THE CARDIOVASCULAR SYSTEM

The Cardiovascular System
y A closed system of the heart and blood vessels
y The heart pumps blood y Blood vessels allow blood to circulate to all parts of the body

y The function of the cardiovascular system is to deliver oxygen and nutrients and to remove carbon dioxide and other waste products
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The Heart

y Location
y Thorax between the lungs y Pointed apex directed toward left hip

y About the size of your fist

3

The Heart

Figure 11.1

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Overview: Heart
‡ ‡ ‡ ‡ ‡ Muscular pumping organ of the body Occupies most of the L mediastinum Weighs < 1 lb; approx. 300-400 g Resembles a closed fist Covered by serous membrane
± Pericardium (parietal and visceral) - Serous fluid fills the space between the layers of pericardium ± Pericardial fluid = 10-20 cc; prevents friction rub

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Overview: Heart
Layers ‡ Epicardium- outermost ‡ Myocardium- middle ‡ Endocardium- innermost

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The Heart: Heart Wall y Three layers y Epicardium y Outside layer y Connective tissue layer y Myocardium y Middle layer y Mostly cardiac muscle y Endocardium y Inner layer y Endothelium 7 .

The Heart: Coverings y Pericardium ± a double serous membrane y Visceral pericardium y Next to heart y Parietal pericardium y Outside layer 8 .

External Heart Anatomy 9 .

lower -pumping/contracting/ discharging chambers 10 .upper -receiving/collecting chambers ‡ 2 Ventricles.Chambers ‡ 2 Atria.

The Heart: Chambers y Right and left side act as separate pumps y Four chambers y Atria y Receiving chambers y Right atrium y Left atrium y Ventricles y Discharging chambers y Right ventricle y Left ventricle 11 .

12 .

Valves ‡ Prevent blood backflow ‡ Promote unidirectional flow Overview: Heart ‡ AV valves ± Tricuspid and Mitral ‡ Guards opening between atria and ventricles ‡ Closure p S1 sound ‡ Semilunar valves ± Pulmonic and Aortic ± Closure p S2 sound *Extra heart sounds: S3 (Ventricular gallop) p CHF S4 (Atrial gallop) p MI 13 .

The Heart sounds 1. S1.due to increased ventricular filling 4.due to closure of the AV valves 2. S4. S2.due to forceful atrial contraction 14 .due to the closure of the semilunar valves 3. S3.

15 .

The Heart: Valves y Allow blood to flow in only one direction y Four valves y Atrioventricular valves ± between atria and ventricles y Bicuspid valve (left) y Tricuspid valve (right) y Semilunar valves between ventricle and artery y Pulmonary semilunar valve y Aortic semilunar valve 16 .

The Heart: Valves y Valves open as blood is pumped through y Held in place by chordae tendineae (³heart strings´) y Close to prevent backflow 17 .

Operation of Heart Valves 18 .

Blood Circulation 19 .

Blood Circulation Pulmonary circuit (from the heart to lungs then back to heart) RA Tricuspid Valve RV Pulmonic Valve PA Lungs PV LA Mitral Valve LV Aortic Valve Systemic Circuit circulation of blood to all body tissues via aorta parts of the body 20 .

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Coronary Circulation y Blood in the heart chambers does not nourish the myocardium y The heart has its own nourishing circulatory system y Coronary arteries y Cardiac veins y Blood empties into the right atrium via the coronary sinus 23 .

Overview: Heart Coronary Arteries ‡ Arises from base or aorta ‡ R and L main coronary arteries p supplies blood to myocardium (for nourishment) 24 .

Right coronary artery 2. Left coronary artery 25 .The Cardiovascular System The Blood supply of the heart comes from the Coronary arteries 1.

the POSTERIOR septal wall and AV (90%) and SA node (55%) 26 . posterior interventricular b. marginal artery .supplies the RIGHT atrium. RIGHT ventricle. Right coronary artery a.Blood Vessels 1. inferior portion of the LEFT ventricle.

2. Left anterior descending artery ± anterior wall of the LEFT ventricle. Left coronary artery ‡ anterior interventricular a. the anterior septum and the Apex of the left ventricle 27 .left atrium and the posterior LEFT ventricle b. circumflex arteries .

The Coronary Arteries Coronary Artery and its Branches Portion of Myocardium Supplied Portion of Conduction System Supplied Right ‡ Posterior descending ‡ Right margin (AV nodal) Left ‡ Anterior descending (LAD) ‡ Circumflex (LCX) ‡ Right atrium ‡ Inferior wall of right ventricle ‡ ½ anterior surface of left ventricle ‡ Anterior surface of left ventricle ‡ Left atrium ‡ Lateral wall of left ventricle ‡ Part of right ventricle ‡ AV node (90% of population) ‡ SA node ( > 55%) ‡ Bundle of His ‡ Posterior division of left bundle branch ‡ AV node (10%) ‡ SA node (45%) ‡ All bundle branches 28 .

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Cardiac veins 2.The Cardiovascular System The venous drainage of the heart 1. Coronary sinus cardiac veins drain into the coronary sinus which in turn drain into right atrium 30 .

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continuous way 32 . in a regular.The Heart: Conduction System y Intrinsic conduction system (nodal system) y Heart muscle cells contract.

Myocardial Cells Myocardial Cell Types Kinds of Cardiac Cells Myocardial cells Where Found Primary Function Primary Property Contractility Contraction and Myocardium Relaxation Electrical conductio n system Generation and conduction of electrical impulses Specialized cells of the electrical conduction system Automaticity Conductivity 33 .

The Heart: Conduction System y Special tissue sets the pace y Sinoatrial node y Pacemaker y Atrioventricular node y Atrioventricular bundle y Bundle branches y Purkinje fibers 34 .

35 .

To allow ventricular filling ‡ Bundle of His ± Located at interventricular septum ± Divides into R and L main bundle branches ‡ Purkinje fibers ± Located at the walls of ventricles p ventricular contraction Overview: Heart 36 .Conduction System ‡ SA node ± Located at the junction of SVC and RA ± Primary pacemaker p 60-100 bpm ‡ AV node ± Located at interatrial septum ± There is a delay of electrical impulse of 0.08 millisec.

Heart Contractions y Contraction is initiated by the sinoatrial node y Sequential stimulation occurs at other auto rhythmic cells 37 .

SA Node ‡ natural pacemaker for the heart ‡ 60-100 impulses/min ‡ Junction of the right atrium and SVC ‡ sends the electrical impulse that triggers each heartbeat. 38 .

AV Node ‡ Located at the right atrial wall near tricuspid valve ‡ 40-60 impulses/min ‡ Receives impulse from the sinoatrial node ‡ atrioventricular node in turn sends an impulse through the nerve network to the ventricles. 39 .

Purkinje system ‡ Bundle of His ‡ Right and left bundle branch ‡ Purkinje fibers 40 .

Na moves inside. K goes outside to begin Depolarization (electrical activation of cell) ‡ Inside cell membrane. inside cell membrane (-). more (+) ‡ Stimulus incites neighboring cells to depolarize as well ‡ Contraction follows 41 .Physiology of conduction ‡ Electrical activity due to movement of ions ‡ Resting state. outside cell membrane (+) ‡ Initiation of electrical impulse.

