We are not given any further data on the patient except that she is in shock (tissue hypoperfusion) and on introducing a Swan-Ganz catheter we find a low cardiac index (<2), elevated PCP (25mmHg) and elevated systemic resistances (normal: 600-1200 dyne/m2). These data are compatible with cardiogenic origin of shock.

Woman with hypotension and tissue hypoperfusion in whom the following parameters are objectified after insertion of a Swan-Ganz catheter: cardiac index 1.4 L/min/m2, pulmonary capillary wedge pressure 25 mmHg and systemic vascular resistances 2000 dynes/m2. The type of shock presented by the patient is:

Cardiac function and peripheral circulatory adjustments in patients with acute myocardial infarction. Observations during the early stage of AMI.

Since little is known concerning the effect of different types of cardiac dysfunction on the peripheral circulation in acute myocardial infarction, cardiac and peripheral circulatory hemodynamics were measured simultaneously and sequentially in the Coronary Care Unit in 40 patients with acute myocardial infarction (AMI) using a Swan-Ganz catheter and venous occlusion plethysmography. Patients were classified by clinical assessment (Killip) and into four hemodynamic subsets (HS) according to pulmonary capillary wedge pressure (PCWP) and cardiac index (CI) measures obtained by invasive central hemodynamic monitoring (Forrester): uncomplicated AMI, HS-I (PCWP less than or equal to 18 mmHg, CI greater than 2.2 L/min/m2) 15; pulmonary congestion, HS-II (PCWP greater than 18 mmHg, CI greater than 2.2 L/min/m2) 15; peripheral hypoperfusion, HS-III (PCWP less than or equal to 18 mmHg, CI less than or equal to 2.2 L/min/m2) 4; cardiogenic shock, HS-IV (PCWP greater than 18 mmHg, CI less than or equal to 2.2 L/min/m2) 6. Measurements taken within 48 hours after the onset of AMI showed significantly lower calf blood flow (p less than 0.05) and calf venous capacitance (p less than 0.01) and higher calf vascular resistance (p less than 0.05) in all AMI classifications compared to 10 normal subjects. In uncomplicated AMI group (Killip I and HS-I) calf blood flow and venous capacitance were significantly reduced while calf vascular resistance remained unchanged from normal. In AMI complicated by pulmonary congestion (Killip II and HS-II), in addition to reduced calf venous capacitance, calf blood flow was further significantly reduced (p less than 0.05) due, in part, to a rise in calf vascular resistance (p less than 0.05). In AMI complicated by severe heart failure and shock (Killip III, VI and HS-IV), mean changes in the periphery were not statistically different from those seen in patients with pulmonary congestion alone. In patients with AMI complicated by poor peripheral perfusion (HS-III), the peripheral changes did not show significant differences from those seen in uncomplicated AMI (HS-I). Significant correlations were found between calf blood flow and PCWP (r = -0.37, p less than 0.05) and CVP (r = -0.31, p less than 0.05); calf vascular resistance and PCWP (r = +0.36, p less than 0.05) and systemic vascular resistance (r = +0.43, p less than 0.01). Sequential daily peripheral hemodynamic changes in 14 H-I patients not requiring specific therapy showed that calf blood flow took 5 days, calf vascular resistance 3 days and calf venous capacitance 7 days to return to within normal levels.(ABSTRACT TRUNCATED AT 400 WORDS)

[Use of norepinephrine in the treatment of septic shock].

