CARDIOVASCULAR SYSTEM

• EMERITA C. MENDOZA, • R.N., M.D.

Scope
• • • • Anatomy and Physiology Assessment Diagnostic and Lab Disorders

“Closer look”

Anatomy Key Points!
• Layers • Chambers • Valves • Conduction • Blood Supply • Circulatory System • Accessory Structures

Layers
• Epicardium outer • Myocardium middle • Endocardium inner (enclosed by the pericardium) • Pericardial sac space between the pericardium and epicardium

Chambers
• Left and right atrium • Left and right ventricles (thick muscles) inter-atrial septum – divides the left and right atrium inter-ventricular septum – divides the left and right

Valves
• AV atrioventricular valves
– Tricuspid – Mitral or bicuspid

• Semilunar valves
– Aortic – Pulmonic PAMT

Conduction System and Innervation
• SA and AV node are innervated by . . . ANS

Conduction System and Innervation
• • • • SA pacemaker of the heart located at the posterior wall of RA 70-80 beats per minute (atrial contraction)

Conduction System and Innervation
• Bachmann’s bundle • Internodal pathways
– Anterior – Middle (wenckebach’s), – Posterior (thorel’s)

Conduction System and Innervation
• • • • AV Node Reserved generator Located at the interventricular septum 40-60 beats/min

Conduction System and Innervation
• • • • • Purkinje system Bundle of His Right and left bundle Purkinje fibers Purkinje network

BLOOD SUPPLY TO MYOCARDIUM
• COMMON CORONARY ARTERY • RIGHT AND LEFT C.A. Circumflex branch – left ventricle

Arch of the AORTA

Accessory Structures
• Pericardium • Mediastinum • Thoracic Cavity

The Pericardium
• A membrane that surrounds the heart and great vessels

The Mediastinum
• The space between the lungs, which includes the heart pericardium aorta and vena cava.

The Thoracic Cavity
• The chest wall composed of the sternum and the rib cage • The cavity is separated by the diaphragm, the most important respiratory muscle

Vascular System
• Composed of the arteries, veins and capillaries • Transport blood to all parts of the body and back to the heart • Inner layer – tunica intima • Middle layer – tunica medialis • Outer layer – tunica adventitia

Blood Circulation
• Pulmonary circuit from the heart to lungs then back to heart • RA → Tricuspid Valve → RV • → Pulmonic Valve • PA → Lungs → 4 PV • LA → Mitral Valve → LV • → Aortic Valve • Systemic Circuit

Blood Supply to:
• Bone – Haversian canal and Volkmann’s canal • Blood Vessel – vasa vasorum • Heart – coronary arteries • Brain – common carotid artery – external and internal carotid artery, anterior, middle and posterior cerebral artery (Circle of Willis) • Upper Extremities – basillic – cephalic – brachial – radial and ulnar

Blood Supply to:
• Eyes – choroids (between sclera and retina) cornea gets 02 from the atmosphere • Kidneys – renal artery – interlobar artery – arcuate artery – interlobular artery – afferent arteriole – glomerulus – efferent arteriole - vasa recta – back to the heart • Liver – celiac artery – hepatic artery and hepatic portal vein (food laden) -

Regulation of Arterial BP and Distribution of Blood :
• Vasomotor and Cardiac Center in the Medulla Oblongata ↑ or ↓ BP • Pressor area – causes vasoconstriction to increase BP • Depressor area - causes vasodilation to decrease BP • Cardioinhibitor – parasympathetic stimulation to decrease BP • Cardioaccelerator – sympathetic

REGULATIONS
• The Baroreceptor Reflex to increase BP Decreased BP initiates ADH secretion and increases HR to increase BP. • The Chemoreceptor Reflex to increase BP Lack of oxygen – vasoconstriction to increase BP It is only activated when BP is below 60 mm Hg

REGULATIONS
• The CNS Ischemic Response • When CO2 is elevated in the blood and there is insufficient blood supply to the brain the vasomotor becomes very hyperactive causing peripheral vasoconstriction to increase BP.