42 .

protect heart from tetany 1. Absolute refractory period ± cannot be restimulated regardless of strength of stimuli 2. Relative refractory period ± stronger than normal stimulus can incite muscle to contract 43 .‡ ‡ Repolarization (resting state) Refractory period ± phase where muscle cannot be restimulated to contract.

CARDIAC CYCLE ‡ sequence of events that occur when the heart beats 44 .

then ventricles contract y Diastole = relaxation y Systole = contraction 45 .The Heart: Cardiac Cycle y Atria contract simultaneously y Atria relax.

46 .

atria contract d/t SA node Atrial pressure rises ejecting blood to ventricles 47 .diastole ‡ ‡ ‡ ‡ ‡ Ventricles are relaxed AV valves open Blood empties to atria then to ventricles End of diastole.

ventricular pressure decreases ‡ Pulmonary and aortic pressure decreases ‡ Closure of semilunar valves 48 .systole ‡ 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.

Filling of Heart Chambers ± the Cardiac Cycle 49 .

pushing out blood y Early diastole ± atria finish re-filling. ventricular pressure is low 50 .The Heart: Cardiac Cycle y Cardiac cycle ± events of one complete heart beat y Mid-to-late diastole ± blood flows into ventricles y Ventricular systole ± blood pressure builds before ventricle contracts.

The Heart: Cardiac Output y Cardiac output (CO) y Amount of blood pumped by each side of the heart in one minute y CO = heart rate x stroke volume y CO = HR x SV 51 .

Cardiac Output Regulation 52 .

amount of blood ejected per heartbeat ± Average resting stroke volume: 70 ml 53 .‡ Stroke volume ± Volume of blood pumped by each ventricle in one contraction.

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.STROKE VOLUME 1. dec by diuretics 2. Afterload ± amount of resistance to ejection of blood from ventricle ‡ Also called systemic vascular resistance ‡ Inverse relationship with stroke volume 54 .

dopamine and dobutamine 55 . Contractility ± force generated by contracting myocardium . digitalis.3.Enhanced by SNS.

baroreceptor activity.HEART RATE ± affected by ANS. cathecolamines. thyroid hormone ‡ Tachycardia > 100 bpm ‡ Bradycardia < 60 bpm 56 .

The Heart: Regulation of Heart Rate y Increased heart rate y Sympathetic nervous system y Crisis y Low blood pressure y Hormones y Epinephrine y Thyroxine y Exercise y Decreased blood volume 57 .

The Heart: Regulation of Heart Rate ‡ Decreased heart rate ± Parasympathetic nervous system ± High blood pressure / blood volume ± Decreased venous return 58 .

59 .

ADH. aldosterone.Blood Pressure ‡ Cardiac output X peripheral resistance ‡ Control is neural (central and peripheral) and hormonal ‡ Hormones. ANF/ ANP can decrease BP ‡ Baroreceptors in the carotid and aorta 60 . epinephrine can increase BP.

contraction.Baroreceptor reflexes . constriction of renal arterioles and increased aldosterone 61 .causes vasoconstriction and increased blood pressure Dec arterial pressure SNS inc cardiac rate. contractility. circulating blood volume.carotid sinus and aortic arch .

increased pressure on the arteries due to the contraction of the ventricles (heart pumping) .systolic pressure..diastolic pressure. 62 . .decreased pressure due to the relaxation of the ventricles (heart resting) .Blood pressure is measured in mm mercury. . with the systole in ratio to the diastole.

inc BP 63 . when increased along w/ cardiac output.‡ 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.

Blood Pressure y Measurements by health professionals are made on the pressure in large arteries y Systolic ± pressure at the peak of ventricular contraction y Diastolic ± pressure when ventricles relax y Pressure in blood vessels decreases as the distance away from the heart increases 64 .

Blood Pressure: Effects of Factors y Neural factors y Autonomic nervous system adjustments (sympathetic division) y Renal factors y Regulation by altering blood volume y Renin ± hormonal control 65 .

Blood Pressure: Effects of Factors y Temperature y Heat has a vasodilation effect y Cold has a vasoconstricting effect y Chemicals y Various substances can cause increases or decreases y Diet 66 .

Factors Determining Blood Pressure Figure 11.19 67 .

dorsalis pedis a.‡ ARTERIAL PULSE . and emotions ‡ temporal. radial. facial. creates a wave w/c travels through entire arterial system ‡ ‡ 60. femoral. popliteal. postural changes.alternating expansion and recoil of an artery w/ each beat of the left ventricle. brachial. 68 . carotid.100 bpm influenced by activity. posterior tibial.

35 .Pulse y Pulse ± pressure wave of blood y Monitored at ³pressure points´ where pulse is easily palpated 69 Slide 11.

Vascular System 70 .

right lymphatic duct ‡ lymphoid organs 71 . Lymph vascular system ‡ lymphatic capillaries ‡ lymphatic vessels ‡ main lymphatic trunks: thoracic duct. Blood vascular system Taking blood to the tissues and back y y y y y Arteries Arterioles Capillaries Venules Veins B.COMPONENT PARTS A.

they connect the veins and arteries ‡ lymphatic system collects extravasated fluid from the tissues and returns it to the blood 72 .‡ arteries are vessels that carry blood away from the heart to the periphery ‡ The veins are the vessels that carry blood to the heart ‡ The capillaries are lined with squamous cells.

tibial. radial. popliteal. External. dorsalis pedis) 73 . brachial. ). thoracic and abdominal aorta) ‡ Abdominal aorta branches into Common iliac ± internal and external iliac artery (femoral. descending branch ‡ Subclavian artery ± axilary. left subclavian and brachioephalic trunk gives rise to right common carotid and right subclavian. arch (left carotid. ulnar ‡ Common carotid artery .MAJOR ARTERIES OF THE SYSTEMIC CIRCULATION ‡ Aorta ± ascending.(internal.

11 74 .Major Arteries of Systemic Circulation Figure 11.

External and Internal jugular veins drain the head and neck into the superior vena cava 2. pelvis & lower limbs 3. Superior vena cava drains the head and upper extremities 2. coronary sinus is large vein draining the heart muscle back into the heart Veins of the Head and Neck 1.MAJOR VEINS OF THE SYSTEMIC CIRCULATION 1. Inferior vena cava drains the abdomen. Dural venous sinuses empty into internal jugular vein 75 .

Major Veins of Systemic Circulation 76 .

yBLOOD VESSEL: ANATOMY yThree layers (tunics) yTunica intima ySingle layer of smooth endothelial cells yTunica media ySmooth muscle cells yControlled by sympathetic nervous system yAllows vessel to vasoconstrict and vasodilate yTunica adventitia/ externa yMostly fibrous connective tissue 77 .

The Vascular System Figure 11.8b 78 .

Differences Between Blood Vessel Types y Walls of arteries are the thickest y Lumens of veins are larger y Skeletal muscle ³milks´ blood in veins toward the heart y Walls of capillaries are only one cell layer thick to allow for exchanges between blood and tissue 79 .

Movement of Blood Through Vessels y Most arterial blood is pumped by the heart y Veins use the milking action of muscles to help move blood (valves) 80 Slide 11.27 .

Capillary Beds y Capillary beds consist of two types of vessels y Vascular shunt ± directly connects an arteriole to a venule 81 .

