Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
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This document discusses direct jaundice and neonatal cholestasis. It begins by defining direct jaundice and noting that it indicates cholestasis and hepatobiliary dysfunction. The causes of neonatal cholestasis are then outlined, including extrahepatic (e.g. biliary atresia), intrahepatic (e.g. PFIC), and hepatocellular disorders (e.g. metabolic and infections). The diagnostic evaluation, management, and specific conditions like biliary atresia and choledochal cyst are then reviewed over multiple sections.
1. This patient presented with periodic paralysis caused by both hyperthyroidism (thyrotoxic periodic paralysis) and renal tubular acidosis. The hyperthyroidism prevented symptoms from manifesting until after delivery when potassium levels dropped further.
2. The initial nerve conduction study showed demyelination likely due to the previous episode being treated as a demyelinating disease.
3. Going forward, the patient will need long-term management of their hyperthyroidism, renal tubular acidosis, and further evaluation for Sjogren's syndrome. Potassium and bicarbonate supplementation as well as thyroid medication will be required.
Cerebral salt-wasting syndrome is characterized by hyponatremia and extracellular fluid depletion due to impaired sodium reabsorption in the kidney caused by brain injury or disease. It mimics the lab findings of SIADH but can be distinguished by clinical signs of volume depletion. Treatment involves correcting the volume depletion with intravenous saline and sodium replacement, along with mineralocorticoid therapy when needed. The condition usually resolves within a few weeks but accurate diagnosis is important since management differs from SIADH.
This document provides an approach to evaluating a case of quadriparesis (weakness of all four limbs). It discusses obtaining a detailed history regarding onset and progression of weakness, risk factors, and family history. A neurological examination including assessment of upper and lower motor neuron signs is recommended. Various etiologies are considered depending on examination findings such as compressive vs. non-compressive myelopathy, motor neuron disease, subacute combined degeneration, anterior spinal artery syndrome, and myasthenia gravis. Differential diagnoses are formulated based on characteristics such as sensory involvement, reflex changes, symmetry of weakness, and associated symptoms.
This document provides guidance on evaluating and managing patients presenting with chest pain. It outlines the general approach which includes ensuring patient stability, providing oxygen and analgesia. It describes performing a focused history and physical exam, as well as relevant investigations. It discusses life-threatening causes of chest pain including acute coronary syndrome, cardiac tamponade, pulmonary embolism, tension pneumothorax, and aortic dissection. For each condition, it details symptoms, signs, diagnostic tests, and general treatment approaches.
Shock is characterized by reduced systemic tissue perfusion and oxygen delivery, creating an imbalance between oxygen delivery and consumption. Prolonged oxygen deprivation can lead to cellular hypoxia and biochemical derangements. There are several types of shock including hypovolemic, cardiogenic, septic, neurogenic, and hypoadrenal shock. Mean arterial pressure depends on cardiac output and systemic vascular resistance. Parameters like lactate, blood pressure, heart rate, respiratory rate, urine output are used to classify shock into compensated, decompensated, and irreversible stages. Treatment involves identifying and treating the underlying cause while aggressively resuscitating with fluids and vasopressors.
The document provides an overview of liver anatomy and functions, clinical features of liver disease, causes of jaundice, signs of alcohol-related liver damage, common tests used to evaluate liver function, and investigations for liver disease. Key points include that the liver performs important roles in metabolism, detoxification, and protein and hormone synthesis. Clinical features can vary depending on the type of liver disease and include fatigue, jaundice, abdominal pain, and bleeding issues. Biochemical tests and imaging help diagnose and characterize liver injury.
This document discusses direct jaundice and neonatal cholestasis. It begins by defining direct jaundice and noting that it indicates cholestasis and hepatobiliary dysfunction. The causes of neonatal cholestasis are then outlined, including extrahepatic (e.g. biliary atresia), intrahepatic (e.g. PFIC), and hepatocellular disorders (e.g. metabolic and infections). The diagnostic evaluation, management, and specific conditions like biliary atresia and choledochal cyst are then reviewed over multiple sections.
1. This patient presented with periodic paralysis caused by both hyperthyroidism (thyrotoxic periodic paralysis) and renal tubular acidosis. The hyperthyroidism prevented symptoms from manifesting until after delivery when potassium levels dropped further.
2. The initial nerve conduction study showed demyelination likely due to the previous episode being treated as a demyelinating disease.
3. Going forward, the patient will need long-term management of their hyperthyroidism, renal tubular acidosis, and further evaluation for Sjogren's syndrome. Potassium and bicarbonate supplementation as well as thyroid medication will be required.
Cerebral salt-wasting syndrome is characterized by hyponatremia and extracellular fluid depletion due to impaired sodium reabsorption in the kidney caused by brain injury or disease. It mimics the lab findings of SIADH but can be distinguished by clinical signs of volume depletion. Treatment involves correcting the volume depletion with intravenous saline and sodium replacement, along with mineralocorticoid therapy when needed. The condition usually resolves within a few weeks but accurate diagnosis is important since management differs from SIADH.
This document provides an approach to evaluating a case of quadriparesis (weakness of all four limbs). It discusses obtaining a detailed history regarding onset and progression of weakness, risk factors, and family history. A neurological examination including assessment of upper and lower motor neuron signs is recommended. Various etiologies are considered depending on examination findings such as compressive vs. non-compressive myelopathy, motor neuron disease, subacute combined degeneration, anterior spinal artery syndrome, and myasthenia gravis. Differential diagnoses are formulated based on characteristics such as sensory involvement, reflex changes, symmetry of weakness, and associated symptoms.
This document provides guidance on evaluating and managing patients presenting with chest pain. It outlines the general approach which includes ensuring patient stability, providing oxygen and analgesia. It describes performing a focused history and physical exam, as well as relevant investigations. It discusses life-threatening causes of chest pain including acute coronary syndrome, cardiac tamponade, pulmonary embolism, tension pneumothorax, and aortic dissection. For each condition, it details symptoms, signs, diagnostic tests, and general treatment approaches.
Shock is characterized by reduced systemic tissue perfusion and oxygen delivery, creating an imbalance between oxygen delivery and consumption. Prolonged oxygen deprivation can lead to cellular hypoxia and biochemical derangements. There are several types of shock including hypovolemic, cardiogenic, septic, neurogenic, and hypoadrenal shock. Mean arterial pressure depends on cardiac output and systemic vascular resistance. Parameters like lactate, blood pressure, heart rate, respiratory rate, urine output are used to classify shock into compensated, decompensated, and irreversible stages. Treatment involves identifying and treating the underlying cause while aggressively resuscitating with fluids and vasopressors.
