIa inhibitors MOA
-Block receptor protein GP IIb/IIIa that occurs in the platelet wall membranes
Aspirin indications for use
-CAD
-First line of defense for acute coronary syndrome
-Chronic stable angina
-Post PCI, CABG, prosthetic valve insertion, TIA, & cardiac endarterectomy
-Patients with PAD, secondary prevention for venous thrombosis events
-Daily doses of 75 mg to 160 mg
Dipyridamole indications for use
-Used with warfarin to prevent postoperative thromboembolisms
Clopidogrel indications for use
-Post AMIs prevention of thrombosis, reducing thrombotic strokes
Pentoxifylline indications for use
-Peripheral vascular disease
GP IIb/IIIa inhibitors indications for use
-UA & AMI, angioplasty procedures (typically have arrhythmias after PCI)
Antiplatelet contraindications
-Thrombocytopenia, leukemia
-Traumatic injury, GI Bleed, recent stroke
-Vitamin K deficiency
Aspirin adverse events (CNS)
Drowsiness, dizziness, confusion, flushing
Aspirin adverse events (GI)
-N/V, bleeding, diarrhea
Aspirin adverse events (hemotalogical)
-Thrombocytopenia, leukopenia, neutropenia, hemolytic anemia, agranulocytosis, bleeding
Clopidogrel adverse events (CV)
-Chest pain, edema
Clopidogrel adverse events (CNS)
-Flu-like symptoms, fatigue, headache, dizziness
Clopidogrel adverse events (GI)
-Abdominal pain, diarrhea, nausea
Clopidogrel adverse events (miscellaneous)
Epistaxis, rash, pruritus
Ticagrelor adverse events (respiratory & miscellaneous)
Dyspnea (on initiation)
Elevated uric acid levels
GP IIb/IIIa inhibitors adverse events (CV)
-Bradycardia, hypotension, edema
GP IIb/IIIa inhibitor adverse events (CNS)
Dizziness
GP IIb/IIIa inhibitor adverse events (hematological)
-Bleeding, thrombocytopenia
Antiplatelet nursing considerations
-aBleeding
-Withhold drugs 5-7 days prior to surgical procedures
-Perform baseline CV assessment for medications and document pre-existing chest pain, edema, headache, dizziness, epistaxis or flu like symptoms
Aspirin contraindications
-Aspirin not to be used in young ppl or patients with with any bleeding disorder, vit K deficiency or with peptic ulcer disease
Antiplatelets + Pt teaching
-2-3 months for therapeutic effect
-Change position slowly d/t dizziness and orthostatic hypotension
Thrombolytics overview
-“Clot Busters”
-Streptokinase, tissue plasminogen activator [t-PA (alteplase and Tenecteplase (TNK)]
Thrombolytics indactions for use
-MI, arterial thrombosis, DVT, PE
-Occlusion of catheter or shunts
-Acute ischemic stroke
Thrombolytic adverse effects
-Internal, intracranial, and superficial bleeding
-N/V, hypotension, dysrhythmias
Thrombolytic interactions
-Increased bleeding tendency from use of anticoagulants, antiplatelet, or other drugs that affect platelet function
Anti-thrombolytics
-Tranexamic acid
-Aprotinin
-DDAVP
Thrombolytic nursing considerations
-Monitor IV sites, no IM injections
-Monitor bleeding from wounds or from the GI, GU, or respiratory tract
-Monitor for internal bleeding (decreased BP, restlessness, increased pulse)
Thrombolytic nursing considerations when monitoring labs (aspirin)
Monitor CBC (Hgb, hematocrit, platelet counts), PTT and INR
Nursing considerations when monitoring labs: Clopidogrel
-Monitor CBC (Hgb, hematocrit, platelet counts), PTT and INR
-Contact healthcare provider if platelet levels are less than 90 x 109 /L
Nursing considerations when monitoring labs: GP IIb/IIIa inhibitor
-Monitor PTT levels
Nursing considerations when monitoring labs: Thrombolytics
Monitor CBC (Hgb, hematocrit, platelet counts), PTT and INR, fibrinogen levels
Antilipemic medications overview