Capillary Bed Diffusion at Capillary Beds y True capillaries ± exchange vessels y Oxygen and nutrients cross to cells y Carbon dioxide and metabolic waste products cross into blood 82 .

ASSESSMENT 83 .

ASSESSMENT Subjective Data Objective Data 84 .

The Cardiovascular System Cardiac History ‡ Interview ‡ Focused assessment 85 .

CARDIAC ASSESSMENT Health History ‡ Obtain description of present illness and the chief complaint Chest pain or discomfort Shortness of breath/ dyspnea Edema and weight gain Palpitations Fatigue Dizziness and syncope or LOC ‡ Assess risk factors 86 .

Precipitated by stress or can be relieved by Nitroglycerin (NTG) ‡ In MI. it is more intense. angina.Cardiovascular Assessment Cardiac signs and symptoms Chest Pain ‡ Most common ‡ Due to Ischemia or MI. valvular disease ‡ Angina. suspect respiratory problems 87 . unrelated to activities and can¶t be relieved by NTG ‡ If it occurs during breathing.

eating. successful reperfusion of blocked coronary artery 88 . may radiate to inside of arm. may have pain in shoulders and hands ‡ >15 min ‡ Occurs spontaneously or sequela to unstable angina ‡ Relieved by Morphine SO4. nitroglycerine. neck. cold ‡ Relieved with rest. may spread widely throughout the chest. emotion. or jaw ‡ 5-15 min ‡ Usually related to exertion.Cardiac & Non Cardiac Causes of CHEST PAIN ANGINA PECTORIS ‡ Substernal/ retrosternal spreasing across the chest. oxygen MYOCARDIAL INFARCTION ‡ Substernal pain or pain over the precordium.

treatment of underlying cause. coughing. substernal. swallowing. arms and back ‡ Intermittent ‡ Sudden. time. increases with inspiration ‡ Relieved with rest.CHEST PAIN PERICARDITIS ‡ Sharp. antiinflammatory medications PLEURITIC PAIN ‡ Pain arises from inferior portion of pleura. may be referred to costal margins or upper abdomen. severe. to the left of the sternum. bronchodilators 89 . may be referred to neck. increases with inspiration. may be felt in the epigastrium. patient may be able to localize pain ‡ 30+ min ‡ Occurs spontaneously. rotation of the trunk ‡ Relieved by analgesia. sitting upright.

may occur spontaneously ‡ Relieved with food/ antacid. hiatal hernia) ‡ Substernal pain. liquids. cold. may be projected around chest to shoulders ‡ 5-60 min ‡ Precipitated by recumbency. exercise. may be variable.CHEST PAIN ANXIETY ‡ Pain over chest. emotion ‡ Relieved with removal of the stimulus. tingling of the hands and mouth ‡ 2-3 min ‡ Stress. NTG relieves spasm 90 . does not radiate. relaxation ESOPHAGEAL PAIN (Reflux esophagitis or spasm. patient may complain of numbness.

‡ Any sudden or acute dyspnea may be a sign of Pulmonary Embolism ‡ Paroxysmal nocturnal dyspnea (PND): person suddenly awakens. suspect Pulmonary Edema. ‡ Orthopnea (DOB while lying down) is related to blood pooling in the pulmonary bed. 91 . HF ‡ Dyspnea on exertion is due to increased O2 myocardial demand. is sweating and is having DOB.Dyspnea ‡ Difficulty of breathing ‡ subjective feeling (inability to get enough air) ‡ May be due to MI.

Cyanosis ‡ Bluish discoloration of the skin and mucous membrane ‡ Sat O2 is below 94% Fatigue ‡ May be due to Anemia or related to decreased Cardiac Output. severe cardiovascular disorder 92 .

Palpitations ‡ Awareness of rapid or irregular heart beat ‡ Autonomic Nervous System and Adrenal Glands response (stress) Syncope ‡ Transient loss of consciousness ‡ Due to decreased cerebral tissue perfusion 93 .

Edema ‡ May be due to HF ‡ Due to: Increased Hydrostatic Pressure (HP) ‡ Decreased Colloidal Oncotic Pressure (COP) ‡ Obstructed Lymphatic or Vascular System ‡ Related to Inflammatory reaction 94 .

‡ Bilateral edema = CHF or Renal Failure ‡ Unilateral edema = Vascular or Lymphatic obstruction ‡ Non-pitting edema = Inflammatory ‡ Pitting edema = HP and COP derangement 95 .

HF) -straining/ Valsalva maneuver dec HR ‡ Activity and exercise ± changes in pattern of activity in the last 6 -12 months. lab results. risk factors ‡ Nutrition and metabolism ± height. weight. eating habits.impt: dietary modification.how patient perceives his current health status. BP. hyperlipidimia. exercise. weight loss (HPN. fod preferences . exercise/ cardiac rehab program 96 .History ‡ Health perception and management . hyperglycemia) ‡ Elimination ± nocturia (awakening at night to urinate.

changes in sexual activity: fear of another attack/ sudden death. impotence.read/ comprehend (determine the patient¶s mental capacity to manage safe and effective selfcare) ‡ Self perception & self concept ± Type A behavior ‡ Roles and relationships ± support systems ‡ Sexuality and reproduction.stressors and coping ability ‡ Prevention strategies.identify patient¶s modifiable risk factors and measures taken by the patient to prevent disease 97 . untoward symptoms.History ‡ Sleep and rest ± PND (awakening short of breath at night).HF ‡ Cognition and perception. nocturnal angina (awakening with angina) . advised against pregnancy ‡ Coping and stress tolerance. depression.

RISK FACTORS FOR HEART DISEASE NONMODIFIABLE RISK FACTORS ‡ (+) Family History for premature coronary artery disease ‡ Gender ( men and postmenopausal women) ‡ Race (> incidence in African Americans than in Caucasians) 98 .

DM) ‡ Obesity ‡ Physical inactivity ‡ Type A personality characteristics.RISK FACTORS FOR HEART DISEASE MODIFIABLE RISK FACTORS ‡ Hyperlipidemia ‡ Hypertension ‡ Cigarette smoking ‡ Elevated blood glucose level (ie. particularly hostility ‡ Use of oral contraceptives 99 .

CARDIAC ASSESSMENT Physical Examination . Effectiveness of the heart as a pump (dec if ± reduced pulse pressure.Should include the evaluation of the following: a.Performed to confirm the data obtained in the health history . murmurs and gallop) 100 . cardiac enlargement.

CARDIAC ASSESSMENT b.Estimated by the degree of jugular vein distention and the presence or absence of congestion in the lungs. Filling volumes and pressures . peripheral edema and postural changes in BP that occur when the individual sits up or stands 101 .

102 .

CARDIAC ASSESSMENT c. heart rate. Compensatory mechanisms e. pulse.g.Reflected by cognition. pressure.. color and texture of the skin and urine output d. Cardiac output . to help maintain cardiac outputincreased filling volume and elevated heart rate 103 .

such as hemodynamic monitoring (use of monitoring devices to measure cardiovascular function..CARDIAC ASSESSMENT ‡ Findings on PE -correlated with data obtained from diagnostic procedures. e.g. CVP) 104 .

7. 4.CARDIAC ASSESSMENT Physical examination covers: 1. 6. 2. 3. 8. General appearance Cognition Skin Blood pressure Arterial pulses Jugular venous pulsation and pressures Heart Extremities Lungs abdomen 105 . 9. 10. 5.

