Scenario 1

A woman age 60 years complained of fatigue and shortness of breath quickly as spicy. He can not do activities at home for longer without frequent rest with difficulty breathing. Ankles swell during the day and less at night. On examination the doctor, discovered the existence of rapid breathing, heard on auscultation examination of the sound crackles. Pulse regular and systemic blood pressure within normal limits, but there is a dam neck veins while in an upright position. Ictus Cordis palpable in the left anterior axillary line / intercostal space V. Chest X-ray picture shows the CTR of 0.69 and visible pulmonary vascular dam. Patients treated with digoxin and diuretics so that reduced patient complaints.

Difficult words

1. Crepitations (crackles) is a short sound, not continuous, not a musical, much heard during inspiration. Sound crackles like the sound made by rubbing the hair on the ear or the sound when put salt into the fire. Crepitus was found in lung edema, congestive heart failure and pulmonary fibrosis.

2. Ictus Cordis is the structure corresponding to the location of the apex Cordis, namely the lower end of the left ventricle which is usually located between the ribs on the left medioclavicularis V linea. Ictus Cordis is the place to listen to heart sounds of mitral valve.

3. CTR (Cardiothoracix ratio) is the ratio between heart size with the size of the cavum thoracix. Normal heart size if the value of ≤ 50% CTR. CTR is also called CTI (Cardiothoracix index), but the CTI of a decimal number. CTI values that show normal heart size is ≤ 0.5.

4. Digoxin5. Diuretik

Questions

1. Describe the anatomy, histology, physiology, and biochemistry of cardiovascular! 2. Why people feel tired and breathless after the move and the factors that cause shortness

of breath? 3. Why ankles swell during the day and less at night? 4. Why is there sound on auscultation examination crepitations? 5. What is the mechanism of dam jugular vein? 6. How the influence of digoxin and diuretics at reducing symptoms?7. Explain the Differential Diagnosis (DD) and its management?

Answers

1. Anatomy, histology, physiology, and biochemical cardiovascular.

a. Cardiovascular anatomy

The heart (cor) is the main organ in the cardiovascular system. The heart is a muscular organ shaped or pear-Conus fist for fist, rests on the diaphragm thoracis. The heart is located

in the mediastinum in the chest cavity, between the two lungs of caudalis. Two-thirds of the heart is located to the left of the breastbone and a third on the right. The location of the heart in such a way that the top (apex Cordis) facing toward the left caudoventral. In adults, the size of the cast is 12 cm long, 8-9 cm wide, and 6 cm thick. In the male heart weight is 280-340 g and 230-280 g in women. In pathological conditions, the heart size may exceed the normal size.

The projection of the heart on the ventral wall of the thorax is as follows:

· The left edge is located next to the cranial edge of the caudal pars pars on costa cartilaginis sinister, that is 1 cm lateral to the edge of the sternum.

· The left edge next to the caudal is at room intercostalis 5, which is approximately 9 cm to the left of the median linea or 2 cm medial to the left linea medioclavicularis

· Right next to the cranial edge is at the edge of the cranial pars cartilaginis dextra costa III, approximately 1 cm from the lateral edge of the sternum.

· Right next to the caudal edge is at costa cartilaginis pars VI dextra, approximately 1 cm on the lateral edge of the sternum. 

The heart is wrapped by a membrane called the pericardium. Pericardium consists of two layers, the fibrous layer, which is located in the outer pouch to form the fibrous and serous layers are located next to the deep pockets of serous form. Serous membrane lining or covering the surface of the heart called the pericardium form the epicardium and visceral serous layer found on the surface of the fibrous layer to form the parietal pericardium. The second layer is called the limit of a cavity pericardialis cavity. The transition between the visceral pericardium to pericardium parietale called reflexi pericardii. Pericardii cavity containing lubricating fluid called the wetting liquid sereus serous membrane surface, which serves to reduce friction and make freely moving heart systole and diastole at the time. The parietal pericardium is attached to the sternum next to the front, and the vertebral column in the back, while down on the diaphragm. Visceral pericardium directly attached to the surface of the heart. Heart wall consists of three layers, namely:

· Layers supeficial called epycardium

· Intermediate layer called the myocardium

· The deep layer is called endocardium

The heart consists of four chambers, namely the right atrium and the left and right and left ventricles. Atria is a room that is located at the top to receive blood from all over the body and lungs. Ventricle is the heart's chambers are located at the bottom. The right ventricle pumps blood to the lungs while the left ventricle pumps blood throughout the body. The heart of the upper room, atrium, anatomically separate from the room next to the heart, or ventricle, by an annulus fibrosus.