-Reduce lipid levels
-Ezetimibe (Ezetrol)- cholesterol inhibitor
-PCSK9 Inhibitors Monoclonal Antibodies (Evolocumab and Airocumab); for abnormal accumulation of lipids
-For patients at risk of atherosclerotic CVD
Classes of antilipemic medications
-HMG-CoA reductase inhibitors (statins)
-Bile acid sequestrants
-Vitamin B niacin (nicotinic acid)
-Fibric acid (fibrates)
Antilipemic medications are prescribed for people with…
-Decreased cholesterol
-Increase HDL
-Decrease LDL
Antilipemics: HMG-CoA reductase inhibitors
-Inhibit enzyme that catalyzes the rate-limiting step in the synthesis of cholesterol
-“statins”
-First line drug post AMI
Antilipemics: HMG-CoA reductase inhibitors (statins): Contraindications
-Pregnant or breastfeeding
-Liver dysfunction or elevated transaminase levels
-Elevated liver enzymes
Atorvastatin Ca+: Half-life, onset, peak, duration
-Half-life: 13-16 hours
-Onset: 1-2 hours
-Peak: 2 weeks
-Duration: Unknown
Atorvastatin Ca+ (does what, administered when, approved for who, available in what)
-Lowers total cholesterol LDL and triglycerides, raises HDL
-Administered in the evening
-Only statin approved for use in children
-Available in combination with calcium channel blocker amlodipine (Caudet)
Antilipemics: HMG-CoA reductase inhibitors (statins): Adverse effects
-Myopathy (muscle pain) which may progress to a serious condition known as rhabdomyolysis
-Rhabdomyolysis involves the breakdown of muscle protein leading to myoglobinuria
-Excretion of this abnormal urinary protein can lead to acute kidney failure
-Report muscle pain or discomfort
Antilipemics: Ezetimibe (half-life, onset, peak, duration)
-Half-life: 22 hours
-Onset: Unknown
-Peak: 4-12 hours
-Duration: Unknown
-Only cholesterol absorption inhibitor
Functions of ezetimibe
-Selectively inhibits absorption of cholesterol and related sterols in the small intestine
-Reduces total cholesterol, LDL-C, Apo B, and triglycerides
-HDL-C serum level increase
-These beneficial effects are enhanced when combined with a STATIN
Contraindications of ezetimibe
-Active liver disease or unexplained elevations in liver enzymes
Antilipemic lab nursing considerations
-Monitor liver function tests (bili, AST, ALT, Alk Phos, GGT) for toxicity, cholesterol lab test (TG, TC, HDL, LDL) for treatment outcomes, and creatinine, BUN, GFR for kidney dysfunction
Antilipemic nursing considerations + CV adverse events/diabetes
-Monitor for CV events & diabetes (troponin, fasting blood glucose)
Antilipemic nursing considerations + HMG-CoA reducase inhibitors adverse events
-Monitor for rhabdomyolysis (muscle soreness, changes in urine color, fever, malaise, & N/V). If rhabdomyolysis is suspected, CK levels will be drawn
Antilipemic nursing considerations (adverse events)
-GI upset
-Increased liver enzymes
-Hepatomegaly
-Myalgias
Acute HF management goals
-Improve ventricular function, gas exchange, oxygenation & CO
-Decrease preload, afterload & intravascular volume
Clinical presentations of HF (respiratory)
-Dyspnea, decreased SpO2
-Crackles/wheezing
Clinical presentations of HF (CV)
-Low BP, weak pulse
-Edema, JVD, ascites
-Infarct, S3 gallop, tachycardia
Clinical presentations of HF (neurological)
-Anxiety, confusion, fatigue, dilated pupils
Clinical presentations of HF (integumentary)
-Cool, moist, pale, gray or cyanotic
Clinical presentations of HF (GI/GU)
-N/V
-Enlarged spleen & liver
-Decreased urine output
Pharmacological management goals in heart failure
-Improve ventricular function
-Decrease intravascular volume
-Decrease preload
-Decrease afterload
-Improve gas exchange and oxygenation
