SEARCH RESULTS FOR: tamponade

Pericardial Effusion and Tamponade: Pathogenesis and Clinical Findings

jvp-kussmals-sign-explained

Yu Yan - JVP explained - FINAL.pptx Myocardium of right ventricle becomes fibrotic and stifferKussmaul's sign: JVP increases with inspirationJugular Venous Pressure (JVP): Kussmal's Sign explainedExcessive pericardial fluid compresses heart walls on all sidesLegend:Published January 7, 2013 on www.thecalgaryguide.comMechanismPathophysiologySign/Symptom/Lab FindingComplicationsAuthor: Yan YuReviewers:Sean SpenceJason BasermanJason Waechter** MD at time of publication? Right ventricle wall complianceConstrictive pericarditisRight ventricle prevented from fully expanding ? ability of the right ventricle to accommodate higher venous returnBackup of venous blood into right atrium and preceding internal jugular veinsRestrictive cardiomyopathyInflamed, fibrotic pericardium restricts expansion of heartRight ventricle myocardial infarct Cardiac tamponade (rare)InspirationMore venous blood tries to enter the low-pressure thoracic cavity via the right ventricle? pressure in thoracic cavity JVP should return to normal within 3 respiration cyclesJugular Venous Pressure (JVP): Physical Exam FeaturesExerts less force against vesselsTilting the head of the bed:Low pressure, & the thinner walls of the internal jugular veins, are less able to keep lumen open when compressedLegend:Published January 7, 2013 on www.thecalgaryguide.comMechanismPathophysiologySign/Symptom/Lab FindingComplicationsAuthor: Yan YuReviewers:Sean SpenceJason BasermanJason Waechter** MD at time of publicationBlood in internal jugulars settles to bottom of the vein (analogy: half-full tube of water is turned vertically)Visible waves in the JVP correspond to stages of the cardiac cycleNon-palpableBiphasic waveform? JVP The Jugular Venous Pressure (JVP) Blood pressure in the internal jugular veinsV-waveA-waveRight atrial contractionBlood passively fills right atrium during ventricular systole? JVP? JVPIn: ? intrathoracic pressurePressing hard on abdomen (overlying the liver), or doing a valsalvaFacing lower afterload, Right heart more readily pumps blood into pulmonary circulation? abdominal pressure? venous blood forced up into right atriumVenous blood pressure is normally very lowOccludableNote: Since the internal jugular veins are continuous with the right atrium, the JVP is a reliable estimate of right atrial blood pressure (Central Venous Pressure). The JVP on the right side is a better

AAA-Clinical-Findings-and-Complications

Abdominal Aortic Aneurysm (AAA): Clinical Findings and Complications AAA = Abnormal, irreversible dilation of a focal area of abdominal aorta (area of aorta between diaphragm & aortic bifurcation) to twice the diameter of adjacent normal artery segments Asymptomatic, non-ruptured aneurysm: Most AAAs are asymptomatic until rupture or days before impending rupture Asymptomatic AAAs are only detectable on imaging or by palpation Given their structural weakness, AAAs are at risk of rupture (risk ↑ with ↑ size of aneurysm) Ruptured AAA: a medical emergency Aorta lies in between the peritoneal and retroperitoneal space Symptomatic, non-ruptured aneurysm: rarely, an unruptured AAA can cause symptoms or complications (0.1%-1% of AAAs) Authors: Olivia Genereux, Davis Maclean, Yan Yu* Reviewers: Jason Waechter*, Amy Bromley*, Sandeep Aggarwal*, Gregory Samis* *MD at time of publication Posterior aortic wall rupture Retroperitoneal hemorrhage Sudden and severe abdominal and/or back pain Anterior aortic wall rupture Peritoneal hemorrhage Peritoneal space is larger and holds larger volumes of blood Peritoneal hemorrhages are large (entire blood volume can pool in the peritoneal space in minutes) Prior to rupture, the adventitia (thin outermost collagenous layer of the aorta) may dilate significantly Adventitia is the only layer of the aorta that contains sensory innervation à nociceptors there can be activated by adventitia dilation Very rarely (0.1%), areas of stagnant blood flow within the AAA allow for blood & clotting factors to accumulate Thrombi (blood clots) develop in these aneurysms Thrombi may dislodge and travel (embolize) to distal vasculature, cutting off blood- flow to these areas This process (referred to as tamponade) is crucial in preventing catastrophic blood loss, allowing for a window of opportunity for treatment Compensated Hypovolemic Shock: Low blood pressure & poor organ perfusion, but blood loss has temporarily stopped. This state of shock is compatible with life if patient is otherwise healthy (e.g. no coronary artery disease) ↓ space for blood to accumulate in the retroperitoneal space (compared to the peritoneal space) Rapid pressure ↑ in retroperitoneal space overcomes the pressure in aorta Since blood will only travel from areas of ↑ pressure to areas of ↓ pressure, this pressure gradient prevents further blood loss from ruptured aorta Massive hemorrhage due to high blood flow volume through aorta Hypotension and rapid progression to hypovolemic shock Abdominal and/or àorgan ischemia back pain The most common symptom of a symptomatic non- ruptured aneurysm, and may be the first sign of an impending aneurysm rupture Death within minutes (rare) If low blood pressure is now (inappropriately) treated with fluid resuscitation, the blood pressure will ↑ Differential pressure gradient is reversed (aortic blood pressure > pressure in retroperitoneal space) Bleeding into retroperitoneal space resumes Decompensation of hypovolemic shock Possible death Kidney ischemia Lower limb ischemia Time exists to transfer patient to tertiary care center for surgical treatment Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Re-Published February 28, 2021 on www.thecalgaryguide.com

