Lets imagine, that during Medicine ward posting, attending Medicine OPD, you note that a patient comes to the Physician with his medical test reports which were previously prescribed by the Physician, while writing the prescription to the patient the physician tells you to observe the findings in that patient…

You notice that patient is a male, nearly 60 year old, overweight, having dyspnoea, you also notice peripheral edema, with basal crepitation’s (Congratulations, you know how to use your stethoscope) and tender hepatomegaly…..

You also observe that in his medical report he is carrying Chest X Ray, ECG, ABG and Echocardiography with routine blood tests (well good, you are attentive too).

you submit your findings and Physician tells you that it was a case of Acute Congestive Heart Failure and he also tells you that the patient has been admitted in hospital and prescribed with Inj. Furosemide 80 mg IV stat repeated after 3 hours with other medications.

Now watching you, straight into your eyes and with a smile on face, he asks you ” Why Furosemide is given to this patient”?

can you tell the answer…. if you are thinking about the “diuretic action of furosemide“, yes its partial correct answer but it cannot describe the dramatic quick response seen in congestive heart failure patients especially Left ventricular heart patients…..to know the answer ..lets dive deeper……

High ceiling diuretics (Furosemide,bumetenide) are used for mobilizing edema fluid (as this a condition of heart failure….heart is fail in doing its normal work and there is accumulation of fluid in the lungs and the peripheral organs leading to congestive symptoms)

As we know that IV furosemide is given in the congestive heart failure and it quickly relives the congestive symptoms even before its diuretic action, the reason is…….. furosemide increases the prostaglandin formation and cause systemic venodilation and the fluid present in the pulmonary circulation now shifts to the systemic circulation, this provide a quick relief from the dyspnoea and patient feels better, later on the diuretic action of furosemide starts (yes, you were right too) and the excessive fluid from the body is execrated providing further symptomatic relief.

So, for the early quick response, credit goes to the Prostaglandin releasing effect of furosemide which cause venodilation…….

Some Interesting facts related to this topic–

1. This type of symptomatic relief can be achieved by use of Morphine also https://pharmacology.life/2021/08/20/use-of-morphine-in-acute-left-ventricular-failure/
2. After prolonged use resistance may develop to the high ceiling diuretics and to overcome this resistance we add spironolactone.

Use of furosemide/ Morphine provide only symptomatic relief, ACE inhibitors or ARB,s are given concurrently to retard the progression of disease and to decrease mortality (along with other drugs as per the stage of CHF).

Q. In Acute left ventricular failure Morphine is used by intravenous route and it provides nearly dramatic relief why?

Explanation- As Morphine has vasodilatory action (Due to histamine release and depression of vasomotor center)…….it reduces preload of blood, and there is shifting of blood from pulmonary site to systemic circuits (due to greater vasodilation in the systemic blood vessels) which ultimately relives pulmonary congestion and edema

Morphine acts also by its calming effects and thus decreasing the sympathetic stimulation and finally it reduces the cardiac work.

Morphine is used specifically in acute left heart failure…..as it only helps to shift blood from lungs to systemic circuit

Hope you understand the concept…….Happy learning

A male name Ramesh,42 years, bank clerk, was bought in Community Health Center emergency department at 9:00 pm with complaints of chest pain from evening, which was radiating to the left shoulder, vomiting, sweating, shortness of breath were also present.

On examination he seems pale and fearful, his BP was 110/70 mm hg, ECG shows typical ST elevation and cardiac marker (Troponin-T) is also increased.

Q. If you were in place of that doctor, how will you manage this patient before referring him to higher center?

So, in this hypothetical scenario, the patient is suffering from ST segment elevated MI (STEMI), we can save this patient by –

a) Reliving pain and apprehension

b) Preventing further damage produced by the infarct and also reduce the infarct size

c) Preventing complications and further attack

So we give…………….

1. Morphine 10 mg, Intravenous route – you can administer IM also, because time is the key here. it act by reliving pain, and by decreasing preload and afterload. Sometime, if morphine is not available then we use Diazepam IV to reduce anxiety, but morphine is preferred (as morphine control apprehension, has positive effect by decreasing preload and afterload, and also excellent pain control)
2. Glyceryltrinitrate (GTN) 0.5 mg sublingual is administered quickly and repeat after five minutes, upto three doses if needed (Monitor BP, as patient can go into hypotension as in this case, start the IV infusion of saline/dextrose to maintain blood volume, but take care of volume overload also)
3. Streptokinase 1.5 million units infusion given over 1 hour. As we know that it is thrombolytic agent which is antigenic in nature (because it is obtained from beta hemolytic streptococci), so it can produce allergic reactions, but still used at primary and secondary referral units (irrespective availability of better, non antigenic thrombolytic agents like Alteplase), because of its low cost (Streptokinase costs nearly 2,000 INR compared to alteplase which costs nearly 40,000 INR). Note- contraindications of the thrombolytic therapy are – recent history of surgery, stroke, bleeding disorders etc.
4. Aspirin 300 mg orally , to be given immediately. It is an antiplatelet drug and can reduce mortality and should be continued even after recovery.
5. Metoprolol (first IV then orally), if given at early stage can reduce the infarct size and possible consequences and has effect of reducing arrhythmias and mortality (if no contraindications eg. Asthma)
6. ACE inhibitor – Enalapril 5 mg two times a day orally, to be given as early as patient is stable hemodynamically (do not give in hypotensive patient), they afford survival benefit in long term by reducing progression of heart failure and preventing cardiac remodelling.