-Increase CO
Drugs to increase CO in heart failure
-Loop diuretic→ Furosemide
-O2, nitro patch, ACE I
-Digoxin, beta blockers
-In critical care: Dobutamine and nitro infusions
Investigations in HF
-Chest x-ray, ECG
-Echocardiogram to assess ejection fraction; transthoracic echocardiogram
Labs to monitor in HF
-CBC
-Kidney function tests
-Electrolytes
-BUN
-Creatinine
-Glucose
-Hemoglobin
-Liver enzyme
-Lipid
-Thyroid function tests
Disorders of the heart wall
Acute pericarditis, pericardial effusion, cardiac tamponade
Acute pericarditis diagnostic indicators
-12-lead ECG (ST elevation) & chest pain that is relieved by sitting forward
Management of acute pericarditis
-NSAIDs (Ibuprofen 600 mg TID)
-ASA
-Corticosteroids
-Proton pump inhibitor to prevent GI bleed
Pericardial effusion diagnostic tests
-Echocardiogram to identify presence of fluid
-CT chest or cardiac MRI
Pericardial effusion medications
-NSAIDs
-ASA
-Corticosteroids
-PPI
Pericardial effusion labs
-CRP
-Troponin
-WBCs if on corticosteroids
Cardiac tamponade management
-Pericardiocentesis guided by ultrasound
-Post procedure monitor for infection and leaking of fluid from the site
Cardaic tamponade medications
-NSAIDs
-ASA
-Corticosteroids
-PPI
All disorders of the heart wall (pericarditis, pericardial effusions & cardiac tamponade) have what in common?
Medications
DVT lab values
-CBC: Hemoglobin, hematocrit, platelets
-Coagulation: ACT, PTT, INR, D-dimer (to rule out PE)
Invasive investigations for DVT
-CT
-Venography
DVT interventions
-TED stockings
-Intermittent pneumatic compression device
DVT management to prevent DVT (prophylaxis)
-Prophylaxis tx: Heparin or LMWH sc injections, “abans”, and dabigatran
DVT management after diagnosis
-Heparin IV, thrombolytics
-Venous thrombectomy or insertion of a filter to prevent movement of the embolus
-Pain management
DVT patient teaching
-Modify risk factors for developing another clot
-Explain S&S (sudden onset of dyspnea, tachypnea, and pleuritic chest pain)
-Create medication regime including dosages, actions, adverse effects, reason for routine blood tests, and symptoms to report
-Avoid activities with high risk for trauma
-If injury occurs, instruct patient and family to apply pressure to wound for 10-15 minutes
-Well-balanced diet→ calcium and vitamin E
Modified risk factors for developing another clot
-Encourage mobility
-Compression stockings
-Smoking cessation
-Discontinue birth control or oral hormone replacement therapy
-Avoid stagnation
Aortic aneurysm diagnostic studies
-Chest x-ray, EKG, Echocardiography, CT scan, MRI, and angiography
Collaborative care for an aortic aneurysm
-Hydraton and all electrolyte, coagulation and hematocrit abnormalities corrected prior to surgery
-Surgery with goal of normal tissue perfusion, intact motor and sensory function, and no complications related to surgical repair
-ICU post op
Endovascular abdnominal aortic aneurysm repair
-Most common complication from EVAR is endoleak; the seepage of blood back into the old aneurysm
-May require open surgical repair
-Discovered by inserting a catheter and using a transducer system
Aortic aneurysm: Abdominal compartment syndrome
Patients may also develop intra-abdominal hypertension associated with abdominal compartment syndrome; reduces blood flow to the viscera
Aortic aneurysm repair: Post operative care
-Monitor for abdominal compartment syndrome & BP for graft patency
-Infection
-CV&GI status
Monitoring BP graft for patency
-Hypotension may lead to the graft clotting; IV fluids and blood products for adequate blood flow. Monitor urine output.