Right Atrium

The right atrium is a thin wall serves as a repository of blood, and to channel blood from the veins into the systemic circulation of the right ventricle and then into the lungs. Blood from this vein into the right atrium through the superior vena cava, inferior, and the coronary sinus. In the mouth of the vena cava no real valves. Vena cava separating the atria of the heart valves or folds are only rudimentary vocal muscles. Because of this increase in right atrial pressure due to dams in the right heart blood will reverse back into the venous systemic circulation.

Right ventricular

On ventricular contraction, then each ventricle must generate forces large enough to be able to pump the blood it receives from the atrium to the pulmonary circulation or systemic circulation or. Right ventricular unique crescent-shaped, in order to produce a low-pressure contraction, which is enough to draw blood into the pulmonary artery. Pulmonary circulation is a low-pressure blood flow system with a much smaller resistance to the flow of blood from the right ventricle, compared to the high pressure systemic circulation of the blood flow from the left ventricle. Therefore, the workload of the right ventricle is much lighter than the left ventricle. As a result, right ventricular wall thickness is only one-third of the left ventricular wall thickness.

Left Atrium

The left atrium receives blood that has been dioksigenasi from the lungs through the pulmonary vein to the fourth. Between the pulmonary vein and left atrium there is no real valve. Therefore, changes in left atrial pressure is easy to flip retrogard into the lung vessels. Increased left atrial pressure that will cause acute lung dam.

Left ventricular

The left ventricle must generate high enough pressure to overcome the resistance of the systemic circulation, and maintain blood flow to peripheral tissues. Left ventricle has a thick muscles and shape that resembles a circle, facilitate the formation of high pressure during ventricular contraction. Even limiting the ventricular septum also help strengthen the pressure generated by the entire ventricular contractions.

Inside the heart are functioning valves directing blood flow to the appropriate direction. They open at the time the heart contracts and closes to prevent reverse blood flow during relaxation. Between the atria and ventricles are valves between the ventricles and atrioventrikuler and major blood vessels there (aorta and pulmonary artery) are semilunar valves.

Valve Atrioventrikularis

Atrioventrikularis valve leaves smooth but durable. Trikuspidalis valve located between the atrium and right ventricle has three cusps. Mitralis valve separates the left atrium and ventricle, a bicuspid valve with two cusps.

Valve semilunaris

Both valves semilunaris same shape, consisting of three symmetrical cusps resembles a funnel, which is anchored firmly in the annulus fibrosus. Aortic valve is located between the left ventricle and aorta, while the pulmonary valve is located between the right ventricle and the pulmonary artery. Semilunaris valve prevents back flow of blood from the aorta or pulmonary artery into the ventricle, while the ventricles in a resting state.

Efficiency of the heart as a pump depends on the nutrition and oxygenation of the heart muscle. Coronary circulation covers the whole surface of the heart, bringing oxygen and nutrients to the myocardium through the branches of a small intramiokardial. Coronary artery is first branch of the systemic circulation. Mouth of the coronary artery was found in the sinus Valsalva in the aorta, just above the aortic valve. Coronary circulation consists of left and right coronary artery. The left coronary artery has two major branches, the left anterior descending artery and left circumflex artery.

b. Histology of cardiovascular

The cells contained in the heart of the specialized cells whose function is to support cardiac activity in carrying out its functions. These cells are:

1) the heart muscle or myocardial cells in the atria and ventricles that serves to cardiac contraction. These cells have also been demonstrated produce ANP (atrial natriuretic peptide), adrenomedullin, and oxytocin.

2) pacemaker cells contained in the SA and AV node, which is responsible for initiating the heart's electrical activity.

3) Purkinje fibers that spread to the rest of the electrical stimulation of heart muscle cells.

