Clients Cardiovascular Dysfunctions
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Transcript of Clients Cardiovascular Dysfunctions
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Anatomy and Physiology of the
heart
Heart
Is a hollow muscular organlocated n the center of thethorax, it occupies spacebetween the lungs and reston the diaphragm
Pumps blood to the tissues,supplying them withoxygen and nutrients
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3 layers:
Endocardium - consists ofendothelial tissue and lines the
inside of the heart and valves Myocardium made up of muscle
fibers and is responsible forthe pumping action
Epicardium exterior layer of theheart
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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; atough fibrous tissues that attaches to the great vessels,diaphragm, sternum and vertebral column and supportsthe heart in the mediastinum
The space of these two layers is called pericardial space,which is normally filled with about 20ml of fluid whichlubricates the surface of the heart and reduces frictionduring systole.
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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 fromthe veins of the body
Left atrium receives freshly oxygenated blood
from the lungs through the pulmonary veins
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Discharging chambers:
Right atrium receives deoxygenated blood from theright atrium and pmps it to the pulmonary arteryto the lungs for oxygenation
Left ventricle receives freshly oxygenated blood from
the left atrium and pumps it out the aorta to thearterial circulation.
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Heart valves
permits blood to flow in only one direction
are composed of thin leaflets of fibrous tissue, openand close in response to the movement of blood and
pressure changes within the chambers.
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Atrioventricular valves: separate the atria from the
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 whichare shaped like half moons.
Pulmonic valve > valve between the right ventricle andpulmonary artery
Aortic valve > valve between the right ventricle andaorta
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Coronary arteries
>supplies blood to the heart muscles
Left coronary artery
3 branches:
Left main artery
Left anterior descending artery > courses down the anterior wallto 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 throughthe posterior descending artery
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ACUTE CORONARY SYNDROME
>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 unstablevagina
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Pathophysiology:
Pathologic mechanisms:
Intracoronary thrombus formationPre-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
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Clinical manifestations:
Chest pain or discofort
Pressure or tightness
Jaw or neck painLeft arm ache/involvemet
Epigastric discomfort
Scapular or back pain
Nausea and vomiting Dyspnea
Dysrrhythmias
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Diagnostic test:
Elevated troponin I,T, CK-MB
ST elevation on ECG
Decrease ejection on 2D echo
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Management: Optimize blood flow to the myocardium
Medical: Decrease activity of the coagulation system with pharmacologic therapy Antiplatelet agents: Aspirln, Clopidogrel Antithrombin agents: Heparin
Increase ventricular filling time
Beta blockers (Metroprolol) Bed rest
Decrease preload and after load Nitrates Diuretics Morphine sulfate ACE inhibitor
Gold in treating Myocardial infarction MONA(Morphine, Oxygen, Nitroglycerine, Aspirin Sulfate)
emergency protocol for MI
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Prevent complications associated with coronaryobstruction
recurrent ischemia, new infarction, reinfarction continue pharmacologic reintervention
Assess for chest pain
continuous cardiac monitoring
Minimize potential for heart failure
Minimize myocardial oxygen consumption avoid increase of metabolic rate
decrease left ventricle afterload (ACE inhibitor)
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Alleviate pain
Pain relief improves coronary blood flow by decreasingthe level of circulating cathecolamines
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
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Surgical management:
Percutaneous coronary interventions balloon angioplasty
cardiac catheterization with the addition of balloonapparatus 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 ormore coronary vessels or in th case of significant maincoronary disease
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CARDIOGENIC SHOCK
Results when the heart is
unable to pump enough blood
to meet the oxygen, nutrientsneeds of the body
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Pump failure is caused by variety of factors:
MI with resultant cell death in significant portion
Rupture of the ventricle secondary to MI
Myocardial contusions
Cardiomyopathy
End-stage chronic heart failure
D t k l d d di t t
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Pathophysiology:
LV pump failure
Inability of the LV to empty adequate and maintainforward flow
