Diagnosis
Diagnosis is made based on history, physical examination, and examination support.
A. Anamnesis
The clinical manifestations
Mild and moderate heart failure:
- Feelings of discomfort when lying on a flat surface in minutes.
- Systolic blood pressure to normal or high.
Severe heart failure:
- The patient must sit up straight
- Shortness of breath
- Unable to utter a complete sentence because of the difficulty felt
- Systolic blood pressure decreased LV dysfunction à because of heavy
Increased adrenergic activity leads to:
- Cyanosis of the lips and nails
- Sinus tachycardia (a nonspecific sign)
Pulse pressure may be reduced or disappear à indicates a decrease in stroke volume
Peripheral vasoconstriction causes peripheral coldness of the extremities
B. Examination: inspection of the stomach may bulge, can be found hepatomegaly palpation, percussion, and auscultation of bowel sounds are usually normal
C. Investigation:
A. Chest X-ray
Leads to cardiomegaly, LVH heart enlarged to the left, hit the apex of the diaphragm (embedded), RVH enlarged heart with the apex up to the left of the diaphragm, heart uneven waist or stand out, and there is a double image contours.
Describe pulmonary vascular Corakan kranialisasi
Kerley lines A / B
Pulmonary infiltrates second precordial
Pleural effusion
2. EKG to see the underlying disease such as myocardial infarction and arrhythmia. Left ventricular hypertrophy where S d V1 + R in V5/V6 ≥ 35 mm, arrhythmias such as atrial fibrillation where there is a distance R to R 'is not uniform.
D. Other examinations: examination of Hb, electrolytes, echocardiography for valve abnormalities, angiography, renal function, and thyroid function tests performed on indication.
Laboratory:
A. Renal physiology:
+ Urine:
- The density of <
- The volume of urine decreased
- Decreased urine Na, increased aldosterone renin
Blood +:
- U increased and creatinine clearance decreased, it showed severe heart failure.
- Na, Bl and albumin decreased, thereby increasing blood volume and edema fluid due to increased renin and aldosterone.
- Metabolic acidosis: pH decreased, HCO3 down, it indicates heart failure and kidney failure.
2. Heart physiology
Bilirubin blood, urine and increased Urobilinogen
LED off
LDH increased, especially LDH5
Alkaline phosphatase increased (mild / severe)
Protombin slightly up
Pulmonary physiology
O2 pressure drop due to impaired gas exchange, pulmonary edema
Respiratory alkalosis: pH increased, pCO2 down, then going to hyperventilation, the response to hypoxemia
Respiratory acidosis: pH decreased, pCO2 go up, they can lead to acute pulmonary edema that causes the failure of ventilation and CO2 retention.
Framingham criteria can also be used to established diagnosis of congestive heart failure, which is found to exist at least one major criterion and 2 minor criteria.
Major criteria:
Paroxysmal nocturnal dyspnea
Distended neck veins
Increased jugular venous pressure
Smooth wet Rongki not loud
Cardiomegaly
Acute pulmonary edema
S3 Gallop
Reflux hepatojugular
Minor criteria:
Extremity edema
Nighttime cough
Dyspnea d'effort
Hepatomegaly
Pleural effusion
Decrease in vital capacity 1/3 of normal
Tachycardia (> 120x/menit)
Criteria for major or minor
Weight loss> 4.5 kg in 5 days of treatment.
Management
A. Activity
Although physical activity is not recommended in severe heart failure, a mild routine exercise proved beneficial in heart failure patients with NYHA class I-III. Euvolemik patients should be encouraged to do regular isotonic exercise such as walking or riding a bicycle ergometer static, which can be tolerated. Some research on physical exercise yielded positive results with reduced symptoms, improved exercise capacity, and improve the quality and duration of life. The benefits of weight reduction in caloric intake restriction has not been known clearly
2. Diet
Low-salt diet (2-3 g per day) is recommended in all patients with heart failure.