4) transitional cells connecting tissue that conduct electrical stimulation to the muscle cells around the atria and ventricles.

All the cells mentioned above are basically derived from muscle, but the pacemaker cells and Purkinje cells did not develop kontraktilnya components and smaller.Heart muscle cells have a structure similar to skeletal muscle. In the ventricles of mammals, ranging from 75-100 mm in length and 15-20 mm in diameter. In the cell size is smaller atria. Cell membrane, sarkolemma, covered by a layer of electrically charged glycocalyx negative. Sarkolemma invagination into the cell to form a tubular-t at a meeting between band A and band-I. T-tubules in cardiac muscle cells have a diameter larger than the skeletal muscle and is also covered by glycocalix. Sarcomeres cardiac muscle cells have a structure similar to

skeletal muscle cells. Mengadung cardiac muscle cell myofibril and mitochondria in large numbers. Each cardiac muscle cells connected to one disc lainnyaoleh interkalatum (intercalated disk) so as to form a syncytium. Interkalatum disc contains a lot of gap junctions, adherens desmose and fascia which is a component of intercellular communication. SA node cells and AV have a smaller size of the heart muscle cells. SA node cells come together to form a triangular mass, in which there is essentially padakrista terminalis and the peak in the direction of the superior vena cava. Cells surrounded by connective tissue. Connective tissue is increasing rapidly with increasing age and penggatian nodal cells by connective tissue that causes the occurrence of sick sinus syndrome.

c. Cardiovascular physiology

The main function of the heart is pumping blood throughout the body via the aorta and pulmonary artery vessels. Ability of the heart muscle to pump blood around the body is made possible by the walls of the heart consisting of cardiac muscle cells (myocardium). Contraction activity of the heart to pump blood around the body is always preceded by electrical activity. Electrical activity begins in the sinoatrial node (SA node) which lies in the gap between the superior vena cava and right atrium. Pacemaker cells (pacemaker) in the SA node spontaneously started the wave of depolarization, thereby causing an action potential is propagated through the muscle cells of the atria, atrioventrikuler node (AV node) bundle of His, Purkinje fibers, and finally to all the muscles of the ventricles. Therefore, the SA node is called the primary pacemaker.

This electrical activity called an action potential. Action potential in cardiac muscle consists of five phases, namely:

• Phase 0 (upstroke, fast depolarization)

This rapid phase of depolarization due to Na + ions flow into the cell (INA) via the activation gate (m gate). At the time of membrane potential (Vm) of 30 mV-40 mV occurred inactivation process of Na + channels, inactivation gate (h gate) began to close. The process of Na + channel inactivation underlies the refractory period.

• Phase 1 (early repolarization)

This is an early repolarization phase of short duration. Phase is due to Na + channel inactivation and activation of K + channels. Akifasi K + channels leads to the movement of K + out of cells of short duration (Ito, transient outward current). This phase is particularly prominent in the action potential in Purkinje fibers.

• Phase 2 (plateau)

This phase is the longest phase. Phase is due to the INA, Ica and IK, IK1 and Ito. ICA entry through L type Ca2 + channels and T. ICA plays a role in the process of cardiac contraction by triggering the release of intracellular Ca2 + in the sarcoplasmic reticulum (Ca2 +-induced Ca2 + release). Modified ICA through Ca2 + channels by drugs may reduce or increase the contraction of the heart.

• Phase 3 (fast repolarization)T

his phase occurs when the flow of K + out of cells exceeds the influx of Ca2 + currents (Ica). Ito determines the length of the initial phase 2 or phase 3, especially in the atria. IK1 (inwardly Rectified), the most important role in the repolarization process.

• Phase 4 (resting membrane potential)

In this phase of the action potential returned to resting membrane potential ranged from -80 mV to -90 mV in ventricular muscle, muscle is more positive in the atria, AV node and SA node. This phase is determined by the movement of K + ions out of cells, and Na +-pump activity of K + (Na +-K + pump).

