**4. Diagnosis and clinical presentation**

The diagnosis of CS requires a high index of suspicion due to its high morbidity and mortality. It should be noted that up to 70% of patients with CS will develop shock later during their hospital stay [4].

Most patients with CS are critically ill and might complain of chest pain and/or dyspnea. There are physical exam findings that are more specific to CS than other types of shock, such as elevated jugular venous pressure (JVP), S3 gallop and the presence of pulmonary rales. In fact, the presence of elevated JVP > 8 cmH<sup>2</sup> O and rales more than one-third of the lung bases predicted CS with very high sensitivity and specificity [14]. The risk factors that are associated with a higher risk of CS in ACS patients are female gender, diabetes mellitus, anterior wall MI, prior history of MI and older age [14, 15].

Other signs and symptoms of CS are generally those of tissue hypoperfusion, such as the presence of hypotension (SBP < 90 mmHg or MAP < 65 mmHg) in addition to tachycardia, altered mentation, decreased urine output and cold and clammy skin.

Electrocardiogram (ECG) and chest X-ray (CXR) should be obtained in all patients presenting with shock. CXR in CS may show pulmonary edema, pleural effusion, pulmonary vascular congestion or enlarged cardiac silhouette. Cardiac troponin is also mandatory for all patients with suspicion of shock from cardiac causes at the time of presentation and then repeated within 3–6 h [16].

ECG can help diagnose acute STEMI, Q waves or any active cardiac ischemia; although in a routine general practice only about 50% of patients with suspected NSTEMI will have ECG changes that are diagnostic of myocardial infarction at the time of presentation [17].

The presentation ECG carries prognostic information, as well, and can identify high-risk patients. In an analysis from the SHOCK trial [17], which included CS patients caused by AMI, a higher baseline heart rate was associated with a higher one-year mortality. Also, in CS patients secondary to inferior MI who received medical management, a longer QRS duration and a higher sum of ST segment depression in all leads were associated with a higher oneyear mortality [17].

Echocardiography is of utmost importance in the evaluation of shock patients especially when the etiology of shock is not well established. It is noninvasive and readily available at bedside. It helps identify severe valvular regurgitant or stenotic lesions, evaluate for ventricular or septal rupture post-AMI and check for cardiac tamponade.

Two-dimensional echocardiography allows for the identification of LV ejection fraction, assessment of segmental wall motion abnormalities and RV function. Doppler echocardiography allows for the assessment of early mitral filling velocity (E) and the mitral annulus tissue velocity (e') which greatly helps the clinician identifying elevated LV filling pressures with excellent sensitivity and specificity. E:e' > 15 correlates with LVEDP > 14 mmHg and E/e' < 8 correlates with normal LVEDP [18, 19].

Pulmonary artery (PA) catheterization—Swan-Ganz catheter—is an excellent tool for confirming the diagnosis and guiding the medical and mechanical management. In CS, there is an increase in the right atrial (RA) pressure, RV systolic and diastolic pressures and pulmonary capillary wedge pressure (PCWP), and a decrease in the cardiac output and index (**Figure 3**). SVR can also be calculated using the PA catheter and is frequently elevated in CS patients. Currently, the main indication for PA catheter use is to establish the diagnosis of CS when the

**4. Diagnosis and clinical presentation**

embolism; PAH, pulmonary arterial hypertension.

fact, the presence of elevated JVP > 8 cmH<sup>2</sup>

prior history of MI and older age [14, 15].

hospital stay [4].

144 Interventional Cardiology

within 3–6 h [16].

The diagnosis of CS requires a high index of suspicion due to its high morbidity and mortality. It should be noted that up to 70% of patients with CS will develop shock later during their

**Figure 2.** The most common causes of cardiogenic shock. (A) ACS represents 80% of CS cases, (B) non-ACS etiologies, which represent 20% of CS causes. ACS, acute coronary syndrome; LV, left ventricle; RV, right ventricle; HCM, hypertrophic cardiomyopathy; ADHF, acute decompensated heart failure; CMP, cardiomyopathy; PE, pulmonary

Most patients with CS are critically ill and might complain of chest pain and/or dyspnea. There are physical exam findings that are more specific to CS than other types of shock, such as elevated jugular venous pressure (JVP), S3 gallop and the presence of pulmonary rales. In

predicted CS with very high sensitivity and specificity [14]. The risk factors that are associated with a higher risk of CS in ACS patients are female gender, diabetes mellitus, anterior wall MI,

Other signs and symptoms of CS are generally those of tissue hypoperfusion, such as the presence of hypotension (SBP < 90 mmHg or MAP < 65 mmHg) in addition to tachycardia,

Electrocardiogram (ECG) and chest X-ray (CXR) should be obtained in all patients presenting with shock. CXR in CS may show pulmonary edema, pleural effusion, pulmonary vascular congestion or enlarged cardiac silhouette. Cardiac troponin is also mandatory for all patients with suspicion of shock from cardiac causes at the time of presentation and then repeated

ECG can help diagnose acute STEMI, Q waves or any active cardiac ischemia; although in a routine general practice only about 50% of patients with suspected NSTEMI will have ECG

changes that are diagnostic of myocardial infarction at the time of presentation [17].

altered mentation, decreased urine output and cold and clammy skin.

O and rales more than one-third of the lung bases

**Figure 3.** The pressure volume loop in cardiogenic shock. The left loop is that of a normal individual while the right one is the CS loop. In CS, there is an increase in LVEDP and LVDEV; there is a decrease in contractility and SV. LVEDP, left ventricular end diastolic pressure; LVESP, left ventricular end systolic pressure; LVEDV, left ventricular end diastolic volume; SV, stroke volume; AVO, aortic valve opens; AVC, aortic valve closes; MVO, mitral valve opens; MVC, mitral valve closes; IVC, isovolumetric contraction; IVR, isovolumetric relaxation.

clinical picture is not clear, or when hemodynamic stabilization is not achieved despite escalating doses of vasopressors and inotropes. PA catheter is also recommended when mechanical circulatory support devices are considered. It should be noted that the routine use of PA catheter is discouraged in patients with a confirmed diagnosis and those who stabilize rather quickly [20].
