A) Link to patient details:
1.What is the difference btw heart failure with preserved ejection fraction and with reduced ejection fraction?
ANS: The amount of blood pumped out of the heart with each beat is called the ejection fraction (EF). A normal EF is usually around 55 to 70 percent, but it can be lessened in some forms of heart failure.-People with heart failure with reduced ejection fraction (HFrEF) have an EF that is 40 to 50 percent or lower. This is also called systolic heart failure. People with heart failure with preserved ejection fraction (HFpEF) do not have much of a change in their ejection fraction. This is often called diastolic heart failure.
-HFrEF were often diagnosed earlier in life and right after a heart attack.
HFpEF were diagnosed later in life and first experienced symptoms of heart failure between the ages of 65 and 69. Many of those with HFpEF also shared that they have other health problems that led to their diagnosis. Many of them also live with additional health conditions, including acid reflux (GERD), high blood pressure, kidney disease, and sleep disorders.
-HFrEF shared that they feel depressed and/or anxious about their heart failure diagnosis. Risk factors for those in this group include genetics or a family history of heart failure.
HFpEF shared that they are still able to do the things they enjoyed before their heart failure diagnosis.risk factors, including:
Sedentary lifestyle
High blood pressure
Sleep apnea
Other heart conditions
-HFrEF are more likely to have had surgery, including surgery to implant a pacemaker or other heart rhythm control device.HFrEF shared that they currently use a combination therapy to treat their heart failure.
HFpEF have never had surgery to treat their heart failure or had a device implanted.
-HFrEF are men who live in rural areas.
However, most respondents with HFpEF are women who live in urban areas.
2.Why haven't we done pericardiocenetis in this pateint?
ANS;
Pericardiocentesis is done when the pericardial effusion is not resolving on its own . Here the pericardial fluid which has accumulated was resolving on its own , at the time of admission it was 2.4mm and when discharged it was 1.9 mm . Therefore we did not do pericardiocentesis in this pt.
3.What are the risk factors for development of heart failure in the patient?
ANS: IN THIS PATIENT:
NON MODIFICABLE:
age
gender
MODIFIABLE:
hypertension
smoking
type 2 diabetes .
kidney disease.
4.What could be the cause for hypotension in this patient?
ANS:
The pt. was anemic with Hb of 8gm/dl . One of the severe complication of anemia is tissue hypoxia which further lead to hypotension. B) Link to patient details
1.What are the possible causes for heart failure in this patient?
ANS:
Obesity
alcohol
diabetes
hypertension
2.what is the reason for anemia in this case?
ANS: Alcoholics frequently have defective red blood cells that are destroyed prematurely, possibly resulting in anemia. Alcohol also interferes with the production and function of white blood cells, especially those that defend the body against invading bacteria. Consequently, alcoholics frequently suffer from bacterial infections.
3.What is the reason for blebs and non healing ulcer in the legs of this patient?
ANS:
The pt. had recurrent blebs and ulcer on lower limbs (foot). This is due to Type to diabetes mellitus.
Diabetic foot ulcers generally arise as a result of poor circulation in the foot region. While high blood sugar levels and nerve damage or even wounds in the feet may result in foot ulcers in many cases.
In cases of poor circulation of blood, the foot ulcers take quite a bit of time to heal as the blood efficiency in the foot region is at a low level. Furthermore, many develop a bit of reduced sensation on the feet as a result of nerve damage or more.
There are many risk factors that may lead to foot ulcers at the end.
Poor quality or fitting of the footwear.
Unhygienic appearance of foot.
Improper care of the nails of the toe.
Heavy intake of alcohols and tobacco.
Obesity and Weight-related
Complication arising from Diabetes like eye problems, kidney problems and more.
Although aging or old age can also be counted among them.
4. What sequence of stages of diabetes has been noted in this patient?
ANS: alcohol------obesity------impaired glucose tolerance------diabetes mellitus------microvascular complications like triopathy and diabetic foot ulcer-------macrovascular complications like coronary artery disease , coronary vascular disease and peripheral vascular disease. 1Q) what is the evolution of the symptomatology in this patient interms of an event timeline and where is the anatomical localisation for the problem and what is the primary etiology of the patient problem ?
C) Link to patient details:
https://preityarlagadda.blogspot.com/2021/05/biatrial-thrombus-in-52yr-old-male.html
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans:Patient was apparently asymptomatic 2 days ago when he developed Shortness of breath Grade II (on exertion) which progressed to Grade IV (at rest) for which he visited local RMP and was referred to our hospital.Patient also complains of decreased urine output since 2 days and Anuria since morning.
