20249138
Descripción
Fichas por Sam Adeyiga, actualizado hace más de 1 año
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Creado por Sam Adeyiga
hace alrededor de 5 años
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| Pregunta | Respuesta |
| S/S of HF | Sym: dyspesia and fatigue Signs: Edema and rale (crackles) |
| Causes of HF? | 1. Systolic dysfunction = decrease in vent. contractility 2. Diastolic dysfunction = restriction in vent. filling = relaxation mechanism. |
| MAP = ? | CO * TPR |
| The impt. of Frank-Starling mechanism = ? | 1. Involves ability of heart to alter the forces of contractility based on the level of preload. 2. involves relationship of the length-tension w/ relationship of myocardial muscle 3. involves cardiac sarcomere length (determined by end diastolic volume; EDV) 4. Use in compensatoty mechanisms |
| Increased Sarcomere length = decreassed space btw myo and actin = ------ cross-bridge/overlap | increase |
| Increased sarcomere = ------- tension ------- calcium in the cell | increase, increase |
| 1. Sympathetic activation will do what to the myocardium? 2. Parasympathetic activation will do what to myocardium? | 1. Contractile of heart 2. decrease frequency of HR = decrease HR |
| What are the initiating events of HF? | MI HTN Ischemia Edema/Vol overload * These will cause cardiac injury wh/ is the 1st step of HF **This will result in compensatory mechanisms. |
| What do you look for in presented HF patients? Including the lab? | Productive cough JVD S3 gallop Pitting Edema or Peripheral Edema Weight gain |
| compensatory mechanisms involves: | 1. Sympathetic stimulation = NoEpi. 2. Cardiac modeling = Cardiac hypertrophy and dilation |
| How does RAAS activation affects Preload, Contractility and Afterload? | RAAS will increase contractility by increasing volume overload |
| How does Cardiac hypertrophy activation affects Preload, Contractility and Afterload? | Cardiac hypertrophy activation increased contractility |
| In Diastolic dysfunction what factors are affected? | 1. Venous return = RAAS = increased blood volume = increased venous returns. 2. Compliance = stretch during diastole = stiffness as a result of hypertrophy = decreased EDV. 3. Extent and rate of myocardial relaxation = Ca removal by sarcoplasmic reticulum Ca2+ adenosine triphosphatase (SERCA2a) = slowing myocardial relaxation |
| In Systolic dysfunction, as the ability to contract decreases, what happen to end systolic volume, CO, EDV and pressure? | 1.End systolic volume increase 2. Cardiac Output decrease 3. EDV increase 4. Pressure increase |
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