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

e 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

- increased pressure on the arteries due to the contraction of the ventricles (heart pumping) - systolic pressure. - decreased pressure due to the relaxation of the ventricles (heart resting) - diastolic pressure. - Blood pressure is measured in mm of mercury, with the systole in ratio to the diastole.

PERIPHERAL RESISTANCE - amount of friction encountered by blood as it flows through blood vessels -increased by constriction of blood vessels d/t SNS activity/ atherosclerosis, blood viscosity, blood volume; when increased along w/ cardiac output, inc BP Coronary Artery Disease (CAD) Accumulation of fatty deposits in the inner layer of coronary arteries.

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- 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; relieved by rest, drugs; severity does not change

Unstable Occurs unpredictably during exertion and emotion; 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 - Substernal or retrosternal pain that radiates to arms, shoulders, back, neck and jaws - Squeezing, heavy, burning, tight chest - Precipitated by cold, eating, emotions, exertion - 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, uncertain prognosis and threatening environment

Management Relieve pain Place in comfortable position Administer O2 Decrease Anxiety PTCA - percutaneous transluminal coronary angioplasty To compress the plaque against the vessel wall, increasing the arterial lumen CABG - coronary artery bypass graft To improve the blood flow to the myocardial tissue Explain the reasons for hospitalization, diagnostic tests and therapies

Give antianginal drugs

Aspirin- prevent thrombus formation Beta-blockers- reduce BP and HR Calcium-channel blockers- dilate coronary artery and reduce vasospasm Nitrates- to dilate the coronary arteries Put one nitroglycerin tablet under the tongue Wait for 5 minutes If not relieved, 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. CAD 2. Coronary vasospasm 3. Coronary artery occlusion by embolus and thrombus 4. Conditions that decrease perfusion- hemorrhage, shock Risk factors 1. Hypercholesterolemia 2. Smoking 3. Hypertension 4. Obesity 5. Stress 6. 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, steady crushing and squeezing substernal pain

Radiates to the neck, arm, jaw and back

Not relieved by rest or NTG May continue for 15-30 minutes May produce anxiety and fear resulting to increased HR, BP and RR dyspnea Diaphoresis cold clammy skin N/V restlessness, 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, CK MB, LDH CBC- 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

The Cardiovascular System LABORATORY PROCEDURES CARDIAC Proteins and enzymes

Lactic Dehydrogenase (LDH) Elevates in MI in 24 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- 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 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!

levels

Early and late diagnosis can be made!

The Cardiovascular System LABORATORY PROCEDURES SERUM LIPIDS Lipid profile measures the serum cholesterol, triglycerides and lipoprotein Cholesterol= 200 mg/dL Triglycerides- 40- 150 mg/dL

The Cardiovascular System LABORATORY PROCEDURES SERUM LIPIDS

LDL- 130 mg/dL HDL- 30-70- 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

No special preparation is needed

The Cardiovascular System LABORATORY PROCEDURES Stress Test

Pre-test: consent may be required, adequate rest , eat a light meal or fast for 4 hours and avoid smoking, alcohol and caffeine The Cardiovascular System LABORATORY PROCEDURES Post-test: instruct client to notify the physician if any chest pain, dizziness or shortness of breath . 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, avoid alcohol, 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, 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

Oxygen therapy Provide adequate rest periods Minimize metabolic demands Provide soft diet Provide a low-sodium, 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 - Dissolve clots in the coronary artery allowing blood to

ie TPA tissue plasminogen activator (Alteplase), Streptokinase (streptase), Urokinase * S/E: bleeding and urticaria

Have aminocaproic acid ready( fibrinolysis inhibitor) Anticoagulant prevents formation of new blood clots ie Heparin, Warfarin S/S: fever, chills(hypersensitivity), rash, bleeding, diarrhea Monitor blood work (INR, PT-warfarin, PTT-heparin) Avoid ASA and invasive procedures Bleeding precautions Subcutaneous heparin- abdomen, do not aspirate or massage antidotes: Antiplatelet hypersensitivity to aspirin ie Ticlopidine, Clopidogrel

Beta adrenergic blocking agents reduce myocardial O2 demand by blocking sympathetic stimulation; dec HR, contractility, BP ie Propranolol

Calcium channel blockers dec contraction, HR; relax blood vessels ie Diltiazem Morphine - reduces pain and anxiety - Relaxes bronchioles to enhance oxygenation

ACE Inhibitors - Prevents formation of angiotensin II w/c causes vasoconstriction; dec O2 demand Limits the area of infarction