REGULATIONS
• The Renin-Angiotensin-Aldosterone Responses RAAP • A decreased blood flow to the kidneys activates JGA to release RENIN enzyme to increase BP. • Renin → liver → angiotensinogen → angiotensin I → adrenal cortex • → aldosterone → • Angiotensin I → lungs → angiotensin II

REGULATIONS
• The Atrial Natriuretic Peptide • Stored in the atrial cells, opposes the RAAP, decreasing intravascular blood volume by excreting water into the kidneys

TERMS
• CARDIAC OUTPUT • STROKE VOLUME • BLOOD PRESSURE • PULSE • PULSE DEFICIT • PULSE PRESSURE

ASSESSMENT
• Chest pain • Cyanosis • Fatigue • Syncope • Arrhythmia • Gallop rub Dyspnea Pallor Palpitations Edema Murmur Pericardial friction

ASSESSMENT
• Chest Pain • Most common • Due to Ischemia or Myocardial Infarction • Precipitated by stress or can be relieved by Nitroglycerin (NTG) • In MI it is more intense unrelated to activities and can’t be relieved by NTG

ASSESSMENT
• 2. Dyspnea • Labored breathing • Dyspnea on exertion is due to increased O2 demand of myocardium. • Orthopnea is related to blood pooling in the pulmonary bed, suspect Pulmonary Edema • Any sudden or acute dyspnea may be a sign of Pulmonary Embolism

ASSESSMENT
• 3. Cyanosis • Bluish discoloration of the skin and mucous membrane • Sat O2 is below 94% • 4. Fatigue • Maybe due to Anemias or related to decreased Cardiac Output

ASSESSMENT
• 5. Palpitations • Awareness of rapid or irregular heart beat • Autonomic Nervous System and Adrenal Glands response (stress) • 6. Syncope • Transient loss of consciousness • Due to decreased cerebral tissue perfusion

ASSESSMENT
• 7. Edema • Increased Hydrostatic Pressure (HP) • Decreased Colloidal Oncotic Pressure (COP) • Obstructed Lymphatic or Vascular System • Anasarca

ASSESSMENT
• Bilateral edema = CHF or Renal Failure • Unilateral edema = Vascular or Lymphatic obstruction • Non-pitting edema = Inflammatory related • Pitting edema = HP and COP derangement

ASSESSMENT
• 8. Skin • Color, temperature, hair growth, nails, capillary refill, • clubbing or spooning of fingers evaluation.

ASSESSMENT
• • • • • • 9. Cardiac rate and rhythm Tachycardia Bradycardia Heart block Arrhythmias Sinus arrest

ASSESSMENT
• • • • S1 closure of AV valves (lub) S2 closure of SL valves (dup) S3 & S4 diastolic filling sound S3 is heard after S2, if present suspect CHF • S4 is heard prior to S1, if present suspect noncompliant ventricles although this is common among elderly

ASSESSMENT
• Murmurs turbulence of blood flow, if positive watchout FEV, this is normal until 1 year old • Pericardial Friction Rub “squeking sound” suspect pericardial effusion and pericarditis if this is heard • Muffled Heart Sound Deadening sound, if this is positive rule out Cardiac Tamponade and other similar problem like Effusion

ASSESSMENT

ASSESSMENT

Dx and Lab Tests
• Cardiac enzymes • Serum analysis • CARDIAC CATH
– Angiography (technetium 99, thallium) – CVC – SWAN-GANZ

• • •

EKG Pacemaker PTCA

Disorders
• • • • • Hyperlipidemia Coronary Artery Disease Angina Myocardial Infarction Congestive Heart Failure

Coronary Artery Disease CAD
• fatty deposits in the inner layer of coronary arteries. • mainly from hypercholesterolemia

Coronary Artery Disease
• • • • • • • • • Risk Factors: Hypertension Cigarette Smoking Diabetes Mellitus Obesity Sedentary Lifestyle Stress Atherosclerosis Hyperlipidemia

Coronary Artery Disease
• Incomplete occlusion of the coronary arteries lead to Angina (ischemia) • Complete occlusion of the coronary arteries lead to Myocardial Infarction

Angina
• Diminished O2 supply to the myocardium • Types: • Stable – ↑activity = pain, relieved by rest • Unstable – ↑activity = pain, relieved by NTG • Pre infarction – pain at rest, relieved by NTG

Angina
• Diagnostic Evaluation: • Characteristic of chest pain: • Substernal or retrosternal pain that radiates to arms neck and jaws • Squeezing, heavy, tightness of the chest • Precipitated by cold, eating, emotions and exertion • Lasts a few minutes and then subsides

