cardiovascular Heart • complex muscular pump that maintains O2 and blood circulation through the lungs and the

rest of the body • Size of a clenched fist • Beats 60-100 per minute • The heart pumps about 7200 liters/day. Layers of the wall • Endocardium – innermost layer

• • • •

Myocardium – middle, thickest; contracting layer Epicardium – outer layer Pericardium encloses epicardium; divided into visceral and parietal part Pericardial sac - space between the 2 layers

Chambers, Valves • AV atrioventricular valves – Tricuspid – Mitral or bicuspid

Semilunar valves – Aortic – Pulmonic Blood Vessels 1. Right coronary artery a. posterior interventricular b. marginal artery - supplies the RIGHT atrium, RIGHT ventricle, inferior portion of the LEFT ventricle, the POSTERIOR septal wall and AV (90%) and SA node (55%) 2. Left coronary artery

• • •

anterior interventricular circumflex arteries - left atrium and the posterior LEFT ventricle

Left anterior descending artery – anterior wall of the LEFT ventricle, the anterior septum and the Apex of the left ventricle 3. cardiac veins -drain into the coronary sinus w/c in turn drain into right atrium

2 TYPES OF CONTROL SYSTEMS OF THE HEART: • Neural regulation – autonomic nervous system Sympathetic- accelerates & strengthen heartbeat\ Parasympathetic- slows down 2. Electrical Conduction System/Nodal System - network of nerve fibers coordinate the contraction and relaxation of the cardiac muscle tissue to obtain an efficient, wave-like pumping action of the heart. Physiology of conduction • Electrical activity d/t movement of ions

• • • •
• •

Resting state, inside cell membrane (-); outside cell membrane (+)

Initiation of electrical impulse, Na moves inside, K goes outside to begin Depolarization (electrical activation of cell) • Inside cell membrane, more (+) Stimulus incites neighboring cells to depolarize as well Contraction follows

Repolarization (resting state) Refractory period – phase where muscle cannot be restimulated to contract; protect heart from tetany • Absolute refractory period – cannot be restimulated regardless of strength of stimuli • Elative refractory period – stronger than normal stimulus can incite muscle to contract CARDIAC CYCLE


systole

sequence of events that occur when the heart beats

• • •

Ventricular pressure rises AV valves close Blood ceases flowing from atria into ventricles and regurgitation into atria is prevented • Rise in ventricular pressure opens semilunar valves • Blood ejected into pulmonary artery and aorta • End of systole, ventricular pressure decreases • Pulmonary and aortic pressure decreases • Closure of semilunar valves diastole • Ventricles are relaxed

• • • •

AV valves open Blood empties to atria then to ventricles End of diastole, atria contract d/t SA node Atrial pressure rises ejecting blood to ventricles

Cardiac Output, Sroke Volume and Heat Rate

• • •

STROKE VOLUME – amount of blood ejected per heartbeat

HEART RATE – affected by ANS, baroreceptor activity, cathecolamines, thyroid hormone CARDIAC OUTPUT - amount of blood pumped out by each ventricle in 1 minute - product of heart rate and stroke volume STROKE VOLUME • Preload – degree of stretch at the end of diastole • Inc volume inc stretch inc preload greater contraction and inc stroke volume • Increased by inc blood volume and exercise, dec by diuretics 2. Afterload – amount of resistance to ejection of blood from ventricle • Also called systemic vascular resistance • Inverse relationship with stroke volume 3. Contractility – force generated by contracting myocardium - Enhanced by SNS, digitalis, dopamine and dobutamine Blood Pressure • Cardiac output X peripheral resistance

• •
BP

Control is neural (central and peripheral) and hormonal Hormones- ADH, aldosterone, epinephrine can increase BP; ANF can decrease Baroreceptors in the carotid and aorta

Baroreceptor reflexes - carotid sinus and aortic arch - causes vasoconstriction and increased blood pressure Dec arterial pressure SNS inc cardiac rate, contraction, contractility, circulating blood volume, constriction of renal arterioles and increased aldosterone

• PERIPHERAL RESISTANCE .diastolic pressure.Males and post-menopausal females • Race • Family History • Hypertension • Cigarette Smoking • Diabetes Mellitus • Obesity • Sedentary Lifestyle • Stress • Atherosclerosis Pathophysiology Fatty streak formation in the vascular intima  T-cells and monocytes ingest lipids in the area of deposition atheroma narrowing of the arterial lumen  reduced coronary blood flow  myocardial ischemia Angina • Chest pain resulting from coronary atherosclerosis or myocardial ischemia Types: • Stable – exertional.systolic pressure. inc BP Coronary Artery Disease (CAD) • Accumulation of fatty deposits in the inner layer of coronary arteries. drugs. relieved by rest. . with the systole in ratio to the diastole. blood viscosity. • • • • • • due to hypercholesterolemia Incomplete occlusion of the coronary arteries lead to Angina (ischemia) Complete occlusion of the coronary arteries lead to Myocardial Infarction Manifestations depend on the severity of coronary arterial occlusion Risk Factors Age above 45/55 Sex. ..decreased pressure due to the relaxation of the ventricles (heart resting) .Blood pressure is measured in mm of mercury.increased pressure on the arteries due to the contraction of the ventricles (heart pumping) . severity does not change . when increased along w/ cardiac output. blood volume.amount of friction encountered by blood as it flows through blood vessels -increased by constriction of blood vessels d/t SNS activity/ atherosclerosis.