perikarderguss-tamponade-pathogenese-und-klinische-befunde

perikarderguss-tamponade-pathogenese-und-klinische-befunde

Death Cardiovascular Respiratory and Neurologic Mechanisms

Death: Cardiovascular, Respiratory and Neurologic Mechanisms Mitochondria in tissues unable to utilize O2 Reduced hemoglobin in blood to carry O2 Low oxygen content in blood (CaO2) Hypoxemia (Type I Respiratory Failure): low dissolved oxygen in blood (PaO2) Lungs can’t oxygenate blood fast enough Lungs can’t rid blood of CO2 fast enough Hypercapnia / hypercarbia (Type II Respiratory Failure): elevated dissolved CO2 in blood (PaCO2) Cerebral vasodilation Toxins: e.g. cyanide, pesticides, arsenic Severe anemia Distributive problems: Systemic inflammation (sepsis, anaphylaxis, pancreatitis), adrenal insufficiency, vasodilatory drugs Obstructive problems: Cardiac tamponade*, tension pneumothorax* or massive pulmonary embolism* Hypovolemic* problems (low blood volume): Hemorrhage, dehydration, widespread skin disruption or burns Cardiac valve dysfunction Myocardial infarction* or cardiomyopathy Cardiac arrhythmia or heart block Disturbed electrical activity in cardiomyocytes Peripheral metabolic disturbances Hypokalemia*, Hyperkalemia* Acidosis* (including renal failure) Hypothermia* Toxins* (e.g. cocaine, beta blockers, tricyclics) Severe thyroid derangement Inappropriate systemic vasodilation Adjacent forces impair heart filling Low cardiac preload Low stroke volume (SV; depends on valves, contractility, preload) Decreased systemic vascular resistance (SVR) Low blood pressure (BP = CO x SVR) Decreased cardiac output (CO = SV x HR) Disseminated intravascular coagulationàwidespread thrombi that occlude blood flow (also causes hemorrhage, see relevant box at left) Methemoglobinemia: some hemoglobin gets stuck in a state that can’t carry O2 Hemoglobin has reduced capacity to carry or release O2 Drugs: e.g. dapsone, nitrates Carbon monoxide poisoning Circulatory collapse / shock: inadequate perfusion of tissue with blood Respiratory collapse: blood has insufficient useable O2 content Ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT) Hypoxia*: inadequate O2 delivery or utilization in tissues Hypoxia creates metabolic disturbances that impair cardiac cells. Alternatively, any of the preceding conditions marked with (*) can directly trigger cardiac arrest first Pulseless Electrical Activity (PEA): organized activity on ECG with no cardiac output (can be preceded or mimicked by pseudo-PEA, in which there is still some output on ultrasound) Low atmospheric pressure or oxygen content Severe lung disease Asthma, COPD, interstitial lung disease, congestive heart failure, pulmonary hypertension, pulmonary embolism, lung collapse / atelectasis Acute respiratory distress syndrome Pneumonia, aspiration pneumonitis, inhalational injury, systemic inflammation, drowning Severe hypoventilation Respiratory fatigue, advanced COPD, chest wall disorders, neuromuscular disorders, upper airway obstruction, toxins (e.g. opioids, botulism) Can degenerate at any time Asystole: no cardiac electrical activity or output Death Respiratory arrest: cessation of breathing Inability to protect airway Decreased level of consciousness Note This is a broad overview of the many scenarios that can result in death. For detailed explanations of the various disease mechanisms, refer to the corresponding slides. * = reversible causes of cardiac arrest (Hs and Ts) Author: Ben Campbell Reviewers: Yan Yu* Huma Ali* * MD at time of publication Bradycardia (low heart rate, HR) Unopposed parasympathetic stimulation of heart (can also cause vasodilation, see Distributive problems) Disruption of spinal cord sympathetic control Injury to cervical or upper thoracic spinal cord Irreversible cessation of cardiac, respiratory, and brain function Prolonged seizure initially causes increased cardiovascular activity, until the system fatigues Disruption of respiratory control center in medulla Expanding skull contents squeeze brainstem (herniation) Increased intracranial pressure Edema from intracranial hemorrhage, trauma, brain mass Edema, inflammation, hypoxia and/or metabolic derangements cause diffuse neuron dysfunction Central nervous system infection Dementia, particularly with delirium Massive ischemic stroke Seizure activity prevents or alters breathing Metabolic disturbances that affect the central nervous system Hypoglycemia Hypocalcemia, hypercalcemia Hyponatremia, hypernatremia Uremia Acute liver failure (hyperNH4) Many drugs / toxins Withdrawal (e.g. EtOH) Status epilepticus Brainstem lesion (e.g. stroke, neoplasm, inflammatory) Nervous System Insult Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published November 11, 2023 on www.thecalgaryguide.com Respiratory System Insult Cardiovascular System Insult Cardiogenic problems