3. Diuretics
Most of the clinical manifestations of moderate to severe heart failure caused by fluid retention leading to volume expansion and congestive symptoms. Diuretics are the only pharmacologic agent that can control the fluid retention in severe heart failure, and should be used to restore and maintain the volume status in patients with congestive symptoms (shortness of breath, orthopnea, and edema) or signs of increased filling pressure (rales, distended veins jugular, peripheral edema). Furosemide, torsemide, and bumetanide work on the loop of Henle (loop diuretics) with menginhibisi reabsorption of Na +, K +, and Cl - in the ascending to the loop of Henle; thiazide and metolazone reduces the reabsorption of Na + and Cl-in the early part of the tubule convoluted distal, and potassium-sparing diuretic such as spironolactone work on the duct koligens.
4. Vasodilator
Vasodilator indicated for acute heart failure as first-line Therapy, if hypoperfusion but adequate blood pressure and signs of congestion with little diuresis, to open the peripheral circulation and reduces pre-load. Examples of vasodilators Glyceryl trinitrate 5-mononitrat, Isosorbid dinitrat, Nitropusid, and Nesitirid.
5. ACE Inhibitors (ACEI)
There is much evidence to suggest that ACE inhibitors should be used in symptomatic and asymptomatic patients with EF (ejection fraction) decreased. ACE inhibitors affect the renin-angiotensin system with menginhibisi enzyme that contribute to the conversion of angiotensin into angiotensin II. Not only that, because the ACE inhibitor (ACEI) can also inhibit kininase II, which would cause an increase in Bradykinin, which will enhance the beneficial effect of angiotensin suppression. ACEI stabilize LV remodeling, relieve symptoms, reduce the likelihood of hospitalization, and prolong life expectancy. Because fluid retention can reduce the effects of ACEI, it is recommended to be given a diuretic before starting ACEI therapy. However, it is important to reduce the dose of diuretic during the beginning of the ACEI in order to reduce the possibility of symptomatic hypotension. ACEI should be started with low doses, followed by a gradual increase in dose if lower doses can be tolerated.
Adverse events were mostly related to the suppression of the renin angiotensin system. Decrease in blood pressure and mild azotemia may occur during therapy and usually well tolerated so that the dose does not need to be lowered. However, if hypotension or dizziness accompanied by renal dysfunction becomes more severe, it is important to reduce the dose. On the retention of potassium that do not respond to diuretics, ACE dose also needs to be reduced.
6. Angiotensin Receptor Blocker (ARB)
The drug is well tolerated in patients who can not be given ACE as coughing, skin rash, and angioedema. Although ACEI and ARBs inhibit the renin-angiotensin system, both classes of drugs work in different mechanisms. ACEI block the enzymes that play a role in converting angiotensin I into angiotensin II, ARBs block the effects of angiotensin II on the angiotensin receptor type I. Several clinical studies indicate therapeutic benefits from the addition of ARB to ACEI therapy in patients with chronic HF.
Both ACE inhibitors and ARBs have similar effects on blood pressure, kidney function, and potassium. So that the side effects of both drugs are similar.
7. β-Adrenergic Receptor Blockers
Beta blocker therapy demonstrated major advances in the treatment of patients with reduced EF. This drug affects the harmful effects of prolonged activation of adrenergic systems with competitively blocking one or more adrenergic receptors (α1, β1, and β2). Although there are three potential benefits in blocking these receptors, most of the effect of decreasing the activation of adrenergic receptors is mediated by β1. If given in conjunction with the ACEI, beta blocker inhibits LV remodeling process, relieve patient symptoms, prevent hospitalization, and prolong life expectancy. Thus the beta blocker is indicated in symptomatic or asymptomatic HF patients with decreased EF (<40%).
Side effects of beta blockers are usually associated with complications arising from the reduction in adrenergic nervous system. These reactions usually occur a few days after the initiation of therapy and usually responsive after the dose is reduced. Betabloker therapy can cause bradykardia and / or exacerbation of heart block. Thus, the beta blocker dose should be reduced if the heart rate decreased to <50> 1 receptor which can lead to vasodilatation effect.