At the heart muscle, as well as in skeletal muscle mechanism of contraction and relaxation consists of five stages: 1) the action potential in the cell membrane to open channels of Ca that occurred increased the flow of Ca2 + into the cytoplasm with consequent concentration of Ca2 +, 2) bound Ca2 + to TNC which would alter the confirmation of troponin-tropomyosin complex with actin, 3) change confirmation is causing crossridge causing contractions, 4) in the absence of stimulus, Ca2 + will be re-uptake into the reticulum sarcoplasmic and teradi separation between Ca2 + to TNC; 5) filament thin will come back to the beginning where Gen. konfgurasi will cover parts that will interact with the actin-myosin head. The overall mechanism is known as excitation-contraction coupling atauexcitation-contraction coupling.

• The mechanism of excitation

In short, if the depolarization process occurs in heart muscle cells, with a quick wave of excitation will spread throughout the heart muscle through gap junctions. Skilful excitation spread to the inside of the cell through the T-tubules are invaginations into the muscle fibers to the heart on the line Z. In the second phrase the depolarization, Ca2 + channels in cell membranes and the tubular-T will open and Ca2 + entry into the cell due to concentration differences. Ca2 + into the cells stimulates the release of Ca2 + from the reticulum sarcoplasma. This mechanism is known as the Ca2 +-induced Ca2 + released. Intracellular free Ca2 + concentration will increase from 10-7M to 10-6 to 10-5 M during the excitation process, and Ca2 + will be bound by the TNC. Although basically the excitation-contraction coupling mechanism in cardiac muscle similar to skeletal muscle, there is a difference in the effect of Ca2 + on the contraction process. T tubules in cardiac muscle has a volume 25 times greater than skeletal muscle. In addition, the T tubules also found a number of mucopolysaccharide which have negative charge and binds Ca2 + reserves more. This is to ensure that Ca2 + is always available in sufficient quantities that will diffuse into the inside of the heart muscle fibers in the event of an action potential. Because the structure of the T tubules in cardiac muscle has an open end toward the outside, resulting in the relationship between the extracellular space. As a result, the concentration of Ca2 + for contraction is strongly influenced by the concentration of Ca2 + in the extracellular fluid.

Any mechanism that increases the concentration of Ca2 + increases the contraction of heart muscle, and that lower concentrations of Ca2 + will decrease the heart contraction. For example, catecholamines are bound to the beta adrenergic receptor will phosphorylate Ca2 + channels via cAMP-dependent protein kinase A. This phosphorylation of Ca2 + channels will open up so many of Ca2 + into the cell. Increased intracellular Ca2 + can also be done by blocking the pump Na + - K + by digitalis. Digitalis will inhibit Na + expenses resulting accumulation of intracellular Na +. Increased intracellular Na + would inhibit the exchange of Na + and Ca2 +, which means that less Ca2 + released from the cell. This leads to the accumulation of intracellular Ca2 + so that the contraction increases.

• Changes in troponin-tropomyosin complex and actin

Interaction between Ca2 + with troponin-tropomyosin complex to shift the position of tropomyosin from actin. TNC is the only place bound Ca2 + from troponin-tropomyosin complex. When Ca2 + concentration reaches a high enough level, allosteric interactions between Ca2 +-TNC will cause tropomyosin and tropomyosin will shift -10 Å deeper into the grooves of actin. This movement will open the interaction between actin and myosin allows the formation of cross-bridge, and thus muscle contraction.

• Cross-Bridge

CycleIn the resting state, the head of myosin S1 binding to ATP. ATP-ase activity of myosin S1 head is menghidrolisa ATP to ADP and P. In the resting state as well, myosin does not bind to actin and myosin head orientation perpendicular to the actin. When the muscle is stimulated, an increase in intracellular Ca2 + would cause a conformational change of troponin-tropomyosin complex and the subsequent occurrence of cross-bridge memungkan. Bonding between myosin heads and actin in these processes lead to changes in myosin head tilted position due to the conformation of 90omenjadi peubahan 45o. This conformational change to minimize energy requirements. This change causes the hydrolysis of ATP to ADP and P. The energy that was captured off and cause the power to pull actin. In the place of release of ADP, a new ATP molecule is bound, in which ATP is used to release actin from the myosin head. A condition known as rigor mortis or muscle stiffness in people who have meningal due to lack of cross-bridge ATP that is settled.