Decrease stroke volume and decease cardiac output
Decrease BP and decrease tissue perfusion
Decrease stroke volume and decease cardiac outputDecrease BP and decrease tissue perfusion
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Stages and clinical manifestations:
Initial stage represents the first cellular changesresulting from the decrease in oxygen delivery to the
tissues
Compensatory stage involves a number ofphysiologic events that represents an attempt to
compensate for the decrease cardiac output andrestore adequate oxygen and nutrient to the tissues
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>nervous system response - activation producesvasoconstriction of peripheral circulation thus shifting
of blood to vital organs
>Hormonal response causes activation of RAASmechanism and catecholamine release
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Release of Renin
Combines with angiotensinogen
Production of angioltensin 1
Potent vasoconstriction conversion to angiotensin II
Vasoconstriction
Aldosterone ->Na and K retention ->water retentionADH -> retention
Increase BP, intravascular volume
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Compensatory mechanisms are effective for finite
periods of time:
Increase HR
Increase RR
Cool clammy skin may be cyanotic
Weak moderate strong pulses
Concentrated scant urine
Increase blood glucose Restlessness, agitation
Normal to slightly low BP
P i t
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Progressive stage
Compensatory changes are no longer effective and severe hypoperfusion follows
Signs and symptoms: Unresponsive to painful stimuli
Increase HR
Increase BP
Increase RR Cold, cyanotic, molted skin
Weak thread absent of peripheral pulses
Scanty urine output
Absent of bowel sounds
Refractory stage irreversible stage of shock
Cell death has progressed and cell death is imminent
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Management: Correct the underlying cause
Remove coronary obstruction and restore blood f low
Improve oxygenation
Assess patients airway and intubate
Administer 100 % FiO2
Restore adequate perfusion
Administer plasma expander Initiate vasoactive drug therapy
Initiate vasoactive drug therapy
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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
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Classification of Aortic Aneurysm according to location:
ascending
transverse
descending
thoracoabdominal
Causes and risk factors:
atherosclerosis
genetics / congenital abnormality
HPN Trauma to chest
P th h i l
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Pathophysiology:
Degeneration of smooth muscle cells and elastic tissue in the medial layeror 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
Compensation of the central cavity
Compromised blood flow
Rupture
occurs when all 3 layers of the aorta are disrupted and massivehemorrhage
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Clinical manifestations:
Thoracic aneurysm
>ripping, tearing or splinting pain anterior or posteriorchest, intense or excruciating in nature
Dyspnea Dysphagia
Hoarseness, cough
Different blood pressure
Different pulses
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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
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Aortic dissection
Sudden increase in chest or back pain Dyspnea
Syncope
Abdominal discomfort / bloating
Extreme weakness
Oliguria / hematuria
Hemiparesis / hemiplegia
Paraplegia Speech or visual disturbance
Decrease hemoglobin
Decrease hematocrit
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Aortic rupture
Sudden cessation of pain
Reoccurrence of pain
Signs of shock
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Diagnostic test:
Chest x-ray dilate aorta, wide mediastinum,mediastinal mass
CT scan, MRI determine the size or the aorta andaneurysm, extent of dissection lumen and diameter
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Management:
Relieve pain and anxiety
Narcotics
Relaxation therapy
Deep breathing exercise
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Decrease stress on the aneurysm wall
Decrease afterload Vasodilators (Nicardipines) - to lower BP, BP is maintained as
low as possible (s: 90-120) without compromising organperfusion
Avoid valsalva- maneuver/ straining
Decrease preload Limit oral fluids
Decrease sodium intake
Diuretic
Decreased myocardial Beta blockers (Propanolol)
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Vascular surgery Repair for aortic aneurysm
Indicated for: Acute aneurysm rupture
Aortic dissection refractory to medical therapy Assymptomatic patients with fusiform aneurysm more than 6cm in
diameter
Aortic aneurysm is resected and a prosthetic graft is sutured inplace
If acute dissection or rupture occurs: Administer narcotics for pain
Nitrate vasodilators
Administer fluids
Administer blood
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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
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CONGESTIVE HEART FAILURE>Inability or the heart to pump
sufficient blood to meet the oxygenation
and nutrients requirements to the body
>Effective cardiac output depends on
adequate functional muscle mass and the
ability of the ventricles to work together.
