clients cardiovascular dysfunctions

8/2/2019 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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