Now a days Primary Percutaneous coronary intervention (PCI) with stenting/ coronary angioplasty is preferred in place of fibrinolytic agents, but availability of Infrastructure and Clinician are major issues especially at primary and secondary level

Hope you enjoyed the topic…………. Happy learning

Five Points you Must know (about ACE inhibitors) –

1. These are the First Line Antihypertensive drugs in all Grades of Hypertension. As the name suggest, they inhibit the Angiotensin converting Enzyme in Renin Angiotensin Aldosterone System (RAAS). This RAAS physiologically regulates the electrolyte balance and plasma volume of body.
2. Captopril, Enalapril, Lisinopril, Perindopril, Fosinopril, Ramipril, Benazepril are example of ACE inhibitors.
3. All ACE inhibitors are Prodrugs (Except Captopril and Lisinopril).
4. ACE inhibitors are used in – (a) Hypertension– first line drugs in all grades of Hypertension (b) Congestive cardiac failure -Standard therapy for all grades of CHF, as they provide symptomatic improvement, decreased mortality as well as Hospitalization (c) Myocardial infarction – When given within 24 hours of an attack and then continued, then they reduce early and long term mortality (d) Diabetic nephropathy – long term therapy is proven useful in preventing progression of renal disease as well as proteinuria in diabetic patients. (e) Chronic renal failure– delays the progression of failure. (f) scleroderma renal crisis– it is an medical emergency in rheumatology, presented as acute onset renal failure with marked hypertension and ACE inhibitors have life saving effect in this condition (as this crisis is mediated by Angiotensin II)
5. Major side effects are– (a) Cough -Due to increased level of bradykinin, often discontinuation of the drug is needed and Angiotensin -II receptor antagonist like Telmisartan can be used in place of ACE inhibitors (b) Hypotension (c) Hyperkaliemia – cautious use with other drugs which increase K+ like NSAIDs (d) Teratogenicity – ACE inhibitors are contraindicated in pregnancy. Fetal growth retardation and hypoplasia of organs and fetal death can occur especially if given during second or third trimester of pregnancy. (e) Renal artery stenosis patients– ACE inhibitors can precipitate acute renal failure ion patients with renal artery stenosis hence contraindicated in same.

So lets recall once again, ACE Inhibitors like enalapril are first line drugs in hypertension, they are contraindicated in pregnancy and dry cough is their common side effect.

Hope this will help you to remember the concept easily…………………… Have a great day

Five Must Know points about Statins-

(1) HMG- COA reductase inhibitors AKA Statins are Most commonly used hypolipidemic drugs.( As they are best tolerated and most efficacious among hypolipidemic drugs)

They act by Inhibiting enzyme HMG COA reductase, this enzyme is important in cholesterol synthesis, as it inhibit conversion of HMG-COA into mevalonate which is rate limiting step during cholesterol synthesis.

(2) Lovastatin, Simvastatin, Atorvastatin, Rosuvastatin, Pravastatin, Pitavastatin are the examples of statins.

Statins are usually given at bedtime as HMG COA reductase activity (cholesterol synthesis) is maximum at midnight.

Atorvastatin and Rosuvastatin are longer acting statins (t1/2 nearly 16 and 20 hours respectively) they can be given anytime for treatment of hyperlipidemia.

(3) Cholesterol is needed by our body for bile acid and steroid hormones synthesis.

After taking statins, the cholesterol synthesis is decreased, and liver respond to this situation by increasing the uptake of LDL from plasma (LDL is low density lipoprotein contains only cholesteryl esters)

So, statins reduce the LDL and cholesterol levels significantly, they also reduce Triglyceride and VLDL slightly and there is slight increase in the HDL (good cholesterol).

(4) Mostly statins are taken orally, their main adverse effects are myopathy and hepatotoxicity.

That’s why concurrent use of any other drugs causes myopathy (like Fibrates, niacin, amiodarone and verapamil etc.) or hepatotoxic drugs/ Alcohol should be avoided.

Other side effects are GI disturbances, allergic reactions, rhabdomyolysis.

(5) So, if we talk about the uses of statins-

• The statins are the first choice drugs for the patients with raised LDL levels and total Cholesterol levels (First line drugs for the familial and secondary hyperlipidemias).

• They also produce multiple other beneficial effects (Pleotropic effects).

They reduce the platelet aggregation, reduce inflammation, decrease arterial smooth muscle proliferation etc. due to their antioxidant property.

As a result they are useful in lowering mortality and morbidity in patients of coronary heart disease (especially in all type of atherosclerotic cardiovascular diseases).

• They are commonly used in patients with Myocardial infarction (afford secondary prophylaxis), thrombotic stroke, peripheral arterial disease, new onset angina etc.

In brief –

Atorvastatin is commonly used hypolipidemic drug with additional antioxidant properties, can cause myopathy and hepatotoxicity.

Hope this post will make you understand the concept more easily…………………..Happy learning ……