The document provides an overview of liver anatomy and functions, clinical features of liver disease, causes of jaundice, signs of alcohol-related liver damage, common tests used to evaluate liver function, and investigations for liver disease. Key points include that the liver performs important roles in metabolism, detoxification, and protein and hormone synthesis. Clinical features can vary depending on the type of liver disease and include fatigue, jaundice, abdominal pain, and bleeding issues. Biochemical tests and imaging help diagnose and characterize liver injury.
This document provides information on the clinical and pathological approach to jaundice. It defines jaundice as a yellowish discoloration of the skin and mucous membranes due to increased bilirubin levels in the blood. Jaundice is categorized as pre-hepatic, hepatic, or post-hepatic. Pre-hepatic causes include various hemolytic anemias. Hepatic causes include physiologic jaundice of newborns and hepatitis. Post-hepatic causes involve issues with the bile ducts. The document outlines clues for diagnosing different types of jaundice and discusses evaluation and management of neonatal jaundice.
This document provides guidance on evaluating patients presenting with paraplegia. It outlines the key components of the clinical history and neurological examination needed to determine the cause and level of spinal cord injury. The history should ascertain details of onset and any associated symptoms. The exam focuses on assessing sensory and motor function at different dermatomal and myotomal levels to localize the lesion. Together this information can indicate if the injury is acute, subacute, or chronic, and identify potential etiologies like trauma, infection, inflammation, compression, or vascular causes. The goal is to arrive at a diagnosis and localization of injury within the spinal cord or vertebrae.
This document discusses potassium management and provides key details about hypokalemia and hyperkalemia. It covers:
- Causes of hypokalemia including redistribution, extrarenal loss, and renal loss. Redistribution can be caused by alkalosis, medications, or increased sympathetic tone. Extrarenal losses include diarrhea, laxative abuse, and sweating. Renal losses are associated with metabolic acidosis or alkalosis.
- Treatment of hypokalemia focuses on replacing deficits orally or intravenously, while also treating underlying causes.
- Causes of hyperkalemia include increased intake, pseudohyperkalemia, transcellular shifts during conditions like tumor l
Portal-systemic encephalopathy is a brain disorder caused by liver dysfunction that allows toxins to reach the brain. It is characterized by alterations in mental status, neurological abnormalities, and distinctive EEG changes. The main underlying mechanism involves increased levels of ammonia in the bloodstream from the gut that are normally processed by the liver. Treatment focuses on reducing ammonia production in the colon through medications like lactulose and restricting protein intake. Prognosis depends on the underlying liver disease and can range from fully treatable acute episodes to chronic and potentially fatal cases.
A 38-year-old female presented with sudden onset loss of consciousness and a severe headache. Her medical history included untreated hypertension. On examination, her blood pressure was extremely high and her Glasgow Coma Scale was low. A CT scan revealed an acute hemorrhage in the right pons and cerebellum. She was treated in the ICU and showed signs of the one-and-a-half syndrome along with right facial nerve palsy, indicating a lesion in the dorsal pons involving critical structures. This rare combination of symptoms, called the eight-and-a-half syndrome, was caused by her hypertensive pontine hemorrhage.
Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver dysfunction and portosystemic shunting of blood flow. The leading theories for its cause are ammonia toxicity, inflammation, and imbalances in neurotransmitters. It ranges from mild cognitive impairment to coma. Treatment involves identifying and treating precipitants, a low-protein diet, non-absorbable disaccharides to reduce ammonia, and antibiotics to suppress gut bacteria. For persistent cases, additional therapies include branched-chain amino acids, probiotics, and transplantation for severe cases.
history and examination in pediatric CVSRaghav Kakar
This document provides guidance on performing a thorough history and physical examination for pediatric patients with suspected cardiovascular disease. Key aspects to assess include symptoms, timing of onset, family history, pre/postnatal history, examination of pulse, blood pressure, jugular venous pressure, precordial examination including auscultation of heart sounds and murmurs. Specific congenital heart defects should be considered based on findings. Investigations are guided by physical exam. A complete cardiovascular exam is essential for accurate diagnosis of heart disease in children.
This document defines and describes Fulminant Hepatic Failure (FHF), also known as Acute Liver Failure (ALF). It provides definitions for different types of liver failure based on duration and presence of pre-existing liver disease. The document discusses the etiology, pathogenesis, clinical manifestations and stages of hepatic encephalopathy in FHF. It outlines the diagnostic workup and management approach for FHF, including initial stabilization, monitoring for complications, supportive care to maximize survival, and consideration of liver transplantation.
This document provides an overview of heart failure, including evaluation and management. It begins with definitions of heart failure and discusses etiology and pathogenesis. It then covers the period of compensation, clinical manifestations, classification of severity, and stages of development. Diagnosis of HFrEF versus HFpEF is explained. Treatment of HFpEF focuses on symptom management while treatment of HFrEF emphasizes guideline directed medical therapy including ACEi/ARB, beta-blockers, ARNi, diuretics, aldosterone antagonists, and SGLT2 inhibitors. Management is aimed at controlling symptoms and congestion through pharmacological optimization and treatment of comorbidities.
Examination of neck veins(CLINICAL MEDICINE)Sue Ting Lim
The document discusses examination of the neck veins, with a focus on differentiating arterial and venous pulsations. It also outlines causes of elevated and low JVP, abnormalities in different neck vein waveform components, and signs related to jugular vein examination including Kussmaul's sign, Friedrich's sign, and hepatojugular reflux. Causes of elevated JVP include cardiac issues like congestive cardiac failure and non-cardiac issues like pulmonary embolism. Causes of low JVP include dehydration, hemorrhage, and hypovolemic shock.
Aluminum phosphide is a commonly used pesticide that has become a major cause of poisoning in India. It releases phosphine gas in the stomach, which causes cellular damage through oxidative stress and inhibits mitochondrial function. Clinical features include nausea, vomiting, hypotension, arrhythmias, and multi-organ failure. Treatment involves decontamination, hemodynamic support, magnesium supplementation, and managing complications like acidosis, arrhythmias and respiratory failure. Prognosis is poor, with mortality rates as high as 100% for ingestions over 1.5g. Poor prognostic factors include shock, ECG abnormalities, hyperglycemia and elevated serum phosphine levels.
Hepato Renal Syndrome (HRS) is a form of kidney failure that occurs in patients with advanced chronic liver disease. It results from intense renal vasoconstriction caused by interactions between the systemic and portal circulatory systems. HRS has no underlying kidney pathology and typically develops spontaneously or in response to precipitating events like infections, bleeding, or large volume paracentesis. Diagnosis is based on criteria and HRS carries the worst prognosis of all liver disease complications. Treatment involves terlipressin and liver transplantation provides a definitive cure.