8. Aldosterone antagonist
Although classified as a potassium-sparing diuretics, drugs that block the effects of aldosterone (spironolactone or eplerenon) has a beneficial effect independent of the effects of sodium balance. Although ACEI can decrease aldosterone secretion is transient, with long-term therapy, aldosterone levels will return to pre-ACEI therapy is performed. Therefore, administration of aldosterone antagonists is recommended in patients with NYHA class III or class IV who had a decreased EF (<35%).
The main problem is the administration of aldosterone antagonists increased risk of hyperkalemia, which is more likely to occur in patients receiving potassium supplement therapy or had previous renal insufficiency. Aldosterone antagonist is not recommended if serum creatinine> 2.5 mg / dL (or creatinine clearance <30> 5.0 mmol / L.
9. Anticoagulants and Antiplatelet
HF patients have an increased risk of incident thromboembolik. In the clinical penilitan, the incidence of stroke ranging from 1.3 to 2.4% per year. Decrease in LV function believed to result in relatively static blood in dilated cardiac chamber with an increased risk of thrombus formation. Treatment with warfarin is recommended in patients with HF, paroxysmal atrial fibrillation, or with a history of systemic or pulmonary emboli, including stroke or transient ischemic attack (TIA). Patients with symptomatic or asymptomatic ischemic kardiomyopati and have a history of MI in the presence of LV thrombus should be treated with warfarin with the onset of 3 months after MI, unless there are contraindications to its use.
Aspirin is recommended in HF patients with ischemic heart disease to avoid the occurrence of MI and death. However, low-dose aspirin (75 or 81 mg) may be selected because of the possibility of worsening HF at higher doses.
Bibliography
A. Ahlquist David A, Camilleri M. Harrison's Principles of Internal Medicine. 15th edition. Braunwald, Fauci, Kasper et all (Editor). , 2008.
2. Simadibrata K, Daldiyono. Textbook of Medicine. Aru Sudoyo W (Editor), Publisher Center UI. Jakarta, 2006.
3. The full text of internal medicine. Annual Scientific Meeting of medicine in 2007.
Diagnosis is made based on history, physical examination, and examination support.
A. Anamnesis
The clinical manifestations
Mild and moderate heart failure:
- Feelings of discomfort when lying on a flat surface in minutes.
- Systolic blood pressure to normal or high.
Severe heart failure:
- The patient must sit up straight
- Shortness of breath
- Unable to utter a complete sentence because of the difficulty felt
- Systolic blood pressure decreased LV dysfunction à because of heavy
Increased adrenergic activity leads to:
- Cyanosis of the lips and nails
- Sinus tachycardia (a nonspecific sign)
Pulse pressure may be reduced or disappear à indicates a decrease in stroke volume
Peripheral vasoconstriction causes peripheral coldness of the extremities
B. Examination: inspection of the stomach may bulge, can be found hepatomegaly palpation, percussion, and auscultation of bowel sounds are usually normal
C. Investigation:
A. Chest X-ray
Leads to cardiomegaly, LVH heart enlarged to the left, hit the apex of the diaphragm (embedded), RVH enlarged heart with the apex up to the left of the diaphragm, heart uneven waist or stand out, and there is a double image contours.
Describe pulmonary vascular Corakan kranialisasi
Kerley lines A / B
Pulmonary infiltrates second precordial
Pleural effusion
2. EKG to see the underlying disease such as myocardial infarction and arrhythmia. Left ventricular hypertrophy where S d V1 + R in V5/V6 ≥ 35 mm, arrhythmias such as atrial fibrillation where there is a distance R to R 'is not uniform.
D. Other examinations: examination of Hb, electrolytes, echocardiography for valve abnormalities, angiography, renal function, and thyroid function tests performed on indication.
Laboratory:
A. Renal physiology:
+ Urine:
- The density of <
- The volume of urine decreased
- Decreased urine Na, increased aldosterone renin
Blood +:
- U increased and creatinine clearance decreased, it showed severe heart failure.
- Na, Bl and albumin decreased, thereby increasing blood volume and edema fluid due to increased renin and aldosterone.