Anatomical localization is heart
Primary etiology is atrial fibrillation
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans; 1) INJ. Dobutamine 3.6ml/hr was given to maintain the falling BP up to a MAP of 55 mmHg.
Mechanism of action: Dobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the ß receptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects. It does not cause the release of endogenous norepinephrine, as does dopamine
.2) TAB. Digoxin 0.25mg OD 5/7 and INJ. Unfractionated Heparin 5000 IU TID.
Mechanism of action: Digoxin has two principal mechanisms of action which are selectively employed depending on the indication: Positive Ionotropic: It increases the force of contraction of the heart by reversibly inhibiting the activity of the myocardial Na-K ATPase pump, an enzyme that controls the movement of ions into the heart
3[INJ. Unfractionated Heparin Infusion @5ml/hr
Mechanism of action: It produces its major anticoagulant effect by inactivating thrombin and activated factor X (factor Xa) through an antithrombin (AT)-dependent mechanism. ... By inactivating thrombin, heparin not only prevents fibrin formation but also inhibits thrombin-induced activation of platelets and of factors V and VIII.Other medications used during the course in hospital -
1. TAB. Cardivas3.125mg PO/BD
2. TAB. Dytor 10mg PO/OD
3. TAB Pan D 40mg PO/OD
4. TAB. Taxim 200mg PO/OD
5. INJ. Thiamine 100mg in 50ml NS IV/TID
6. INJ. HAI S.C 8U-8U-6U
3) What is the pathogenesis of renal involvement due to heart failure (cardio renal syndrome)? Which type of cardio renal syndrome is this patient?
Ans; The pathophysiology of CRS can be attributed to two broad categories of "hemodynamic factors" such as low cardiac output, elevation of both intra-abdominal and central venous pressures, and non-hemodynamic factors or "cardiorenal connectors" such as neurohormonal and inflammatory activation.[5] It was previously believed that low cardiac output in heart failure patients result in decreased blood flow to the kidneys which can lead to progressive deterioration of kidney function. As a result, diuresis of these patients will result in hypovolemia and pre-renal azotemia.
In addition, CRS has been observed in patients with diastolic dysfunction who have normal left ventricular systolic function.[3]Therefore, there must be additional mechanisms involved in the progression of CRS. Elevated intra-abdominal pressures resulting from ascites and abdominal wall edema may be associated with worsening kidney functions in heart failure patients. Several studies have shown that as a result of this increased intra-abdominal pressure there is increased central venous pressure and congestion of the kidneys' veins, which can lead to worsening kidney function.[3]
In addition, many neurohormonal and inflammatory agents are implicated in the progression of CRS. These include increased formation of reactive oxygen species, endothelin, arginine vasopressin, and excessive sympathetic activity which can result in myocardial hypertrophy and necrosis.
Other cardiorenal connectors include renin-angiotensin-system activation, nitric oxide/reactive oxygen species imbalance, inflammatory factors and abnormal activation of the sympathetic nervous system, which can cause structural and functional abnormalities in both heart and/or the kidney. There is a close interaction within these cardiorenal connectors as well as between these factors and the hemodynamic factors which makes the study of CRS pathophysiology complicated.
4) What are the risk factors for atherosclerosis in this patien
Ans; High cholesterol and triglyceride levels.
High blood pressure.
Smoking.
Type 1 diabetes.
Obesity.
Physical inactivity.
High saturated fat diet.t?
5) Why was the patient asked to get those APTT, INR tests for review?
Ans; Standard coagulation screening tests such as activated partial thromboplastin time (APTT), prothrombin time (PT), and the international normalized ratio (INR) are important constituents of basic examinations in clinical laboratories. APTT can be used as an indicator of intrinsic coagulation pathway activity, and a short APTT is linked to increased thrombin generation and increased risk for thrombosis.
D) Link to patient details: https://daddalavineeshachowdary.blogspot.com/2021/05/67-year-old-patient-with-acute-coronary.html?m=1
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
TIMELINE OF EVENTS-
• Diabetes since 12 years - on medication
• Heart burn like episodes since an year- relieved without medication
• Diagnosed with pulmonary TB 7 months ago- completed full course of treatment, presently sputum negative.
• Hypertension since 6 months - on medication
• Patient presented with Shortness of Breath
Anatomical localisation - Cardiovascular system
Etiology: The patient is both Hypertensive and diabetic and these may result in the development of atherosclerosis.