This document discusses diabetic ketoacidosis (DKA), providing information on its pathophysiology, classification, precipitating factors, signs and symptoms, laboratory investigations, management, and goals of treatment. It classifies DKA as mild, moderate or severe based on plasma glucose, arterial pH, serum bicarbonate, urine ketones, and anion gap. The key aspects of management include fluid resuscitation to restore intravascular volume, insulin therapy to reduce glucose and ketone levels, and potassium supplementation to correct deficiencies. Bicarbonate supplementation is only recommended if the pH is less than 6.9.
This document provides guidelines for the management of diabetic ketoacidosis (DKA). It defines DKA and classifies its severity. The main goals of treatment are rehydration, electrolyte replacement, and insulin administration to lower blood glucose levels slowly. Treatment involves initial fluid resuscitation followed by intravenous fluids and insulin. Potassium levels must be closely monitored and replaced as needed. Fluids are given over 48 hours and patients transition to subcutaneous insulin before discharge. Complications like cerebral edema are risks that require careful monitoring of fluid, electrolyte and glucose levels during treatment.
A 17-year old girl presented with abdominal pain, vomiting, black stools, and weakness after ingesting copper sulfate. She was diagnosed with copper sulfate poisoning based on her symptoms and laboratory results showing kidney and liver damage. She received supportive care including dialysis and blood transfusions. After 12 dialysis sessions over one month, her kidney function recovered and she was discharged.
This document discusses drug-induced liver injury (DILI) caused by anti-tuberculosis (ATT) drugs. It notes that ATT drugs, particularly isoniazid, rifampin, and pyrazinamide, are common causes of DILI. Isoniazid metabolism varies depending on acetylator status, and its toxicity may be due to reactive metabolites. Rifampin induces liver enzymes and its toxicity is often seen in combination with other ATT drugs. Pyrazinamide toxicity depends on dose and can cause fatty liver. Presentations of ATT-induced DILI range from asymptomatic elevations in enzymes to acute liver failure. Careful screening and monitoring of patients on ATT is needed to prevent DILI
Approach to a_patient_presenting_with_hemiplegiaalyaqdhan
1) A 60-year-old man presented with sudden onset right-sided hemiplegia upon waking.
2) On examination, he had right-sided weakness and sensory loss consistent with involvement of the left middle cerebral artery territory.
3) Brain imaging revealed an acute ischemic stroke in the left middle cerebral artery distribution, likely due to thrombotic occlusion of that vessel.
Mrs. Gyani Maya Tamang, a 44-year-old woman, presented with jaundice and easy fatigability for 1 month. On examination, she had pallor, icterus, hepatosplenomegaly, and elevated bilirubin. Testing found hemolytic anemia with spherocytes on blood smear and a positive osmotic fragility test, consistent with hereditary spherocytosis. Further workup ruled out other potential causes of hemolytic anemia such as G6PD deficiency, sickle cell disease, autoimmune hemolytic anemia, and drug or toxin-induced hemolytic anemia.
The document discusses the Law of Discordance for left bundle branch block (LBBB), stating that in a normal LBBB the ST segments should be isoelectric or go in the opposite direction from the dominant part of the QRS. It then outlines the Modified Sgarbossa Criteria for diagnosing STEMI in the presence of LBBB, including concordant ST changes or discordant ST elevation greater than 1/4 the amplitude of the S wave. Finally, it notes that these criteria also apply to ventricular paced rhythms and stresses the importance of documentation for ECG interpretations.
The document outlines the components of a neurological examination, including:
1) Gathering a patient history with details of present illness, past medical history, family history, and socioeconomic status.
2) Performing a physical exam including vital signs, general exam, and focused neurological exam of cranial nerves, motor and sensory systems.
3) Evaluating mental status, cognition, and primitive reflexes.
4) Localizing neurological deficits based on involved pathways, tracts, and regions of the brain or spinal cord.
Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
This document provides an overview of several common critical medical conditions including respiratory failure, ARDS, acute MI, CHF, GI bleed, DKA, shock, and sepsis. It defines each condition and discusses signs and symptoms, causes, complications, treatments, and nursing interventions. Respiratory failure can result from ventilation-perfusion mismatching or intrapulmonary shunting. ARDS causes damage to the alveolar-capillary interface leading to pulmonary edema. Acute MI is caused by coronary artery obstruction from thrombus or plaque. CHF occurs when the heart cannot pump sufficient blood to meet metabolic needs.
This document provides information on the clinical and pathological approach to jaundice. It defines jaundice as a yellowish discoloration of the skin and mucous membranes due to increased bilirubin levels in the blood. Jaundice is categorized as pre-hepatic, hepatic, or post-hepatic. Pre-hepatic causes include various hemolytic anemias. Hepatic causes include physiologic jaundice of newborns and hepatitis. Post-hepatic causes involve issues with the bile ducts. The document outlines clues for diagnosing different types of jaundice and discusses evaluation and management of neonatal jaundice.
This document provides guidance on evaluating patients presenting with paraplegia. It outlines the key components of the clinical history and neurological examination needed to determine the cause and level of spinal cord injury. The history should ascertain details of onset and any associated symptoms. The exam focuses on assessing sensory and motor function at different dermatomal and myotomal levels to localize the lesion. Together this information can indicate if the injury is acute, subacute, or chronic, and identify potential etiologies like trauma, infection, inflammation, compression, or vascular causes. The goal is to arrive at a diagnosis and localization of injury within the spinal cord or vertebrae.
This document discusses potassium management and provides key details about hypokalemia and hyperkalemia. It covers:
- Causes of hypokalemia including redistribution, extrarenal loss, and renal loss. Redistribution can be caused by alkalosis, medications, or increased sympathetic tone. Extrarenal losses include diarrhea, laxative abuse, and sweating. Renal losses are associated with metabolic acidosis or alkalosis.
- Treatment of hypokalemia focuses on replacing deficits orally or intravenously, while also treating underlying causes.
- Causes of hyperkalemia include increased intake, pseudohyperkalemia, transcellular shifts during conditions like tumor l
Portal-systemic encephalopathy is a brain disorder caused by liver dysfunction that allows toxins to reach the brain. It is characterized by alterations in mental status, neurological abnormalities, and distinctive EEG changes. The main underlying mechanism involves increased levels of ammonia in the bloodstream from the gut that are normally processed by the liver. Treatment focuses on reducing ammonia production in the colon through medications like lactulose and restricting protein intake. Prognosis depends on the underlying liver disease and can range from fully treatable acute episodes to chronic and potentially fatal cases.
