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Heart
Is a hollow muscular organ
located n the center of the thorax, it occupies space between the lungs and rest on the diaphragm Pumps blood to the tissues, supplying them with oxygen and nutrients
3 layers:
Endocardium - consists of
endothelial tissue and lines the inside of the heart and valves Myocardium made up of muscle fibers and is responsible for the pumping action Epicardium exterior layer of the heart
Pericardium the heart is encased in a thin, fibrous sac called the pericardium which is composed of two layers
Visceral pericardium adheres to the epicardium Parietal pericardium envelops visceral pericardium; a
tough fibrous tissues that attaches to the great vessels, diaphragm, sternum and vertebral column and supports the heart in the mediastinum The space of these two layers is called pericardial space, which is normally filled with about 20ml of fluid which lubricates the surface of the heart and reduces friction during systole.
Heart chambers: >the pumping action of the heart is accomplished by the rhythmic relaxation and contraction of the muscular walls of its four chambers.
Receiving chambers: Right atrium receives deoxygenated blood from
the veins of the body Left atrium receives freshly oxygenated blood from the lungs through the pulmonary veins
Discharging chambers:
Right atrium receives deoxygenated blood from the
right atrium and pmps it to the pulmonary artery to the lungs for oxygenation Left ventricle receives freshly oxygenated blood from the left atrium and pumps it out the aorta to the arterial circulation.
Heart valves
permits blood to flow in only one direction
and close in response to the movement of blood and pressure changes within the chambers.
ventricle Tricuspid valve > separates tight atrium and right ventricle Mitral or bicuspid valve > separates left and left ventricle
Semilumanar valves: are composed of 3 leaflets which
are shaped like half moons. Pulmonic valve > valve between the right ventricle and pulmonary artery Aortic valve > valve between the right ventricle and aorta
to the heart Circumflex artery > circles around to the lateral left of the heart
Right coronary artery
which leads to the inferior wall of the heart Posterior descending coronary artery the posterior wall to the heart receives its blood supply through
>any condition brought about on by a sudden reduced blood flow to the heart >usually of the 3 diseases involving the coronary arteries: ST elevation MI, non-ST elevation MI and unstable vagina
Pathophysiology:
Pathologic mechanisms: Intracoronary thrombus formation Pre-existing atherosclerosis Coronary wall spasm Triggers: HPN,high blood glucose level, stress Rupture of plaque Activation of clotting factors Formation of thrombosis Obstruction of blood flow Ischemia of heart muscle Infarction
Clinical manifestations:
Chest pain or discofort
Pressure or tightness Jaw or neck pain Left arm ache/involvemet Epigastric discomfort Scapular or back pain
Diagnostic test:
Elevated troponin I,T, CK-MB ST elevation on ECG Decrease ejection on 2D echo
Management:
Optimize blood flow to the myocardium Medical:
Decrease activity of the coagulation system with pharmacologic therapy Antiplatelet agents: Aspirln, Clopidogrel Antithrombin agents: Heparin Beta blockers (Metroprolol) Bed rest Nitrates Diuretics Morphine sulfate ACE inhibitor
Alleviate pain
Pain relief improves coronary blood flow by decreasing
Nitrates dilates coronary artery Morphine Sulfate potent Narcotic and vasodilator
Reduce anxiety
To reduce catecholamine secretion
Relief of pain Relaxation techniques Proper and clear instructions Visitor presence
Surgical management:
Percutaneous coronary interventions balloon angioplasty cardiac catheterization with the addition of balloon apparatus at the tip of the catheter for revascularating the myocardium intracoronary stents Coronary Artery Bypass Grafting (CABG) Generally used in patient with atherosclerosis of 3 or more coronary vessels or in th case of significant main coronary disease
CARDIOGENIC SHOCK Results when the heart is unable to pump enough blood to meet the oxygen, nutrients needs of the body
MI with resultant cell death in significant portion Rupture of the ventricle secondary to MI Myocardial contusions Cardiomyopathy End-stage chronic heart failure
Inability of the LV to empty adequate and maintain forward flow Decrease stroke volume and decease cardiac output Decrease BP and decrease tissue perfusion
Pathophysiology:
LV pump failure
Inability of the LV to empty adequate and maintain forward flow Decrease stroke volume and decease cardiac output Decrease BP and decrease tissue perfusion
physiologic events that represents an attempt to compensate for the decrease cardiac output and restore adequate oxygen and nutrient to the tissues
>nervous system response - activation produces vasoconstriction of peripheral circulation thus shifting of blood to vital organs >Hormonal response causes activation of RAAS mechanism and catecholamine release
Release of Renin
Progressive stage Compensatory changes are no longer effective and severe hypo perfusion follows
Management:
Correct the underlying cause Remove coronary obstruction and restore blood flow Improve oxygenation Assess patients airway and intubate Administer 100 % FiO2 Restore adequate perfusion Administer plasma expander Initiate vasoactive drug therapy Initiate vasoactive drug therapy
AORTIC ANEURYSM >an area of the aortic wall dilatation representing an underlying weakness in the wall of the aorta at the location of the aneurysm most prevalent in 50 60 years old generally classified type: >fusiform distention of the entire circumference of the affected portion of the aorta >saccular - distention of one side of the aorta