General Appearance and Cognition Indication of heart¶s ability to propel oxygen to the brain (cerebral perfusion) ‡ Patient¶s level of distress ‡ Level of consciousness ‡ Thought processes ‡ Put the anxious patient at ease. (Emotional effects on CV status) 106 .

may be normal in peripheral vasoconstriction associated with a cold environment ‡ Central cyanosis. extremities and earlobes. pulmonary edema.decreased flow rate of blood to a particular area. serious cardiac disorder.lack of oxyhemoglobin. bluish tinge of the nails. eg.Inspection of the skin ‡ Pallor. anxiety. result of anemia or decreased arterial perfusion ‡ Peripheral cyanosis. skin of the nose. CHD 107 . venous blood passes through the pulmonary circulation without being oxygenated. lips. in HF.bluish tinge in the tongue and buccal mucosa.

normal: skin is warm and dry.dehydration and aging ‡ Temperature and moistness. MI: diaphoresis 108 .yellowish.Inspection of the skin ‡ Xanthelasma. under stress: cool and moist. cardiogenic shock: cold and clammy. slightly raised plaques in the skin. along the nasal portion of 1 or both eyelids and may indicate elevated cholesterol levels (hypercholesterolemia) ‡ Reduced skin turgor.

yellow or brown over time -blood outside the vessels.adequate healing.PT & PTT) ‡ Wounds. purplish-blue color fading to green. thinning (erosion) 109 . unexplained ecchymosis in patients with anticoagulant therapy (prolonged clotting time.bruise. caused by trauma. scars and tissue surrounding implanted devices.Inspection of the skin ‡ Ecchymosis.

BP ‡ Affected by cardiac output. volume. velocity and viscosity of the blood ‡ Normal adult values: ‡ (?) 100/60 to 140/90 mmHg ‡ Hypertension ‡ hypotension 110 . distention of arteries.

111 .

HPN) ‡ Decreased in -abnormal condition reflecting reduced SV. ejection velocity (shock. mitral regurgitation) or obstruction to the blood flow during systole (mitral/ aortic stenosis) 112 . aging. reduce systemic vascular resistance (fever). exercise. reduce distensibility of the arteries (atherosclerosis.Pulse pressure ‡ ‡ ‡ ‡ Difference b/w systolic and diastolic pressures Normal: 30 ± 40 mmHg How well the patient maintains cardiac output Increased in . hypovolemia. bradycardia). HF.conditions that elevate the SV (anxiety.

Postural Blood Pressure Changes Postural orthostatic hypotension ‡ BP drops significantly after the patient assumes an upright position accompanied by dizziness. or syncope ‡ Normal: HR inc of 5.20 bpm above resting rate unchanged systolic pressure or slight decrease of up to 10 mmHg slight increase of 5 mmHg in diastolic pressure 113 . lightheadedness.

Postural Blood Pressure Changes ‡ Suspect decrease in the amount of blood or fluid increased HR and either a decrease in systolic pressure by 15 mmHg or a drop in diastolic pressure by 10 mmHg 114 .

heart block) ‡ Pulse Quality: 0 .+4 (absent to strong/ bounding ‡ Pulse configuration 115 . atrial flutter. PVC.Arterial Pulses ‡ Pulse rate ‡ Pulse rhythm ± pulse deficit: radial vs apical (atrial fibrillation.

116 .

acute massive pulmonary embolism) 117 .Jugular Venous pulsations ‡ Internal jugular vein ‡ Not apparent ± 30 degrees ‡ (+) obvious distention with the patient¶s head at 45 ± 90 degrees: abnormal increase in volume of the venous system ‡ Right sided HF (less common: obstruction of BF to SVC.

Heart Inspection & Palpation

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119

Surface Anatomy

Auscultation

Tricuspid Valve

lies behind right half of the right half of the lower end sternum; opposite the 4th of the body of the ICS sternum lies behind the left half of apex beat (5th LICS MCL) the sternum; opposite the 4th costal cartilage Lies behind the medial end Medial end of the 2nd left of the 3rd left costal cartilage ICS & the adjoining part of the sternum Behind left half of sternum; Medial end of the 2nd right opposite 3rd ICS ICS
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Mitral Valve

Pulmonary Valve

Aortic Valve

Cardiac IPPA
‡ Inspection and Palpation ± PMI (left 5th ICS MCL) ‡ Bruits and Thrills ± murmurlike; vascular in origin ‡ palpate a thrill, auscultate a bruit ‡ Percussion ± displaced apical pulse
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122

123

HPN. heard after S2. aortic stenosis 124 .closure of SL valves (dub). associated w/ CAD. atrial contraction. apex of heart ‡ S2 .closure of AV valves (lub). may be heard when ventricles fail to eject all of their blood on systole ‡ S4 is heard prior to S1. normal in children and young adults. base of the heart ‡ S3 ± rapid diastolic filling.Heart Sounds ‡ S1 .

125 .

126 .

127 .

suspect pericardial effusion if this is heard ‡ Muffled Heart Sound .Heart Sounds ‡ Murmurs . if positive watch out for FVE and regurgitation. normal until 1 year old ‡ Pericardial Friction Rub -³grating sound´.if positive rule out Cardiac Tamponade and other similar problems like Effusion 128 .turbulence of blood flow.

loss of pulse. pain. decrease in temperature. edema. vascular changes (numbness.Extremities ‡ Extremities ± capillary refill. pallor) ‡ Clubbing ± CHD 129 .

130 .

OTHER SYSTEMS: ‡ Abdomen ± hepatomegaly d/t RVF .HF Wheezing.pulmonary edema 131 .decreased urine output ‡ Lungs: tachypnea (HF/ pain) hemoptysis (acute pulmonary edema) Cheyne¶s Stokes respiration ± LVF dry hacking cough ± HF pulmonary congestion Crackles.liver engorgement .

CARDIAC ASSESSMENT 3. Laboratory and diagnostic studies ‡ CBC ‡ Cardiac catheterization ‡ Lipid profile ‡ Arteriography ‡ Cardiac enzymes and proteins ‡ CXR ‡ CVP ‡ ECG ‡ Holter monitoring ‡ Exercise ECG 132 .

To assist in diagnosing MI 2. To identify abnormalities 3.The Cardiovascular System Laboratory Test Rationale 1. To assess inflammation 133 .

To monitor serum level of medications 6. To assess the effects of medications 134 .The Cardiovascular System Laboratory Test Rationale 4. To determine baseline value 5.

LABORATORY PROCEDURES CARDIAC Proteins and enzymes CK.MB ( creatine kinase) Elevates in MI within 4 hours. peaks in 18 hours and then declines till 3 days 135 .

LABORATORY PROCEDURES CARDIAC Proteins and enzymes CK.MB ( creatine kinase) Normal value is 0-7 U/L 136 .

peaks in 48-72 hours Normally LDH2 is greater than LDH1 137 .LABORATORY PROCEDURES CARDIAC Proteins and enzymes Lactic Dehydrogenase (LDH) Elevates in MI in 24 hours.

LABORATORY PROCEDURES CARDIAC Proteins and enzymes Lactic Dehydrogenase (LDH) MI.LDH1 greater than LDH2 (flipped LDH pattern) Normal value is 70-200 IU/L 138 .