A 38-year-old female presented with sudden onset loss of consciousness and a severe headache. Her medical history included untreated hypertension. On examination, her blood pressure was extremely high and her Glasgow Coma Scale was low. A CT scan revealed an acute hemorrhage in the right pons and cerebellum. She was treated in the ICU and showed signs of the one-and-a-half syndrome along with right facial nerve palsy, indicating a lesion in the dorsal pons involving critical structures. This rare combination of symptoms, called the eight-and-a-half syndrome, was caused by her hypertensive pontine hemorrhage.
Hepatic encephalopathy is a neuropsychiatric syndrome caused by liver dysfunction and portosystemic shunting of blood flow. The leading theories for its cause are ammonia toxicity, inflammation, and imbalances in neurotransmitters. It ranges from mild cognitive impairment to coma. Treatment involves identifying and treating precipitants, a low-protein diet, non-absorbable disaccharides to reduce ammonia, and antibiotics to suppress gut bacteria. For persistent cases, additional therapies include branched-chain amino acids, probiotics, and transplantation for severe cases.
history and examination in pediatric CVSRaghav Kakar
This document provides guidance on performing a thorough history and physical examination for pediatric patients with suspected cardiovascular disease. Key aspects to assess include symptoms, timing of onset, family history, pre/postnatal history, examination of pulse, blood pressure, jugular venous pressure, precordial examination including auscultation of heart sounds and murmurs. Specific congenital heart defects should be considered based on findings. Investigations are guided by physical exam. A complete cardiovascular exam is essential for accurate diagnosis of heart disease in children.
This document defines and describes Fulminant Hepatic Failure (FHF), also known as Acute Liver Failure (ALF). It provides definitions for different types of liver failure based on duration and presence of pre-existing liver disease. The document discusses the etiology, pathogenesis, clinical manifestations and stages of hepatic encephalopathy in FHF. It outlines the diagnostic workup and management approach for FHF, including initial stabilization, monitoring for complications, supportive care to maximize survival, and consideration of liver transplantation.
This document provides an overview of heart failure, including evaluation and management. It begins with definitions of heart failure and discusses etiology and pathogenesis. It then covers the period of compensation, clinical manifestations, classification of severity, and stages of development. Diagnosis of HFrEF versus HFpEF is explained. Treatment of HFpEF focuses on symptom management while treatment of HFrEF emphasizes guideline directed medical therapy including ACEi/ARB, beta-blockers, ARNi, diuretics, aldosterone antagonists, and SGLT2 inhibitors. Management is aimed at controlling symptoms and congestion through pharmacological optimization and treatment of comorbidities.
Examination of neck veins(CLINICAL MEDICINE)Sue Ting Lim
The document discusses examination of the neck veins, with a focus on differentiating arterial and venous pulsations. It also outlines causes of elevated and low JVP, abnormalities in different neck vein waveform components, and signs related to jugular vein examination including Kussmaul's sign, Friedrich's sign, and hepatojugular reflux. Causes of elevated JVP include cardiac issues like congestive cardiac failure and non-cardiac issues like pulmonary embolism. Causes of low JVP include dehydration, hemorrhage, and hypovolemic shock.
Aluminum phosphide is a commonly used pesticide that has become a major cause of poisoning in India. It releases phosphine gas in the stomach, which causes cellular damage through oxidative stress and inhibits mitochondrial function. Clinical features include nausea, vomiting, hypotension, arrhythmias, and multi-organ failure. Treatment involves decontamination, hemodynamic support, magnesium supplementation, and managing complications like acidosis, arrhythmias and respiratory failure. Prognosis is poor, with mortality rates as high as 100% for ingestions over 1.5g. Poor prognostic factors include shock, ECG abnormalities, hyperglycemia and elevated serum phosphine levels.
Hepato Renal Syndrome (HRS) is a form of kidney failure that occurs in patients with advanced chronic liver disease. It results from intense renal vasoconstriction caused by interactions between the systemic and portal circulatory systems. HRS has no underlying kidney pathology and typically develops spontaneously or in response to precipitating events like infections, bleeding, or large volume paracentesis. Diagnosis is based on criteria and HRS carries the worst prognosis of all liver disease complications. Treatment involves terlipressin and liver transplantation provides a definitive cure.
This document discusses diabetic ketoacidosis (DKA), providing information on its pathophysiology, classification, precipitating factors, signs and symptoms, laboratory investigations, management, and goals of treatment. It classifies DKA as mild, moderate or severe based on plasma glucose, arterial pH, serum bicarbonate, urine ketones, and anion gap. The key aspects of management include fluid resuscitation to restore intravascular volume, insulin therapy to reduce glucose and ketone levels, and potassium supplementation to correct deficiencies. Bicarbonate supplementation is only recommended if the pH is less than 6.9.
This document provides guidelines for the management of diabetic ketoacidosis (DKA). It defines DKA and classifies its severity. The main goals of treatment are rehydration, electrolyte replacement, and insulin administration to lower blood glucose levels slowly. Treatment involves initial fluid resuscitation followed by intravenous fluids and insulin. Potassium levels must be closely monitored and replaced as needed. Fluids are given over 48 hours and patients transition to subcutaneous insulin before discharge. Complications like cerebral edema are risks that require careful monitoring of fluid, electrolyte and glucose levels during treatment.
A 17-year old girl presented with abdominal pain, vomiting, black stools, and weakness after ingesting copper sulfate. She was diagnosed with copper sulfate poisoning based on her symptoms and laboratory results showing kidney and liver damage. She received supportive care including dialysis and blood transfusions. After 12 dialysis sessions over one month, her kidney function recovered and she was discharged.
This document discusses drug-induced liver injury (DILI) caused by anti-tuberculosis (ATT) drugs. It notes that ATT drugs, particularly isoniazid, rifampin, and pyrazinamide, are common causes of DILI. Isoniazid metabolism varies depending on acetylator status, and its toxicity may be due to reactive metabolites. Rifampin induces liver enzymes and its toxicity is often seen in combination with other ATT drugs. Pyrazinamide toxicity depends on dose and can cause fatty liver. Presentations of ATT-induced DILI range from asymptomatic elevations in enzymes to acute liver failure. Careful screening and monitoring of patients on ATT is needed to prevent DILI
Approach to a_patient_presenting_with_hemiplegiaalyaqdhan
1) A 60-year-old man presented with sudden onset right-sided hemiplegia upon waking.
2) On examination, he had right-sided weakness and sensory loss consistent with involvement of the left middle cerebral artery territory.
3) Brain imaging revealed an acute ischemic stroke in the left middle cerebral artery distribution, likely due to thrombotic occlusion of that vessel.
Mrs. Gyani Maya Tamang, a 44-year-old woman, presented with jaundice and easy fatigability for 1 month. On examination, she had pallor, icterus, hepatosplenomegaly, and elevated bilirubin. Testing found hemolytic anemia with spherocytes on blood smear and a positive osmotic fragility test, consistent with hereditary spherocytosis. Further workup ruled out other potential causes of hemolytic anemia such as G6PD deficiency, sickle cell disease, autoimmune hemolytic anemia, and drug or toxin-induced hemolytic anemia.
