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Preparations for treatment of hypertensive crisis

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  3. HYPERTONIC CRISIS (HC)
  4. Intravascular and surgical methods of AMI treatment
  5. Preparations for acidosis correction
  6. TREATMENT OF ACUTE RENAL FAILURE
  7. Treatment of ARF
  8. TREATMENT OF ARRHYTHMIAS
  9. Treatment of cardiogenic shock

 

Preparations Method of administra­tion Start of action Duration of action Notes
         
Vasodilators:
Sodium nitroprusside 50-100 mg i/v drop-by-drop 0.25-10 mg/kg per min in 5% glucose 250-500 ml Immediately 1-3 min. While administrating-AP control
Nitroglycerin 50-200 //g/min i/v drop-by-drop 2-5 min. 3-5 min. Particularly effective in acute cardiac failure, myocardial infarction.
           
           
           
Nicardipine hydrochloride 5-15 mg/h drop-by-drop 5-10 min 1-4 h. Do not apply in patients with cardiac insufficiency, in patientswith IHD — with caution.  
Verapimil I/v 5-10 mg, it may be conti­nued drop-by-drop 3-25,«g/h 1-5 min. 10-30 min. It is contraindicated in cardiac insufficiency and for persons taking /^-blockers  
Hydralazine I/v as a bolus 20 mg per 20 ml physiologic solution, i/v drop-by-drop 0.5 mg/min. or i/m 10-15 mg 10-20 min. 2-6 hrs. Primarily in eclampsia. Administration may be repeated in 2-6 hours.  
Enalprilate I/v 1.25-5 mg 15-30 min. 6 hrs. It is effective in acute left ventricular failure  
Nimodipine I/v - drop-by-drop 15 mg/ kg/h 10-20 min. 2-4 hrs. In subarachnoidal hemorrhages  
Antiadrenergic preparations:  
Labetalol I/v as a bolus 20-80 mg at the rate of 2 mg/min or i/v drop-by-drop 50-300 mg. 5-6 min. 4-8 hrs. Do not apply in patients with cardiac insufficiency  
Propranolol I/v 2-5 mg drop-by-drop at the rate of 0.1 mg/min. 10-20 min. 2-4 hrs. Primarily in dissecting aortic aneurysm and coronary syndrome  
Esmolol I/v 250-500,wg/kg per min. drop-by-drop, then 50-100 1-2 min. 10-20 min. It is the preparation of choice in dissecting aortic aneurysm and after operational hypertension  
Trimethafan I/v 1-4 mg/min drop-by-drop (1 ml per 250 ml 5% glucose or physiologic solution) Immediately 1-3 min. In crises with edema of the lungs, brain, dissecting aortic aneurysm  
                   

 

         
Clonidine I/v 0.5-1 ml 0.01% i/m 0.5-2.0 ml 5-15 min. 2-6 hrs. It is undesirable in cerebral insult
Pentamin I/v 0.2-0.75 ml - titrated administration, i/m 0.3-1.0 ml 5% solution 5-15 min. 2-4 hrs. It causes orthostatic hypertension, it is undesirable for patients of elderly age
Phentol-aminum I/v or i/m 5-15 mg 1-2 min. 3-10 min. Pheochromocytoma, syndrome of clop-helinum cancellation
Other preparations:
Furosemid (lasix) I/v as a bolus 200 mg 5-30 min. 6-8 hrs. In HC with acute cardiac or renal failure
Magnesium sulfate I/v 25% -5-20 ml 30-40 min. 3-4 hrs. In convulsions, eclampsia of pregnancy.

In case of impossibility to carry out immediate intravenous administration of preparations one may use some nitrates sublingually, nifedipin, clonidine, captopril, blockers or intramuscularly clophelinum, phentolaminum or dibazolum. The preference is given to sodium nitroprusside, nitroglycerine and trimethaphan.

The optimal is the decrease of AP by 25% from the initial level. A lower decrease of AP may cause a decrease of the cerebral blood flow, up to coma development, angina pectoris, myocardial infarction, particularly in elderly persons with pronounced atherosclerosis.

In uncomplicated HC they apply clonidine (contraindicated in persons receiving cardiac glycosides, with disturbance of cardiac conduction), nifedipin, captopril — inhibitor of angiotensin-converting enzyme (ACE), as well as dibazolum i/m, pyroxanum, droperidol.

ACUTE MYOCARDIAL INFARCTION (AMI)

Acute myocardial infarction is the main cause of death of those suffering from IHD. Studies of AMI pathogenesis have shown that in 90% of patients an obstructive thrombus is formed at the place of rupture of atherosclerotic plaque of coronary artery that quickly leads to a reduction of the coronary artery lumen. This leads to a change of laminar blood flow in the vessel that becomes turbulent. The turbulence of blood flow contributes to adhesion, thrombocyte aggregation and thromboplastin activation the latter triggers a process of thrombogenesis. Under the influence of thromboplastin prothrombin is converted into thrombin that, in its turn, transforms a soluble fibrinogen into insoluble fibrin (Fig. 41).

 



Organized thrombus consists of fibrin and formed elements of blood that get into the cells of fibrinous network. Different factors and proenzymes of fibrinolytic system may form a part of thrombus composition. When a thrombus arises the endogenic fibrinolytic system is activated the basic physiologic role of which is in lysis of thrombi. Endogenic fibrinolytic system consists of the inactive proenzyme — plasminogen that can be converted into the active form — plasmin by means of different plasminogen activators (tissue plasminogen activator, plasminogen activator of urokinase type). Plasmin is the powerful proteolytic enzyme splitting the basic thrombus substrate — fibrin into small soluble fragments (products of fibrin degradation) contributing to vascular recanalization. Besides, plasmin is able to split fibrinogen and other hemostatic plasma proteins.

Natural inhibitors of fibrinolytic system are:

— at the level of plasminogen activators — plasminogen activator inhibitor (PAI-1);

— at the level of plasmin — a2 antiplasmin (a2 PI) preventing a generalized fibrinolysis (Fig. 42).

Endogenic fibrinolysis is often insufficient and the application of exogenic thrombolytic agents is required for a thrombus lysis.

Application of exogenic plasminogen activators is based on the transformation of inactively circulating and bound with thrombus plasminogen into active plasmin.

When endogenic and exogenic thrombolysis joins in the process, lysis occurs both inside and outside a thrombus.

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