• Re-uptake Reticulum Ca2 + by sarcoplasmic

At the end of systole, the influx of Ca2 + is reduced, and there is no stimulus for intracellular Ca2 + release from the sarcoplasmic reticulum. When the concentration of intracellular Ca2 + decreased due to re-uptake of Ca2 + into the sarcoplasmic reticulum in relaxation will occur. Sarcoplasmic reticulum membrane Ca2 + pump contains a lot of the mechanisms of action triggered by fosfolamban who have undergone phosphorylation. Through this pump, two moles of Ca2 + will be transported into the sarcoplasmic reticulum for every one mole of ATP hydrolysis. These pumps maintain low concentrations of Ca2 + in the cell. In addition, low concentrations of Ca2 + in cells is also influenced by the Ca pump located in the heart muscle cell membrane and the activity of Na-Ca exchanger is exchanging 3 Na + for one Ca2 +.

d. Biochemical cardiovascular

To perform its functions normally, the heart hanging suspended from the supply of oxygen and energy. Oxygen and energy shortages due to disruption of coronary blood flow will lead to heart dysfunction which can be fatal. The main source of energy needed to maintain the function of the heart's contraction comes from adenosine triphosphate (ATP). At heart, ATP is mainly derived from the metabolism of carbohydrates and fatty acids. Glucose metabolism has two main components, glycolysis and glucose oxidation. Glycolysis, which is the first step of glucose metabolism pathway has the advantage in the formation of ATP, which does not require oxygen. However, the formation of ATP from glycolysis contributes only 1-5% of the entire supply of ATP in the normal heart in aerobic condition. It seems that the ATP generated from glycolysis has a special role to maintain the ionic homeostasis in cardiac muscle cells. Another component of glucose metabolism contribute to the ATP is the oxidation of glucose, in which pyruvic acid from glycolysis is further metabolized taken up by mitochondria to produce ATP. Pyruvate can also be obtained from lactic acid in the healthy heart. The main enzyme involved in the oxidation of glucose and lactate are pyruvate dehydrogenase, which converts pyruvate to acetyl CoA in the mitochondria. Acetyl CoA enters the Krebs cycle, in which he will dioksiasi and used to generate NADH for electron transport chain. The presence of oxygen electron transport chain to pump protons out of mitochondria to memecu phosphorylation of ADP to ATP, a process known as oxidative phosphorylation. ATP is then used as the energy of chemical for muscle contraction and to maintain the homeostatic ionic in the cell, such as: 1) pump Ca2 + from reticulum sarcoplasmic after the contraction ends, 2) pump Na + and K + through the membrane to maintain the environmental ionic appropriate for the formation of action potentials. Fatty acid oxidation is a major source of acetyl CoA in the mitochondria. In the normal heart, 60-90% acetyl CoA derived from fatty acids. However, although fatty acids are the main source of ATP production in the heart, fatty acids requires 11% more oxygen than glucose to generate ATP in the same amount. Thus, from the point of consumption of oxygen, fatty acids are not as efficient as glucose as an energy source. In addition, with increased contribution of fatty acid oxidation to form acetyl CoA, the contribution of glucose oxidation decreased. It is not desirable, especially during or after ischemia, by kaena toxic materials resulting from the process of glycolysis (lactate and protons) and had accumulated. Attempts to remove such materials requires considerable ATP, but ATP is required for kontaksi, this will lead to impaired ATP utilization efficiency.

2. Patients feel tired and breathless after the move and the factors that cause shortness of breath.

a. Patients feel tired

Fatigue is a common symptom of reduced cardiac output (COP) or cardiac output. Decreased cardiac output causes decreased perfusion to the amount of blood or skeletal muscle. This causes reduction in the amount of oxygen carried to the muscle cells so that the process of cell metabolism is inhibited. Inhibited metabolism causes the number of high-energy molecules, namely ATP (Adenosine Triposphat) produced decreases. The resulting

decrease in ATP causes the energy to move is also reduced. So that patients feel tired easily while on the move. Patients with congestive heart failure and mitral valve disease often complain of tired. However, fatigue is not specific to heart disease. Common causes of fatigue are anxiety and depression. Other conditions associated with anemia and fatigue is a chronic disease.