Antihyperlipidemics- lowers serum lipids by decreasing triglycerides or cholesterol Ex. HMG-CoA reductase( statins), Fibrates( Gemfibrozil), bile acid sequestrants( cholestyramine) S/E: N/V, diarrhea, musculskeletal injury, hepatic toxicity, rash, reduced absorption of fat and fat-soluble vitamins. Visual disturbances(lovastatin & gemfibrozil) Administer statins at HS to inc absorption, other meds wt meals to dec GI irritation, cholestyramine shld be mixed wt full glass of liquid Surgical revascularization: Percutaneous Transluminal Coronary Angioplasty (PTCA);

coronary artery bypass graft (CABG ) After the condition had been stabilized: - CBR without BP (complete bedrest without bathroom privilege) - Gradual resumption of ADL to full recovery

1-2. Give 2 examples of preloaders 3. Captopril can ______ the afterload Increases

Decrease

No effect 4. What is the pacemaker of the heart? 5. Nitrates is best stored in refrigerator

Amber colored glass In open containers The garden

6. A patient complained of chest pain. 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. Thrombolytic agents are given in MI. What is the antidote Aminocaproic acid

Aminobutyric acid Protamine sulfate

Vt. K 9. Partial occlusion usually results in Ischemia Infarction Necrosis death

10. This is a type of angina felt at rest ,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

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, kidney and other tissues oliguria, dizziness PATHOPHYSIOLOGY RIGHT ventricular failure blood pooling in the venous circulation increased hydrostatic pressure peripheral edema

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

Limit fluid intake Monitor daily weight and report signs of fluid retention

Complications: Acute Pulmonary Edema Treatment: Bed rest and maintain high fowlers 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- caused by rapid vasodilation and subsequent pooling of blood within the peripheral system( drugs, 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, vasopressors and inotropics such as DOPAMINE and DOBUTAMINE, diuretics, nitrates


pain

Administer O2 Morphine is administered to decrease pulmonary congestion and to relieve

Assist in intubation, mechanical ventilation, PTCA, CABG, insertion of Swan-Ganz cath and IABP Monitor urinary output, BP and pulses Risk Factors

Cardiac trauma Complication of Myocardial infarction Pericarditis Cancer metastasis

Manifestations BECKs Triad- Jugular vein distention, hypotension and distant/muffled heart sound Pulsus paradoxus

Increased CVP decreased cardiac output Syncope anxiety dyspnea Percussion- Flatness across the ant. chest

Diagnostics Echocardiogram

CXR Management Assist in PERICARDIOCENTESIS

Administer IVF Monitor ECG, urine output and BP

Monitor for recurrence of tamponade Vascular Disorders Venous Thrombosis

CVI Arterosclerosis Raynauds 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 - greater and lesser saphenous veins affected.

Deep vein thrombosis - deep veins affected; pulmonary embolism is a complication Manifestations (+) Homans 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

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. Venous return is decreased chronic venous stasis edema formation veins becomes distorted or tortuous (varicosities) stasis ulcer, 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

Raynauds Phenomenon Arteriolar vasospastic disease with unusual sensitivity to cold or emotional stress. cause is unknown but may be secondary to Autoimmune Diseases ASSESSMENT Pallor then cyanosis

Hyperemia when blood returns to digits after vasospasm

Numbness, 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. Atherosclerosis-common type of arteriosclerosis due to atheromas.

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

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- 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= Marfans 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:

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, 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, NSAIDs, steroids) Malignant Hypertension It is a combination of both which is BP is uncontrolled. Risk Factors Old age

male

Race Overweight Family History Smoking Sedentary Lifestyle Diabetes Mellitus

Manifestations 1. Headache 2. Visual changes 3. chest pain 4. dizziness 5. N/V Diagnostic Evaluation Monitor BP EKG, Blood Sugar, Blood Chem etc.

Management: Control of all risk factors:. Lose weight, limit alcohol, cut sodium to 2.4 g/day, stop smoking, reduce dietary saturated fat and cholesterol, reduce coffee intake.

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, nutrition, weight, diet (low fat, low Na), cessation of smoking treatment regimen ie drugs BP monitoring Follow up

Cardiovascular Drugs:

Anti Anginal Opiate Analgesic Morphine Sulfate cardiac workload and BP, improve LOC and sedative effect Vasodilators Nitroglycerin NTG, hydralazine, nitroprusside Relax smooth muscle, dec. BP and alleviate headache Increase blood vessel diameter and improves blood flow S.E. dizziness and flushing, B6, B12 dec Can be given SL or IV (Isordil) and topical (Nitrobid) Calcium Channel Blockers Nifidepine (Procardia) Diazepam (Cardizem) Decrease muscle tone, interferes contraction, decrease BP S.E. bradycardia, diarrhea and rashes Beta Blocking Agent Propranolol Decrease workload Blocks beta receptors and capable of decreasing HR S.E. vomiting, nausea and depression

