Introduction Sudden cardiac death (SCD) is a world wide health problem resulting in one-fifth of unexpected deaths in the western world. Ventricular fibrillation (VF) is one of the life-threatening arrhythmias contributing to the increasing number of individuals needing urgent medical assistance (Wellens, Gorgels & Munter, 2013). The following case study will explore a complex critically ill patient who has suffered from a ventricular tachycardia (VT) and VF due to dilated left ventricle (LV) with severe segmental systolic function. The case study will review the pathophysiology of the patient’s current health problem and will further investigate the primary interventions in relationship to evidence based practice.
Sudden Cardiac Death SCD …show more content…
Patient X experienced VF for the reason that he previously had experienced acute myocardial infarct (AMI). Myocardial scar tissue occurs with AMIs and comprises a combination of fibrosis and surviving myocytes to provide a path of re-entry for VT which can cause SCD (Stevenson & John, 2011).
Pathophysiology of poor LV function HF is an intricate clinical syndrome that is caused by any systemic or functional impairment of ventricular filling or blood discharge (Yancy et al., pp. 246, 2013), for instance, from injury to the myocardium causing decreased CO. Patient X’s HF is due to IHD, hypertension and smoking. Valvular disease, cardiomyopathy, infections and diabetes can also cause HF. As CO decreases, dyspnoea, peripheral oedema, ascites and fatigue may occur. There are several compensatory mechanisms which occur due to decreased CO (Kemp & Conte, 2012). The first compensatory mechanism is the Frank Starling mechanism which commences as stroke volume (SV) decreases. Higher muscle contraction/stretch and SV intensifies left ventricular end-diastole pressure (LVEDP) hence increasing CO. Patient X’s CA showed a high LVEDP of 28 and a dilated LV with severe global dysfunction (Holubarsch et al., …show more content…
This process involves three key components. The first is renin which stimulates the formation of angiotensin which in turn stimulates the conversion of angiotensin to angiotensin II (AII). AII increases systemic vascular resistance (SVR) and arterial pressure, and stimulates the release of aldosterone causing sodium reabsorption and water retention in the body (Klabunde, 2014). As sodium and fluid retention occurs, preload increases CO thus increasing blood pressure and renal perfusion (Andrew, 2002). AII and aldosterone lead to cardiac muscle apoptosis resulting in fibroblast activation, myocardial scarring and cardiac remodelling, causing worsening of HF (Unger & Li,
Sudden Cardiac Death SCD …show more content…
Patient X experienced VF for the reason that he previously had experienced acute myocardial infarct (AMI). Myocardial scar tissue occurs with AMIs and comprises a combination of fibrosis and surviving myocytes to provide a path of re-entry for VT which can cause SCD (Stevenson & John, 2011).
Pathophysiology of poor LV function HF is an intricate clinical syndrome that is caused by any systemic or functional impairment of ventricular filling or blood discharge (Yancy et al., pp. 246, 2013), for instance, from injury to the myocardium causing decreased CO. Patient X’s HF is due to IHD, hypertension and smoking. Valvular disease, cardiomyopathy, infections and diabetes can also cause HF. As CO decreases, dyspnoea, peripheral oedema, ascites and fatigue may occur. There are several compensatory mechanisms which occur due to decreased CO (Kemp & Conte, 2012). The first compensatory mechanism is the Frank Starling mechanism which commences as stroke volume (SV) decreases. Higher muscle contraction/stretch and SV intensifies left ventricular end-diastole pressure (LVEDP) hence increasing CO. Patient X’s CA showed a high LVEDP of 28 and a dilated LV with severe global dysfunction (Holubarsch et al., …show more content…
This process involves three key components. The first is renin which stimulates the formation of angiotensin which in turn stimulates the conversion of angiotensin to angiotensin II (AII). AII increases systemic vascular resistance (SVR) and arterial pressure, and stimulates the release of aldosterone causing sodium reabsorption and water retention in the body (Klabunde, 2014). As sodium and fluid retention occurs, preload increases CO thus increasing blood pressure and renal perfusion (Andrew, 2002). AII and aldosterone lead to cardiac muscle apoptosis resulting in fibroblast activation, myocardial scarring and cardiac remodelling, causing worsening of HF (Unger & Li,