Shock and Cardiac Arrest
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Shock and Cardiac Arrest - Marcador
Shock and Cardiac Arrest - Detalles
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| 🇬🇧 | 🇬🇧 |
| Why does arterial blood pressure fall generally in shock | This can because of decrease in cardiac output and decrease in total peripheral resistance |
| What can cause fall in cardiac output | Hypovolaemia Loss of contractility Reduced filling of the cardium |
| What causes the fall in Total Peripheral Resistance | Profound vasodilation |
| What are some causes of hypovolemic shock | Blood loss due to hemorrhage Gastro-intestinal loss Burns Third space loss → fluid losses into spaces that are not visible, such as the bowel lumen (in bowel obstruction) |
| What is the pathophysiology behind hypovolemic shock | Decreased blood volume leads to fall in venous pressure leading to reduced end-diastolic volume so there is reduced stroke volume which leads to fall in CO so a fall in mean arterial blood pressure Reduction in arterial BP is sensed by baroreceptors Which triggers a number of compensatory mechanisms: RAAS system Sympathetic system Internal transfusion |
| For the 3 compensatory mechanisms for hypovolemic shock, what is the pathophysiology behind that | Increased sympathetic activity --> Increase HR, Increase contractility, Vasoconstriction , Venoconstriction RAAS --> angiotensin II leads to aldosterone release, Na+ reabsorption , vasoconstriction , releases noradrenaline to increase sympathetic activity and release of ADH from the anterior pituitary gland Internal Transfusion --> Increase in TPR leads to decrease hydrostatic pressure of the capillary which leads to net flow of fluid into the capillaries |
| What can prolonged shock lead to | Imparied tissue perfusion Tissue hypoxia release of metabolic vasodilators Fall in TPR further fall in mean arterial BP Vital organs are no longer perfused |
| What are some clinical features of hypovolemic shock | Tachycardia Sweating Weak peripheral pulses Prolonged CRT Pale skin Cold / clammy extremities Drowsiness / confusion / irritability Tachypnoea → high resp rate |
| Management of hypovolemic shock | ABCDE management : Give oxygen Replace what is lost i.e. blood or fluid Fix underlying cause e.g. surgery |
| If there is pulmonary embolism, how can that lead to shock | A massive, proximal pulmonary embolism can occlude a large pulmonary artery, which means Right ventricle cannot empty Reduced return of the blood onto the left side of the heart Reduced left EDV Reduced Stroke Volume Reduced CO Fall in mean arterial pressure |
| Clinical picture of PE and management | Shortness of Breath, Pleuritic chest pain, haemoptysis Raised JVP Tachycardia, hypotension, pale, sweaty Management --> warfarin and other blood thinners , also any replace any fluid |
| What is cardiac tamponade | When the heart cannot fill because there is a buildup in the pericardial space restricting filling Which leads to reduced EDV --> SV --> CO --> fall in Arterial BP |
| What are some causes of cardiac tamponade and clinical picture and also management | Causes --> Blunt / penetrating chest trauma or Myocardial rupture Clinical picture --> Becks Triad: ↓ BP + ↑ JVP + Muffled heart sounds, Tachycardia, SOB etc – features of compensation Management --> pericardiocentesis |
| What is cardiogenic shock/causes | Caused by a fall in contractility so the ventricles are unable to empty properly Can be caused by : MI Acute worsening of heart failure Arrhythmias ( loss of coordinated pump action ) |
| Pathophysiology of cardiogenic shock | Heart fills but fails to pump effectively which results in Reduced SV Reduced CO fall in mean arterial BP Central venous pressure could be raised or normal |
| What is septic shock | Circulating bacteria release endotoxins which stimulates a systemic inflammatory response, causing Vasodilation which leads to fall in TPR increased vascular permeability -> fall in intravascular fluid volume -> fall in CO Leads to fall in mean Arterial BP Baroreceptors detect drop in arterial pressure triggering increased SNS activity Increased HR + SV Vasoconstriction overridden by endotoxin effects This could also be a cause of distributive shock |
| What is anaphylatic shock | Anaphylaxis = severe allergic reaction Hypersensitive response from the immune system to usually harmless substances Known as allergens e.g. peanuts etc. Results in release of histamine from mast cells Histamine is a potent vasodilator Fall in TPR and fall in mean arterial BP Histamine also causes bronchospasm and laryngeal oedema = difficulty breathing This could also be a cause of distributive shock |
| Management of anaphylatic shock | ABCDE management Adrenaline, hydrocortisone, chlorphenamine |
| What is cardiac arrest | Heart suddenly stops pumping effectively – loss of cardiac output Due to a loss of effective electrical or mechanical activity Patient presents with loss of consciousness, loss of pulse, loss of breathing |
| Management of cardiac arrest | CPR and defibrillation / drugs electrical current delivered to the heart depolarises all cells potential for coordinated electric activity to restart Drugs – adrenaline, amiodarone |