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Results from a number of underlyingetiologies:
Coronary atherosclerosis
Valvular heart disease
Hyperstension
Cardiomyopathy
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Pathophysiology
Phase 1
Initiating event
Damage loss of myocytes
Compromised ventricular function
Decreased stroke volume
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Phase 2
Referred to as compensatory phase
Decrease cardiac output
Sympathetic nervous system activation
Arterial and venous constriction
Increase in blood volume, heart rate and venousrupture
Result in phase II:Increase blood volumeIncrease vascularresistanceWeakened myocyteVentricularhypertropgyIncrease ventricularwall stress
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Later on
Myocardial hypertrophy
Overstretching of the ventricles
decompensation
Phase III Occurs when adaptive mechanism in phase II fails and
the clinical syndrome of the heart failure follows
Characterized by progressive deterioration ofcardiovascular function
Result: s/s of Heart failure, decrease function status
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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
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Management:
Limit initial management and treatment of underlyingcause Most effective but most difficult: Fibronolytic therapy PCI
Manage f luid volume restriction Diuretics Sodium and fluid restriction 2g/day or less of Sodium ;
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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 life-
threatening, medical emergencies
while artery may cause minor
symptoms
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Classified by: Site of origin:
Atrial SA node
Ventricular AV node, bundle bruch
Junctional bundle of his
Rate Normal
Tachycardia
Bradycardia
Mechanism
Flutter
Fibrillation
Atria ysr yt mia
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Atria ysr yt mia
Premature atrial contractions (PACs)
a.k.a. premature atrial complexes
characterized by premature heart beats, originatingfrom the atria
may caused by caffeine, alcohol, nicotine, ischemia,anxiety, hyperdynamic compromised
treatment not necessary because they do not causehemodynamic compromise
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Atrial fibrillation
extremely rapid and disorganized pattern ofdepolarization in the atria(usually involvingboth atria)
rate of 400-600bpm or faster
Occurs in Rheumatic heart disease, congestiveheart failure, valve disease
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Congestive heart failure, valve disease
Quivering atria
Rapid ventricular response decrease cardiacoutput
Stasis of blood thrombus formation
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Treatment:
IV calcium channel blockers
Beta Blockers
Digitalis
Anti- coagulants
Cardioversion
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Junctional Arrythmias
Junctional Rhythm
Occurs if the sinus rate falls below the rate of the AV
junctional pacemaker or when atrial conductionthrough the AV junction has been disrupted
Occurs with ischemia to the atria
Treatment:
Atropine anticholinergic
Cardoversion
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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, increasecatecholamines, caffeine, alcohol
Treatment:
Low dose beta-blockers
IV lodocaine
Amiodarone
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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 becomesomnolent and pulseless
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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 patternthroughout ventricles
Treatment:
Immediate fibrillation
CPR performed until defribrillation is intiated
IV lidocaine, cordarone
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Patients Profile
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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
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History :
2 weeks of inability to ambulate due to pain over thighmuscles and hips. Prior to admission patient noted rightanterior chest wall pains and had difficulty in fallingasleep. Decrease urine output and history of 1 weekinfected wound on the right heel. Hemodialysis 3x a
week for 1 year.
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Medications: Ketoanalogues(Ketorosil) Caltrate Plus
Autab
Sinvastatin Trimetazidine(Trimetar)
Montra
Gabapentin
Fluconazole
Bisacodyl
Sucralfate
Hemostan
Metoclopramide Omeprazole
Dexamthasone
Epoitin Dobutamine
Dopamine
Levophed
PNSS
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