Pulsus Paradoxus

Pulsus Paradoxus: Pathogenesis and Clinical Findings Inspiration: Diaphragm and intercostal muscles contract Author: Yan Yu, Victória Silva, Layla Al-Yasiri Reviewers: Sean Spence, Laura Craig, Juliette Hall, Raafi Ali, George Tadros. Shahab Marzoughi Nanette Alvarez* * MD at time of publication Vascular pathology (rare) Thoracic cavity expands Lungs expand and intrathoracic pressure ↓ Physiologic: ↑ Venous return to right (R) heart ↑ R heart preload (volume of blood inside the ventricle right before it contracts) ↑ Blood pools in the right side of the heart Obstructive lung diseases (e.g., COPD**, asthma**) Hyperinflated lungs ↑ Stretching of pulmonary vessels at rest On inspiration, ↑↑ stretching of pulmonary vessels ↑↑ Blood pools within pulmonary vasculature ↓↓ Flow to L heart Pathologic: Constrictive pathologies (e.g., cardiac tamponade**, constrictive pericarditis**) Decreased pericardial compliance Constriction of ventricles On inspiration, ↑ venous return to R heart (normal) R ventricle unable to fully expand due to ↓ compliance Septum bows into L ventricle L ventricle unable to fully expand ↓↓ Filling of L heart ↓↓ L ventricular end diastolic volume ↓↓ L heart stroke volume ↓↓ Cardiac output Pulsus Paradoxus Exaggerated ↓in systolic BP on inspiration (>10mmHg) Air flows into the lungs Pulmonary vessels are physically stretched/pulled ↑ Blood pools in pulmonary vessels ↓ Return of blood to left (L) heart ↓ L heart preload ↓ L heart stroke volume ↓ Cardiac output Obstruction of superior or inferior vena cava (e.g., clot) ↓↓ Venous return to R heart at rest ↓↓ Right heart filling ↓↓ Blood flow to pulmonary arteries Pulmonary embolism** Clot occludes pulmonary arteries/ arterioles ↓↓ Flow to pulmonary veins At rest, ↓↓ flow to L heart On inspiration, ↓↓↓ flow to L heart ↓ Systolic blood pressure (BP) of < 10mmHg on inspiration BP = cardiac output x systemic vascular resistance **See corresponding Calgary Guide slides Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published Jan 21, 2013; updated Dec 3, 2024 on www.thecalgaryguide.com

心包积液及心包填塞

心包积液及心包填塞: 发病机制及临床表现