- Metabolic acidosis: pH decreased, HCO3 down, it indicates heart failure and kidney failure.
2. Heart physiology
Bilirubin blood, urine and increased Urobilinogen
LED off
LDH increased, especially LDH5
Alkaline phosphatase increased (mild / severe)
Protombin slightly up
Pulmonary physiology
O2 pressure drop due to impaired gas exchange, pulmonary edema
Respiratory alkalosis: pH increased, pCO2 down, then going to hyperventilation, the response to hypoxemia
Respiratory acidosis: pH decreased, pCO2 go up, they can lead to acute pulmonary edema that causes the failure of ventilation and CO2 retention.
Framingham criteria can also be used to established diagnosis of congestive heart failure, which is found to exist at least one major criterion and 2 minor criteria.
Major criteria:
Paroxysmal nocturnal dyspnea
Distended neck veins
Increased jugular venous pressure
Smooth wet Rongki not loud
Cardiomegaly
Acute pulmonary edema
S3 Gallop
Reflux hepatojugular
Minor criteria:
Extremity edema
Nighttime cough
Dyspnea d'effort
Hepatomegaly
Pleural effusion
Decrease in vital capacity 1/3 of normal
Tachycardia (> 120x/menit)
Criteria for major or minor
Weight loss> 4.5 kg in 5 days of treatment.
Management
A. Activity
Although physical activity is not recommended in severe heart failure, a mild routine exercise proved beneficial in heart failure patients with NYHA class I-III. Euvolemik patients should be encouraged to do regular isotonic exercise such as walking or riding a bicycle ergometer static, which can be tolerated. Some research on physical exercise yielded positive results with reduced symptoms, improved exercise capacity, and improve the quality and duration of life. The benefits of weight reduction in caloric intake restriction has not been known clearly
2. Diet
Low-salt diet (2-3 g per day) is recommended in all patients with heart failure.
3. Diuretics
Most of the clinical manifestations of moderate to severe heart failure caused by fluid retention leading to volume expansion and congestive symptoms. Diuretics are the only pharmacologic agent that can control the fluid retention in severe heart failure, and should be used to restore and maintain the volume status in patients with congestive symptoms (shortness of breath, orthopnea, and edema) or signs of increased filling pressure (rales, distended veins jugular, peripheral edema). Furosemide, torsemide, and bumetanide work on the loop of Henle (loop diuretics) with menginhibisi reabsorption of Na +, K +, and Cl - in the ascending to the loop of Henle; thiazide and metolazone reduces the reabsorption of Na + and Cl-in the early part of the tubule convoluted distal, and potassium-sparing diuretic such as spironolactone work on the duct koligens.
4. Vasodilator
Vasodilator indicated for acute heart failure as first-line Therapy, if hypoperfusion but adequate blood pressure and signs of congestion with little diuresis, to open the peripheral circulation and reduces pre-load. Examples of vasodilators Glyceryl trinitrate 5-mononitrat, Isosorbid dinitrat, Nitropusid, and Nesitirid.
5. ACE Inhibitors (ACEI)
There is much evidence to suggest that ACE inhibitors should be used in symptomatic and asymptomatic patients with EF (ejection fraction) decreased. ACE inhibitors affect the renin-angiotensin system with menginhibisi enzyme that contribute to the conversion of angiotensin into angiotensin II. Not only that, because the ACE inhibitor (ACEI) can also inhibit kininase II, which would cause an increase in Bradykinin, which will enhance the beneficial effect of angiotensin suppression. ACEI stabilize LV remodeling, relieve symptoms, reduce the likelihood of hospitalization, and prolong life expectancy. Because fluid retention can reduce the effects of ACEI, it is recommended to be given a diuretic before starting ACEI therapy. However, it is important to reduce the dose of diuretic during the beginning of the ACEI in order to reduce the possibility of symptomatic hypotension. ACEI should be started with low doses, followed by a gradual increase in dose if lower doses can be tolerated.