The effects of noradrenaline were studied in 16 patients, with either a hyperkinetic septic shock syndrome or a septic shock resistant to dobutamine treatment. The study aimed to restore normal tissue perfusion pressure, assessed by a return to normal of urine output or blood pressure. An optimal left ventricular filling pressure, estimated by the pulmonary capillary wedge pressure, was obtained for each patient using a Swan-Ganz catheter. The administration of 10.6 +/- 0.5 micrograms.kg-1.min-1 dobutamine (starting dose: 6 micrograms.kg-1.min-1) was started when the cardiac index (CI) was less than 3.3 l.min-1.m-2 after vascular filling with plasma expanders. Patients became eligible for noradrenaline treatment when they fulfilled the following conditions: arterial systolic pressure (Pasys) less than or equal to 90 mmHg; systemic vascular resistances less than or equal to 600 dyn.s.cm-5; CI greater than 3.5 l.min-1.m-2; persistent oliguria (less than 30 ml.h-1). This drug was given at a constant rate with a starting dose of 0.5 micrograms.kg-1.min-1, increased every 10 min by 0.3 to 0.6 micrograms.kg-1.min-1 according to the effects on Pasys and hourly urine output. Eight patients received noradrenaline alone; the efficient dose was 0.9 +/- 0.2 micrograms.kg-1.min-1, and it was used for a mean 5.1 +/- 1 days. CI increased in those patients who were given both noradrenaline and dobutamine. Thirteen out of the 16 patients had a dramatic increase in urine output; only three patients remained oliguric. There were no effects on serum creatinine concentration, anion gap, intrapulmonary shunt and oxygen consumption.(ABSTRACT TRUNCATED AT 250 WORDS)

Increasing mean arterial pressure in cardiogenic shock secondary to myocardial infarction: effects on hemodynamics and tissue oxygenation.

There are very few data regarding the effects of norepinephrine uptitration on global and regional hemodynamics in cardiogenic shock. We studied 25 patients with shock secondary to myocardial infarction successfully treated with percutaneous coronary intervention. Before the inclusion, 16 of 25 patients presented a cardiac arrest in the presence of medical staff. Norepinephrine was titrated to increase mean arterial pressure (MAP) from 65 to 85 mmHg during 1 h. Swan-Ganz variables, arterial and mixed venous blood gases, lactate, and thenar near-infrared spectroscopy variables (muscle tissue oxygen saturation [StO2] and its changes during a vascular occlusion test) were measured before, 1 h after norepinephrine uptitration, and 1 h after norepinephrine downtitration. To obtain a MAP at 85 mmHg, norepinephrine was increased from 0.6 (0.28-1.2) to 1.53 µg · kg · min (0.76-2.6 µg · kg · min) (P < 0.00001) (median and interquartile range), with no change in heart rate. Norepinephrine uptitration significantly increased cardiac index (2.3 ± 0.5 to 2.8 ± 0.1 L · min · m), cardiac power index (0.40 ± 0.1 to 0.55 ± 0.1 W/m), mixed venous oxygen saturation (69% ± 9% to 73% ± 9%), and coronary perfusion pressure (32 ± 3 to 43 ± 4 mmHg). Lactate level decreased from 2.6 ± 1.7 to 1.6 ± 0.4 mmol/L (P < 0.05). Pulmonary artery occlusion pressure remained unchanged. Regarding near-infrared spectroscopy variables, all values except StO2 were significantly pathological when compared with healthy volunteers. The StO2 recovery slope and delta StO2, respectively, increased from 3.0% ± 1.3%/s to 3.6% ± 1.3%/s and 10% ± 3% to 14% ± 4%, whereas StO2 did not change (83% ± 6% to 83% ± 7%). After H1, norepinephrine was decreased to basal values, and all variables returned to baseline. In conclusion, a short-term increase in MAP with norepinephrine in resuscitated cardiogenic shock complicated by postreperfusion disease is associated with better cardiac performance and improved microcirculatory variables.

Dobutamine in severe scorpion envenomation: effects on standard hemodynamics, right ventricular performance, and tissue oxygenation.