exertion . shoulders.Precipitated by cold.• Unstable – Occurs unpredictably during exertion and emotion. emotions.Lasts a few minutes and then subsides • • • • • • • • • • • Diaphoresis Nausea and vomiting Cold clammy skin Sense of apprehension and doom Dizziness and syncope Diagnostic Tests • NTG test (relief from pain) ECG (ST depression and T wave elevation) Cardiac catheter – atherosclerotic lesions Thallium 201 Imaging Technetium Imaging Nursing Diagnosis • Pain related to imbalance in myocardial oxygen demand Decreased cardiac output related to reduced preload and afterload Anxiety related to pain. heavy. neck and jaws .Substernal or retrosternal pain that radiates to arms. eating.Squeezing. severity increases with time and pain may not be relieved by rest and drug • Prinzmetal (variant) – pain at rest with vasospasm Manifestations • Characteristic of chest pain .percutaneous transluminal coronary angioplasty – To compress the plaque against the vessel wall. increasing the arterial lumen • CABG . uncertain prognosis and threatening environment Management • Relieve pain • Place in comfortable position • Administer O2 • Decrease Anxiety • PTCA . tight chest . burning. back. diagnostic tests and therapies .coronary artery bypass graft – To improve the blood flow to the myocardial tissue • Explain the reasons for hospitalization.

prevent thrombus formation Beta-blockers. shock Risk factors 1.dilate coronary artery and reduce vasospasm Nitrates. Obesity 5. steady crushing and squeezing substernal pain • Radiates to the neck. arm. jaw and back .Give antianginal drugs • • • • • • • • • Aspirin. take another tablet and wait for 5 minutes Another tablet can be taken (third tablet) If unrelieved after THREE tablets seek medical attention Myocardial Infarction • • • Absence of O2 supply to the myocardium Necrosis or death to the myocardial tissue Attack may be sudden or gradual Etiology 1. Conditions that decrease perfusion.reduce BP and HR Calcium-channel blockers. CAD 2. Stress 6. Hypertension 4. Coronary artery occlusion by embolus and thrombus 4. Hypercholesterolemia 2. Sedentary lifestyle Pathophysiology Interrupted coronary blood flow myocardial ischemia anaerobic myocardial metabolism for several hours myocardial death  depressed cardiac function  triggers autonomic nervous system response  further imbalance of myocardial O2 demand and supply Chest pain: • Severe.to dilate the coronary arteries Put one nitroglycerin tablet under the tongue Wait for 5 minutes If not relieved. Coronary vasospasm 3.hemorrhage. Smoking 3.

sense of doom tachycardia or bradycardia hypotension dysrhythmias • • • • • • • • Diagnostic Evaluation • Chest pain cannt be relieved by NTG • ST segment elevation and T wave inversion. Q wave • Cardiac enzymes: increased Troponin. BP and RR dyspnea Diaphoresis cold clammy skin N/V restlessness. CK MB.may show elevated WBC count The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes   CK.MB ( creatine kinase) Elevates in MI within 4 hours. peaks in 24 hours and then declines till 3 days The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes   CK.MB ( creatine kinase) Normal value is 0-7 U/L . LDH • CBC.• • • Not relieved by rest or NTG May continue for 15-30 minutes May produce anxiety and fear resulting to increased HR.

The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes    Lactic Dehydrogenase (LDH) Elevates in MI in 24 hours. peaks in 4-24 hours and persists for 7 days to 3 Normal value for Troponin I is less than 0.6 ng/mL weeks! The Cardiovascular System LABORATORY PROCEDURES Troponin I and T • REMEMBER to AVOID IM injections before obtaining blood sample! .LDH2 greater than LDH1 (flipped LDH pattern) Normal value is 70-200 IU/L The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes Myoglobin    Rises within 1-3 hours Peaks in 4-12 hours Returns to normal in a day The Cardiovascular System LABORATORY PROCEDURES Troponin I and T • • • Troponin I is usually utilized for MI Elevates within 3-4 hours. peaks in 48-72 hours Normally LDH1 is greater than LDH2 The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes    Lactic Dehydrogenase (LDH) MI.

