**3.1 Cardiac reserve and response after lower limb revascularization related to MACE**

The blood flow rate which feed to the end organs are determined by the cardiovascular system. Each organ can adjust their vascular resistance or afterload which maintaining the blood flow and pressure to their vascular bed by the autoregulation mechanisms. Therefore, revascularization procedures which result in the reduction of afterload rapidly are significantly increased blood flow to the lower

#### **Figure 3.**

*The normal physiologic changes of cardiovascular system and cardiac response after lower limb revascularization. BP, blood pressure; CO, cardiac output; TPR, total peripheral resistant; SV, stroke volume; HR, heart rate.*

*Cardiovascular Complications Related to Lower Limb Revascularization and Drug-Delivering… DOI: http://dx.doi.org/10.5772/intechopen.107973*

extremities [39, 42, 43]. The preoperative cardiac reserve and cardiac response after lower limb revascularization are the important risk factors of perioperative MACE [14, 37, 43]. The rapidly increasing of the lower limb perfusion after revascularized procedures causes the alteration of cardiac physiology and activation of autoregulation process [3, 41, 42]. The cardiac responsibility is dependent on the increasing of blood flow rate to the revascularized limb which is determined by the degree of revascularization. If the revascularization is successful, almost stenotic, or occlusive lesions are well recanalization by endovascular therapy or open vascular bypass procedure which is cross all vascular lesions from the good inflow to the good run-off vessel, the after load of the lower limb are decreasing rapidly. The decreasing afterload leads to the reduction of total peripheral resistance (TPR) (**Figure 3**).

In the normal cardiac reserve patients, the immediate cardiac response to maintain the mean arterial blood pressure (MAP) is increasing of the cardiac output (CO) by the mechanoreceptors, known as baroreceptor reflex which are in the aortic arch and carotid sinus. The baroreceptors activity is decreasing lead to the reduction of impulse toward to the cardiovascular center. The increasing of sympathetic activity and the reduction of parasympathetic activity cause the increasing of CO (Eq. (1)). The increasing of CO is performed by the increasing of stroke volume (SV) and heart rate (HR) which are regulated by an autonomic nervous system (ANS) and a hormonal system though the positive chronotropic substances in human body. (Eq. (2)) (**Figure 3**).

$$\mathbf{MAP} = \mathbf{CO} \times \mathbf{TPR} \tag{1}$$

$$\text{MAP} = (\text{SV} \times \text{HR}) \times \text{TPR} \tag{2}$$

The good cardiac reserve patients with good ejection fraction (EF) are regulated the SV by increasing of cardiac contractility and venous return (Eq. (3)). The increasing of cardiac contractility is activated by the neurohormonal system through the positive inotropic substances. The venous return which is regulated by the blood volume and venous tone are increased by the renin-angiotensin-aldosterone system (RAAS) activation, antidiuretic hormone (ADH) releasing, sympathetic nervous system, and central nervous system (Eq. (4)) (**Figure 3**).

$$\text{MAP} = \text{(cardiac contraction} \times \text{venous return)} \times \text{HR} \times \text{TPR} \tag{3}$$

$$\text{MAP} = \text{cardiac contraction} \times \text{(blood volume} \times \text{venous tone}) \times \text{HR} \times \text{TPR} \tag{4}$$

During the lower limb revascularization in patients with CLTI, the cardiac response by the increasing of SV through the cardiac contractility and increasing of HR are requiring the adequate perfusion of a myocardium which is more than resting cardiac metabolic requirement in non-revascularization of lower limb patients. So, the good functional status and cardiac reserve by the coronary artery perfusion which feeding to the myocardium is very important to prevent perioperative MI. In addition, the normal cardiac response and autoregulation process are controlling the MAP to keep a constant blood flow to the other vital organ including the brain and renal to prevent perioperative stroke and acute kidney injury (AKI), respectively (**Figure 3**) [37, 41, 42].

For poor functional status and poor cardiac reserve patients, the cardiac response after revascularization though the increasing of heart rate and cardiac contractility to maintain MAP which increase the perfusion demand of myocardium are risk of acute

#### **Figure 4.**

*The physiologic disturbance of cardiovascular system after lower limb revascularization in patients with coexisting coronary artery disease. BP, blood pressure; CO, cardiac output; TPR, total peripheral resistant; SV, stroke volume; HR, heart rate; ACS, acute coronary syndrome; UA, unstable angina; MI, myocardial infarction.*

coronary syndrome (ACS) (Eq. (3)). The coexisting CAD or HF causes the limitation of blood supply to the myocardium and poor ejection fraction (EF) cause the insufficient perfusion to the heart and other organ. Therefore, the MI and acute HF are usually precipitated during revascularization procedure in CLTI patients with cardiac comorbidities. The ACS including UA, STEMI, and NSTEMI. After the mismatch of cardiac demand–supply, the severity of myocardial ischemia can present from the UA without myocardial necrosis to the myocardial infarction (MI) which there is myocardial ischemia with detectable myonecrosis by the releasing of cardiac biomarkers such as creatine kinase, troponin, myoglobin in the systemic circulation (**Figure 4**) [41, 42].

The consequence of MI or acute HF are systemic poor perfusion and cardiogenic shock. The autoregulation process to keep the adequate perfusion to the brain is the vital role to prevent stroke for this situation. The concomitant significant arterial occlusive disease of the carotid and vertebral arterial system can precipitate the perioperative stroke after revascularization because the decompensate in cardiac responsibility and autoregulation process which lead to the failure to maintain the constant blood flow to the brain. For this reason, the concomitant CAD, HF or CVD in patient with CLTI are high risk of MACE during lower limb revascularization. The early detection, optimization of the functional status, aggressive medical treatment in the preoperative phase before lower limb revascularization should be performed intensively to decrease the risk of perioperative MACE and to increase the chance of a functional limb salvage and long-term ambulatory status which effect on quality of life and cardiovascular mortality in patients with CLTI [19, 20].