To document the effects of dobutamine on standard hemodynamics and right ventricular (RV) performance in patients exhibiting pulmonary edema following severe scorpion envenomation, and to characterize the tissue oxygenation profile in patients sustaining scorpion envenomation-related shock. Prospective cohort study. An ICU in a university hospital. Nineteen consecutive patients were admitted to the ICU for severe scorpion envenomation; all 19 patients exhibited hemodynamic pulmonary edema, and 10 patients had peripheral shock. All patients underwent a hemodynamic study with a Swan-Ganz catheter. In 8 of 19 patients, the thermodilution catheter was equipped with a fast-response thermistor. Standard hemodynamic parameters were recorded on admission and following the infusion of dobutamine in all patients at a dosage, from 7 to 20 microg/kg/min, intended to achieve the best hemodynamic and tissue oxygenation compromise. RV ejection fraction (RVEF) and RV volumes were simultaneously recorded in 8 patients, and tissue oxygenation parameters were assessed in the 10 patients with peripheral shock. The clinical signs of tissue hypoperfusion improved, and optimal hemodynamic parameters were achieved at a mean +/- SD dobutamine dosage of 17 +/- 7 microg/kg/min. Dobutamine infusion evoked statistically significant increases in cardiac index, from 2.3 +/- 0.6 to 3.6 +/- 0.7 L/min/m2; stroke volume index, from 18 +/- 5 to 31 +/- 10 mL/m2; and systemic arterial pressure, from 64 +/- 12 to 78 +/- 14 mm Hg. Pulmonary artery occlusion pressure (PAOP) and venous admixture decreased significantly: from 23 +/- 4 to 15 +/- 6 mm Hg and from 29 +/- 7% to 20 +/- 5%, respectively. With respect to RV function, dobutamine infusion significantly increased the RVEF, from 24 +/- 7% to 42 +/- 9%, without significantly changing the RV end-diastolic volume index, reflecting an enhanced RV contractility. In patients with peripheral circulatory failure, the baseline tissue oxygenation profile was consistent with cardiogenic shock, showing increased oxygen extraction as a consequence of a striking depression in oxygen delivery (DO2). After dobutamine infusion, DO2 improved significantly, from 386 +/- 104 to 676 +/- 156 mL/min/m2, with a significant decrease in oxygen extraction, from 34 +/- 8% to 24 +/- 6%. In severe scorpion envenomation, dobutamine infusion improves impaired heart function. The effects involve both left ventricular and RV dysfunction. Impaired tissue oxygenation is also improved.

[Short term effects of hypertonic saline during severe sepsis and septic shock].

Assessment of haemodynamic effects of 250 ml hypertonic saline 7.5% (HS) perfusion in critically ill patients with severe sepsis or septic shock. Observational study. Twelve mechanically ventilated patients with severe sepsis or septic shock requiring a pulmonary artery catheter and volume loading. Two hundred and fifty millilitres HS were given over 15 min. Were measured: heart rate (HR), mean arterial pressure (MAP) and pulmonary artery pressure (MPAP), pulmonary capillary wedge pressure (PCWP), right atrial pressure (RAP), cardiac index (CI), indexed systemic vascular resistance (ISVR), indexed pulmonary vascular resistance (IPVR), plasma sodium, chloride, protein and haemoglobin concentrations and arterial blood lactate. Studied parameters were assessed at baseline (T(0)) and 5 (T(0)) and 105 min (T(120)) after the end of HS infusion. MAP, HR and RAP were not altered. HS increased PAPM (25 +/- 5-30 +/- 6 mmHg), PCWP (13 +/- 3-18 +/- 4 mmHg) and CI (3.5 +/- 1.2-4.6 +/- 1.1 l/min per m(2)) at T(20) (P < 0.05). ISVR and IPVR were decreased at T(20). Protein and haemoglobin were decreased at T(20). Sodium and chloride were increased at T(20) (from 136 +/- 4 to 147 +/- 4 and from 110 +/- 6 to 123 +/- 6 mmol/l, respectively, P < 0.01) and T(120). In patients with severe sepsis or septic shock, 250 ml HS transiently (<120 min) increases CI and PCWP and induces an increase in sodium and chloride concentrations.