The document discusses the Law of Discordance for left bundle branch block (LBBB), stating that in a normal LBBB the ST segments should be isoelectric or go in the opposite direction from the dominant part of the QRS. It then outlines the Modified Sgarbossa Criteria for diagnosing STEMI in the presence of LBBB, including concordant ST changes or discordant ST elevation greater than 1/4 the amplitude of the S wave. Finally, it notes that these criteria also apply to ventricular paced rhythms and stresses the importance of documentation for ECG interpretations.
The document outlines the components of a neurological examination, including:
1) Gathering a patient history with details of present illness, past medical history, family history, and socioeconomic status.
2) Performing a physical exam including vital signs, general exam, and focused neurological exam of cranial nerves, motor and sensory systems.
3) Evaluating mental status, cognition, and primitive reflexes.
4) Localizing neurological deficits based on involved pathways, tracts, and regions of the brain or spinal cord.
Approach to evaluating and treating Chronic Heart Failure and Acute Heart Failure
Reference: Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
This document provides an overview of several common critical medical conditions including respiratory failure, ARDS, acute MI, CHF, GI bleed, DKA, shock, and sepsis. It defines each condition and discusses signs and symptoms, causes, complications, treatments, and nursing interventions. Respiratory failure can result from ventilation-perfusion mismatching or intrapulmonary shunting. ARDS causes damage to the alveolar-capillary interface leading to pulmonary edema. Acute MI is caused by coronary artery obstruction from thrombus or plaque. CHF occurs when the heart cannot pump sufficient blood to meet metabolic needs.
This document discusses heart failure with preserved ejection fraction (HFpEF). It begins by defining HFpEF and noting that approximately half of heart failure patients have normal or near-normal ejection fractions. The document then reviews various classification systems for HF, diagnostic criteria, echocardiographic assessment of HFpEF, risk factors, and challenges in diagnosing and treating HFpEF. It concludes by discussing current and potential future treatment approaches for HFpEF, including drugs targeting comorbid conditions that are common in HFpEF patients.
This document discusses heart failure with preserved ejection fraction (HFpEF). It defines HFpEF and describes the pathophysiology as being related to diastolic dysfunction from impaired relaxation and stiffness of the left ventricle. Common causes include hypertension, coronary artery disease, and obesity. Patients typically present with signs and symptoms of congestion. Echocardiography is used to diagnose HFpEF by showing preserved ejection fraction and evidence of diastolic dysfunction. Treatment focuses on controlling hypertension, congestion with diuretics, and some evidence that ARBs and spironolactone may reduce hospitalizations for HFpEF patients.
A 22-year-old male presented with complaints of easy fatigability, abdominal discomfort, leg swelling, and shortness of breath with exertion over the past 6-8 months. Examination found edema, elevated jugular venous pressure, hepatomegaly, and cachexia. Testing showed elevated liver enzymes and BNP. Echocardiogram demonstrated thickened pericardium with ventricular interdependence and equal diastolic pressures, consistent with constrictive pericarditis. The patient was diagnosed with constrictive pericarditis likely due to a prior unknown infection or inflammatory process causing thickening and scarring of the pericardium.
The third presentation in my ACEM Fellowship Summary series. Focuses on the aetiology, diagnosis and management of acute heart failure in its many forms.
Acute Decompensated Heart Failure : What is New ?drucsamal
1. The document discusses drug trials for acute decompensated heart failure and their results. Many trials tested drugs like nesiritide, milrinone, tezosentan, levosimendan, tolvaptan, and rolofylline but did not show clinical benefit.
2. It proposes classifying patients based on their clinical profile into those with volume overload, reduced cardiac output, or a combination, to help determine optimal treatment which may include diuretics, vasodilators, inotropes, or renal preservation agents.
3. The management of acute heart failure is divided into initial, in-hospital, and discharge phases, with goals like establishing diagnoses, treating precip
The document discusses shock in children, defining it as circulatory system failure to supply oxygen and nutrients to meet cellular demands. It covers circulatory physiology, classifications of shock, evaluation, treatment including fluid resuscitation and vasoactive drugs, and specific types of shock such as hypovolemic, cardiogenic, obstructive, and distributive shock. Metabolic issues associated with shock like acid-base and electrolyte abnormalities are also reviewed.
1) Pulmonary hypertension is defined as a systolic pulmonary artery pressure >35mmHg or mean pulmonary artery pressure >25mmHg and is classified into 5 groups. Group 1 includes pulmonary arterial hypertension which can be idiopathic or associated with other conditions.
2) Pulmonary hypertension results from an imbalance between vasoconstrictors like endothelin-1 and vasodilators like nitric oxide leading to vascular remodeling and increased pulmonary pressures. Acute pulmonary hypertension in the ICU is often caused by conditions like pulmonary embolism, lung disease, heart disease or sepsis.
3) Diagnosis involves clinical exam, imaging like echocardiogram and right heart catheterization. Treatment goals are to reduce pulmonary pressures
This document discusses pulmonary hypertension (PH), including its definition, classification, pathophysiology, diagnosis, and management in intensive care patients. It defines PH as a mean pulmonary artery pressure >25 mmHg and outlines the various causes classified under five groups. The pathophysiology of PH involves vasoconstriction, vascular remodeling, thrombosis and endothelial dysfunction. Diagnosis involves history, physical exam, imaging like chest X-ray and ECG, as well as right heart catheterization. Management focuses on treating the underlying cause, using vasodilators, inotropes to support the right ventricle, diuretics, oxygen therapy and potentially surgery in refractory cases. PH increases mortality and deteriorations can be rapid
This document summarizes key information about pulmonary hypertension (PH) management including: median survival rates; clinical presentation; diagnostic testing including echocardiogram, right heart catheterization, and biomarkers; risk assessment; and therapy. Median survival is 2.8 years for adults and 10 months for pediatric patients with PH. Clinical presentation includes symptoms of exertional shortness of breath, fatigue, and right ventricular failure. Diagnostic testing is aimed at confirming the diagnosis, assessing severity, and identifying the cause of PH. Risk assessment evaluates factors like functional capacity, right ventricular function, and complications to determine low, intermediate, or high risk status. Therapy involves general measures, PH-specific drug therapy, and interventional procedures in advanced cases.
This document summarizes a clinical case report of a 79-year-old female patient admitted for heart failure with acute exacerbation likely due to infection. Key details include:
- The patient has a history of hypertension, atrial fibrillation, hyperuricemia, and impaired glucose tolerance.