Diuretics- K- waster, sparer S/E: hyponatremia, GI irritration, hyperurecemia, hypomagnesemia, dec. Ziinc( except K- sparers) Furosemide- competes w/ ASA for renal excretioninc. ASA levels Hypocalcemia- sparers (spirinolactone, amiloride, triamterene) Thiazides and loop diuretics- hyperglycemia in pxs w/ DM All drugs are better administered in AM

Digitalis, Digoxin - Positive Inotropic (Increases contraction of the heart) - Increase emptying capacity of the heart - Negative chronotropic (Decreases HR) AV node control - Increase CO (improves stroke volume) S.E. GIT disturbance, CNS depression and flashes of light

Dopamine diuresis effect - Increase Na excretion (kidney) Dobutamine - Increase CO - 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, contractility and automaticity Quinidine for atrial fib

Thrombolytic/Fibrinolytic Agent - Streptokinase lyses the clot (20T IU IV bolus or 4T IU/min drip) - 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 Dont give to pregnant women Antidote Vitamin K Cardiac catheterization The Cardiovascular System LABORATORY PROCEDURES

Pretest: Ensure Consent, assess for allergy to seafood and iodine, NPO, document weight and height, baseline VS, blood tests and document the peripheral pulses The Cardiovascular System LABORATORY PROCEDURES

Pretest: Fast for 8-12 hours, teachings, medications to allay anxiety The Cardiovascular System LABORATORY PROCEDURES

Intra-test: inform patient of a fluttery feeling as the catheter passes through the heart; 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, 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. 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. CLinical Manifestations: - fatigue, shortness of breath, light-headedness, dizziness, syncope, palpitations, chest pain and anxiety. May also be asymptomatic.

Assessment and Diagnostics: extra heart sound referred to as Mitral click Management- symptomatic relief and control. In advance cases mitral valve repair and replacement may be necessary.

2. Mitral Regurgitation involves flowing back from the let ventricle to the left atrium during systole Maybe caused by problems in one of more leaflets, chorda tendinae, annulus or the papillary muscles.

Assessment and diagnostics: - (+) systolic murmur, high pitched blowing sound at the apex Echocardiography - diagnose and monitor progression

Management: -medical management-congestive heart failure. -mitral valve replacement or valvuloplasty.

3. Mitral stenosis It is an obstruction of blood flowing from the left atrium to the left ventricle. It is most often caused by the rheumatic endocarditis, which progressively thickens the leaflets and chorda tendinae. Leaflets often fuse together narrowing the orifice and progressively obstructing blood flow into the ventricle.

Clinical manifestations - DOB on exertion - May expectorate blood - cough - Recurrent repiratory infections due to venous pulmonary hypertension. Assessment and Diagnosis: - PE-weak, irregular pulse, low pitched rumbling diastolic murmur heard at the apex. - Echocardiography is used to diagnose. - ECG and cardiac catheterization are used to determine severity. Management: - antibiotic prophylaxis- to prevent recurrence of infections. - Anticoagulants - to decrease risk for developing atrial thrombus. - valvuloplasty.
4. Aortic Regurgitation It is the flow of blood back from the aorta back into the left ventricle during diastole. It maybe caused by inflammatory lesions that deform the leaflets preventing them from closing the orifice.

 Clinical Manifestations: - usually asymptomatic - forceful heartbeat in the head and neck - visible or palpable temporal pulsations - exertional dyspnea - fatigue. Assessment and Diagnostics (+)high pitched, blowing sound diastolic murmur heard at the 3rd to 4th intercostals space at left sternal area.(+) widened pulse pressure, water-hammer pulse. Diagnosis confirmed by echocardiography, radionucleide imaging, ECG, MRI and cardiac catheterization. Management: use of antibiotic prophylaxis prior to any invasive and dental procedure. 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.

5. Aortic Stenosis It is the narrowing of the orifice between the left ventricle and the aorta. In adults, stenosis may involve congenital leaflet malformation or abnormal number of leaflets or it may result from rheumatic endocarditis or cusp calcification of unknown cause. Clinical manifestations: - Many are asymptomatic. - exertional dyspnea - Dizziness or syncope due to reduced blood flow to the brain - angina pectoris results from increased O2 demand of a hypertrophied left ventricle.

