Cardiac chamber asmfm 2019
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This document discusses how to obtain views of the fetal cardiac chambers and describe normal anatomy and anomalies. It provides an overview of obtaining the apical, right lateral, left lateral, and basal views to assess the situs, size, axis, atria, veins, ventricles, valves, and contractility. Common anomalies that can be diagnosed include atrioventricular septal defect, hypoplastic left heart syndrome, Ebstein's anomaly, total anomalous pulmonary venous return, coarctation of the aorta, and tumors. Proper orientation and standardized description of the views are important for diagnosing any anomalies present.
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This document discusses considerations for caring for adult patients with congenital heart disease. It outlines common congenital heart defects classified as simple, moderately complex, or highly complex. It describes defects, complications, and treatments. Common reasons for hospitalization include heart failure, arrhythmias, and valve disease. Adult congenital heart patients have increased risks of comorbidities and require lifelong specialized care. Nurses should consult the adult congenital heart team and consider the psychological and social impacts of living with congenital heart disease.
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2-Fetal Echo part 2 Dr Ahmed Esawy
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Ultrasound Markers
soft ultrasound markers
Minor markers
Nuchal fold
Echogenic bowel
Ventriculomegaly
Echogenic cardiac focus
Choroid plexus cyst
Single umbilical artery
Enlarged cisterna magna
Renal pyelectasis
Trisomy 21: Down’s Syndrome
Trisomy 18 Edward Syndrome
Trisomy 13
Molar Tooth Sign
Fetal Echocardiography
1st Step: Check the heart is beating
2nd Step: M-mode heart rate - should be between 120 and 180 beats per minute
3rd step : Situs-
4th step four chamber view.
5th and 6th Step Outflow Tracts
5th step : LVOT
6TH step : RVOT
7th step : 3 Vessel View
8th step: Interventricular Septum
IVS (a false positive for septal defect).
It should be assessed in both B-mode and Colour Doppler.
9th step : Aortic Arch
The 'arches' are best assessed when the foetus is prone.
10th step : Ductal Arch
This is the ductus arteriosus:
Fetal bradycardia
• Fetal sinus bradycardia
• Fetal bradyarrythmias
Fetal Tachyarrhythmia
Fetal premature atrial contraction (PAC)
Fetal Complete Atrioventricular block
Supraventricular tachycardia
Communications between systemic and pulm. Circuits LT RT. shunt.
• Inter-atrial communications. Patent F. oval , ost. 1 defect, sinus venosus, ost.2 defect, endocarial cushin defect.
• Inter-ventricular communications.
-simple VSD.
-VSD with AI
-Single ventricle
-Gerbode defect
-Endocar. Cushion
• Aorto-pulmonary communications:
a. Persistent ductus arteriosus (P.D.A.)
b. Aorto-pulmonary window.
c. Truncus arteriosus.
d. Ruptured sinus of valsalva.
e. Coronary arterio-venous fistula.
Ventricular Septal Defect (VSD)
Endocardial Cushion Defect
Complete atrioventricular canal
Truncus arteriosus
ductus Arteriosus
Valvular and Obstructive lesions
Coarctation of aorta
Vascular rings
Aortic stenosis.
AI, MS, hypopalstic heart.
Cotriatrium
Fallot (F5,F4, F3.)
Pulmonary. Atresia
PULMONARY STENOSIS
Ebestien anomaly
Transposition of great vessels
Tetralogy of fallot
Double outlet right ventricle
Pulmonary atresia with a VSD
Common arterial trunk
Absent pulmonary valve syndrome
Tricusped atresia
Tricuspid dysplasia
Tetralogy of Fallot
Normal Fetal HEAD
SEPTUM PELLUCIDUM
Choriod plexus cyst
Agenesis of the corpus callosum
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- An atrial septal defect (ASD) is an opening in the wall separating the left and right atria of the heart that was not present at birth.
- The most common type is an ostium secundum defect, which accounts for 70-75% of ASDs.
- Small ASDs may close on their own, but larger defects require closure to prevent long term complications like heart failure and pulmonary hypertension.
- Echocardiography is the primary diagnostic test used to identify the size, location and type of ASD.