40.mg/dL NPO post midnight (usually 12 hours) The Cardiovascular System LABORATORY PROCEDURES ELECTROCARDIOGRAM (ECG) A non-invasive procedure that evaluates the electrical activity of the heart Electrodes and wires are attached to the patient The Cardiovascular System LABORATORY PROCEDURES Holter Monitoring • A non-invasive test in which the client wears a Holter monitor and an ECG tracing recorded continuously over a period of 24 hours The Cardiovascular System LABORATORY PROCEDURES ECHOCARDIOGRAM • Non-invasive test that studies the structural and functional changes of the heart with the use of ultrasound .150 mg/dL • • The Cardiovascular System LABORATORY PROCEDURES SERUM LIPIDS • • • • • LDL.30-70. triglycerides and lipoprotein Cholesterol= 200 mg/dL Triglycerides.130 mg/dL HDL.• • levels Early and late diagnosis can be made! The Cardiovascular System LABORATORY PROCEDURES SERUM LIPIDS Lipid profile measures the serum cholesterol.

fear of death and threatening environment Decreased cardiac output related to impaired contraction of the heart Altered tissue perfusion (myocardial) related to coronary stenosis Activity intolerance related to insufficient oxygenation Risk for injury (bleeding) related to dissolution of clots Ineffective individual coping related to threats to self esteem Management .• No special preparation is needed The Cardiovascular System LABORATORY PROCEDURES Stress Test • • Pre-test: consent may be required. Instruct client to avoid taking a hot shower for 10-12 hours after the test The Cardiovascular System LABORATORY PROCEDURES Pharmacological stress test • • • • • • • • • • • Use of dipyridamole Maximally dilates coronary artery Side-effect: flushing of face The Cardiovascular System LABORATORY PROCEDURES Pharmacological stress test Pre-test: 4 hours fasting. adequate rest . alcohol and caffeine The Cardiovascular System LABORATORY PROCEDURES Post-test: instruct client to notify the physician if any chest pain. caffeine Post test: report symptoms of chest pain Nursing Diagnosis • Pain related to an imbalance in oxygen supply and demand Anxiety related to chest pain. eat a light meal or fast for 4 hours and avoid smoking. avoid alcohol. dizziness or shortness of breath .

Warfarin S/S: fever. diarrhea Monitor blood work (INR. bleeding. do not aspirate or massage antidotes: Antiplatelet – hypersensitivity to aspirin ie Ticlopidine. dec HR. PTT-heparin) Avoid ASA and invasive procedures Bleeding precautions Subcutaneous heparin.• • • – – • Oxygen therapy Provide adequate rest periods Minimize metabolic demands Provide soft diet Provide a low-sodium. Urokinase • * S/E: bleeding and urticaria • • • • • • • • Have aminocaproic acid ready( fibrinolysis inhibitor) Anticoagulant – prevents formation of new blood clots ie Heparin.Dissolve clots in the coronary artery allowing blood to ie TPA tissue plasminogen activator (Alteplase).abdomen. PT-warfarin. low cholesterol and low fat diet Passive ROM Minimize anxiety Reassure client and provide information as needed Check fluids – overload is dangerous if CO is compromised Avoid anaerobic exercise and exposure to cold • – • • • • flow Post-MI: recognize risk of sensory overload Pharmacologic Therapy Thrombolytic agents . rash. BP ie Propranolol . chills(hypersensitivity). Clopidogrel • • Beta adrenergic blocking agents – reduce myocardial O2 demand by blocking sympathetic stimulation. Streptokinase (streptase). contractility.

• coronary artery bypass graft (CABG ) After the condition had been stabilized: . relax blood vessels ie Diltiazem • Morphine .Relaxes bronchioles to enhance oxygenation • ACE Inhibitors . HR. What is the pacemaker of the heart? 5. Visual disturbances(lovastatin & gemfibrozil) • Administer statins at HS to inc absorption. Fibrates( Gemfibrozil). Nitrates is best stored in • refrigerator • • • Amber colored glass In open containers The garden .reduces pain and anxiety . reduced absorption of fat and fat-soluble vitamins.CBR without BP (complete bedrest without bathroom privilege) .• Calcium channel blockers – dec contraction. Captopril can ______ the afterload • Increases • • Decrease No effect 4. hepatic toxicity.lowers serum lipids by decreasing triglycerides or cholesterol • Ex. cholestyramine shld be mixed wt full glass of liquid Surgical revascularization: • Percutaneous Transluminal Coronary Angioplasty (PTCA). rash. bile acid sequestrants( cholestyramine) • S/E: N/V. musculskeletal injury. HMG-CoA reductase( statins). diarrhea. Give 2 examples of preloaders 3. dec O2 demand – Limits the area of infarction • Antihyperlipidemics.Prevents formation of angiotensin II w/c causes vasoconstriction. other meds wt meals to dec GI irritation.Gradual resumption of ADL to full recovery 1-2.