Angina
• • • • NTG test (relief from pain) ECG (ST and T wave changes) Thallium 201 Imaging Technetium-99 Imaging

Angina
• Nursing Diagnosis: • Pain related to imbalance in myocardial oxygen demand • Decreased cardiac output related to reduced preload and after load • Anxiety related to pain, uncertain prognosis and threatening environment

Angina
• • • • • Management: Give antianginal drugs Administer O2 Maintaining cardiac output Decreasing Anxiety

Myocardial Infarction
• Absent of O2 supply to the myocardium • Necrosis or death to the myocardial tissue • Attack may be sudden or gradual

Myocardial Infarction

Myocardial Infarction
• • • • • • Chest pain: Severe, steady crushing and squeezing Not relieved by rest or NTG May continue for 15 minutes Levine’s sign May produce anxiety and fear resulting to increased HR, BP and RR • Diaphoresis, cold clammy skin, facial pallor

Angina
• Diagnostic Evaluation: • Characteristic of chest pain: • Substernal or retrosternal pain that radiates to arms neck and jaws • Squeezing, heavy, tightness of the chest • Precipitated by cold, eating, emotions and exertion • Lasts a few minutes and then subsides

Myocardial Infarction
• Diagnostic Evaluation: • Chest pain can’t be relieved by NTG • ST segment depression and T wave inversion • Cardiac enzymes: increased • Troponin-T (CT and T) • CK MB (CREATINE PHOSPHOKINASE) • LDH (lactate dehydrogenase) • AST (aspartate aminotransferase)

CK -MB
• it rises in serum within 2 to 8 hours of onset of acute myocardial infarction. • Serial measurements every 2 to 4 hours for a period of 9 to 12 hours after the patient is first seen will provide a pattern to determine whether the CK-MB is rising, indicative of myocardial injury.

Myocardial Infarction
• 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

Myocardial Infarction
• 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

Myocardial Infarction
• • • • • • • Management: CBR without BP Oxygen therapy Pain control Morphine or Meperidine Vasodilator (NTG) Anxiolytic (Benzodiazepine)

Myocardial Infarction
• • • • • • • • • Pharmacologic Therapy Thrombolytic Agents TPA tissue plasminogen activator Streptokinase (streptase) Urokinase Anticoagulant Heparin Warfarin Beta adrenergic blocking agents

Myocardial Infarction
• Surgical revascularization: • PTCA Percutaneous Transluminal Coronary Angioplasty • CABG coronary artery bypass graft

Congestive Heart Failure
• inability of the heart to pump blood into the circulatory system. • usually due to inability of the ventricles to pump blood • leading to • ↓ • Pulmonary congestion • ↓ • Pulmonary hypertension

CHF
• left sided heart failure will manifest • ↓ • Pulmonary in Nature • dyspnea, labored breathing, orthopnea, • moist hacking cough, bi-basilar crackles, • increased PAWP • ↓

CHF
• right ventricle will pump harder just to • pass blood into the congested pulmonary capillaries • ↓ • resulting to right ventricular hypertrophy • Right Ventricular Failure (Cor Pulmonale) • ↓

CHF
• blood will be congested into the right side • ↓ • right sided heart failure will follow • ↓ • Venous congestion • distended neck veins, hepatomegaly,

CHF
• venous pooling in the lower extremities • bi-pedal edema, varicosities, DVT • ↓ • until all venous system becomes congested with fluid • ↓ • periorbital edema or • generalized edema • ANASARCA

CHF
• • • • • • • Predisposing Factors: Myocardial Infarction Arrhythmias Pregnancy Pulmonary Embolism Anemia Renal Failure

CHF
• Diagnosing CHF: • Daily weighing reveals unexplained weight gain • Abdominal girth measurement shows ascites • EKG detects heart strain • Chest X-ray may highlights cardiomegaly and pleural effusion • CVC Central Venous Catheter and

SWAN-GANZ

CHF
• Nursing Considerations: • The goal of treatment is to improve pump function and reverse the compensatory mechanism of the heart. • Observe complete bed rest and reduce myocardial oxygen demand. • Employ FEV (forced expired volume) management and prevent the complications to occur. • Give Diuretics and Digoxin (0.5 – 2.0

CHF
• • • • 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

CHF
• Complications: • Cardiac Arrhythmias • Disturbances in regular rate and rhythm due to changes in electrical automaticity or conduction • Irregular HR, rhythm and regularity

