Cardiac causes of acute cardiogenic pulmonary edema
-hypoxia
-CHF
-MI
-LVF
-valvular incompetence - not all the blood is ejected from the ventricle in the right direction
-chronic HT -> hypertrophy - cardiac muscle thickness and reduces the size of th exchanger less blood can be injected
-cardiac tamponade-> large amount of blood in the pericardial sack impending stretch of the myocardium
-dysrhtymias
Other causes of acute cardiogenic pulmonary edema
-over dose
-CVA
-near drowning
-irritant gas inhalation
-rapid IV infusion
-blood disorders
-intracranial haemorrhage
-ARDS
-PE
-shock/ sepsis
-eclampsia
-pancreatic
-lymphatic disorder
-capillary epithelium disorder
Patho of acute caridogenic pulmonary edema
-acute pulmonary edema of left ventricular dysfunction with pulmonary venous HTN & alveolar flooding
-LV failure occurs due to primary cardiac/ hypoxia event, means it becomes unstable to effectively receive blood form the RSH and pump into systemic circulation
-the left ventricle stiffens due to hypoxia and cannot stretch
-reduced elasticity of the LV lead to dismissed cardiac output (frank starling law)
-LV pressure increases and is transmitted back into the atria and then into the pulmoanry venous circulation and pulmoanry capillaries
-Hydrostatic pressure exceeds onotic
*under normal condition the lymphatic drianaing would remove excess fluid in the intersitial of the lung
Pt presentaiton in acute cardiogenic pulmoanry edema
-dyspnea
-pale or cyanosed
-crackles
-tachcyardia
-elevated BP
-diaphoretic
-shallow rapid respirations
-chest pain
-coughing pin frothy sputum
-wheeze
-peirphal edema
-JVD
Patho of anaphylaxis
-exposure to allergen
-causes IgE production
-allergen introduced
-local response causes allergen activate the immune system to provide large amount of IgE
-large amount of IgE bind to receptor on surface of mast cell remain inactive till there is repeat exposure
-when allergen and cross links to IgE sensitized to mast cell & basophils histamine is release
What are some immediate histamine relase causes in anaphylaxis:
-respiratory
-cardio
-GI
-CNS
-skin
Respiratory
-bronchospasm
-mucus plug
-inflammation and airway swelling
Cardio
-periphearl vasodilation
-increased capillary permeability -> leakage/ loss of plasma form circulation
GI
-increased GI activity
-increased mucus secretion/ fluid in gut -> N/V, diarrhea, cramps and increased salvia production
CNS
-impaired gas exchange and shock causing CNS
-deteriorate of neurological funciton
Skin
-sign of secondary to vasodilation
-erythema and utiracria
-itching
What are the 2 stages of anaphylaxis?
Stage 1
-primary - vasodialtion and vascular leakage and smooth muscle contraction
-5-30 mins post exposure subsides after 60 mins
Stage 2
-secondary - more intense infiltration of tissue with acute and chronic inflammatory cells in addition to epithelial cell damage
-2-8 hours later and last up to several days
Examples of extrinsic and intrinsic bronchospasm and asthma
Extrinsic (allergy)
-allergens
-pollen
-animal dandier and dust mites
Intrinsic (non allergic)
-exercise
-cold air
-smoke
-aspirin/ NSAID/ other meds
-emotional stres
=infection
How is asthma different than anaphylaxis?
Asthma
-primary failure is in the airway wall
Anaphylaxis
-primary failure is in the immune system -> circulation and capillary bed
Cor pulmonale in related to COPD
-right sided heart failure caused by lungs disease
Step 1
-COPD alveoli destroyed airway are inflamed and narrowed, ga exchange poor
Step 2
-low alveolar O2 -> pulmonary arterioles constriction (hypoxia pulmonary vasoconstriction)
Step 3
-resistance in the pulmonary circulation increases
Step 4
-RV must pump against it higher resistance
Step 5
-RV is designed for low pressure so this cause RV hypertrophy
Metabolic causes for cardiac arrest
-hyperkalmeia (excess potassium) leads to winding of the QRS and peaked T waves that may decorate into VT, VF, asystole or PEA
What is PEA for cardiac arrest?