- Exams and tests show signs of congestive heart failure including jugular vein distension and crackles in the lungs. Echocardiogram finds diastolic dysfunction.
- She is treated with antibiotics, diuretics, and other heart failure medications. Her symptoms improve with treatment and she is discharged with medications including valsartan and furosemide.
1) Congestive heart failure results from any structural or functional abnormality that impairs the ventricle's ability to eject or fill with blood.
2) The renin-angiotensin-aldosterone system plays a role in the vicious cycle of congestive heart failure by stimulating sodium and water retention.
3) Treatment for systolic heart failure involves correcting underlying factors, lifestyle modifications, and maximizing medications like loop diuretics, ACE inhibitors, beta blockers, and aldosterone antagonists.
The document provides information on competencies for nurses caring for patients with heart failure. It defines heart failure and describes the different clinical classifications. It discusses identifying the underlying causes, nursing management including monitoring clinical parameters, diagnostic tests and biomarkers, medical management with diuretics and inotropes, and lifestyle modifications including diet and risk factor reduction for chronic heart failure patients.
1) Congestive heart failure results from any structural or functional abnormality that impairs the ventricle's ability to eject or fill with blood.
2) The renin-angiotensin-aldosterone system plays a role in the vicious cycle of congestive heart failure by stimulating sodium and water retention.
3) Treatment for systolic heart failure involves lifestyle modifications, medications like diuretics, ACE inhibitors, beta blockers, and devices or transplantation for refractory cases.
This document discusses two cases involving heart transplantation:
1. Case 1 involves a 57-year-old woman with non-ischemic cardiomyopathy, pulmonary hypertension, and history of blood clots who is being evaluated for heart transplantation. Right heart catheterization found severe pulmonary hypertension.
2. Case 2 involves a 61-year-old woman who received a heart transplant 9 months ago after having an LVAD placed. She is now presenting for complications including shock, arrhythmias, and possible transplant rejection.
Cyanosis OVERVIEW # MBBS#BDS#BPTH#ALLIED SCIENCESPandian M
Cyanosis can be caused by conditions that increase the amount of reduced hemoglobin or involve abnormal hemoglobin in the bloodstream. The document outlines an approach to evaluating cyanosis in newborns, including defining the condition, discussing mechanisms, diagnostic testing, and classifications of cardiac lesions that can cause cyanosis. A thorough clinical evaluation is important for diagnosis, and stabilization and monitoring of the newborn is critical when congenital heart disease is suspected.
Heart failure is a clinical syndrome where the heart cannot pump enough blood to meet the body's needs. It affects over 64 million people worldwide and is a leading cause of hospitalization. It can be caused by structural or functional issues with the heart. Heart failure is classified based on whether the left side, right side, or both ventricles are affected, and ejection fraction. Common causes include coronary artery disease and hypertension. Symptoms include dyspnea, fatigue, edema and reduced exercise capacity. Treatment involves medications to reduce preload, afterload, heart rate and prevent remodeling, as well as diuretics, device therapies, surgery and transplantation in advanced cases.
Calcium released from the sarcoplasmic reticulum in cardiac myocytes stimulates contraction. Calcium is reuptaken into the sarcoplasmic reticulum and effluxed from the cell, lowering intracellular calcium as contraction peaks. Heart failure is defined by symptoms such as breathlessness and signs such as elevated jugular venous pressure. It requires evidence of structural heart abnormality and impaired function.
1. Sepsis is a life-threatening organ dysfunction caused by a dysregulated immune response to infection. It can progress to septic shock, which involves circulatory and metabolic abnormalities increasing the risk of death.
2. Initial management of sepsis involves screening, resuscitation, infection control, hemodynamic support, and empiric antibiotics within 1-3 hours while obtaining cultures. Ongoing care focuses on organ support, source control, and monitoring for complications.
3. Long term goals include preventing disability, addressing psychosocial needs, and smooth transition to post-acute care and follow up. Prompt recognition and treatment can reduce mortality from this medical emergency.
1. The document discusses various cardiac arrhythmias including supraventricular tachycardias, atrial fibrillation, ventricular tachycardia, and ventricular fibrillation.
2. It provides details on characteristics, causes, diagnosis, and treatment of these arrhythmias based on American and European cardiology guidelines.
3. The treatment discussed includes electrical cardioversion, antiarrhythmic medications, catheter ablation, and implantable cardioverter defibrillators.
This document provides an overview of atrial fibrillation (AF) and paroxysmal supraventricular tachycardia (PSVT). It defines these conditions and describes their typical ECG patterns, mechanisms, clinical presentations, diagnostic evaluations, and treatment approaches including medications, procedures like cardioversion and ablation. Key points include: AF can be paroxysmal, persistent or permanent, and is caused by mechanisms like reentry and ectopic automaticity; evaluation involves assessing thromboembolic risk with scores like CHA2DS2-VASc; treatment focuses on rate or rhythm control with medications or ablation, while preventing thromboembolism with anticoagulation; PSVT often presents with abrupt
A 24-year-old woman presented with headache and left-sided weakness. Imaging showed cerebral venous thrombosis involving the superior sagittal sinus and draining veins. She was diagnosed with antiphospholipid syndrome based on recurrent pregnancy loss and positive lupus anticoagulant. She was treated with anticoagulation and anticonvulsants and showed gradual improvement over 10 days with residual mild weakness. Her long-term management plan includes lifelong anticoagulation and screening for recurrent thrombosis.
A 68-year-old male farmer presented with post-traumatic T3-T4 compression fracture and paraplegia in January 2022. He developed recurrent UTIs, hemorrhagic pleural effusion, and a retropharyngeal cyst requiring debulking. In early March, he developed cough, dyspnea, stridor and altered sensorium. He was diagnosed with right lower lobe pneumonia, sepsis and respiratory failure. Treatment included antibiotics, ventilation, and supportive care. He later developed bilateral vocal cord palsy and was discharged at family's request before further evaluation.
Chronic myeloid leukemia (CML) is a stem cell disorder caused by the Philadelphia chromosome, which results from the fusion of the BCR gene on chromosome 22 and the ABL gene on chromosome 9. This fusion produces the BCR-ABL protein which exhibits uncontrolled tyrosine kinase activity, driving excessive proliferation of CML cells. CML progresses through chronic, accelerated and blast crisis phases as additional genetic mutations accumulate. Tyrosine kinase inhibitors (TKIs) target the BCR-ABL protein and have significantly improved survival, with a 10-year survival of 85% with TKI therapy. Monitoring response through cytogenetics, FISH and molecular testing guides treatment decisions such as changing or adding other TKIs.