caused by vasospasm • Stable • • • Variant Unstable Semi-stable Congestive Heart Failure CHF • A syndrome of congestion of both pulmonary and systemic circulation caused by inadequate cardiac function and inadequate cardiac output to meet the metabolic demands of tissues Predisposing Factors • Myocardial Infarction • Arrhythmias . Thrombolytic agents are given in MI. K 9. This is a type of angina felt at rest .6. A patient complained of chest pain. Partial occlusion usually results in • Ischemia Infarction Necrosis death 10. What is the antidote • Aminocaproic acid • • • • • • Aminobutyric acid Protamine sulfate Vt. This is true angina if the ECG reading showed • ST depression • • • • • ST elevation Q wave invertion T wave invertion 7. IM injections should be avoided_____ taking cardiac enzymes specimen • Before After never 8.

• • • • • • • • • Pregnancy Pulmonary Embolism Anemia Renal Failure CAD Valvular heart diseases Hypertension Cardiomyopathy Pericarditis and cardiac tamponade New York Heart Association Class 1 • Ordinary physical activity does NOT cause chest pain and fatigue • No pulmonary congestion • Asymptomatic • NO limitation of ADLs Class 2 • SLIGHT limitation of ADLs • NO symptom at rest • Symptom with INCREASED activity • Basilar crackles and S3 Class 3 • Markedly limitation on ADLs • Comfortable at rest BUT symptoms present in LESS than ordinary activity Class 4 • SYMPTOMS are present at rest PATHOPHYSIOLOGY • LEFT Ventricular pump failure back up of blood into the pulmonary veins increased pulmonary capillary pressure pulmonary congestion LEFT ventricular failure decreased cardiac output decreased perfusion to the brain. dizziness PATHOPHYSIOLOGY • RIGHT ventricular failure  blood pooling in the venous circulation  increased hydrostatic pressure peripheral edema . kidney and other tissues  oliguria.

vasodilators and hypolipidemics • LOW sodium diet . Pulmonary crackles/rales 5. hepatomegaly 5.heart strain • Chest X-ray . Body weakness 7. Cool extremities 8. Anorexia.cardiomegaly and pleural effusion • CVC Central Venous Catheter and Swan-Ganz Catheter are able to record high pressure in the chambers and pulmonary capillaries. Ascites 6. liver and GIT LEFT SIDED CHF ASSESSMENT FINDINGS 1. signs of cerebral anoxia RIGHT SIDED CHF ASSESSMENT FINDINGS 1. Orthopnea 4. • complete bed rest and reduce myocardial oxygen demand. cough with Pinkish. • Echocardiogram may show hypokinetic heart • ABG and Pulse oximetry may show decreased O2 saturation Nursing Considerations • goal of treatment .improve pump function and reverse the compensatory mechanism of the heart. Oliguria 12. Fatigue 11. PND 3. Weight gain 3. Dyspnea on exertion 2. decreased peripheral pulses 10. Distended neck vein 4. frothy sputum 6. pitting edema 2. • FVE management and prevent complications • Diuretics and Digoxin. Peripheral dependent.RIGHT ventricular failure blood pooling venous congestion in the kidney. Pulsus alternans Diagnostics • EKG . Tachycardia 7. Cyanosis 9. nausea 8.

nitrates . vasopressors and inotropics such as DOPAMINE and DOBUTAMINE.caused by rapid vasodilation and subsequent pooling of blood within the peripheral system( drugs.• • Limit fluid intake Monitor daily weight and report signs of fluid retention Complications: • Acute Pulmonary Edema Treatment: Bed rest and maintain high fowler’s position O2 therapy Morphine administration to dilate blood vessels Dopamine to increase myocardial contractility and ↑ CO Diuretics to reduce blood volume Steroids to reduce inflammation Shock • • Hypovolemic.occurs 2 to loss of fluid resulting in decrease perfusion Neurogenic. spinal anesthesia etc) • Anaphylactic.caused by an allergic reaction which cause histamine releasevasodilation • Septic-2 to infection which cause plasma leakage ASSESSMENT FINDINGS • HYPOTENSION • • • • • • • oliguria (less than 30 ml/hour) tachycardia narrow pulse pressure weak peripheral pulses cold clammy skin changes in sensorium/LOC pulmonary congestion LABORATORY FINDINGS • – Increased CVP Normal is 4-10 cmH2O Management • modified Trendelenburg (shock ) position • IVF. diuretics.

chest Diagnostics • Echocardiogram • CXR Management • Assist in PERICARDIOCENTESIS • • • Administer IVF Monitor ECG. CABG. insertion of Swan-Ganz cath and IABP • Monitor urinary output. mechanical ventilation.• • pain Administer O2 Morphine is administered to decrease pulmonary congestion and to relieve • Assist in intubation.Jugular vein distention. urine output and BP Monitor for recurrence of tamponade Vascular Disorders • Venous Thrombosis . BP and pulses Risk Factors • • • • Cardiac trauma Complication of Myocardial infarction Pericarditis Cancer metastasis Manifestations • BECK’s Triad. hypotension and distant/muffled heart sound • Pulsus paradoxus • • • • • • Increased CVP decreased cardiac output Syncope anxiety dyspnea Percussion.Flatness across the ant. PTCA.