-Hypertensive periods may cause leaking or rupture suture lines; Furosemide or IV antihypertensive medications (nitroprusside, esmolol, and labetalol)
Monitoring CV status post aortic aneurysm repair
-Monitor for AMI d/t decreased myocardial O2 supply or increased demands
-Monitor for cardiac dysrhythmias d/t electrolyte imbalances, hypoxemia, hypothermia, or MI
-ECG, ABG draws, pain control, IV antidysrhythmic and antihypertensive meds
Monitoring for infection post aortic aneurysm repair
-Administer broad spectrum antibiotics cefazolin (Ancef)
-Monitor Labs and wound for signs of infection
Monitoring GI status post aortic aneurysm repair
-Paralytic ileus may occur; nasogastric tube may be placed
-Monitor for pain (ischemic gut or bowel infarction due to low blood supply)
Aortic aneurysm repair: Post operative care overview
-Close monitoring of neurological status
-Maintenance of peripheral & renal Perfusion
Aortic aneurysm labs to monitor
-CBC
-Coagulation factors
-Electrolytes
-Kidney function tests
-Specialty labs
-ABG
Aortic dissection nursing management
-HR, BP control & pain management
-Maintain MAP >65 mm Hg (diastolic pressure ~ 44 mm Hg (antihypertensives))
-Cardiac monitoring
-Monitor urine output, peripheral pulses & capillary refill
Preoperative and postoperative care for an aortic dissection
-Maintain quiet, calm environment
-SF position (HF increases stroke volume)
Discharge teaching following an aortic dissection
antihypertensive therapy for life, regular follow-up, emergency treatment if pain recurs
Types of congenital heart disease
-Acyanotic
-Cyanotic
Acyanotic shunting of blood
-Left to right
Acyanotic cyanosis
Not usual (unless CHF)
Acyanotic surgery
-Usually done in one stage
Acyanotic prognonsis
Very good/excellent
Acyanotic types
-Ventricular septal defect
-Coarctation of the aorta
Cyanotic shunting of blood
Right to left
Cyanotic cyanosis
Always “blue babies”
Cyanotic surgery
Usually done in several stages
Cyanotic prognosis
Guarded
Cyanotic types
-Tetralogy of Fallot
-Transposition of the great arteries (TGA)
Congenital heart disease (acyanotic)
-Defects with increased pulmonary blood flow; ventricular septal defect (VSD)
-Obstructive defects; coarctation of the aorta
Ventricular septal defect (VSD) surgical treatments
-Palliative- Pulmonary artery banding
-Complete repair: Small defects repaired with sutures. Large defects usually require that a knitted patch be sewn over the opening.
-Cardiopulmonary bypass is used for both procedures
Nonsurgical treatment of ventricular septal defect (VSD)
Device closure during cardiac catheterization
Obstructive defects: Coarctation of the aorta (surgical treatment)
-Resection of the coarctation portion with an end-to-end anastomosis of the aorta or enlargement of the constricted section using a graft of prosthetic material or a portion of the left subclavian artery
-Percutaneous balloon angioplasty techniques have proved to be effective in relieving residual postoperative coarctation gradients
Obstructive defects: Coarctation of the aorta surgical treatment & post operative HTN management
-IV Na+ nitroprusside, esmolol, or milrinone followed by PO ACE I or beta blockers
-To prevent HTN, elective surgery for COA is advised within the first 2 years of life
Nonsurgical treatment of coarctation of the aorta
-Balloon angioplasty is being performed as a primary intervention for COA in older infants and children
-In adolescents, stents may be placed in the aorta to maintain patency
Congential heart disease: Cyanotic
-Defects with decreased pulmonary blood flow; tetralogy of fallot
-Mixed blood flow; transposition of great arteries (TGA)
Defects with decreased pulmonary blood flow: Tetralogy of Fallot (surgical treatment)
-Palliative shunt- Provides blood flow to the pulmonary arteries from the left or right subclavian artery via a tube graft