b. Factors that cause shortness of breath

• Heart disease: left ventricular failure and mitral stenosis

• Lung disease: obstructive pulmonary disease, asthma, restrictive lung disease, pulmonary embolism, and pulmonary hypertension

• Emotional: anxiety and depression

• Exposure to high places: the reduced oxygen pressure • Anemia: decreased oxygen-carrying capacity

c. Pulmonary vascular dam and shortness of breath after activity

Shortness of breath (dispnue) is associated with subjective complaints of difficulty breathing. Mild shortness of breath may be a complaint that really subjective, but if more severe shortness of breath, the condition may be accompanied by objective evidence of any attempt to increase the frequency of breathing. Complaints dispnue very important. Patients will describe that he was "shortness of breath" or that he "did not get air in sufficient quantity". Dispnue usually associated with heart disease and lung cancer. In the case, shortness of breath caused by left heart failure. Left heart failure causes blood in the right ventricle is not pumped completely so that the amount of blood that remains in the left ventricle more than the normal amount. This will led to more blood being pumped phase of ventricular systole to the next so that the pressure in the ventricle increases which in turn can increase the pressure and end diastolic volume. Increased right ventricular pressure causes increased pressure in the left atrium and pulmonary veins. Pressure in the pulmonary venous retrograde deployed on vessels in the lungs smaller. Actually increase the pressure on the pulmonary vessels is an adaptive mechanism to protect the lungs from congestion. However it can not last long. Due to a more negative pressure in the area and perivaskuler prebronkial intersisial and the increased ability of these nonalveolar intersititium, liquids are often increased in number in this place when the pumping ability of the lymphatic channels are redundant. If the displacement of fluid from the blood into the alveoli intertitial or to refund excess amounts of fluid into the blood vessels and the flow of fluid into the lymphatic system there will be a pulmonary vascular congestion. Pulmonary vascular congestion will reduce spasticity and improve pulmonary airflow resistance so that the work of breathing will increase. It causes shortness of breath.

3. Ankles swell during the day and less at night.

a. The cause of edema in the ankles.

Ankle edema caused by heart failure. Heart failure causes the activation of the renin-angiotensin-aldosterone (RAA). This mechanism would increase systemic vascular resistance but lower cardiac output. An increase in renin secretion in cells juxta-renal glomerulus. Renin will break circulation angiotensinogen to form angiotensin I which is then rapidly broken down by the angiotensin converting enzyme bound to the endothelial cells to form angiotensin II, a powerful vasoconstrictor. With the rise of angiotensin II, there was arteriolar vasoconstriction, increased total peripheral resistance, this will help to maintain systemic blood pressure. Angiotensin II is also working on adrenalis cortex to increase aldosterone secretion. This spurred the hormone aldosterone sodium reabsorption of sodium and water from renal tubules into the circulation and help to increase intravascular volume. It causes water retention terajdinya kidney nephron. As a result, the displacement of fluid from the blood into the space that exceeds the amount of refund intertitial fluid into the blood vessels and the flow of fluid into the lymphatic system there will be edema in the dependent regions.

b. Cause Edema increased during the day and decreases at night.

Edema increased during the day and decreases at night due at noon everyday activities that use more legs and is often performed than at night.

4. The cause of the crackles on auscultation examination.

Crepitus arise when there is fluid in the inner bronchial and distal airway collapse there and alveoli. Equalization of pressure rise suddenly crackles. A more coarse crepitations related to the larger airways. Sound crackles like the sound made by rubbing the hair near the ears.

5. The mechanism of dam jugular vein.

Dam jugular vein caused by right heart failure. Right heart failure causes blood in the right ventricle is not pumped completely so that the amount of blood that remains in the right ventricle more than the normal amount. This will led to more blood being pumped phase of ventricular systole to the next so that the pressure in the ventricle increases which in turn can increase the pressure and end diastolic volume increases. Increased right ventricular pressure causes increased pressure in the right atrium and the superior and inferior vena cava. Pressure in the superior and inferior vena cava in retrograde spread on vessels smaller including jugular vein. That caused the dam jugular vein.

