Table 2. Typical drugs for treatment of the various types of shock.
| Drug | Indication | Main effect | Important adverse effects | Dosage |
| Blood and coagulation products | ||||
| Red cell concentrates (RCC) | Hemorrhagic shock, traumatic hemorrhagic shock, all other types of shock in patients with signs of anemic hypoxia | Replace lost red blood cells, increase blood oxygen concentration, increase blood coagulability | Hyperkalemia (check length of storage of RCC), acute transfusion reaction, sensitization in case of non-identical subgroup infection (cytomegaly, HIV, hepatitis A, B, C, E) | According to effect, need, and transfusion trigger in the individual case, 1 RCC raises Hb value by approx. 1 g/dL. In patients with massive hemorrhage: RCC:FFP:PC = 4:4:1 |
| Fresh frozen plasma (FFP) | Hemorrhagic shock, traumatic hemorrhagic shock, all other types of shock in patients with acquired coagulopathy and bleeding | Replaces coagulation factors and volume | Anaphylaxis, acute transfusion reaction, sensitization in case of non-identical subgroup infection, volume overload, TRALI, infection (cytomegaly, HIV, hepatitis A, B, C, E) | Initially 20 mL/kg, then according to effect and individual need. 1 mL/kg raises the coagulation factor(s) concerned by approx. 1%.. In patients with massive hemorrhage: RCC:FFP:PC = 4:4:1 |
| Coagulation factors (fibrinogen, PPSB = F II, VII, IX and X) | Hemorrhagic shock, traumatic hemorrhagic shock, all other types of shock in patients with acquired coagulopathy and bleeding | Selectively replace individual factors after loss/use of vitamin K inhibitor and NOAC-induced hemorrhage | Risk of thromboembolism, contraindication: HIT2 | 1 IU/kg causes the relevant factor to rise by approx. 0.5–1% |
| Platelet concentrates (PC) | Trauma and hemorrhage-induced coagulopathy with thrombocytopenia | Replaces platelets | Acute transfusion reaction, sensitization in case of non-identical subgroup infection, anaphylaxis | 1 apheresis PC raises the platelet count by approx. 20 G/dL. In patients with massive hemorrhage: RCC:FFP:PC = 4:4:1 |
| Tranexamic acid | Hemorrhagic shock, traumatic hemorrhagic shock, peripartum hemorrhage | Inhibits plasmin activation, reduces hyperfibrinolysis | Diarrhea, vomiting, nausea, allergic dermatitis; administration later than 3 h after trauma may be harmful | Early (<3 h) in patients with hemorrhage, especially when peripartum or due to trauma: 1–2 g i. v. |
| Solutions for infusion | ||||
| Isotonic balanced full electrolyte solutions | All types of shock, when cardiac preload is concomitantly reduced due to intravascular volume depletion or obstruction | Replaces fluids lost due to electrolyte imbalance or volume shift, increases stroke volume by raising cardiac preload | Volume overload, pulmonary edema, peripheral edema | Initially 10–20 mL/kg i. v. repeatedly according to effect and volume response |
| Vasoconstrictors, positive inotropic agents, and vasodilators | ||||
| Epinephrine*1,* 2 | All types of shock, when use of other catecholamines fails to achieve adequate vasoconstriction and increased inotropy: cardiopulmonary resuscitation, anaphylactic shock | α1-Receptor-mediated vasoconstrictionβ1-Receptor-mediated positive inotropia β2-Receptor-mediated bronchodilation | Myocardial ischemia, stress cardiomyopathy, tachyarythmias, oliguria/anuria | 0.3–0.6 mg i.m. (autoinjector in anaphylaxis cases), continuously according to effect and need: 0.05 to 1.0 (up to a maximum of 5.0) µg/kg per min i. v.Bolus doses: 5–10 µg i. v.; with CPR: 1 mg i. v. every 3–5 min |
| Dobutamine*2 | Cardiogenic shock, all types of shock with insufficient ventricular pump function | Predominantly β1-receptor-mediated positive inotropic effect | Rise in heart rate ≥ 30/min, rise in BP ≥ 50 mmHg, headache, cardiac arrhythmias, possible drop in BP due to β2-receptor-mediated vasodilation | Continuously according to effect and need: 2.5 to 5 (up to a maximum of 10) µg/kg per min i. v. |