-Complete repair- Closure of the VSD and resection of the infundibular stenosis, with placement of a pericardial patch to enlarge the right ventricular outflow tract. In some repairs the patch may extend across the pulmonary valve annulus (transannular patch), making the pulmonary valve incompetent
-Procedure requires a median sternotomy and the use of cardiopulmonary bypass
Mixed defects: Transposition of the great arteries (TGA)
-Therapeutic management (to provide intracardiac mixing)- IV prostaglandin E1. During cardiac catheterization or under echocardiographic guidance, a balloon atrial septostomy
-Surgical treatment; an arterial switch procedure
-Rastelli procedure—This procedure is the operative choice in infants with TGA, VSD, and severe pulmonic stenosis (PS)
Acquired heart disease
-Kawasaki disease
-Rheumatic fever
Kawasaki disease treatment
-IV immunoglobulin; single large infusion of 2g/kg over 10-12 hours
-Steroids (prednisone)
-ASA; 80-100 mg/kg/day in divided doses every 6 hours to control then after fever, continued as an antiplatelet doses (3-5 mg/kg/day) until platelet count as returned back to normal (6-8 weeks)
-Clopidogrel, enoxaparin or Warfarin may be indicated for medium-size or giant coronary artery aneurysms
Kawasaki disease: Nursing considerations
-Echo to monitor for coronary artery aneurysms
-Encourage fluids and nutrition. Administer fluids cautiously d/t usual finding of myocarditis
-Clear liquids and soft foods
-Assess child for HF
-Provide symptomatic relief
-Family support due to irritability of child (hallmark sign of Kawasaki disease)
Kawasaki disease: Patient teaching
-Follow-up monitoring
-Irritability to persist up to 2 months after onset of symptoms
-Monitor for arthritis
-Defer live immunizations after as antibodies may not form
-CPR training, monitor for AMI and cardiac ischemia in child
Rheumatic fever treatment
-Eradication of hemolytic streptococci
-Prevention of recurrences & mitral stenosis
-Symptom relief
Pharmacological intervention of rheumatic fever
-Penicillin with erythromycin as a substitute
-Salicylates, naproxen, or prednisone; controls inflammatory response (especially in the joints), and reduces fever and discomfort
Rheumatic fever patient teachings
-Chorea is transitory and all manifestations eventually form into a disease
Rates of the conduction system
-SA node; 60-100 times/min
-AV junction; 40-60 times/min
-Purkinje fibers; 20-40 times/min
Paroxysmal supraventricular tachycardia
-150-250 bpm and regular
-Abnormal P shape (may be hidden)
-Variable P-R interval
Clinical significance of SVT
-In a prolonged episode with a HR >180 bpm may decrease cardiac output resulting in hypotension, dyspnea, and angina
SVT treatment
-Vagal maneuvers
-Adenosine
-Beta adrenergic & calcium channel blockers
-Amiodarone
-Defibrillation
Atrial flutter
-Atrial: 250-350 bpm and regular
-Ventricular: >100 bpm and irregular
-Sawtooth P wave shape
-Variable P-R interval
Clinical significance of atrial flutter
-Decrease cardiac output; HF
-Stroke
Treatment of atrial flutter
-Calcium channel blockers, beta adrenergic blockers
-Defibrillation
-Amiodarone, propafenone, and ibutilide
-Radiofrequency ablation; catheter in the right atrium in between the IVC and tricuspid valve. Tissue is ablated and dysrhythmia is terminated
Atrial fibrillation
-Atrial: 350-600 bpm and irregular
-Ventricular: >100 bpm and irregular
-Chaotic fibrillatory P wave
-P-R interval is absent
Clinical significance of atrial fibrillation
-Decreased cardiac output because of loss of atrial kick
-Stroke
Treatment of atrial fibrillation
-Calcium channel blockers and beta adrenergic blockers
-Amiodarone
-If clots are present defibrillation is contraindicated
Junctional rhythms
-40-140 bpm and regular
-P wave inverted (may be hidden)
-P-R interval is variable
Clinical significance of junctional rhythms
-Decreased cardiac output
Treatment of junctional dysrhythmias
-Atropine
-Beta adrenergic blockers, calcium channel blockers and amiodarone
First-degree AV heart block
