Sei sulla pagina 1di 61

Anatomy and Physiology of the heart

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

are composed of thin leaflets of fibrous tissue, open

and close in response to the movement of blood and pressure changes within the chambers.

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 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

Coronary arteries >supplies blood to the heart muscles


Left coronary artery 3 branches:
Left main artery Left anterior descending artery > courses down the anterior wall

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

the posterior descending artery

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 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

Nausea and vomiting Dyspnea Dysrrhythmias

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

Increase ventricular filling time


Decrease preload and after load


Gold in treating Myocardial infarction MONA(Morphine, Oxygen, Nitroglycerine, Aspirin Sulfate)

emergency protocol for MI

Prevent complications associated with coronary obstruction


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)

Alleviate pain
Pain relief improves coronary blood flow by decreasing

the 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

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

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

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

Stages and clinical manifestations:


Initial stage represents the first cellular changes

resulting from the decrease in oxygen delivery to the tissues


Compensatory stage involves a number of

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

Combines with angiotensinogen


Production of angioltensin 1

Potent vasoconstriction conversion to angiotensin II


Vasoconstriction Aldosterone ->Na and K retention ->water retention ADH -> retention Increase BP, intravascular volume

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

Progressive stage Compensatory changes are no longer effective and severe hypo perfusion 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

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

Classification of Aortic Aneurysm according to location:


ascending transverse descending thoracoabdominal

Causes and risk factors:


atherosclerosis genetics / congenital abnormality HPN Trauma to chest

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

Compensation of the central cavity

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

Speech or visual disturbance


Decrease hemoglobin Decrease hematocrit

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

aneurysm, extent of dissection lumen and diameter

Management:
Relieve pain and anxiety
Narcotics Relaxation therapy Deep breathing exercise

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 organ perfusion Avoid valsalva- maneuver/ straining

Decrease preload Limit oral fluids Decrease sodium intake Diuretic


Decreased myocardial Beta blockers (Propanolol)

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 in

place If acute dissection or rupture occurs:


Administer narcotics for pain Nitrate vasodilators Administer fluids

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

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.

Results from a number of underlying

etiologies:
Coronary atherosclerosis Valvular heart disease Hyperstension Cardiomyopathy

Pathophysiology
Phase 1
Initiating event

Damage loss of myocytes


Compromised ventricular function Decreased stroke volume

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

Increase in blood volume, heart rate and venous rupture

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 of cardiovascular function Result: s/s of Heart failure, decrease function status

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

Most effective but most difficult: Fibronolytic therapy PCI

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

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

catecholamines, caffeine, alcohol

Treatment: Low dose beta-blockers IV lodocaine Amiodarone

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

CPR performed until defribrillation is intiated


IV lidocaine, cordarone

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

Potrebbero piacerti anche