greater and lesser saphenous veins affected. Deep vein thrombosis .• • • • • CVI Arterosclerosis Raynaud’s Phenomenon Aneurysm Hypertension Venous Thrombosis Due to: • • • Stasis of blood Injury to the vessel wall Altered blood coagulation High Risk: • Fractures. cast and joint replacement • • • Obesity and smoking Immobilized patient Heart problems May progress to: • Phlebitis-inflammation of the vessel wall • • Superficial thrombophlebitis . pulmonary embolism is a complication Manifestations • (+) Homan’s sign • fever and chills • swelling and cyanosis of the affected leg/arm Diagnostics: • Venous duplex ultrasound • Impedance plethysmography • RF testing (radioactive fibrinogen) fibrinogen I 125 • Venography • Coagulation Profiles: APTT. PT/INR Management • Prevent complications .deep veins affected.

• • • • • • • • Bed rest for 5 days Prevent muscle contraction if possible to prevent dislodging the clot Elevation of affected part 10-20 degree above the heart Anti-embolic stockings Anticoagulant Thrombolytic Green-field filter (IVC) Thrombectomy Chronic Venous Insufficiency • Destruction of the valves because of chronic blood pooling or trauma. cellulites and recurrent thrombosis manifest later Manifestations • Edema • • • • • • • Altered pigmentation Pain Stasis dermatitis Dilated superficial veins Stasis ulcers Management • Elevate legs Elastic compression stockings Skin should be kept clean and dry Raynaud’s Phenomenon • Arteriolar vasospastic disease with unusual sensitivity to cold or emotional stress. Venous return is decreased ↓ chronic venous stasis ↓ edema formation ↓ veins becomes distorted or tortuous (varicosities) ↓ stasis ulcer. • cause is unknown but may be secondary to Autoimmune Diseases ASSESSMENT • Pallor then cyanosis • Hyperemia when blood returns to digits after vasospasm .

tingling and burning pain Management • Avoid primary stimuli (cold. tobacco) • • • Ca channel blocker Nifedipine for vasospasm Safety measures Arteriosclerosis • • hardening of the arterial blood vessel walls related to aging.• Numbness. Aging and atheromas ↓ impeding the lumen of the arterial walls (incomplete or incomplete occlusions ) ↓ systemic effects depending on the blood vessel affected ↓ asymptomatic or may manifest if damaged is obvious ↓ systemic effects ↓ ↑ PVR to heart strain to hypertension weakening the muscles of the wall that leads to aneurysm • • • • • • • TIA to CVA Angina to MI ATN to Renal Failure Retinopathy to Blindness Peripheral Occlusive Disease (TAO) to Gangrene Formation Hepatic Infarction Pulmonary Infarction Diagnostic Evaluation: • Arteriography . Atherosclerosis-common type of arteriosclerosis due to atheromas.

vaporizes the plaque • Embolectomy-removal of clot from the artery • Thrombectomy-removal of thrombus from the artery • Endarterectomy-removal of plaque from the artery • Bypass Graft Aneurysm • Dilation involving an artery formed at a weak point in the vessel wall • • Saccular= when one side of the vessel is affected Fusiform= when the entire segment becomes dilated RISK FACTORS • Atherosclerosis • • • Infection= syphilis Connective tissue disorder Genetic disorder= Marfan’s Syndrome PATHOPHYSIOLOGY Damage to the intima and media weakness outpouching Dissecting aneurysm tear in the intima and media with dissection of blood through the layers Manifestations: .• • • • CT Scan MRI Duplex UTZ EKG Management: • Modification of risk factors (CAD and hyperlipidemia) • Anticoagulants • • • • Antiplatelets Lipid Lowering Agent Antihypertensive Vascular Rehabilitation/Exercise Surgical Intervention: • PTA-Percutaneous Transluminal Angioplasty-introduce a balloon-tipped catheter to the stenosis to reduce or eliminate the obstruction • Laser Angioplasty.

steroids) • Malignant Hypertension • It is a combination of both which is BP is uncontrolled. NSAIDs. Renin-Angiotensin-Aldosterone System. Extracellular Fluid Volume Primary or Essential Hypertension • • • • Other causes are absent Average BP exceeds the upper limits (taken at rest 3x with several days interval) Diastolic is 90 mm Hg or higher Represents 95% of patients with hypertension Secondary Hypertension Due to: • Renal Pathology • Coarctation of the Aorta • Endocrine Disturbance • Drugs (estrogens. sympathomimetics.• • • Asymptomatic Pulsatile sensation on the abdomen bruit Diagnostics • CT scan • Ultrasound • X-ray • Aortography Management • Anti-hypertensives • Synthetic graft Nsg: • • • • Administer medications Emphasize the need to avoid increased abdominal pressure No deep abdominal palpation Remind patient the need for serial ultrasound to detect diameter changes Hypertension • “Silent killer” • • disease of vascular regulation that leads to high blood pressure due to alteration of Central Nervous System. Risk Factors • Old age • male .