[Comparison of clinical assessment and invasive evaluation of hemodynamic parameters in septic shock].

The authors compare, in this prospective study, the accuracy of their own clinical assessment of hemodynamic parameters and severity of disease with the findings obtained by right heart catheterization in 50 patients with septic shock. The purpose of the study was to determine whether Swan-Ganz catheter insertion was necessary in all patients with septic shock. As soon as the diagnosis was established, the value of pulmonary capillary wedge pressure was estimated, as well as presence or absence of pathological uptake/supply dependency in all patients. The latter is an excellent indicator of severity of disease. The accurate assessment was noted in 27 (54%) patients (1. investigator), and in 30 (60%) patients (2. investigator). The sensitivity of detection of pathological uptake/supply dependency amounted to 53% and 65%; specificity was 73% and 79%, respectively. The therapy was altered in 21 patients (42%) after catheter insertion. The results were tested with chi2-test (p < 0.01). The findings of this study warrant catheter insertion in patients with septic shock.

Cardiogenic shock

Swan-Ganz catheter The Swan–Ganz catheter or pulmonary artery catheter may assist in the diagnosis by providing information on the hemodynamics. Biopsy When cardiomyopathy is suspected as the cause of cardiogenic shock, a biopsy of heart muscle may be needed to make a definite diagnosis. Cardiac index If the cardiac index falls acutely below 2.2 L/min/m2, the person may be in cardiogenic shock. Treatment Depending on the type of cardiogenic shock, treatment involves infusion of fluids, or in shock refractory to fluids, inotropic medications. In case of an abnormal heart rhythm immediate synchronized cardioversion or anti-arrhythmic agents may be administered, e.g. adenosine.

Hemodynamic and oxygen transport variables in cardiogenic shock secondary to acute myocardial infarction, and response to treatment.

There are few data on oxygen transport in cardiogenic shock after acute myocardial infarction. This prospective study examined oxygen transport variables in 19 such patients and assessed their responses to treatment. Femoral and pulmonary arterial catheters were inserted before any therapy except correction of hypoxemia by mechanical ventilation in 8 patients, defibrillation (3 patients) or pacing (5 patients). In 3 patients mean arterial pressure was greater than 80 mm Hg and cardiac index greater than 2.1 liters/min/m2 with normal mixed venous oxygen saturation despite simultaneous clinical shock. They recovered with no further treatment. Sixteen patients were treated with varying combinations of intravenous fluids and dobutamine (37 +/- 25 mu/kg/min) and 14 survived long enough for a second set of measurements to be completed. Mean heart rate increased from 83 +/- 22 to 101 +/- 20 beats/min and mean cardiac index from 1.4 +/- 0.5 to 2.5 +/- 0.4 liters/min/m2 (p less than 0.001). Oxygen consumption (VO2) was maintained even when oxygen delivery (DO2) was less than 330 ml/min/m2. After treatment DO2 increased from 230 +/- 69 to 397 +/- 60 ml/min/m2 (p less than 0.001) and VO2 from 103 +/- 31 to 124 +/- 27 ml/min/m2 (p less than 0.05). Mean mixed venous oxygen saturation increased from 54 +/- 16 to 69 +/- 8% (p less than 0.001) and mean oxygen extraction ratio decreased from 48 +/- 16 to 31 +/- 6% (p less than 0.001). There was no correlation between cuff systolic blood pressure and mean arterial pressure before or after resuscitation. Thirteen patients survived to hospital discharge. When cardiogenic shock responds to treatment, large increases in DO2 lead to small increases in VO2 but large increases in mixed venous oxygen saturation, reflecting improved tissue oxygen availability.