-Regular rhythm
-Normal P wave
-P-R interval >0.20 seconds, constant
Type I (mobitz type I, Wenckebach’s)
-Atrial: Regular
-Ventricular: Slower and irregular
-Normal P wave
-Progressively lengthened P-R interval
-Normal width with a pattern of one nonconducted QRS complex
Clinical significance of type I (mobitz type I, Wenckebach’s)
-Usually results from myocardial ischemia or infarction
-May indicate AV conduction disturbance
Treatment of type I (mobitz type I, Wenckebach’s)
-Atropine, temporary pacemaker
Type II (Mobitz II)
-Atrial: Regular or irregular
-Ventricular: Slower and regular or irregular
-More P waves than QRS complex
-Normal or prolonged P-R interval
-Widened QRS, preceded by two or more P waves
Type II (Mobitz II) clinical significance
-Decreased cardiac output
-Hypotension and myocardial ischemia
Treatment of type II (Mobitz II)
-Temporary and then permanent pacemaker
Third-degree AV heart block
-Ventricular rate 20-40 bpm
-Normal P wave with no connection to the QRS complex
-No P-R intervals related to the QRS; more P waves than QRS complexes
-Normal or widened QRS with no connection to P waves
Third-degree AV heart block clinical significance
-Reduced cardiac output; ischemia, HF, shock
-Syncope
Treatment of third-degree AV heart block
-Temporary and then permanent pacemaker
-Atropine, epinephrine, isoproterenol, and dopamine
Premature ventricular contraction (PVC)
-6o-100 bpm and irregular
-No P wave
-No P-R interval
-Wide and distorted QRS complex
Clinical significance of PVC
-May reduce cardiac output and cause angina and HF
Ventricular tachycardia
-100-250 bpm and regular or irregular
-No P wave
-No P-R interval
-Wide and distorted QRS complex
Clinical significance of ventricular tachycardia
-Decreased cardiac output
-Hypotension, pulmonary edema, decreased cerebral perfusion, cardiopulmonary arrest
-Ventricular fibrillation may develop
Treatment of ventricular tachycardia
-Amiodarone
-Defibrillation
-Epinephrine
Ventricular fibrillation
-Rhythm not measurable and irregular
-No P wave
-No P-R interval
-Immeasurable QRS complex
Ventricular fibrillation clinical significance
-Unresponsiveness, pulselessness, apneic state
Treatment of ventricular fibrillation
-CPR, defibrillation
Sinus bradycardia
<60bpm
Sinus bradycardia clinical significance
-Pale, cool skin
-Hypotension
-Weakness, angina, dizziness, syncope
-Confusion
-SOB
Treatment of sinus bradycardia
-Atropine, pacemaker
Sinus tachycardia clinical significance
-Depends on patients tolerance of increased HR
-Dizziness, dyspnea, and hypotension
-Angina or increased infarction size may occur if persistent
Premature atrial contraction
-Irregular rhythm
-P wave is different than the one originating from the SA node
-PR interval may be shorter or longer but with normal length
Premature atrial contraction clinical significance
-In people with heart disease, PACs may enhance automaticity of the atria or re-entry mechanism
-May initiate more serious dysrhythmias (SVT)
Antidysrhythmic drugs
-Class I: Na+ channel blockers; Decrease conduction velocity in the atria, ventricles and His-Purkinje system
-Class Ia (procainamide, quinidine); delays repolarization, Widened QRS and prolonged QT interval
-Class Ib (Lidocaine, mexiletine, and phenytoin); accelerates repolarization
-Class Ic (flecainide, propafenone); decrease impulse conduction, Pronounced prodysrhythmic actions, widened QRS, prolonged QT interval
-Class II: Beta adrenergic blockers; Delay repolarization increasing prolonged duration of actional potential and prolonged refractory period, Prolonged PR and QT intervals, widened QRS, bradycardia
-Class IV: Calcium channel blockers; Decrease automaticity of SA node, delay AV node conduction; reduce myocardial contractility, Bradycardia, prolonged PR interval, AV block
-Other antidysrhythmics; Decrease conduction through AV node; reduce automaticity of SA node, ECG effects: Prolonged PR interval, AV block