Cardiac Arrhythmias
• ATRIAL A. • Premature atrial contraction (PAC) – more than 100 bpm • Atrial flutter – 250-300 bpm • Atrial fibrillation – higher than 500 bpm

• VENTRICULAR A. • Premature ventricular contraction

Premature ventricular contraction

• AV Block • Impulse is delayed from SA node to AV node • 1st degree – • 2nd degree –
– Mobitz type I – asymptomatic (ventricular contraction is adequate) – Mobitz type II – critical (atrial contraction is not synchronized with the ventricle)

• Treatment:

• Cardiac Arrest • Heart stops beating or contraction is ineffective • Watch-out for ↓ tissue perfusion manifestations: Restlessness (early sign) Tachycardia and tachypnea Shallow respirations Palpable BP

• Cardiac Arrest • Treatment: • Increase CO • Cardiovascular drugs and mechanical equipment utilization • Cardiovascular Drugs: • IV Dopamine (vasopressor) • IV Dobutamine (diuretic effects)

Disorders
• • • • • Venous Thrombus Chronic Venous Insufficiency Arteriosclerosis Raynaud’s Phenomenon Hypertension

Venous Thrombus
• • • • Due to: Stasis of blood Injury to the vessel wall Altered blood coagulation

Venous Thrombus
• • • • • High Risk: Fractures, cast and joint replacement Obesity and smoking Immobilized patient Heart problems

Venous Thrombus
• May progress to: • Phlebitis-inflammation of the vessel wall • Superficial thrombophlebitis-greater and lesser saphenous veins are affected. • Deep vein thrombosis-deep veins are affected, pulmonary embolism is a known complication of this.

Venous Thrombus
• • • • Manifestations: (+) Homan’s sign fever chills swelling and cyanosis

Venous Thrombus
• • • • Diagnostic: Venous duplex ultrasound Impedance plethysmography RF testing (radioactive fibrinogen) fibrinogen I 125 • Venography • Coagulation Profiles:
– APTT – PT/INR

Venous Thrombus
• • • • 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 • Anticoagulant • Thrombolytic

Chronic Venous Insufficiency
• Destruction of the valves because of chronic blood pooling or trauma. • Venous return is decreased • ↓ • chronic venous stasis • ↓ • resulting to edema and swelling formation • ↓

Arteriosclerosis
• It is hardening of the arterial blood vessel walls related to aging. • Atherosclerosis-common type of arteriosclerosis due to atheromas.

Arteriosclerosis
• Aging and atheromas • ↓ • impeding the lumen of the arterial walls • ↓ • it may be incomplete or incomplete occlusions • ↓ • producing systemic effects

Arteriosclerosis
• maybe asymptomatic or it may manifest only if the damaged is severe ↓ • systemic effects ↓ • 1. ↑ PVR = heart strain to hypertension • 2. weakening the muscles of the wall that leads to aneurysm

Arteriosclerosis
• • • • • 3. TIA to CVA 4. Angina to MI 5. ATN to Renal Failure 6. Retinopathy to Blindness 7. Peripheral Occlusive Disease (TAO) to Gangrene Formation • 8. Hepatic Infarction • 9. Pulmonary Infarction

Arteriosclerosis
• • • • • • Diagnostic Evaluation: Arteriography CT Scan MRI Duplex UTZ EKG

Arteriosclerosis
• Management: Modification of risk factors (CAD and hyperlipidemia) • Anticoagulants • Antiplatelets • Lipid Lowering Agent • Antihypertensive • Vascular Rehabilitation/Exercise

Arteriosclerosis
• Surgical Intervention: • PTA-Percutaneous Transluminal Angioplasty • Laser Angioplasty • Embolectomy-removal of clot from the artery • Thrombectomy-removal of thrombus from the artery • Endarterectomy-removal of plaque

TAO
• THROMBOANGITIS OBLITERANS (TAO) OR Buerger’s Disease • Occlusion of the peripheral blood vessels (lower extremities) • Cause: heavy smokers (common), ARTERIOSCLEROSIS, HYPERLIPIDEMIA, DM

TAO
• Dx: Arteriography • Management: promote collateral circulation (exercise), stop from smoking or control other risk factors, no elevation above the heart, warm compress • DRUGS: anticoagulants, fibrinolytics, vasodilators,

Raynaud’s Phenomenon
• This is a vasospastic disease with unusual sensitivity to cold or emotional stress. • The cause is unknown but it may be secondary to Autoimmune Disease.