Cardiogenic Shock -- Introduction

Cardiogenic shock is defined as a primary cardiac disorder that results in both clinical and biochemical evidence of tissue hypoperfusion. Clinical criteria include a systolic blood pressure of less than or equal to 90 mm Hg for greater than or equal to 30 minutes or support to maintain systolic blood pressure less than or equal to 90 mm Hg and urine output less than or equal to  30 mL/hr or cool extremities. Hemodynamic criteria include a depressed cardiac index (less than or equal to 2.2 liters per minute per square meter of body surface area) and an elevated pulmonary-capillary wedge pressure greater than 15 mm Hg.

InternalMed_Harrison

Cardiogenic shock (CS) is characterized by systemic hypoperfusion due to severe depression of the cardiac index (<2.2 [L/min]/m2) and sustained systolic arterial hypotension (<90 mmHg) despite an elevated filling pressure (pulmonary capillary wedge pressure [PCWP] >18 mmHg). It is associated with in-hospital mortality rates >50%. The major causes of CS are listed in Table 326-1. Circulatory failure based on cardiac dysfunction may be caused by primary myocardial failure, most commonly secondary to acute myocardial infarction (MI) (Chap. 295), and less frequently by cardiomyopathy or myocarditis (Chap. 287), cardiac tamponade (Chap. 288), or critical valvular heart disease (Chap. 283).

Hemodynamic patterns in shock and critically ill patients.

Nine variables were studied in 56 patients to analyze hemodynamic patterns of critically ill and shock patients. The variables were central venous pressure, mean arterial pressure, heart rate, cardiac index, left ventricular stroke work, strok index, total peripheral resistance, arteriovenous oxygen difference, and oxygen consumption. We observed six patterns; three with low cardiac index (hypodynamic) and three with high cardiac index (hyperdynamic). Group IA: Low cardiac index with increased central venous pressure and arteriovenous oxygen differences associated with myocardial infarction, cardiac insufficiency, and postoperative cardiac surgery: Group IB: Low cardiac index with normal arteriovenous oxygen difference associated with myocardial infarction or hypovolemia. Group IC: Low cardiac index and decreased arteriovenous oxygen difference in patients with hypodynamic septic shock. Group IID: High cardiac index and increased arteriovenous oxygen difference in patients with sepsis and stable hemodynamic conditions. Groups IIE and IIF: Increased cardiac index and normal or increased arteriovenous oxygen difference in septic patients, who were hemodymamically unstable or in shock. These hemodynamic observations were found to be useful for understanding physiological compensations, for deciding on therapy, and in evaluating the effectiveness of therapy.

[Hemodynamic effects of intravenous clonidine in patients with acute myocardial infarction].

To assess the hemodynamic effects of Clonidine in hypertensive patients (pts) with an acute myocardial infarction (AMI), we administered the drug to 12 such patients either in a single bolus (75--150 micrograms in 5 min - 8 pts) or by continuous infusion (0.4--5 micrograms/min - 4 pts). Hemodynamic measurements were obtained by means of a Swan-Ganz thermodilution catheter, before and 60 min after the administration of the drug. Clonidine did not significantly affected Heart Rate (from 80.5 +/- 3.9 to 78.4 +/- 5.9 beats/min), Mean Pulmonary Arterial Pressure (from 18.6 +/- 1.7 to 15.1 +/- 1 mmHg), Mean Pulmonary Wedge Pressure (from 12.5 +/- 1.1 to 10.6 +/- 0.7 mmHg), central Venous Pressure (from 4 +/- 0.8 to 3 +/- 0.9 mmHg), Cardiac Index (from 2.6 +/- 0.07 to 2.6 +/- 0.7 L/min/m2), Stroke Volume (from 65.2 +/- 2.8 to 68.5 +/- 5.5 ml/b). Conversely Mean Arterial Pressure fell significantly from 127 +/- 3.1 to 96.2 +/- 7.2 mmHg (P less than 0.001). Left Ventricular Systolic Work Index was reduced from 62.3 +/- 3.3 to 50.4 +/- 4.4 gm/beats/m2 (P less than 0.025), Total Systemic Resistances from 1888 +/- 50 to 1412 +/- 117 dyne sec cm-5 (P less than 0.005) and Tension Time Index from 3536 +/- 495 to 2389 +/- 385 x 10(3) mmHg x sec/min (p less than 0.05). Clonidine is a safe and useful drug to obtain a fall of high blood pressure often complicating AMI, without depressing left ventricular performance, as suggested by no significant changes of CI, WP and LVSWI. The reduction of TTI suggests a beneficial effect on the balance between myocardial oxygen delivery and demand. Clonidine is a hypotensive drug which can be safely used in patients with AMI, without depressing the left ventricular performance.