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Recommended
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This document discusses considerations for caring for adult patients with congenital heart disease. It outlines common congenital heart defects classified as simple, moderately complex, or highly complex. It describes defects, complications, and treatments. Common reasons for hospitalization include heart failure, arrhythmias, and valve disease. Adult congenital heart patients have increased risks of comorbidities and require lifelong specialized care. Nurses should consult the adult congenital heart team and consider the psychological and social impacts of living with congenital heart disease.
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This document discusses various acyanotic congenital heart diseases. It begins by classifying congenital heart disease into cyanotic and acyanotic categories. It then further divides acyanotic congenital heart disease into those with a left-to-right shunt or increased pulmonary blood flow, such as atrial septal defect (ASD), ventricular septal defect (VSD), and patent ductus arteriosus (PDA), and those without a shunt such as coarctation of the aorta. The document then goes on to describe the pathophysiology, clinical features, investigations and management of ASD, VSD, and PDA in more detail. It also briefly discusses Eisenmenger syndrome.
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The document discusses various pathologies that can cause enlargement of different parts of the heart and pulmonary vasculature. It lists conditions such as mitral regurgitation, pulmonary venous hypertension, mitral stenosis, left atrial myxoma, and papillary muscle dysfunction that can lead to enlargement of the left atrium. It also lists increased blood flow, ventricular septal defects, patent ductus arteriosus, pulmonary arterial hypertension, and pulmonary venous hypertension as causes of enlargement of the main pulmonary artery. Finally, it discusses cardiomyopathy, pericardial effusion, multiple valve disease, and coronary artery disease as potential causes of cardiac dilation.
2-Fetal Echo part 2 Dr Ahmed Esawy
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Ultrasound Markers
soft ultrasound markers
Minor markers
Nuchal fold
Echogenic bowel
Ventriculomegaly
Echogenic cardiac focus
Choroid plexus cyst
Single umbilical artery
Enlarged cisterna magna
Renal pyelectasis
Trisomy 21: Down’s Syndrome
Trisomy 18 Edward Syndrome
Trisomy 13
Molar Tooth Sign
Fetal Echocardiography
1st Step: Check the heart is beating
2nd Step: M-mode heart rate - should be between 120 and 180 beats per minute
3rd step : Situs-
4th step four chamber view.
5th and 6th Step Outflow Tracts
5th step : LVOT
6TH step : RVOT
7th step : 3 Vessel View
8th step: Interventricular Septum
IVS (a false positive for septal defect).
It should be assessed in both B-mode and Colour Doppler.
9th step : Aortic Arch
The 'arches' are best assessed when the foetus is prone.
10th step : Ductal Arch
This is the ductus arteriosus:
Fetal bradycardia
• Fetal sinus bradycardia
• Fetal bradyarrythmias
Fetal Tachyarrhythmia
Fetal premature atrial contraction (PAC)
Fetal Complete Atrioventricular block
Supraventricular tachycardia
Communications between systemic and pulm. Circuits LT RT. shunt.
• Inter-atrial communications. Patent F. oval , ost. 1 defect, sinus venosus, ost.2 defect, endocarial cushin defect.
• Inter-ventricular communications.
-simple VSD.
-VSD with AI
-Single ventricle
-Gerbode defect
-Endocar. Cushion
• Aorto-pulmonary communications:
a. Persistent ductus arteriosus (P.D.A.)
b. Aorto-pulmonary window.
c. Truncus arteriosus.
d. Ruptured sinus of valsalva.
e. Coronary arterio-venous fistula.
Ventricular Septal Defect (VSD)
Endocardial Cushion Defect
Complete atrioventricular canal
Truncus arteriosus
ductus Arteriosus
Valvular and Obstructive lesions
Coarctation of aorta
Vascular rings
Aortic stenosis.
AI, MS, hypopalstic heart.
Cotriatrium
Fallot (F5,F4, F3.)
Pulmonary. Atresia
PULMONARY STENOSIS
Ebestien anomaly
Transposition of great vessels
Tetralogy of fallot
Double outlet right ventricle
Pulmonary atresia with a VSD
Common arterial trunk
Absent pulmonary valve syndrome
Tricusped atresia
Tricuspid dysplasia
Tetralogy of Fallot
Normal Fetal HEAD
SEPTUM PELLUCIDUM
Choriod plexus cyst
Agenesis of the corpus callosum
Atrial Septal Defect
- An atrial septal defect (ASD) is an opening in the wall separating the left and right atria of the heart that was not present at birth.