LABORATORY PROCEDURES CARDIAC Proteins and enzymes Myoglobin Rises within 1-3 hours Peaks in 4-12 hours Returns to normal in a day 139 .

LABORATORY PROCEDURES CARDIAC Proteins and enzymes Myoglobin Not used alone Muscular and RENAL disease can have elevated myoglobin 140 .

6 ng/mL 141 .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 weeks! ‡ Normal value for Troponin I is less than 0.

LABORATORY PROCEDURES Troponin I and T ‡ REMEMBER to AVOID IM injections before obtaining blood sample! ‡ Early and late diagnosis can be made! 142 .

LABORATORY PROCEDURES SERUM LIPIDS ‡ Lipid profile measures the serum cholesterol.150 mg/dL 143 .40. triglycerides and lipoprotein levels ‡ Cholesterol= 200 mg/dL ‡ Triglycerides.

mg/dL ‡ NPO post midnight (usually 12 hours) 144 .130 mg/dL ‡ HDL.30-70.LABORATORY PROCEDURES SERUM LIPIDS ‡ LDL.

LABORATORY PROCEDURES ELECTROCARDIOGRAM (ECG) ‡ A non-invasive procedure that evaluates the electrical activity of the heart ‡ Electrodes and wires are attached to the patient 145 .

LABORATORY PROCEDURES ELECTROCARDIOGRAM (ECG) ‡ Tell the patient that there is no risk of electrocution ‡ Avoid muscular contraction/movement 146 .

147 .

148 .

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 149 .

The Cardiovascular System LABORATORY PROCEDURES Holter Monitoring ‡ Instruct the client to resume normal activities and maintain a diary of activities and any symptoms that may develop 150 .

151 .

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 152 .

153 .

LABORATORY PROCEDURES Stress Test ‡ A non-invasive test that studies the heart during activity and detects and evaluates CAD ‡ Exercise test. pharmacologic test and emotional test 154 .

Chest pain causes. drug effects and dysrhythmias in exercise 155 .The Cardiovascular System LABORATORY PROCEDURES Stress Test ‡ Treadmill testing is the most commonly used stress test ‡ Used to determine CAD.

The Cardiovascular System LABORATORY PROCEDURES Stress Test ‡ Pre-test: consent may be required. alcohol and caffeine 156 . adequate rest . eat a light meal or fast for 4 hours and avoid smoking.

dizziness or shortness of breath ‡ Instruct client to avoid taking a hot shower for 10-12 hours after the test 157 .The Cardiovascular System LABORATORY PROCEDURES ‡ Post-test: instruct client to notify the physician if any chest pain.

The Cardiovascular System LABORATORY PROCEDURES Pharmacological stress test ‡ Use of dipyridamole ‡ Maximally dilates coronary artery ‡ Side-effect: flushing of face 158 .

LABORATORY PROCEDURES Pharmacological stress test ‡ Pre-test: 4 hours fasting. caffeine ‡ Post test: report symptoms of chest pain 159 . avoid alcohol.

LABORATORY PROCEDURES CARDIAC catheterization ‡ Insertion of a catheter into the heart and surrounding vessels ‡ Determines the structure and performance of the heart valves and surrounding vessels 160 .

LABORATORY PROCEDURES CARDIAC catheterization ‡ Used to diagnose CAD. assess coronary artery patency and determine extent of atherosclerosis 161 .

assess for allergy to seafood and iodine.LABORATORY PROCEDURES ‡ Pretest: Ensure Consent. baseline VS. NPO. document weight and height. blood tests and document the peripheral pulses 162 .

teachings. medications to allay anxiety 163 .LABORATORY PROCEDURES ‡ Pretest: Fast for 8-12 hours.

inform the patient that a feeling of warmth and metallic taste may occur when dye is administered 164 .LABORATORY PROCEDURES ‡ Intra-test: inform patient of a fluttery feeling as the catheter passes through the heart.

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 165 .

‡ ‡ ‡ ‡ ‡ 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 166 .

LABORATORY PROCEDURES CVP ‡ The CVP is the pressure within the SVC ‡ Reflects the pressure under which blood is returned to the SVC and right atrium 167 .

LABORATORY PROCEDURES CVP ‡ Normal CVP is 0 to 8 mmHg or 4-10 cm H2O 168 .

LABORATORY PROCEDURES CVP ‡ Elevated CVP indicates increase in blood volume. excessive IVF or heart/renal failure 169 .

LABORATORY PROCEDURES CVP ‡ Low CVP may indicate hypovolemia. hemorrhage and severe vasodilatation 170 .

171 . Position the zero point of the CVP line at the level of the right atrium. 4th ICS 3.LABORATORY PROCEDURES Measuring CVP 1. Usually this is at the MAL. Position the client supine with bed elevated at 45 degrees (CBQ) 2. Instruct the client to be relaxed and avoid coughing and straining.

172 .

BP. Cardiac assessment 2. Assess the cardio-pulmonary status VS. Enhance cardiac output ± Establish IV line to administer fluids 173 .CARDIAC IMPLEMENTATION 1.

Promote gas exchange ± Administer O2 ± Position client in SEMI-Fowler¶s ± Encourage coughing and deep breathing exercises 174 .CARDIAC IMPLEMENTATION 3.

Increase client activity tolerance ± Balance rest and activity periods ± Assist in daily activities ± Provide strict bed rest if indicated ± Soft foods ± Assistance in self-care 175 .CARDIAC IMPLEMENTATION 4.

Promote client comfort ± Assess the client¶s description of pain and chest discomfort ± Administer medication as prescribed ‡ Morphine for MI ‡ Nitroglycerine for Angina ‡ Diuretics to relieve congestion (CHF) 176 .CARDIAC IMPLEMENTATION 5.

CARDIAC IMPLEMENTATION 6. Promote adequate sleep 7. Prevent infection ± Monitor skin integrity of lower extremities ± Assess skin site for edema. redness and warmth ± Monitor for fever ± Change position frequently 177 .

fears and concerns ± Answer client questions. Minimize patient anxiety ± Encourage verbalization of feelings. Provide information about procedures and medications 178 .CARDIAC IMPLEMENTATION 8.

Activity Intolerance Monitor TPR and BP Space activities in the day Permit rest periods before activity Limit activity 1 hour before meals Teach energy conservation measures like bed rest Instruct patient to avoid constricting garments Instruct to elevate edematous areas Instruct patient to avoid dependent positions Teach patient to prepare low sodium meals Apply anti-embolic stockings Instruct patient to stop activity when pain occurs Administer nitroglycerine for angina Pace activities within patient¶s limits Instruct patient to avoid cold temperatures and smoking Instruct to report unrelieved pain immediately 179 Edema Pain .

180 .

Cardiac Disorders ‡ ‡ ‡ ‡ ‡ ‡ ‡ CAD Angina MI Cardiac Dysrythmias CHF Cardiogenic shock Cardiac Tamponade 181 .

Hyperlipidemia group of metabolic disorders that lead to: ‡ elevated serum total cholesterol (hypercholesterolemia) ‡ elevated low density lipoprotein ‡ elevated triglycerides (hypertriglyceridemia) 182 .

Secondary: ‡ DM ‡ Hypothyroidism ‡ Nephrotic Syndrome ‡ Liver Disease ‡ Obesity ‡ Dietary Intake ‡ Pregnancy ‡ Use of Beta Blockers and Diuretics 183 .1. Primary: Genetic 2.