reduce dietary saturated fat and cholesterol. weight. Headache 2.• • • • • • Race Overweight Family History Smoking Sedentary Lifestyle Diabetes Mellitus Manifestations 1. limit alcohol. stop smoking. dizziness 5. reduce coffee intake. Blood Chem etc.4 g/day. Visual changes 3. chest pain 4. cut sodium to 2. diet (low fat. Lose weight. N/V Diagnostic Evaluation • Monitor BP • EKG. cessation of smoking – treatment regimen ie drugs – BP monitoring – Follow up . Despite lifestyle changes and BP remains high drug therapy should be started: • Diuretics • • • • • Beta blockers Calcium channel blockers ACE inhibitors A2 Receptor blockers Vasodilators Nursing Management • Health teaching on: – Lifestyle changes ie activities. • – – Management: Control of all risk factors:. low Na). Blood Sugar. nutrition.

Negative chronotropic (Decreases HR) AV node control . – GIT disturbance. ASA levels • Hypocalcemia. hydralazine.Increase CO (improves stroke volume) S. dec. B12 dec Can be given SL or IV (Isordil) and topical (Nitrobid) Calcium Channel Blockers Nifidepine (Procardia) Diazepam (Cardizem) Decrease muscle tone.E. hypomagnesemia. CNS depression and flashes of light .sparers (spirinolactone.E. dec. Digoxin . B6.Cardiovascular Drugs: • – – • – – – Anti Anginal Opiate Analgesic – Morphine Sulfate ↓ cardiac workload and BP. amiloride. – bradycardia.K.competes w/ ASA for renal excretion—inc. hyperurecemia. diarrhea and rashes Beta Blocking Agent Propranolol Decrease workload Blocks beta receptors and capable of decreasing HR S. nausea and depression • – – – • – – – • • Diuretics. BP and alleviate headache Increase blood vessel diameter and improves blood flow S. interferes contraction. – vomiting. Ziinc( except K. triamterene) • Thiazides and loop diuretics.waster.sparers) • Furosemide.Positive Inotropic (Increases contraction of the heart) . GI irritration. nitroprusside Relax smooth muscle. sparer S/E: hyponatremia.Increase emptying capacity of the heart . decrease BP S.E. – dizziness and flushing.E. improve LOC and sedative effect Vasodilators Nitroglycerin NTG.hyperglycemia in pxs w/ DM • All drugs are better administered in AM • Digitalis.

Increase CO . teachings. document weight and height. blood tests and document the peripheral pulses The Cardiovascular System LABORATORY PROCEDURES • Pretest: Fast for 8-12 hours. baseline VS.Streptokinase – lyses the clot (20T IU IV bolus or 4T IU/min drip) . contractility and automaticity Quinidine for atrial fib • – – – – – – • • – • Thrombolytic/Fibrinolytic Agent . medications to allay anxiety The Cardiovascular System LABORATORY PROCEDURES .• • Dopamine – diuresis effect .Urokinase – avtivates plasminogen to plasmin (intracoronary) Blood thinner Heparin – prevent formation of new clot (4-8T IU/30 min) Antidote – Protamine Sulfate Warfarin (Coumadine) – decrease viscosity of blood (PO) home meds Don’t give to pregnant women Antidote – Vitamin K Cardiac catheterization The Cardiovascular System LABORATORY PROCEDURES • Pretest: Ensure Consent.More potent on contraction Anti dysrhythmic drug Lidocaine (Xylocaine) for PVC Atropine for Mobitz type I Isoproterenol (Isuprel) for sinus bradycardia Norepinephrine (Levophed) powerful vasoconstrictor Epinephrine – increase conduction. NPO. assess for allergy to seafood and iodine.Increase Na excretion (kidney) Dobutamine .

inform the patient that a feeling of warmth and metallic taste may occur when dye is administered The Cardiovascular System LABORATORY PROCEDURES Post-test: Monitor VS and cardiac rhythm Monitor peripheral pulses.  Assessment and Diagnostics: extra heart sound referred to as Mitral click  Management. color and warmth and sensation of the extremity distal to insertion site Maintain sandbag to the insertion site if required to maintain pressure Monitor for bleeding and hematoma formation The Cardiovascular System LABORATORY PROCEDURES • • • • • Maintain strict bed rest for 6-12 hours Client may turn from side to side but bed should not be elevated more than 30 degrees and legs always straight Encourage fluid intake to flush out the dye Immobilize the arm if the antecubital vein is used Monitor for dye allergy Thank You! CVS Valvular disorders 1. palpitations. light-headedness. In advance cases mitral valve repair and replacement may be necessary. dizziness. .symptomatic relief and control. May also be asymptomatic. shortness of breath.• • • • • Intra-test: inform patient of a fluttery feeling as the catheter passes through the heart. syncope. chest pain and anxiety. CLinical Manifestations:  .fatigue. mitral valve prolapse  a portion of the mitral valve leaflet balloons back into the atrium during systole. blood then regurgitates from the left ventricle back into the left atrium.