Adverse events were mostly related to the suppression of the renin angiotensin system. Decrease in blood pressure and mild azotemia may occur during therapy and usually well tolerated so that the dose does not need to be lowered. However, if hypotension or dizziness accompanied by renal dysfunction becomes more severe, it is important to reduce the dose. On the retention of potassium that do not respond to diuretics, ACE dose also needs to be reduced.
6. Angiotensin Receptor Blocker (ARB)
The drug is well tolerated in patients who can not be given ACE as coughing, skin rash, and angioedema. Although ACEI and ARBs inhibit the renin-angiotensin system, both classes of drugs work in different mechanisms. ACEI block the enzymes that play a role in converting angiotensin I into angiotensin II, ARBs block the effects of angiotensin II on the angiotensin receptor type I. Several clinical studies indicate therapeutic benefits from the addition of ARB to ACEI therapy in patients with chronic HF.
Both ACE inhibitors and ARBs have similar effects on blood pressure, kidney function, and potassium. So that the side effects of both drugs are similar.
7. β-Adrenergic Receptor Blockers
Beta blocker therapy demonstrated major advances in the treatment of patients with reduced EF. This drug affects the harmful effects of prolonged activation of adrenergic systems with competitively blocking one or more adrenergic receptors (α1, β1, and β2). Although there are three potential benefits in blocking these receptors, most of the effect of decreasing the activation of adrenergic receptors is mediated by β1. If given in conjunction with the ACEI, beta blocker inhibits LV remodeling process, relieve patient symptoms, prevent hospitalization, and prolong life expectancy. Thus the beta blocker is indicated in symptomatic or asymptomatic HF patients with decreased EF (<40%).
Side effects of beta blockers are usually associated with complications arising from the reduction in adrenergic nervous system. These reactions usually occur a few days after the initiation of therapy and usually responsive after the dose is reduced. Betabloker therapy can cause bradykardia and / or exacerbation of heart block. Thus, the beta blocker dose should be reduced if the heart rate decreased to <50> 1 receptor which can lead to vasodilatation effect.
8. Aldosterone antagonist
Although classified as a potassium-sparing diuretics, drugs that block the effects of aldosterone (spironolactone or eplerenon) has a beneficial effect independent of the effects of sodium balance. Although ACEI can decrease aldosterone secretion is transient, with long-term therapy, aldosterone levels will return to pre-ACEI therapy is performed. Therefore, administration of aldosterone antagonists is recommended in patients with NYHA class III or class IV who had a decreased EF (<35%).
The main problem is the administration of aldosterone antagonists increased risk of hyperkalemia, which is more likely to occur in patients receiving potassium supplement therapy or had previous renal insufficiency. Aldosterone antagonist is not recommended if serum creatinine> 2.5 mg / dL (or creatinine clearance <30> 5.0 mmol / L.
9. Anticoagulants and Antiplatelet
HF patients have an increased risk of incident thromboembolik. In the clinical penilitan, the incidence of stroke ranging from 1.3 to 2.4% per year. Decrease in LV function believed to result in relatively static blood in dilated cardiac chamber with an increased risk of thrombus formation. Treatment with warfarin is recommended in patients with HF, paroxysmal atrial fibrillation, or with a history of systemic or pulmonary emboli, including stroke or transient ischemic attack (TIA). Patients with symptomatic or asymptomatic ischemic kardiomyopati and have a history of MI in the presence of LV thrombus should be treated with warfarin with the onset of 3 months after MI, unless there are contraindications to its use.
Aspirin is recommended in HF patients with ischemic heart disease to avoid the occurrence of MI and death. However, low-dose aspirin (75 or 81 mg) may be selected because of the possibility of worsening HF at higher doses.
Bibliography
A. Ahlquist David A, Camilleri M. Harrison's Principles of Internal Medicine. 15th edition. Braunwald, Fauci, Kasper et all (Editor). , 2008.
2. Simadibrata K, Daldiyono. Textbook of Medicine. Aru Sudoyo W (Editor), Publisher Center UI. Jakarta, 2006.
3. The full text of internal medicine. Annual Scientific Meeting of medicine in 2007.
0 Response to "Congestive Heart Failure part II"
Post a Comment