‡ 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 184 .Coronary Artery Disease (CAD) ‡ Accumulation of fatty deposits in the inner layer of coronary arteries.

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 185 .

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 186 .

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 187 .Angina ‡ Chest pain resulting from coronary atherosclerosis or myocardial ischemia Types: ‡ Stable ± exertional. relieved by rest.

Squeezing. neck and jaws .Manifestations ‡ Characteristic of chest pain .Substernal or retrosternal pain that radiates to arms. burning.Precipitated by cold. tight chest . emotions.Lasts a few minutes and then subsides 188 . heavy. eating. exertion .

‡ ‡ ‡ ‡ ‡ Diaphoresis Nausea and vomiting Cold clammy skin Sense of apprehension and doom Dizziness and syncope 189 .

Diagnostic Tests ‡ NTG test (relief from pain) ‡ ECG (ST depression and T wave elevation) ‡ Cardiac catheter ± atherosclerotic lesions ‡ Thallium 201 Imaging ‡ Technetium Imaging 190 .

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 191 .

diagnostic tests and therapies 192 .percutaneous transluminal coronary angioplasty ± To compress the plaque against the vessel wall.Management ‡ ‡ ‡ ‡ ‡ Relieve pain Place in comfortable position Administer O2 Decrease Anxiety PTCA . increasing the arterial lumen ‡ CABG .coronary artery bypass graft ± To improve the blood flow to the myocardial tissue ‡ Explain the reasons for hospitalization.

193 .

reduce BP and HR ‡ Calcium-channel blockers.Give antianginal drugs ‡ Aspirin.to dilate the coronary arteries 194 .dilate coronary artery and reduce vasospasm ‡ Nitrates.prevent thrombus formation ‡ Beta-blockers.

take another tablet and wait for 5 minutes ‡ Another tablet can be taken (third tablet) ‡ If unrelieved after THREE tablets seek medical attention 195 .‡ Put one nitroglycerin tablet under the tongue ‡ Wait for 5 minutes ‡ If not relieved.

Myocardial Infarction Absence of O2 supply to the myocardium Necrosis or death to the myocardial tissue Attack may be sudden or gradual 196 .

CAD 2. Coronary artery occlusion by embolus and thrombus 4. Conditions that decrease perfusion. Coronary vasospasm 3. shock 197 .Etiology 1.hemorrhage.

Stress 6. Sedentary lifestyle 198 .Risk factors 1. Hypertension 4. Hypercholesterolemia 2. Obesity 5. Smoking 3.

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 199 .

jaw and back ‡ Not relieved by rest or NTG ‡ May continue for 15-30 minutes ‡ May produce anxiety and fear resulting to increased HR. steady crushing and squeezing substernal pain ‡ Radiates to the neck. BP and RR 200 .Chest pain: ‡ Severe. arm.

sense of doom tachycardia or bradycardia hypotension dysrhythmias 201 .‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡ dyspnea Diaphoresis cold clammy skin N/V restlessness.

202

Diagnostic Evaluation
‡ Chest pain cannot be relieved by NTG ‡ ST segment depression and T wave inversion, Q wave

‡ Cardiac enzymes: increased Troponin, CK MB, LDH ‡ CBC- may show elevated WBC count
203

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

204

‡ 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
205

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
206

Pharmacologic Therapy
‡ Thrombolytic agents - Dissolve clots in the coronary artery allowing blood to flow ie TPA tissue plasminogen activator (Alteplase), Streptokinase (streptase), Urokinase ‡ Anticoagulant ± prevents formation of new blood clots ie Heparin, Warfarin
207

contractility. relax blood vessels ie Diltiazem 208 .‡ Antiplatelet ± hypersensitivity to aspirin ie Ticlopidine. Clopidogrel ‡ Beta adrenergic blocking agents ± reduce myocardial O2 demand by blocking sympathetic stimulation. HR. BP ie Propranolol ‡ Calcium channel blockers ± dec contraction. dec HR.

‡ Morphine .Relaxes bronchioles to enhance oxygenation ‡ ACE Inhibitors .reduces pain and anxiety . dec O2 demand ± Limits the area of infarction 209 .Prevents formation of angiotensin II which causes vasoconstriction.

Gradual resumption of ADL to full recovery 210 .CBR without BP (complete bedrest without bathroom privilege) . ‡ coronary artery bypass graft (CABG ) After the condition had been stabilized: .Surgical revascularization: ‡ Percutaneous Transluminal Coronary Angioplasty (PTCA).

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 211 .

Predisposing Factors ‡ ‡ ‡ ‡ Myocardial Infarction Arrhythmias Pregnancy Pulmonary Embolism ‡ Anemia ‡ Renal Failure ‡ CAD ‡ Valvular heart diseases ‡ Hypertension ‡ Cardiomyopathy ‡ Pericarditis and cardiac tamponade 212 .

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 213 .

Class 3 ‡ Markedly limitation on ADLs ‡ Comfortable at rest BUT symptoms present in LESS than ordinary activity Class 4 ‡ SYMPTOMS are present at rest 214 .

PATHOPHYSIOLOGY ‡ LEFT Ventricular pump failure back up of blood into the pulmonary veins increased pulmonary capillary pressure pulmonary congestion 215 .

kidney and other tissues oliguria.LEFT ventricular failure decreased cardiac output decreased perfusion to the brain. dizziness 216 .

PATHOPHYSIOLOGY ‡ RIGHT ventricular failure blood pooling in the venous circulation increased hydrostatic pressure peripheral edema 217 .

RIGHT ventricular failure blood pooling venous congestion in the kidney. liver and GIT 218 .

Orthopnea 4. frothy sputum 6. Pulmonary crackles/rales 5.LEFT SIDED CHF ASSESSMENT FINDINGS 1. Tachycardia 219 . Dyspnea on exertion 2. PND 3. cough with Pinkish.

Cyanosis 9. Cool extremities 8. Oliguria 12. Fatigue 11. signs of cerebral anoxia 220 . decreased peripheral pulses 10.7.

Body weakness 7. Anorexia. hepatomegaly 5. nausea 8. Distended neck vein 4. Peripheral dependent.RIGHT SIDED CHF ASSESSMENT FINDINGS 1. Pulsus alternans 221 . Ascites 6. Weight gain 3. pitting edema 2.

heart strain ‡ Chest X-ray .Diagnostics ‡ EKG .cardiomegaly and pleural effusion ‡ CVC Central Venous Catheter and SwanGanz 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 222 .

‡ complete bed rest and reduce myocardial oxygen demand.improve pump function and reverse the compensatory mechanism of the heart. vasodilators and hypolipidemics ‡ LOW sodium diet ‡ Limit fluid intake ‡ Monitor daily weight and report signs of fluid retention 223 . ‡ FVE management and prevent complications ‡ Diuretics and Digoxin.Nursing Considerations ‡ goal of treatment .

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 224 .

Cardiac Arrhythmias ‡ Disturbances in regular rate and rhythm due to changes in electrical automaticity or conduction ‡ Irregular HR. rhythm and regularity 225 .

dec. Calcium and MI ‡ Ventricular tachycardia (vtach) ± 3 or more PVC¶s ‡ Ventricular fibrillation (vfib) ± extremely rapid and erratic impulse formation 226 . K. due to dec.‡ Premature atrial contraction (PAC) ± more than 100 bpm ‡ Atrial flutter ± 250-300 bpm ‡ Atrial fibrillation ± higher than 500 bpm ‡ Premature ventricular contraction (PVC) ± most common.