ECG and cardiac catheterization are used to determine severity.  Clinical manifestations .antibiotic prophylaxis. . low pitched rumbling diastolic murmur heard at the apex.Echocardiography is used to diagnose.PE-weak.  It maybe caused by inflammatory lesions that deform the leaflets preventing them from closing the orifice.  Assessment and Diagnosis: .Recurrent repiratory infections due to venous pulmonary hypertension.DOB on exertion .to prevent recurrence of infections. . Mitral stenosis  It is an obstruction of blood flowing from the left atrium to the left ventricle. annulus or the papillary muscles. irregular pulse.May expectorate blood . .cough . which progressively thickens the leaflets and chorda tendinae.Anticoagulants .    Assessment and diagnostics: .  Management: .diagnose and monitor progression  Management: -medical management-congestive heart failure.(+) systolic murmur. high pitched blowing sound at the apex Echocardiography .  It is most often caused by the rheumatic endocarditis. 3. Mitral Regurgitation  involves flowing back from the let ventricle to the left atrium during systole  Maybe caused by problems in one of more leaflets. . Aortic Regurgitation  It is the flow of blood back from the aorta back into the left ventricle during diastole.to decrease risk for developing atrial thrombus. Leaflets often fuse together narrowing the orifice and progressively obstructing blood flow into the ventricle.2. .valvuloplasty. chorda tendinae. 4. -mitral valve replacement or valvuloplasty.

.usually asymptomatic . ECG. 5. stenosis may involve congenital leaflet malformation or abnormal number of leaflets or it may result from rheumatic endocarditis or cusp calcification of unknown cause. AntiDysrhythmic medications valve replacement (definitive tx) .fatigue. In adults.  Management: Antibiotic prophylaxis to prevent endocarditis.  Assessment and Diagnostics  (+)high pitched.forceful heartbeat in the head and neck . Clinical Manifestations: . water-hammer pulse.  Management: use of antibiotic prophylaxis prior to any invasive and dental procedure.  Clinical manifestations: .Dizziness or syncope due to reduced blood flow to the brain . radionucleide imaging.(+) widened pulse pressure.Many are asymptomatic. Same meds for heart failure Antiarrhythmic drugs Surgery is recommended for any patients with left ventricular hypertrophy regardless of the presence or absence of symptoms.visible or palpable temporal pulsations .exertional dyspnea .  Echocardiography is used to diagnose and monitor progression.  Assessment and diagnostics:  PE.  Diagnosis confirmed by echocardiography. MRI and cardiac catheterization. rough systolic murmur heard at the aortic area (systolic crescendodecrescendo).angina pectoris results from increased O2 demand of a hypertrophied left ventricle. blowing sound diastolic murmur heard at the 3rd to 4th intercostals space at left sternal area.loud.exertional dyspnea . Aortic Stenosis  It is the narrowing of the orifice between the left ventricle and the aorta.

increasing the remaining blood in the ventricle after contraction. Less blood is then able to enter the ventricle during diastole.  The systolic function is usually normal.. 2.  the heart muscle increase in size and mass especially along the septum resulting in dec size of ventricular cavity causing longer relaxation time.Cardiomyopathies 1. poor perfusion to git(nausea). .  Clinical manifestations:  Usually asymptomatic for years.  The cause for this disorder is usually unknown in most cases but in others can often be attributed to amyloidosis and other infiltrative disease.tachycardia and extra heart sounds in early stages. pitting edema)  Echocardiogram  ECG  CXR  Endomyocardial biopsy  Management:  Determine and manage cause. peripheral edema. Hypertrophic Cardiomyopathy  It is a genetic disease. 3. vein distention. exertional dyspnea.  dec amt of blood ejected from the ventricle in systole. symptoms of CHF( pulmonary crackles. Dilated cardiomyopathy  most common form of cardiomyopathy  diminished contractile elements and diffuse necrosis of myocardial cells resulting in poor systolic function. fluid retention. This makes it difficult for the ventricles to be filled with blood during the 1st part of diastole and making them more dependent on atrial contraction for filling. may have s/sxs of heart failure. low salt diet and exercise. Restrictive cardiomyopathy  It characterized by diastolic dysfunction caused by rigid ventricular walls that impair ventricular stretch and diastolic filling. cough. increasing the end-diastolic pressure and eventually increasing the pulmonary pressure. dizziness and syncope with exertion  Assessment and Diagnostics:  PE. orthopnea. chest pain. correction of heart failure with medications.