[Hemodynamic effects of dobutamine in hyperkinetic septic shock treated with norepinephrine].

A prospective study of the haemodynamic effects of dobutamine was carried out in six men and four women suffering from hyperkinetic septic shock, already treated with noradrenaline and dopamine. All ten patients had septic shock, defined as a mean arterial blood pressure of less than 70 mmHg and an urine output under 15 ml.h-1, persisting despite fluid loading, associated with positive blood cultures, increased white blood cell counts, and a septic area. Initial treatment consisted in fluid loading, so as to increase cardiac output whilst keeping pulmonary wedge pressure (Ppw) between 8 and 10 mmHg. Dopamine was then added, up to a dose of 15-20 micrograms.kg-1.min-1, in an attempt to improve coronary and renal blood flows. In patients in whom this failed, the amounts of dopamine were then decreased, down to 3 micrograms.kg-1.min-1, and replaced by noradrenaline. When patients had as steady cardiac index (CI) greater than 3 l.min-1.m-2 and a systemic arterial resistance index (RsaI) of less than 1,800 dyn.s.cm-5.m-2 for more than 60 min, they were included in the protocol. Dopamine was then replaced by increasing doses of dobutamine (0, 5, 7.5, 10, 15 and again 0 micrograms.kg-1.min-1). The usual haemodynamic parameters were measured and calculated once a steady state had been obtained at each dose (within 20 to 30 min). Ppw was kept between 8 and 10 mmHg by fluid loading with a 4% albumin solution. At the beginning of the study, patients had a mean blood pressure of 78 +/- 6 mmHg, a CI of 4.8 +/- 1.5 l.min-1.m-2 and a RsaI of 1,285 +/- 341 dyn.s.cm-5.m-2 RsaI.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac catheterization

Right heart catheterization is often done for pulmonary hypertension, heart failure, and cardiogenic shock. The pulmonary artery catheter can be placed, used, and removed, or it can be placed and left in place for continuous monitoring. The latter can be done an intensive care unit (ICU) to permit frequent measurement of the hemodynamic parameters in response to interventions. Parameters obtainable from a right heart catheterization: Right atrial pressure Right ventricular pressure Pulmonary artery pressure Pulmonary capillary wedge pressure Systemic vascular resistance Pulmonary vascular resistance Cardiac output Blood oxygenation Implantation of a CardioMEMS is done during a right heart catheterization. This device is implanted into the pulmonary artery to permit real-time measurement of the pulmonary artery pressure over time. Coronary catheterization

A Two Parameters for the Evaluation of Hypovolemia in Patients with Septic Shock: Inferior Vena Cava Collapsibility Index (IVCCI), Delta Cardiac Output.