Impulse is delayed from SA node to AV node 1st degree ± atrial impulses conducted slower than normal 2nd degree ± some atrial impulses conducted into ventricles Mobitz type I ± asymptomatic (ventricular contraction is adequate) Mobitz type II ± critical (atrial contraction is not synchronized with the ventricle) 3rd degree ± no atrial impulse conducted to Av node 227 .‡ AV Block .

Treatment ‡ Increase CO ‡ Cardiovascular drugs and mechanical equipment ‡ Cardiovascular Drugs: IV Dopamine (vasopressor) IV Dobutamine (diuretic effects) IV Epinephrine (vasoconstrictor) IV Nitroprusside (vasodilator) 228 .

‡ Mechanical: IABP intra aortic balloon pump (improves coronary perfusion) Defibrilator (arrhythmias can be stopped) Cardiac monitor (to detect arrhythmias) 229 .

CARDIOGENIC SHOCK ‡ Heart fails to pump adequately resulting to a decreased cardiac output and decreased tissue perfusion ETIOLOGY ‡ Massive MI ‡ Severe CHF ‡ Cardiomyopathy ‡ Cardiac trauma ‡ Cardiac tamponade 230 .

‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡ HYPOTENSION oliguria (less than 30 ml/hour) tachycardia narrow pulse pressure weak peripheral pulses cold clammy skin changes in sensorium/LOC pulmonary congestion 231 .

LABORATORY FINDINGS ‡ Increased CVP ± Normal is 4-10 cmH2O 232 .

insertion of Swan-Ganz cath and IABP ‡ Monitor urinary output. mechanical ventilation. nitrates ‡ Administer O2 ‡ Morphine is administered to decrease pulmonary congestion and to relieve pain ‡ Assist in intubation. diuretics. CABG. PTCA. vasopressors and inotropics such as DOPAMINE and DOBUTAMINE. BP and pulses 233 .Management ‡ modified Trendelenburg (shock ) position ‡ IVF.

sudden accumulation of more than 50 ml fluid in the pericardial sac 234 .CARDIAC TAMPONADE ‡ heart is unable to pump blood due to accumulation of fluid in the pericardial sac (pericardial effusion) ‡ restricts ventricular filling resulting to decreased cardiac output ‡ Acute tamponade .

Risk Factors ‡ Cardiac trauma ‡ Complication of Myocardial infarction ‡ Pericarditis ‡ Cancer metastasis 235 .

Jugular vein distention. hypotension and distant/muffled heart sound ‡ Pulsus paradoxus ‡ Increased CVP ‡ decreased cardiac output ‡ Syncope ‡ anxiety ‡ dyspnea ‡ Percussion.Manifestations ‡ BECK¶s Triad.Flatness across the anterior chest 236 .

Diagnostics ‡ Echocardiogram ‡ CXR 237 .

Management ‡ Assist in PERICARDIOCENTESIS ‡ Administer IVF ‡ Monitor ECG. urine output and BP ‡ Monitor for recurrence of tamponade 238 .

CARDIOMYOPATHIES ‡ Heart muscle disease associated with cardiac dysfunction 239 .

CARDIOMYOPATHIES 1. Restrictive cardiomyopathy 240 . Hypertrophic Cardiomyopathy 3. Dilated Cardiomyopathy 2.

Heavy alcohol intake ‡ 2. Idiopathic 241 .DILATED CARDIOMYOPATHY ASSOCIATED FACTORS ‡ 1. Pregnancy ‡ 3. Viral infection ‡ 4.

DILATED CARDIOMYOPATHY PATHOPHYSIOLOGY ‡ Diminished contractile proteins poor contraction decreased blood ejection increased blood remaining in the ventricle ventricular stretching and dilatation. ‡ SYSTOLIC DYSFUNCTION 242 .

Idiopathic 243 .HYPERTROPHIC CARDIOMYOPATHY Associated factors: 1. Genetic 2.

HYPERTROPHIC CARDIOMYOPATHY Pathophysiology ‡ Increased size of myocardium reduced ventricular volume increased resistance to ventricular filling diastolic dysfunction 244 .

Infiltrative diseases like AMYLOIDOSIS 2. Idiopathic 245 .RESTRICTIVE CARDIOMYOPATHY Associated factors 1.

RESTRICTIVE CARDIOMYOPATHY Pathophysiology ‡ Rigid ventricular wall impaired stretch and diastolic filling decreased output ‡ Diastolic dysfunction 246 .

Palpitations 6. Chest pain 5. Orthopnea 3. PND 2. Syncope with exertion 247 .CARDIOMYOPATHIES Assessment findings 1. dizziness 7. Edema 4.

CXR.may reveal cardiomegaly 2.CARDIOMYOPATHIES Laboratory Findings 1. ECHOCARDIOGRAM 3. ECG 4. Myocardial Biopsy 248 .

CARDIOMYOPATHIES Medical Management 1. Pharmacological drugs for symptom relief 249 . pacemaker insertion 3. Surgery= heart transplant 2.

Improve cardiac output ‡ Adequate rest ‡ Oxygen therapy ‡ Low sodium diet 250 .CARDIOMYOPATHIES Nursing Management 1.

CARDIOMYOPATHIES
Nursing Management 2. Increase patient tolerance ‡ Schedule activities with rest periods in between

251

CARDIOMYOPATHIES
Nursing Management 3. Reduce patient anxiety ‡ Support patient ‡ Offer information about transplantations ‡ Support family in anticipatory grieving
252

Infective endocarditis

‡ Infection of the heart valves and the endothelial surface of the heart
253

Infective endocarditis

‡ Can be acute, sub-acute or chronic

254

Infective endocarditis

Etiologic factors 1. Bacteria- Organism depends on several factors 2. Fungi

255

Infective endocarditis
Risk factors 1. Prosthetic valves 2. Congenital malformation 3. Cardiomyopathy 4. IV drug users 5. Valvular dysfunctions
256

Infective endocarditis Pathophysiology Direct invasion of microbes microbes adhere to damaged valve surface and proliferate damage attracts platelets causing clot formation erosion of valvular leaflets and the clot and vegetation can embolize 257 .

back pain and joint pain 4. cough.Infective endocarditis Assessment findings 1. Intermittent high grade fever 2. anorexia. splinter hemorrhages under nails 258 . weight loss 3.

Osler¶s nodes.painful nodules on fingerpads 6.Infective endocarditis Assessment findings 5.pale hemorrhages in the retina 259 . Roth¶s spots.

Heart failure= usually acute heart failure 260 . Heart murmurs 8.Infective endocarditis Assessment findings 7.

bronchoscopy. 261 . surgery. etc.Infective endocarditis Prevention ‡ Antibiotic prophylaxis if patient is undergoing procedures like dental extractions.

Infective endocarditis Prevention ‡ Any invasive procedure that is associated with transient bacteremia may cause the microrganism to lodge in the damaged. irregular valves 262 .