Myocarditis  It is an inflammatory process involving the myocardium. It may also be caused by an Allergic reaction. protozoal.  Clinical manifestations: . Pericarditis  refers to inflammation of the pericardium( membranous sac enveloping the heart).  Clinical manifestations:  Signs and symptoms of valvular regurgitation  Assessment and diagnostics:  PE.  lead to pericardial effusion and increased pressure on the heart leading to cardiac tamponade. s 4. The degree of myocardial involvement determines the degree of hemodynamic effect and resulting signs and symptoms.  Occurs as a result of sensitivity reaction occurring in response to the Streptoccal infection. Infective Endocarditis  It occurs as a direct invasion of the microorganisms to the endocordium.. presence of murmur   Management: eradicate microorganism through long term antibiotic regimen( Penicillin). Rheumatic Endocarditis  It occurs most often in school children following a streptococcal pharyngitis. 2.  Myocarditis results from Viral. 3. A left ventricular assistive device may be used pending the transplant.  primary illness or caused by a variety of medical and surgical disorders.findings will depend on which side of the heart is involved. bacterial. severity depends on the size and location of the lesion. mycotic. spirochetial infection. Frequent or prolonged episodes may also lead to thickening and decreased elasticity that restricts the hearts ability to fill properly (constrictive pericarditis).  Its presentation is similar to the rheumatic endocarditis with the addition of influenza-like symptoms prior to the valvular damage manifestations. Infectious diseases of the heart 1. Surgical management includes heart transplantation when medical management fails.

(+) Homan’s sign b.most characteristic sign  Dyspnea and other signs of heart failure may occur as a result of pericardial compression. myalgia 4. Which examination finding supports your diagnosis? a.        Assessment and Diagnostic findings: Echocardiogram ECG Management: Treat underlying cause Treat complications and symptoms QUIZ  Patient has A Left sided heart failure. usually constant but may worsen with inspiration or when lying down or turning. If this is a case of CHF.M. Patient was diagnosed w/ chronic venous insufficiency. A.Chest pain-most characteristic symptom. Edema d.  Friction rub. Last wk he complained of having chest tightness upon walking 2 miles. what NYHA classification is the patient in?  1  2  3  4 3. used to walk 3 miles a day. fever c. Which of the following should be avoided by a patient with buerger’s disease?  Cold  Hot . The expected assessment finding for this patient includes all of the ff except  Orthopnea  Oliguria  Dizziness  ascites 2.

What is the shock position? 10. What is the Normal CVP?  3-6  4-10  5-8  6-15 . (+) Homan’s sign b. Which of the following is an expected finding in a Patient with venous thrombosis? a. Edema d. Beck’s triad includes all of the following except  Jugular vein distention  hypotension  Flatness across the chest  distant/muffled heart sound 9. The best response is  Your doctor will discuss it with you  You have to change a few things in your life  It is best to modify your lifestyle to help in controlling your BP  Start taking metoprolol 50 mg BID 8. fever c. The patient was initially screened for cardiac tamponade. the patient belongs to which satge?  Stage 1  2  3  4 7. A newly diagnosed hypertensive patient asks you what is the most appropriate treatment for him. She was involved in a car accident and sustained chest injuries. A client was rushed to the hosp. myalgia 6. According to JNC 7 if the patient has a BP of 170/100.  Alcohol nifedipine 5.

. This sound is heard in a patient with mitral valve stenosis?  Mitral click  High pitched systolic murmur  Low pitched diastolic murmur  Loud rumbling sound .11. Which drug-drug interaction should be expected  Aspirin levels will decrease  Aspirin levels will increase  Furosemide levels will decrease  Furosemide levels will increase 15. Furosemide was given in a patient who is taking aspirin. Aneurysms often presents with  Pain  Pulsatile sensations  Assymptomatic  bruits 13. This sound is heard in a patient with mitral valve prolapse?  Mitral click  High pitched systolic murmur  Low pitched diastolic murmur  Loud rumbling sound 16. If you suspect a client to have aneurysm. This sound is heard in a patient with mitral valve regurgitation?  Mitral click  High pitched systolic murmur  Low pitched diastolic murmur  Loud rumbling sound 17. This is a type of cardiomyopathy wherein the contractile proteins are diminsished 12. which assessment intervention should be avoided?  Ascultation  Deep palpation  Percussion  inspection 14.

18. This is referred to as a PULSELESS DISEASE 19. Rheumatic endocarditis is seen in  Patients with active streptococcal infection  All patients w/ arthritis  Following a streptococcal infection  elderly . This is a mainstay for treatment of almost all vasculitis  NSAID  Steroids  COX-2 inhibitor  penicillin 20.

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