-the heart electrical system is working but the hot actually pumping blood
Patho of cardiac arrest
-blood flow and oxygen supply to the coroanry arteries ceases due to one of many possible cause
-oxygen supply and waste removal stops due to cessation of blood flow
-hypoxia leads to anoxia and dysrthymias arise due to heart inherent demand for oxygen for caridac muscle contraction and relaxation and electrical conducigton through use of ATP to power IOn channel pump
-depletion of oxygen and glucose to the brain causes LOC
-global ischemia occurs with consequences at cellular level that affect organ funciton
-body forced into anerobic metoalism , increase lactic acid
-ATP becomes depleted
-in flux of potassium and influx of Na and ca into the cell
-excess sodium in the cell casues cellar edema as water follows sodium into cell
-excess calcium damage mitochondria
Insulin
-stimulate uptake of glucose into the cell
-promote glycegenesis
-inhibits gluconeogenesis
-prevents glycogenolysis
-inhibits lipolysis
Glucagon
-travels from the pancreas via portal vein where it situate glycgenolysis
-maintain BGL between meal and fasting
-stimulate gluconeogenesis
-sitmulates lipolysis
Adrenal cortex in diabetes
-catecholamine , such as Adrenalin is related form the adrenal medulla during periods of hypoglycemia
-adrenal acts ismluar to glucagon and sitmualtes glycenolsysis
-increase lipolysis
-adrenal cortex also relases growth hormone and cortisol in response to prolonged hypoglmeia and sitmualtes gluconeogenes in the absence of glucose
Ketoacidosis
-usually in type 1
-no insulin so it inhibits lipolysis
-fatty acid released fat cells -> convert to ketones in the liver
-fatty acid metoablism -> ketones production -> leads to ketoacidosis
-form of metabolic acidosis
Leads to
-increased resp to correct acidosis
-ongoing dehydraiton leads to circulatory shock
-cardiac dystopias fatal arrhythmias
Somatic pain
-skin and deep tissue are innervated by somatic fibers with tend to sitmalute more intense pain easier to pinpoint
Visceral
-internal organ and blood Vessel are innervated by visceral pain fibers, and tend to be dull/ vague pain harder to localize and pinpoint discomfort, heaviness
What is angina
-Symptoms of CAD resulting a demand/ supply mismatch oxygen delivery and waste removal
-myocardial oxygen demand increases, coroanry artery dilation increases blood flow and oxygen supply but in CAD theses artieores are already chronically dilated distal to the atheroma and cannot further increaed blodo flow
-angina caused by atheorsiclos or vasospams
Vasospastic angina
-casued by coroanry artery spasm restricting myocardial blood flow
-pain can occur at any time including during sleep
-pain is casued by oxygen supply and demand mismatch again leading to anaerobic metoablism and prohibition of lactic acid -> lactic acid simulates nocierpecors and is interpreted as pain
Tachycardia
-chest pain potently may be experienced is in prolonged stated of tachycardia or has rapid tachycardia
-supply and demand mismatch heart pumping to quick defence in filling of coaornay rites in diastole
-coroanry arteries poorly perfused
-cardiac muscel is forced into anaerobic metabolism due to reduced blodo supply and therefore reduced o2 supply, and lactic acid is produced, stimulating nocieptors and causing pain
Bradycardia
-chest pain potently may be experienced in prolonged bradycardia
-heart relate rescued diastole occurs less frequently therefore the coronary arteries are perfused less frequently
-supply/ demand mismatch is present as the supply is reduced
-cardiacs mucle is forced into anaerobic metabolism, lactic acid is produced, nocieptors are stimulated and interpreted as pain
Rigor mortis
—due to lack of ATP, which is required to remove myosin heads form actin, causing muscle relaxation, therefore muscle stays in contracted state