- The most common type is an ostium secundum defect, which accounts for 70-75% of ASDs.
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This document discusses several congenital heart defects:
1) Aortic stenosis is an obstruction to blood flow from the left ventricle to the aorta that can be caused by a muscular obstruction or abnormal aortic valve. Symptoms range from mild to severe depending on the severity of obstruction.
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3) Hypoplastic left heart syndrome involves underdevelopment of the left side of the heart and can cause signs of shock and poor feeding in newborns. The treatment is cardiac transplantation or staged surgical reconstruction.
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This document contains lecture notes from a presentation on reading and interpreting chest x-rays. It discusses various findings that can be observed on a chest x-ray and their potential medical significance, including cardiomegaly, mediastinal widening, the shape of heart borders, lung opacity and plethora, and situs of organs. It also notes some limitations and fallacies of using metrics like cardiothoracic ratio and provides examples of clinical cases to spot diagnoses from chest x-rays.
Congenital Heart Diseases
This document discusses congenital cardiovascular anomalies, specifically atrial septal defects and ventricular septal defects. It provides information on the incidence, causes, classifications, clinical presentations, investigations, and management of these conditions. The key points are that atrial septal defects and ventricular septal defects are the most common congenital heart diseases, accounting for around 30-35% of cases. They typically present with no cyanosis but can cause heart failure if left untreated. Echocardiography is the main investigation used to diagnose them. Small atrial septal defects may close spontaneously while larger defects usually require surgical closure.
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This document discusses valvular heart disease, focusing on the main heart valves: aortic, mitral, tricuspid, and pulmonic. For each valve, the document covers etiologies, pathophysiology, physical exam findings, diagnosis, and treatment approaches for various valve abnormalities such as stenosis and regurgitation. Key valve diseases discussed in depth include aortic stenosis, aortic regurgitation, mitral regurgitation, mitral stenosis, and tricuspid stenosis. The document emphasizes physical exam maneuvers and findings that are important for diagnosing different valvular conditions.
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The document discusses diagnostic radiology of the cardiovascular system. It provides details on basic X-ray features of heart conditions and describes common diseases including rheumatic heart disease, ischemic heart disease, congenital heart diseases like atrial septal defect and Tetralogy of Fallot. For specific conditions like mitral stenosis, it outlines the hemodynamics, typical X-ray appearances and key diagnostic features.
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2nd-generation Antihistaminic Part I.pptx
CLASSIFICATION OF H1 ANTIHISTAMINICS-
FIRST GENERATION ANTIHISTAMINICS-
1)HIGHLY SEDATIVE-DIPHENHYDRAMINE,DIMENHYDRINATE,PROMETHAZINE,HYDROXYZINE 2)MODERATELY SEDATIVE- PHENARIMINE,CYPROHEPTADINE, MECLIZINE,CINNARIZINE
3)MILD SEDATIVE-CHLORPHENIRAMINE,DEXCHLORPHENIRAMINE
TRIPROLIDINE,CLEMASTINE
SECOND GENERATION ANTIHISTAMINICS-FEXOFENADINE,
LORATADINE,DESLORATADINE,CETIRIZINE,LEVOCETIRIZINE,
AZELASTINE,MIZOLASTINE,EBASTINE,RUPATADINE. Mechanism of action of 2nd generation antihistaminics-
These drugs competitively antagonize actions of
histamine at the H1 receptors.
Pharmacological actions-
Antagonism of histamine-The H1 antagonists effectively block histamine induced bronchoconstriction, contraction of intestinal and other smooth muscle and triple response especially wheal, flare and itch. Constriction of larger blood vessel by histamine is also antagonized.
2) Antiallergic actions-Many manifestations of immediate hypersensitivity (type I reactions)are suppressed. Urticaria, itching and angioedema are well controlled.3) CNS action-The older antihistamines produce variable degree of CNS depression.But in case of 2nd gen antihistaminics there is less CNS depressant property as these cross BBB to significantly lesser extent.
4) Anticholinergic action- many H1 blockers
in addition antagonize muscarinic actions of ACh. BUT IN 2ND gen histaminics there is Higher H1 selectivitiy : no anticholinergic side effects
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