| Norepinephrine*2 | All types of shock with reduced peripheral resistance | Predominantly α1-receptor-mediated vasoconstriction, (low) positive inotropic effects | Peripheral ischemia, rise in BP, reflex bradycardia, cardiac arrhythmias | Continuously according to effect and need: 0.1–1.0 µg/kg per min i. v. Bolus administration: 5–10 µg i. v. |
| Milrinone*2 | Cardiogenic shock | PDE-3 inhibitor: positive inotropic and vasodilatory effect | Drop in BP due to vasodilation, ventricular ectopic beats and tachycardia, ventricular fibrillation, headache | Continuously according to effect and need: 0.375–0.75 µg/kg per min i. v. |
| Levosimendan*2 | Cardiogenic shock | Calcium sensitizer | Drop in BP due to vasodilation, ventricular tachycardia, headache, extrasystoles, atrial fibrillation, heart failure, myocardial ischemia, dizziness, gastrointestinal disorders | Single use only: 0.05–0.2 µg/kg per min/24 h i. v. |
| Vasopressin*3 | Shock states, especially septic shock, when norepinephrine alone does not achieve the required vasoconstriction and lost volume has been replaced | V1-mediated (catecholamine-independent) vasoconstriction | Ischemia, reduced cardiac output, bradycardia, tachyarrhythmia, hyponatremia, ischemia | Continuously according to effect and need: 0.01 up to max. 0.03 U/min i. v. |
| Cafedrine hydrochloride 200 mg Theodrenaline-hydrochloride 10 mg*4 | Neurogenic shock | β1-Receptor-mediated inotropy and α1-receptor-mediated vasoconstriction Rise in BP with peripheral resistance unchanged and moderately reduced heart rate | Palpitations, symptoms of angina pectoris, cardiac arrhythmias | ¼–1 ampoule (2 mL) usually diluted with NaCL 0.9% to a total of 10 mL i. v. Maximum: 3 ampoules/24 h |
| Glyceryl trinitrate*2 | Cardiogenic shock | Vasodilation to reduce preload in particular | Development of tolerance | Continuously according to effect and need: 0.3–4 µg/kg per min i. v. |
| Sodium nitroprusside*2 | Cardiogenic shock | Vasodilation to reduce afterload | Risk of cyanide toxicity | Initially: 0.1 µg/kg per min i. v., then: double the dose every 3–5 min up to 10 µg/kg per min i. v. |
| Anti-inflammatory and antiallergic drugs | ||||
| Dimetindene maleate*1 | Anaphylaxis/ anaphylactic shock | Blocks H1-receptor-mediated action of histamine | Drowsiness, fatigue, dizziness, nausea, dry mouth | 4–8 mg over 30 s/24 h i. v. |
| Methylprednisolone*1 | Anaphylaxis/ anaphylactic shock | Synthetic glucocorticoid, potent anti-inflammatory effect | Glucocorticoid-associated adverse effects only when given long-term | 0.5–1 g/24 h i. v. |
| Hydrocortisone*5, *6 | Septic shock with persistent instability after fluid and vasopressor therapy Adrenal insufficiency | Endogenous glucocorticoid, substituted in patients with reduced or no cortisol production | See Methylprednisolone | Initially: 100 mg over 10 min then: 200–500 mg/24 h i. v. |
| Fludrocortisone*7 | Neurogenic shockSeptic shock? | Mineralocorticoid | If given long-term: edema, hypertension, hypokalemia | 0.1–0.2 mg/24 h p. o. |
Sources of dosage recommendations:
*1 Guideline for acute therapy and management of anaphylaxis. S2 guideline (31), *2 German–Austrian S3 guideline “Infarction-related cardiogenic shock—diagnosis, monitoring, and therapy” (37), *3 drug information for Empressin® February 2015, *4 drug information for Akrinor® September 2016, *5 Angus and van der Poll 2013 (24), *6 drug information for Hydrocortison® March 2018, *7 drug information for Astonin-H® June 2014.
DIC, disseminated intravascular coagulation; RCC, red cell concentrates; FFP, fresh frozen plasma; HIT2, heparin-induced thrombocytopenia type 2; i. m., intramuscular;
i. v., intravenous; PC, platelet concentrates; TRALI, transfusion-related acute lung injury; PPSB, prothrombin, proconvertin, Stuart factor, and antihemophilic B factor; CPR, cardiopulmonary resuscitation; BP, blood pressure; PDE-3, phosphodiesterase 3