6. Effect of digoxin and diuretics at reducing symptoms.

a. Effect of Digoxin

Digoxin is a drug positive inotropic and negative kronotropik which can increase the contractility of cardiac muscle. Digoxin increases the contractility of cardiac muscle by

inhibiting the enzyme Na + / K +-ATPase in cardiac myocytes resulting in an increase in myocyte shortening velocity which effectively increases the strength of ventricular contraction.

b. Effect of Diuretics

Diuretics to reduce fluid and salt in the body by reducing the amount of intravascular fluid gradually. Diuretics are also a venoilator direct vasodilator effect immediately react so as to reduce preload.

7. Differential Diagnosis (DD) and its management.

a. differential Diagnosis

In the above case there are several possible diseases suffered by patients with heart failure can cause the left and right heart failure according to the symptoms experienced by patients. Differential diagnosis is as follows:

• Mitral Stenosis

• Aortic Stenosis

• Coronary heart disease

• Dilatation Miokardiopati

b. management

• Non-Pharmacological

• Eliminate the ballast factor

• Reduce the risk factors

• Changing the life style

• Pharmacologic

• Surgical Intervention

Diseases that can cause shortness of breath.

a. Mitral stenosis

Mitral stenosis is a condition in which an interruption of blood flow from the left atrium through the mitral valve due to obstruction at the level of the mitral valve. This leads to structural abnormalities of the mitral opening disorder causing impaired left ventricular filling at diastole. Mitral stenosis is a common cause of endocarditis rheumatica, due to the progressive reaction of rheumatic fever by infection streptokokkus.

b. Aortic stenosis

Aortic stenosis is a condition in which an interruption of blood flow from the left ventricle through the aortic valve due to obstruction at the level of the aortic valve. Etiology of senile calcific aortic stenosis is, a variation of congenital and rheumatic heart disease.

c. Coronary heart disease

Coronary heart disease is one of the main result of arteriosclerosis (hardening of the arteries) which is known as atherosclerosis. At this state of narrowed arteries due to fatty deposits (atheroma and plaques) on didindingnya. Risk factors for the occurrence of this condition are smoking, high blood pressure, elevated cholesterol dioxide in value, stress obesity, diabetes mellitus and a strong family history for coronary heart disease. With increasing age the disease will be more frequent there. men have a higher risk than in women, but this difference with increasing age will increasingly small.

d. Dilatation Miokardiopati

Cardiomyopathy is a type of cardiomyopathy is most commonly found. With descriptions of abnormalities found: right ventricular dilatation and or left, contractility dysfunction in one or both ventricles, arrhythmias are often accompanied by symptoms of emboli and congestive heart failure.

Management of each of Differential Diagnosis

• Mitral Stenosis

Several classes of drugs such as antibiotics penicillin, erythromycin, sulfa, cephalosporins for the prevention of rheumatic fever or endocarditis is often used. Negative inotropic drugs such as β-blocker-blocker atauCa can benefit in patients with sinus rhythm who gave a complaint at the time of heart frequency increases as in exercise. Retriksi salt or provision of intermittent diuretic useful if there is evidence of pulmonary vascular congestion.

In the circumstances the use of digitalis Atrium Fibrillation is an indication, can be combined with beta blockers or calcium antagonists.

anticoagulant warfarin should be used in mitral stenosis with atrial fibrillation or sinus rhythm with a tendency of thrombus formation to prevent thromboembolic phenomena.

percutaneous mitral valvotomy with a balloon. Initially carried out with two balloons but lately with the development in the manufacture of balloons, the procedure is quite satisfactory valvotomy with a balloon procedure.

Surgical intervention, repair or replace the valve. 1950 to 1960 komisurotomi with closed surgery performed through a transatrial and transventrikel. Lately komisurotomi surgery done openly because of the heart-lung machine.

• Aortic Stenosis

Physical activity be avoided in patients with severe AS (<0.5 cm2/m2), although still asymptomatic. NGT is given when there is angina. Diuretics and digitalis given when no signs of heart failure. Statin is recommended to prevent aortic valve calcification leaves. Surgery is performed when the valve area <1 cm2 or 0.6 cm2/m2 (body surface), left ventricular dysfunction (stress test), dilatation of aortic stenosis due to calcification of post usually occurs in older people who have also experienced a decrease in kidney function, liver, and lung. Evaluation of these organs is required prior to surgery.