Assessment and diagnostics: PE- loud, rough systolic murmur heard at the aortic area (systolic crescendodecrescendo). Echocardiography is used to diagnose and monitor progression. Management: Antibiotic prophylaxis to prevent endocarditis. AntiDysrhythmic medications valve replacement (definitive tx)

Cardiomyopathies 1. Dilated cardiomyopathy most common form of cardiomyopathy diminished contractile elements and diffuse necrosis of myocardial cells resulting in poor systolic function. dec amt of blood ejected from the ventricle in systole, increasing the remaining blood in the ventricle after contraction. Less blood is then able to enter the ventricle during diastole, increasing the end-diastolic pressure and eventually increasing the pulmonary pressure.. 2. Hypertrophic Cardiomyopathy It is a genetic disease. the heart muscle increase in size and mass especially along the septum resulting in dec size of ventricular cavity causing longer relaxation time. 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. 3. Restrictive cardiomyopathy It characterized by diastolic dysfunction caused by rigid ventricular walls that impair ventricular stretch and diastolic filling. The systolic function is usually normal. The cause for this disorder is usually unknown in most cases but in others can often be attributed to amyloidosis and other infiltrative disease.

Clinical manifestations: Usually asymptomatic for years, may have s/sxs of heart failure, exertional dyspnea, orthopnea, fluid retention, peripheral edema, cough, poor perfusion to git(nausea), chest pain, dizziness and syncope with exertion Assessment and Diagnostics: PE- tachycardia and extra heart sounds in early stages, symptoms of CHF( pulmonary crackles, vein distention, pitting edema) Echocardiogram ECG CXR Endomyocardial biopsy Management: Determine and manage cause, correction of heart failure with medications, low salt diet and exercise.

 Surgical management includes heart transplantation when medical management fails. A left ventricular assistive device may be used pending the transplant.
Infectious diseases of the heart 1. Rheumatic Endocarditis It occurs most often in school children following a streptococcal pharyngitis. Occurs as a result of sensitivity reaction occurring in response to the Streptoccal infection. Clinical manifestations: Signs and symptoms of valvular regurgitation

Assessment and diagnostics: PE- findings will depend on which side of the heart is involved; severity depends on the size and location of the lesion, presence of murmur
Management: eradicate microorganism through long term antibiotic regimen( Penicillin).

2. Infective Endocarditis It occurs as a direct invasion of the microorganisms to the endocordium. Its presentation is similar to the rheumatic endocarditis with the addition of influenza-like symptoms prior to the valvular damage manifestations. 3. Myocarditis It is an inflammatory process involving the myocardium. Myocarditis results from Viral, bacterial, mycotic, protozoal, spirochetial infection. It may also be caused by an Allergic reaction. The degree of myocardial involvement determines the degree of hemodynamic effect and resulting signs and symptoms. s 4. Pericarditis refers to inflammation of the pericardium( membranous sac enveloping the heart).. primary illness or caused by a variety of medical and surgical disorders. lead to pericardial effusion and increased pressure on the heart leading to cardiac tamponade. Frequent or prolonged episodes may also lead to thickening and decreased elasticity that restricts the hearts ability to fill properly (constrictive pericarditis).

Clinical manifestations:

Chest pain-most characteristic symptom, usually constant but may worsen with inspiration or when lying down or turning. Friction rub- most characteristic sign Dyspnea and other signs of heart failure may occur as a result of pericardial compression.

Assessment and Diagnostic findings: Echocardiogram ECG Management: Treat underlying cause Treat complications and symptoms

QUIZ Patient has A Left sided heart failure. The expected assessment finding for this patient includes all of the ff except Orthopnea Oliguria Dizziness ascites 2. A.M. used to walk 3 miles a day. Last wk he complained of having chest tightness upon walking 2 miles. If this is a case of CHF, what NYHA classification is the patient in? 1 2 3 4 3. Patient was diagnosed w/ chronic venous insufficiency. Which examination finding supports your diagnosis? a. (+) Homans sign b. fever c. Edema d. myalgia

4. Which of the following should be avoided by a patient with buergers disease? Cold Hot

Alcohol nifedipine

5. Which of the following is an expected finding in a Patient with venous thrombosis? a. (+) Homans sign b. fever c. Edema d. myalgia 6. According to JNC 7 if the patient has a BP of 170/100, 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. 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. A client was rushed to the hosp. She was involved in a car accident and sustained chest injuries. The patient was initially screened for cardiac tamponade. Becks triad includes all of the following except Jugular vein distention hypotension Flatness across the chest distant/muffled heart sound 9. What is the shock position? 10. What is the Normal CVP? 3-6 4-10 5-8 6-15

11. This is a type of cardiomyopathy wherein the contractile proteins are diminsished 12. Aneurysms often presents with Pain Pulsatile sensations Assymptomatic bruits 13. If you suspect a client to have aneurysm, which assessment intervention should be avoided? Ascultation Deep palpation Percussion inspection

14. Furosemide was given in a patient who is taking aspirin. Which drug-drug interaction should be expected Aspirin levels will decrease Aspirin levels will increase Furosemide levels will decrease Furosemide levels will increase 15. 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. 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 sound is heard in a patient with mitral valve stenosis? Mitral click High pitched systolic murmur Low pitched diastolic murmur Loud rumbling sound

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