3 culture specimens are obtained and antibiotic sensitivity done 263 .Infective endocarditis LABORATORY EXAM ‡ Blood Cultures to determine the exact organism ±Usually.

heart sounds 2. Long-term antibiotic therapy is given to ensure eradication of bacteria 264 . Regular monitoring of temperature.Infective endocarditis Nursing management 1. Manage infection 3.

Infective endocarditis Medical management 1. Pharmacotherapy ‡ IV antibiotic for 2-6 weeks ‡ Antifungal agents are given ± amphotericin B 265 .

Infective endocarditis Medical management 2. Surgery ‡ Valvular replacement 266 .

Vascular Disorders ‡ ‡ ‡ ‡ ‡ ‡ Venous Thrombosis CVI Arterosclerosis Raynaud¶s Phenomenon Aneurysm Hypertension 267 .

Venous Thrombosis Due to: ‡ Stasis of blood ‡ Injury to the vessel wall ‡ Altered blood coagulation 268 .

cast and joint replacement ‡ Obesity and smoking ‡ Immobilized patient ‡ Heart problems 269 .High Risk: ‡ Fractures.

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

270

Manifestations
‡ (+) Homan¶s sign ‡ fever and chills ‡ swelling and cyanosis of the affected leg or arm Diagnostics: ‡ Venous duplex ultrasound ‡ Impedance plethysmography ‡ RF testing (radioactive fibrinogen) fibrinogen I 125 ‡ Venography ‡ Coagulation Profiles: APTT PT/INR
271

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

272

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
273

Manifestations
‡ ‡ ‡ ‡ ‡ ‡ Edema Altered pigmentation Pain Stasis dermatitis Dilated superficial veins Stasis ulcers

274

Management
‡ Elevate legs ‡ Elastic compression stockings ‡ Skin should be kept clean and dry

275

Raynaud¶s Phenomenon ‡ Arteriolar vasospastic disease with unusual sensitivity to cold or emotional stress. ‡ cause is unknown but may be secondary to Autoimmune Diseases 276 .

tingling and burning pain 277 .ASSESSMENT ‡ Pallor then cyanosis ‡ Hyperemia when blood returns to digits after vasospasm ‡ Numbness.

Management ‡ Avoid primary stimuli (cold. tobacco) ‡ Ca channel blocker ‡ Nifedipine for vasospasm ‡ Safety measures 278 .

‡ Atherosclerosis-common type of arteriosclerosis due to atheromas. 279 .Arteriosclerosis ‡ hardening of the arterial blood vessel walls related to aging.

Aging and atheromas impeding the lumen of the arterial walls (incomplete or incomplete occlusions ) systemic effects depending on the blood vessel affected 280 .

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 281 .

‡ ‡ ‡ ‡ ‡ TIA to CVA Angina to MI ATN to Renal Failure Retinopathy to Blindness Peripheral Occlusive Disease (TAO) to Gangrene Formation ‡ Hepatic Infarction ‡ Pulmonary Infarction 282 .

Diagnostic Evaluation: ‡ ‡ ‡ ‡ ‡ Arteriography CT Scan MRI Duplex UTZ EKG 283 .

Management: ‡ Modification of risk factors (CAD and hyperlipidemia) ‡ Anticoagulants ‡ Antiplatelets ‡ Lipid Lowering Agent ‡ Antihypertensive ‡ Vascular Rehabilitation/Exercise 284 .

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 from the artery ‡ Bypass Graft 285 .

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 286 .

Infection= syphilis 3.RISK FACTORS 1.Connective tissue disorder 4.Genetic disorder= Marfan¶s Syndrome 287 .Atherosclerosis 2.

PATHOPHYSIOLOGY Damage to the intima and media weakness outpouching Dissecting aneurysm tear in the intima and media with dissection of blood through the layers 288 .

bruit Diagnostics ‡ CT scan ‡ Ultrasound ‡ X-ray ‡ Aortography 289 .Manifestations: 1. Pulsatile sensation on the abdomen 3. Asymptomatic 2.

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 290 .

Hypertension ‡ ³Silent killer´ ‡ disease of vascular regulation that leads to high blood pressure ‡ due to alteration of Central Nervous System. Extracellular Fluid Volume 291 . Renin-Angiotensin-Aldosterone System.

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 292 .

NSAIDs.It is a combination of both where in BP is uncontrolled.Secondary Hypertension Due to: ‡ Renal Pathology ‡ Coarctation of the Aorta ‡ Endocrine Disturbance ‡ Drugs (estrogens. 293 . steroids) ‡ Malignant Hypertension . sympathomimetics.

Risk Factors ‡ ‡ ‡ ‡ ‡ ‡ ‡ ‡ Old age male Race Overweight Family History Smoking Sedentary Lifestyle Diabetes Mellitus 294 .

chest pain 4. N/V 295 . dizziness 5.Manifestations 1. Visual changes 3. Headache 2.

Diagnostic Evaluation ‡ Monitor BP ‡ EKG. Blood Chem etc. ± stop smoking.4 g/day. 296 . Blood Sugar. cut sodium to 2. limit alcohol. reduce coffee intake. reduce dietary saturated fat and cholesterol. ‡ Management: Control of all risk factors:. ± Lose weight.

Despite lifestyle changes and BP remains high drug therapy should be started: ‡ ‡ ‡ ‡ ‡ ‡ Diuretics Beta blockers Calcium channel blockers ACE inhibitors A2 Receptor blockers Vasodilators 297 .

weight.Nursing Management ‡ Health teaching on: ± Lifestyle changes ie activities. cessation of smoking ± treatment regimen ie drugs ± BP monitoring ± Follow up 298 . nutrition. low Na). diet (low fat.

dec. improve LOC and sedative effect ‡ Vasodilators ± Nitroglycerin NTG ± Relax smooth muscle.E. ± dizziness and flushing Can be given SL or IV (Isordil) and topical (Nitrobid) 299 .Cardiovascular Drugs: ‡ Anti Anginal ± Opiate Analgesic ± Morphine Sulfate ± cardiac workload and BP. BP and alleviate headache ± Increase blood vessel diameter and improves blood flow S.

nausea and depression 300 . decrease BP ± S.E. ± vomiting.E. ± bradycardia. interferes contraction. diarrhea and rashes ‡ Beta Blocking Agent ± Propranolol ± Decrease workload ± Blocks beta receptors and capable of decreasing HR S.‡ Calcium Channel Blockers ± Nifidepine (Procardia) Diazepam (Cardizem) ± Decrease muscle tone.

Increase Na excretion (kidney) ‡ Dobutamine .Increase CO . ± GIT disturbance.‡ Digitalis.E.Increase CO (improves stroke volume) S.Positive Inotropic (Increases contraction of the heart) .More potent on contraction 301 .Negative chronotropic (Decreases HR) AV node control .Increase emptying capacity of the heart . CNS depression and flashes of light ‡ Dopamine ± diuresis effect . Digoxin .

Furosemide (Lasix) ± K waster ‡ ACE inhibitors ± Captopril (Capoten) 302 .‡ Diuretics .Spironolactone (Aldactone) ± K sparer .

‡ 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 303 .

Urokinase ± avtivates plasminogen to plasmin (intracoronary) 304 .Streptokinase ± lyses the clot (20T IU IV bolus or 4T IU/min drip) .‡ Thrombolytic/Fibrinolytic Agent .

‡ 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 305 .

306 .

307 .

308 .

309 .Salamat po.

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