Cardiomyopathy
-Group of diseases affecting the structural or functional ability of the myocardium
-Primary cardiomyopathy; etiology of disease is unknown (idiopathic)
-Secondary cardiomyopathy; etiology of disease is known and is secondary to another disease process
Causes of secondary cardiomyopathy: Dilated
-Cardiotoxic agents
-Alcohol, cocaine, doxorubicin
-Genetic
-HTN
-Ischemia
-Metabolic disorders
-Muscular dystrophy
-Myocarditis
-Pregnancy
-Valve disease
Causes of secondary cardiomyopathy: Hypertrophic
-Aortic stenosis
-Genetic
-HTN
Causes of secondary cardiomyopathy: Restrictive
-Amyloidosis
-Endomyocardial fibrosis
-Neoplastic tumor
-Post-radiation therapy
-Sarcoidosis
-Ventricular thrombus
Dilated cardiomyopathy manifestations
-Fatigue, weakness, palpitations, dyspnea
-Cardiomegaly
-Contractility decreases
-Valvular incompetence
-Dysrhythmias
-Decreased cardiac output
Hypertrophic cardiomyopathy manifestations
-Exertional dyspnea, fatigue, angina, syncope, palpitations
-Cardiomegaly is mild to moderate
-Decreased or increased contractility
-Mitral valve incompetence
-Atrial and ventricular dysrhythmias
-Normal or decreased cardiac output
-Increased outflow tract obstruction
Restrictive cardiomyopathy manifestations
-Dyspnea & fatigue
-Mild cardiomegaly
-Normal or decreased contractility
-Atrioventricular valve incompetence
-Atrial and ventricular dysrhythmias
-Normal or decreased cardiac output
Cardiomyopathy diagnostic methods
-History & physical exam
-Electrocardiogram
-B-type natriuretic peptide (BNP)
-Chest radiograph
-Echocardiogram
-Nuclear imaging studies
-Cardiac catheterization
-Endocardial biopsy
Cardiomyopathy collaborative therapy
-Nitrates (except in HCM)
-Beta adrenergic blockers
-Antidysrhythmics
-ACE inhibitors
-Diuretics
-Mineralocorticoid receptor antagonist
-Digitalis (except in HCM) (unless used to treat atrial fibrillation)
-Anticoagulants
-Sacubitril valsartan
-Ventricular assist device
-Cardiac cardioverter-defibrillator
-Cardiac transplant
Dilated cardiomyopathy
-Causes heart failure in 25-40% of cases
-Characterized by a diffuse inflammation and rapid degeneration of myocardial fibers
-Causes contractile dysfunction, in contrast to HF the walls do not hypertrophy
-Often follows an infectious myocarditis
Hypertrophic cardiomyopathy
-Asymmetrical left ventricular hypertrophy without ventricular dilation
-Septum between the two ventricles becomes enlarged and obstructs blood flow from the left ventricle
-Often seen in active, athletic individuals
Characteristics of hypertrophic cardiomyopathy
-Ventricular hypertrophy
-Rapid forceful contraction of the left ventricle
-Impaired relaxation
-Obstruction of LVOT
Goals of intervention for hypertrophic cardiomyopathy
Improve ventricular filling by reducing contractility and relieving LVOT obstruction
Treatment of hypertrophic cardiomyopathy
-Beta adrenergic blockers and calcium channel blockers
Restrictive cardiomyopathy
-Impairs diastolic filling and stretch
-No current treatment exists other than trying to improve diastolic filling
Primary varicose veins
caused by congenital weakness of the veins and are more common in women and are idiopathic
Secondary varicose veins
-Typically occurs from a previous VTE
-May occur in the esophagus, vulva, spermatic cords, and anorectal area and as abnormal arteriovenous connections
Reticular veins
smaller varicose veins that appear flat, less tortuous, and bluish green
Telangiectasias (spider veins)
very small visible vessels that appear bluish-back, purple, or red
Etiology of varicose veins
-Increased venous pressure
-Multifactorial and idiopathic
Sclerotherapy
Injection that obliterates varicose veins 5mm or larger in diameter
Nursing management of varicose veins
-Avoid stasis, avoid constrictive clothing and walk daily, deep breathing, and compression stockings
High intakes of vitamin A is associated with
osteoporosis, fracture, and metaphyseal irregularity