Pathophysiology:
Degeneration of smooth muscle cells and elastic tissue in the medial layer or the aorta Weakness of the vessel wall Dilation of all layers caused by a tear in the intima (dissection) Blood leaves the central aorta Flows to the middle layer False lumen
Compromised blood flow Rupture occurs when all 3 layers of the aorta are disrupted and massive hemorrhage
Clinical manifestations:
Thoracic aneurysm
>ripping, tearing or splinting pain anterior or posterior chest, intense or excruciating in nature
Dyspnea Dysphagia Hoarseness, cough Different blood pressure Different pulses
Abdominal aneurysm
Dull, constant abdominal low back or lumbar pain Abdominal mass Pulsation in the abdomen Nausea and vomiting Decrease extremity pulses Decrease blood pressure
Aortic dissection
Sudden increase in chest or back pain Dyspnea Syncope Abdominal discomfort / bloating Extreme weakness Oliguria / hematuria Hemiparesis / hemiplegia Paraplegia
Aortic rupture
Sudden cessation of pain Reoccurrence of pain
Signs of shock
Diagnostic test:
Chest x-ray dilate aorta, wide mediastinum,
mediastinal mass
CT scan, MRI determine the size or the aorta and
Management:
Relieve pain and anxiety
Narcotics Relaxation therapy Deep breathing exercise
Indicated for:
Acute aneurysm rupture Aortic dissection refractory to medical therapy
diameter
Administer blood
Post- operative management: Relieve pain and anxiety Maintain BP Decrease stress on the aortic wall Complete assessment Mechanical ventilation Keep head elevated >45 for the first 2 post-op days Monitor renal function Initiate renal function
etiologies:
Coronary atherosclerosis Valvular heart disease Hyperstension Cardiomyopathy
Pathophysiology
Phase 1
Initiating event
Phase 2
Referred to as compensatory phase Decrease cardiac output Sympathetic nervous system activation Arterial and venous constriction
Result in phase II: Increase blood volume Increase vascular resistance Weakened myocyte Ventricular hypertropgy Increase ventricular wall stress
Later on
Myocardial hypertrophy
Clinical manifestation Present with intravascular and interstitial volume overload and inadequate tissue perfusion Postural nocturnal dyspnea Pulmonary edema Jugular vein distention Chest discomfort and tightness Peripheral edema Cool, pale, cyanotic skin Oliguria Reported weight gain Fatigue Hepatomegaly
Management:
Limit initial management and treatment of underlying
cause
Manage fluid volume restriction Diuretics Sodium and fluid restriction 2g/day or less of Sodium ; <1500mL / 24hrs of all liquids Improve ventricular function Decrease preload and afterload ACE inhibitor Increase myocardial contractility Digoxin Prevent pulmonary embolism - anticoagulants and Beta blockers
CARDIAC DYSRHYTHMIAS
>a.k.a. Arrythmia >term for any large and group of c ondition in which there is an abnormal electrical ability of the heart >some arrhythmias are lifethreatening, medical emergencies while artery may cause minor symptoms
Classified by:
Site of origin: Atrial SA node Ventricular AV node, bundle bruch Junctional bundle of his
Rate
Normal Tachycardia Bradycardia
Mechanism
Flutter Fibrillation
Atrial dysrhythmia
Premature atrial contractions (PACs) a.k.a. premature atrial complexes characterized by premature heart beats, originating from the atria may caused by caffeine, alcohol, nicotine, ischemia, anxiety, hyperdynamic compromised treatment not necessary because they do not cause hemodynamic compromise
Atrial fibrillation
extremely rapid and disorganized pattern of
depolarization in the atria(usually involving both atria) rate of 400-600bpm or faster Occurs in Rheumatic heart disease, congestive heart failure, valve disease
Quivering atria
Rapid ventricular response decrease cardiac output Stasis of blood thrombus formation
Treatment:
IV calcium channel blockers Beta Blockers Digitalis Anti- coagulants Cardioversion
Junctional Arrythmias
Junctional Rhythm
Occurs if the sinus rate falls below the rate of the AV
junctional pacemaker or when atrial conduction through the AV junction has been disrupted Occurs with ischemia to the atria
Treatment:
Atropine anticholinergic Cardoversion
Ventriculal arrhythmias
Premature ventricular contraction
a.k.a. Premature ventricular complexes brought about by premature depolarization Of cells in the ventricular myocardium or purkinjie system caused by hypoxia, ischemia, hypokalemia, increase
Ventricular tachycardia rapid ventricular rhythm at rate greater than 100bpm Treatment: Depends how well the rhythm is tolerated by the patient
Emergency ( if CO2 is low) IV lidocaine Cardioversion Defibrillation and CPR if the patient starts to become somnolent and pulseless
Ventricular fibrillation
Rapid, ineffective quivering of the ventricles that
is fatal without treatment Electrical activity originates in the ventricles and spreads in the chaotic, irregular pattern throughout ventricles
Treatment:
Immediate fibrillation
Patients Profile
Name of patient: Bibera, Gilberto Age: 61 years old Birthday: February 21, 1950 Address: Baybay, Leyte Final diagnosis: Congestive heart failure Pneumonia Chronic Renal Failure Diabetes Mellitus II Date of admission: February 8, 2012
History :
2 weeks of inability to ambulate due to pain over thigh
muscles and hips. Prior to admission patient noted right anterior chest wall pains and had difficulty in falling asleep. Decrease urine output and history of 1 week infected wound on the right heel. Hemodialysis 3x a week for 1 year.
Medications:
Ketoanalogues(Ketorosil) Metoclopramide
Caltrate Plus
Autab Sinvastatin Montra Gabapentin
Omeprazole
Dexamthasone Epoitin Dopamine Levophed
Trimetazidine(Trimetar) Dobutamine
Fluconazole
Bisacodyl Sucralfate
PNSS
Hemostan