LECTURE ON ATRIAL FIBRILLATION TO 9TH TERM MEDICAL STUDENTS REFERENCES: DAVIDSON(2018) HARRISON 20TH ED OF MEDICINE AND 2020 EUROPEAN HEART GUIDELINES ON AF
surviving sepsis guidelines - Notes are made from surviving sepsis guidelines 2016 article to assist medical students and residents to grasp subject in a easy to read format in a step wise manner. Resources: surviving sepsis guidelines 2016 (free access article)
Pulmonary embolism - Notes are made from textbook of Internal medicine to assist medical students and residents to grasp subject in totality. Resources: Harrison's 20thEd, ESC 2019 guidelines on PE
A pulmonary embolism occurs when a blood clot or other material occludes the pulmonary artery or its branches. This most commonly results from a deep vein thrombosis in the lower leg that embolizes to the lung. When a PE occurs, it causes ventilation-perfusion mismatching in the lungs. Diagnosis is difficult due to nonspecific symptoms but evaluation involves a Wells criteria assessment, D-dimer testing, echocardiogram, and CT pulmonary angiogram. Treatment consists of anticoagulation with low molecular weight heparin or novel oral anticoagulants. Fibrinolytic therapy may be used in massive PEs. Prevention focuses on prophylaxis in high risk hospitalized patients.
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Osteoporosis is an increasing cause of morbidity among the elderly.
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Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
1. 10-10-2022
1
Col Bharat Malhotra
Senior Advisor (Medicine)
REFERENCE
Harrison’s Principles of internal medicine Harrison's 21st Ed (2022)
Davidson’s Principlesand practice of Medicine (2018)
AHA & European Guidelines on management of Acute and Chronic Heart Failure (2021 & 2022)
Incidence and Prevalence of HF worldwide
PREVALENCE
Developed Countries: 2%
Asia : 0.1 -7%
India : 0.12- 0.44%
40-60 yrs: 1-2%
> 80 years: 12%
• Complex clinical syndrome
• that results from structural or functional impairment
• of ventricular filling or ejection of blood
• leads to cardinal manifestation of dyspnea and
fatigue and fluid retention
American Heart Association Cardiology Guidelines (2022)
Chronic HF describes those who have had an established
long-standing diagnosis of HF or who have a more gradual
onset of symptoms.
Acute HF is rapid onset of new or worsening of
preexisting HF requiring hospitalization.
In pathophysiological terms
• HF is defined as a syndrome
• characterized by elevated cardiac filling pressures and / or
• inadequate peripheral O2 delivery
• at rest or during stress caused by cardiac dysfunction
STAGE A STAGE B STAGE C STAGE D
AT RISK
HF
PRE HF SYMPTOMATIC
HF
ADVANCED
HF
Symptom + Sign of HF
Structural heart disease
Marked
Symptom + Sign of HF
Structural heart disease
Repeated Hospitalizations
HFrEF HFmrEF HFpEF
Symptoms + Signs Symptoms + Signs Symptoms + Signs
LV EF < 40% LV EF 41% - 49% LV EF > 50%
Objective evidence of
cardiac structural or
functional abnormality
including increase BNP
HF improved EF
(Treatment remains same as that of HFrEF)
2. 10-10-2022
2
DILATED
CARDIOMYOPATHY
CORONARYARTERY
DISEASE
TACHYARRHYTHMIAS
Drug Induced
Alcohol
Metabolic
Endocrinal
Autoimmune
Viral - Myocarditis
VALVULAR DISEASE
Lt –Rt SHUNTING
HYPERTENSION
HYPERTROPHIC
CARDIOMYOPATHY
RESTRICTIVE
CARDIOMYOPATHY
Amylodosis
Sarcoidosis
Haemochromatosis
STENOTIC
VALVULAR DISEASE
HYPERTENSION
ENDOMYOCARDIAL
DISORDERS
CONSTRICTIVE
PERICARDITIS
HIGH OUTPUT STATES
AV Fistula
Chronic Anemia
Thyrotoxicosis
Beri Beri
OTHER FACTORS
Coronary Ischemia
Arrhythmias
Uncontrolled hypertension
Pulmonary embolism
Systemic infection/ sepsis
Patient related factors
Provider related factors
Na & Water RETENTION
INCREASE PRELOAD
VASOCONSTRICTION
INCREASE AFTERLOAD
DECREASES MYOCARDIAL CONTRACTILITY
DECREASES CARDIAC OUTPUT
SVC
IVC
P Artery P Vein
Aorta
Lungs
Lt A
Rt A
Rt V Lt V
Chronic HF describes those who have had an established
long-standing diagnosis of HF or who have a more gradual
onset of symptoms.
3. 10-10-2022
3
The diagnosis of CHF requires the presence of symptoms and/or signs of HF
and objective evidence of cardiac dysfunction
PRO BNP
BNP
ECHO
Chronic Symptoms & signs
of HF
Risk factors for HF
Abnormal ECG/ CXR
Confirm Heart Failure
Define EF & Etiology
EF
Structure
> 125 pg/mL
> 35 pg/mL
Dyspnoea during exercise on less strenuous activity
ultimately may occur at rest
Paroxysmal nocturnal dyspnoea, Orthopnoea
Fatigue, Poor effort tolerance
Ankle edema
Nocturnal cough
Anorexia, nausea, early satiety, Rt upper quadrant
abdominal pain & fullness
Confusion, Disorientation, Oliguria
CONGESTION
RAISED JVP
Prominent P2
Hepatomegaly
Hepatojugular
reflux
Ascites
Pedal edema
Cardiomegaly
S3, S4
Pulmonary crackles
Pleural Effusions
LOW CARDIAC OUTPUT
Lethargy, fatigue, Alter mental state
Cool Extremities
Sinus tachycardia
Narrow pulse pressure
Lower BP
• AKI – Due to poor renal perfusion
• Impair liver function
• Hypokalemia, hyperkalemia
• Hyponatremia
• Thromboembolism
• Atrial or ventricular arrhythmias
• Sudden cardiac death
12 lead ECG
CXR PA View
BNP/ NT Pro BNP test
ECHO
Test for Comorbidities Test for Etiology
CBC
Urea Creatinine
Electrolytes
Fasting Glucose, HBA1c
Lipid Profile
TSH
Iron status – Serum Iron, TIBC, Ferritin
High pretest probability of CAD –PCI