Raynaud’s Phenomenon
• Due to arteriolar constrictions Manifestations: • Coldness • Pain • Pallor of finger tips, toes and tip of the nose • Color changes:
– White - blanching (vasospasm) – Blue - cyanotic (blood pooling)

Raynaud’s Phenomenon
• Diagnostic: • Rule out secondary problem (chronic arterial disease and connective tissue disorder)

Raynaud’s Phenomenon
• Management: • Avoid extreme temperatures Control pain with analgesic, reassure that it is only temporary • Calcium channel blockers is used to reduce vasospasm • NTG or sympatholytics may help • Antiplatelet, Dipyridamole (Persantin) to prevent occlusion

Hypertension
• “Silent killer” • Is a disease of vascular regulation that leads to high blood pressure BP = CO x PR • Mainly due to alteration of:
– Central Nervous System – Renin-Angiotensin-Aldosterone System – Extracellular Fluid Volume

Hypertension
• Primary or Essential Hypertension • Other cause 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

Hypertension
• • • • • • Secondary Hypertension Due to: Renal Pathology Coarctation of the Aorta Endocrine Disturbance Drugs (estrogens, sympathomimetics, NSAIDs, steroids) Malignant Hypertension

Hypertension
• • • • • • • • Risk Factors: Old age Race Overweight Family History Smoking Sedentary Lifestyle Diabetes Mellitus

Classification
• Stage I • Stage II • Stage III = = = 140-159/90-99 160-179/100-109 >or=180/>or=110

Hypertension
• Manifestations: • Usually asymptomatic • Headache, flashes, nausea and vomiting • Monitor the complications
– Heart strain – Aneurysm – Kidney Failure – CVA

Hypertension
• • • • Diagnostic Evaluation: Monitor BP Evaluate all of the risk factors: Eg. EKG, Blood Sugar, Blood Chem etc.

Hypertension
• Management: • Control of all risk factors • Eg. Lose weight, limit alcohol, cut sodium to 2.4 g/day, stop smoking, reduce dietary saturated fat and cholesterol, reduce coffee intake. • Diet, Exercise and Weight reduction • Despite lifestyle changes and BP remains high

• drug therapy should be started: • Diuretics Furosemide (Lasix) • Adrenergic Inhibitor • Peripheral Agent: Reserpine (Serpasil) • Central Alpha-Agonist Methyldopa (Aldomet) • Alpha-Blockers Prazosin HCl (Minipress)

Cardiovascular Drugs
• Anti Anginal • Opiate Analgesic – Morphine Sulfate • ↓ cardiac workload and BP, improve LOC and sedative effect • Vasodilators • Nitroglycerin NTG • Relax smooth muscle, dec. BP and alleviate headache

Cardiovascular Drugs
• Calcium Channel Blockers • Nifidepine (Procardia) Diazepam (Cardizem) • Decrease muscle tone, interferes contraction, decrease BP • S.E. – bradycardia, diarrhea and rashes • Beta Blocking Agent • Propranolol

Cardiovascular Drugs
• 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

Cardiovascular Drugs
• • • • • • • Dopamine – diuresis effect Increase Na excretion (kidney) Vasodilators Norepinephrine effect Dobutamine Increase CO More potent on contraction

Cardiovascular Drugs
• Diuretics • Spironolactone (Aldactone) – K sparer • Furosemide (Lasix) – K waster • Anti hypertensive • ACE inhibitors – Captopril (Capoten)

Cardiovascular Drugs
• • • • 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

Cardiovascular Drugs
• Thrombolytic/Fibrinolytic Agent • Streptokinase – lyses the clot (20T IU IV bolus or 4T IU/min drip) • Urokinase – avtivates plasminogen to plasmin (intracoronary) • TPA – tissue plasminogen activator • Antidote – Amino Caproic Acid

Cardiovascular Drugs
• Blood thinner • Heparin – prevent formation of new clot (4-8T IU/30 min) • Check APTT • Antidote – Protamine Sulfate • Warfarin (Coumadine) – decrease viscosity of blood (PO) home meds

EKG

PACEMAKER

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