• Coronary heart disease

- Angina pectoris stableThe goal of treatment is mainly to prevent deaths and heart attacks (infarction). While

the other is to control angina attacks which improves the quality of life.Treatment consists of:

Pharmacologic:a. Aspirinb. beta blockersc. Angiotensin converting enzyme, especially when accompanied by hypertension or

LV dysfunctiond. The use of drugs to decrease LDL in patients with excess LDLe. Nitroglycerin spray / sublingual to control its angina.f. Ca antagonists or long-term nitrates and beta blockers combination for an

additional beta-blockers contraindicated apabiola, tatau intolerable side effects or fail.

g. Clopidogrel to aspirin substitute the absolute terkontraindikasi

Non-Pharmacological:

a. Provision of Oxygenb. Rest at the time of arrival of angina attacksc. Lifestyle changes include quitting smoking, etc.d. Weight losse. Adjustment of dietf. Regular exercise

- Not Stable Angina pectoris

Patients need treatment in hospital, preferably in the intensive coronary unit, the patient should be rested, given a sedative and Oxygen. Giving morphine or pethidine to patients who still felt the chest pain, despite being received nitroglycerin.

- Acute Myocardial Miocardium.IMA's first treatment goal is relief of pain and anxiety. Both prevent and

treat complications as early as possible (30-40%) of serious heart trouble, arrhythmias, thrombo-embolism, pericarditis, ruptured m. papillary, ventricular aneurysm, right ventricular infarction, recurrent ischemia and sudden death. Sulfas given morphine for pain from 2.5 to 10 mg IV. Pethidin less effective than Morphin and can lead to sinus tachycardia. These drugs are widely used in inferior infarction with chest pain and sinus bradycardia. Dose of 25-50 mg may be repeated after 2-4 hours, slowly, there is chest pain with anterior infarction with LMA mainly sinus tachycardia and systolic blood pressure above 100-100 mm Hg B-Blocker can be used. Small doses of B-Blocker started with 1/2 - 5 mg Inderal. IV. It is said that giving B-blockers in the first five hours when no contra indication to reduce the extent of infarction (1,4,7,12) both sublingual and transdermal nitrates can be used if the chest pain in the days pertama.Nifedipin, C-antagonist that often used when the suspected cause of coronary adalahspasme, specifically angina after the day-to-2 and before returning home. Break, giving 02, low calorie diet and digestibility and ready for serious infusion plug. Giving anti koagulansia only in patients who must be mobilized for a long time such as heart failure, shock and extensive anterior infarction. Approximately 60-70% of myocardial there are no complications and treatment is recommended after 2-3 weeks to test the load latihjantung (ULJB) are modified. If normal for regular rehabilitation but if abnormal coronary arteriogram to be examined to determine the exact state of the coronary arteries so that the optimal position can be determined. If there are complications in trying to classify patients with AMI in clinical and hemodynamic subsets (Forrester) for treatment.Restrictions on the expansion of infarction. As already explained that the myocardial perfusion and metabolic demand should not be harmed by the treatment. Circumstances that may extend the infarct should be prevented or corrected immediately, such as: a. Tachykardia, b. Hypertension, hypotension, d.Aritmia and e. Hipoxemia. Faced with circumstances that required treatment strategies are: Efforts to reduce myocardial 02 requirements by:

• B-Blocker• decrease the afterload of patients with hypertension• Assist with the circulation of IAB Reduced myocardial ischemia by improving the flow of collateral perfusion or

improved so that inventories increased myocardial 02.

- Dilatation MiokardiopatiBecause the causes of dilated Miokardiopati idipatik so special treatment is not

performed. Treatment is aimed fit the clinical picture that arises, in which most of the symptoms of congestive heart failure. So that the standard treatment for congestive heart failure as diuretics are given to reduce symptoms, ACE inhibitors, and beta blockers. Digoxin is a second-line treatment option, in which the optimal doses are to be achieved when serum levels reach 0.5 to 0.8 ng / mL.