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Pharmacological interventions:
TAB MET XL 25 MG/STAT-contains Metoprolol as active ingredient
MOA: METOPROLOL is a cardiselective beta blocker
Beta blockers work by blocking the effects of the hormone epinephrine. Beta blockers have a negative chronotropic effect
and negative inotropic effect.
Beta blockers also have antiarrhythmic effects and also anti ischemic effects. They also inhibit renin.
EFFICACY STUDIES.
In CAD, 12 meta-analyses (93 RCTs, 103,481 patients) showed that beta-blockers reduced mortality in analyses before routine reperfusion, but there was a lack of benefit in contemporary studies where ≥ 50% of patients received thrombolytics or intervention.
Non pharmacological intervention advised to this patient is: PERCUTANEOUS CORONARY INTERVENTION.
Percutaneous Coronary Intervention is a non-surgical procedure that uses a catheter (a thin flexible tube) to place a small structure called a stent to open up blood vessels in the heart that have been narrowed by plaque buildup ( atherosclerosis).
3) What are the indications and contraindications for PCI?
INDICATIONS and CONTRAINDICATIONS:
4) What happens if a PCI is performed in a patient who does not need it? What are the harms of overtreatment and why is research on overtesting and overtreatment important to current healthcare systems?
Although PCI is generally a safe procedure , it might cause serious certain complications like
A)Bleeding
B) Blood vessel damage
C) Allergic reaction to the contrast dye used
D) Arrhythmias
E) Need for emergency coronary artery bypass grafting .
⁃ OVER TESTING AND OVER TREATMENT :
In olden days doctors would so much depend on their intuition as technology was not available .But these days every physician is dependent on laboratory reports.We cannot say it is a bad thing as it would lead to accurate diagnosis, but the point is these should be used logically only where they are required.Or else it would lead to overtesting.And overtesting has its own adverse effects.For example during the recent 2nd wave of Covid Pandemic majority of the Covid Patients including the asymptomatic and patients with mild disease were advised to take CT Scan which lead to unwanted radiation exposure.Even overtreatment has its own adverse effects.So even though all the Therapeutic and Diagnostic Facilities are available at our disposal , Physicians should use them Judiciously or Else they will do more harm than good. E) Link to patient details:
https://bhavaniv.blogspot.com/2021/05/case-discussion-on-myocardial-infarction.html?m=1
Questions:
1) What is the evolution of the symptomatology in this patient in terms of an event timeline and where is the anatomical localization for the problem and what is the primary etiology of the patient's problem?
Ans;Evolution of symptomatology:
Uncontrolled DM2 since 8 years
3 days back Mild chest pain dragging type and retrosternal pain(radiated)
Anatomical localisation: Inferior wall of heart
Primary etiology: Diabetes type 2 (uncontrolled)
high blood glucose from diabetes can damage your blood vessels and the nerves that control your heart and blood vessels
2) What are mechanism of action, indication and efficacy over placebo of each of the pharmacological and non pharmacological interventions used for this patient?
Ans;TAB. ASPIRIN 325 mg PO/STAT
Mechanism of action: The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins.
TAB ATORVAS 80mg PO/STAT
Mechanism of action: Atorvastatin competitively inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. By preventing the conversion of HMG-CoA to mevalonate, statin medications decrease cholesterol production in the liver.
TAB CLOPIBB 300mg PO/STAT
Mechanism of action: The active metabolite of clopidogrelselectively inhibits the binding of adenosine diphosphate (ADP) to its platelet P2Y12 receptor and the subsequent ADP- mediated activation of the glycoprotein GPIIb/IIIa complex, thereby inhibiting platelet aggregation. This action is irreversible.
INJ HAI 6U/IV STAT
VITAL MONITORING.
3) Did the secondary PTCA do any good to the patient or was it unnecessary?
Ans; Repeat PTCA provides a valuable, safe and cost-effective way of management for recurrence of stenosis after initially successful angioplasty. It increased the percent of patients with documented long-term success of angioplasty
Over testing and over treatment can raise a person’s risk of cardiovascular death by as much as four times.
F) Link to patient details:
1. How did the patient get relieved from his shortness of breath after i.v fluids administration by rural medical practitioner?
Because of the fluid lossoccured to the patient
There is
Decreased preload → SOB occured due to decreased cardiac output
IV fluids administered → there is increase in preload → SOB decreased due to better cardiac output
2. What is the rationale of using torsemide in this patient?
Torsemide is used due to abdominal distension
3. Was the rationale for administration of ceftriaxone? Was it prophylactic or for the treatment of UTI?
Treatment for UTI
Rationale - used for any bacterial infection .