Intermediate probability of CAD Stress
ECHO, Exercise testing
Specific disease workup if required
Cardiac – MRI [Infiltrative disorders)
Endomyocardial biopsy
Rt Heart catheterization – done rarely in
evaluation for transplant
ECG – May by abnormal due to ACS, tachyarrhythmias, LBBB, Chamber enlargement
4. 10-10-2022
4
BNP [ >35 pg/mL CHF] [ >100 pg/dLAHF ]
NT Pro BNP [ > 125 pg/mL CHF] [ >400 pg/dLAHF ]
Released from failing heart (sensitive marker for HF)
• Support diagnosis of HF
• Prognosis
• GDMT
• Falsely elevated in acute cardiac illness,
critical illness, Sepsis, PE, AKI
BIOMARKERS: Troponin T (Ischemia)
New diagnosis of HF
Clinical change in patient with known diagnosis of HF
Assess structure, chambers, Valves,
flow dynamics, function, EF
ACEI/ARB/ARNI
B Blocker
MRA
Dapagliflozin/Empagliflozin
Diuretics for fluid retention
LV EF < 35%
QRS WNL
ICD
LV EF > 35%
Device not indicated
If symptom persist
(go to Class II
recommendation)
LV EF < 35%
SR, QRS BROAD
CRT
AIM of Rx
Improve survival
Improve clinical status
ACEI
• Enalapril
• Ramipril
• Lisinopril
ARB
• Losartan
• Valsartan
ARNI
• Sacubitril+
Valsartan
(Combination)
B Blocker MRA SGLT2 Diuretics
Bisoprolol
Metoprolol
Nebivolol
Carvedilol
Spironolactone
Eplerenone
Dapagliflozin
Empagliflozin
Furosemide
Torsemide
Metolazone
ARNI
5. 10-10-2022
5
Reduce HR
further
In Blacks
only
In AF cases Trials Stage
IVABRADINE Hydralazine &
Isosorbide
Digoxin Vericiguat
• Dyslipidemia, Hypertension, diabetes, obesity
Treat risk factors
• CABG/ PCI
CAD
• Anticoagulation, Digoxin
AF
• Assess and treat if required
Sleep Disorders
• IV Ferric Carboxy maltose
Iron deficiency
• Limited Exercise and weight reduction
• Low salt diet, Low fat diet, smoking cessation
Advise
• Influenza
• Pneumococcal
Vaccine
Reduce risk of SCD
LV EF < 35%
QRS WNL
Ischemic origin after 40 d
if survival is > 40 days
Post cardiac arrest
VT with hypotension
Reduce mortality and morbidity in selected patients and
improves cardiac function
LV EF < 35%
QRS wide with LBBB
Sinus rhythm
Symptomatic
HF patients
CABG/
PCI
Valve
Repair
Acute HF is rapid onset of new or worsening of
preexisting HF requiring hospitalization.
6. 10-10-2022
6
PRO BNP
BNP
ECHO
Acute Symptoms & signs
of HF
Risk factors for HF
Abnormal ECG/ CXR/ SpO2
Confirm Heart Failure
Define EF & Etiology
EF
Structure
> 400 pg/mL
> 100 pg/mL
The diagnosis of AHF requires the presence of Rapid onset of HF
or acute decompensation of existing HF
HIGH OUTPUT STATES
Chronic Anemia
Thyrotoxicosis
Beri Beri
OTHER FACTORS
Coronary Ischemia
Arrhythmias
Uncontrolled hypertension
Valvular heart disease
Pulmonary embolism
Systemic infection/ sepsis
Patient related factors
Provider related factors
• Volume overload
Acute Decompensation
(Typical)
• Volume overload
• Hypoperfusion with End organ dysfunction
Acute Decompensation
(Low Output)
• Severe Pulmonary congestion
• Hypoxia
Acute Pulmonary
Edema
• Hypotension with low cardiac output
• End Organ Failure
Cardiogenic Shock
CONGESTION
Orthopnea
Pedal edema
Pleural Effusions
Ascites
Cardiomegaly
S3
Tachypnoea
Pulmonary
crackles
Raised JVP
LOW PERFUSION
Lethargy, fatigue,
Alter mental state
Cool Extremities
Sinus tachycardia
Narrow pulse pressure
Lower BP
End organ dysfunction
Low
P
E
R
F
U
S
I
O
N
CONGESTION
NO YES
NO Warm
Dry
Warm
Wet
YES Cold
Dry
Cold
Wet
Hospitalized
12 lead ECG
CXR PA View, SpO2, ABG
BNP/ NT Pro BNP test
ECHO
Test for Comorbidities Test for Etiology
CBC
Urea Creatinine
Electrolytes
Fasting Glucose, HBA1c
Lipid Profile
Evaluate – coexisting infections
TSH
Iron status – Serum Iron, TIBC, Ferritin
High pretest probability of CAD –PCI
SpO2 monitor
ABG
Swan Ganz Catheter
(Assess PA pressures)
In cardiogenic shock
O2, NIV, Ventilatory support
Congestion/ Fluid overload
• IV Loop Diuretics
• Increase dose - IV loop diuretic,
• Loop diuretic + metolazone
• Renal replacement therapy
Hypoperfusion
• Inotropes – Dobutamine, Dopamine (Milrinone, Levosimendan)
• Vasopressors - Norepinephrine
• Mechanical circulatory support, Emergency PCI
Vasodilators- IV Nitrates , IV Nitroprusside
Other drugs :IV opioids (in acute pulm edema), Anticoagulants (in AF)
7. 10-10-2022
7
DIURETICS
• Furosemide
Continuous
vs Bolus
Add on
• Chlorothiazide
or Metolazone
Refractory or in
Cardiorenal Syndrome
• RRT
Vasodilator Inotropes Vasopressor Other Rx
Nitroglycerine
Na
Nitroprusside
(Reserve drug)
Nesiritide
(Utilizationwaned)
Dobutamine
Dopamine
Milrinone, Levosimendan
(Utilizationwaned)
Norepinephrine ACS
Arrhythmia
Infection
Anemia
Switch to oral Rx
as for HFrEF
Mechanical Circulatory support
ULTRAFILTERATION
EMERGENCY PCI
REFRACTORY HF- CARDIAC TRANSPLANT
69 years old Female
Dyspnoea on exertion - 3 month
Anorexia
Vital Stable
Pedal edema present
Pro BNP 544 pg/mL
ECHO – EF 40% , MR +
65 years Male smoker, diabetes
Progressive dyspnoea 3 days and now dyspnoeic at rest 1 day.
Temp 100 F, Pallor
Pulse 104/min
RR 28/min, Spo2 90%
BP 122/80 mmHg
Warm peripheries
JVP raised
Pedal edema present
Tender hepatomegaly.
Pro BNP 544 pg/mL
ECHO – EF 25% , MR + RWMA +
Trop T positive
52 years Male
Progressive dyspnoea 1 year associated with wheeze
On treatment with bronchodilators from Pvt Nursing home
reported to our hospital due to no improvement in symptoms.
Don’t mistake
cardiac asthma for
bronchial asthma
EXAMINE PATIENT
HAD SIGNIFICANT MURMUR