BACKGROUND The aim of this study was to determine the correlation between inferior vena cava collapsibility index and changes in cardiac output measured during passive leg raising test in patients with spontaneous breathing and septic shock. MATERIAL AND METHODS Fifty-six patients were included in the study. All of these 56 patients were diagnosed with septic shock and had spontaneous breathing under continuous positive airway pressure. Patients exclusions included: patients with cardiac pathology, not septic shock, pregnant, spontaneous breathing, increased intra-abdominal pressure, inferior vena cava could not be visualized, arrhythmia and pulmonary hypertension. Exclusion criteria for the study were as follows: 1) left ventricular systolic dysfunction, 2) cardiomyopathy, 3) medium severe heart valve disease, 4) patients with arrhythmia; 5) pulmonary hypertension, 6) patients without spontaneous breathing (for inferior vena cava collapsibility index, it is not evaluated), 7) patients with >60 mmHg CO₂ in arterial blood gas; 8) pregnant patients; 9) patients with neurogenic shock, cerebrovascular incident or traumatic brain injury, 10) patients whose inferior vena cava and parasternal long axis cannot be visualized, and 11) patients with increased intra-abdominal pressure. Patients were placed in neutral supine position, and the inferior vena cava collapsibility index and cardiac output 1 were recorded. In passive leg raising test, after which the cardiac output 2 is recorded in terms of L/min. The percentage increase between the 2 cardiac outputs was calculated and recorded. RESULTS A moderately positive correlation was also observed between the inferior vena cava collapsibility index and delta cardiac output (r=0.459; r2=0.21), which was statistically significant (P<0.001). The cutoff value for the delta cardiac output was 29.5. CONCLUSIONS In conclusion, we found that the inferior vena cava collapsibility index, which is one of the dynamic parameters used in the diagnosis of hypovolemia in patients with septic shock, is correlated with delta cardiac output after leg raising test. We believe that, based on a clinician's experience, looking at 1 of these 2 parameters is sufficient for the identification of hypovolemia in patients diagnosed with septic shock.

Systemic, pulmonary, and renal hemodynamic effects of endothelin ET(A/B)-receptor blockade in patients with maintained left ventricular function.

Endothelin-1 (ET-1) regulates vascular tone in congestive heart failure and modulates renal function. Its role in patients with normal left ventricular (LV) function and its renal effects are unclear. Cardiac and renal hemodynamics were studied in 24 patients with normal LV function and coronary arteries after single-dose, double-blind, randomized administration of TAK-044 (25, 50, or 100 mg, i.v.), an ET(A/B)-receptor antagonist, or placebo. Hemodynamics were monitored using Swan-Ganz and arterial catheters, and ET levels were measured. Renal function was assessed by clearance techniques. In the absence of a dose-response relation, TAK-044 patients were analyzed as a single group. Most hemodynamic effects occurred during the first 4 h. TAK-044 reduced mean arterial (-9.3 mm Hg, p < 0.001), pulmonary (-1.8 mm Hg, p = 0.01), and pulmonary capillary wedge pressure (-1.6 mm Hg, p < 0.001) between 30 min and 4 h. Mean reduction in systemic vascular resistance was 279 dyne/s/cm2 (p < 0.001), whereas heart rate increased 6.1 beats/min (p < 0.001) and cardiac index by 0.37 L/m2 (p = 0.01). Stroke volume index, right atrial pressure, and pulmonary vascular resistance did not change. TAK-044 increased renal plasma flow in proportion to the increase in cardiac output (+119 ml/min, 4 h after TAK-044; p < 0.05) and ET-1 levels (2.5-fold; p < 0.05). No serious side effects were noted. In patients with normal cardiac function, ET-receptor blockade causes vasodilation and reduces systemic but not pulmonary vascular resistance and increases cardiac index and renal plasma flow.

[Cardiogenic shock].

Cardiogenic shock (CS) is defined as end-organ hypoperfusion as the consequence of primary myocardial dysfunction. Among the diagnostic criteria are a systolic blood pressure < 90 mmHg, acute renal failure (oligoanuria), ischemic hepatitis, cyanosis and cold, clammy skin. Accepted hemodynamic cutoffs are a cardiac index < 2,2 (l/min)/m2 and a pulmonary capillary wedge pressure > 15 mmHg. It should be acknowledged, that a normal blood pressure does not rule out CS; there is a nonhypotensive variant of CS demonstrating all the signs mentioned above (including elevated lactate levels) while the blood pressure is compensated due to vasoconstriction.The single most frequent cause of CS is pump failure in the setting of an acute myocardial infarction and its mortality rate has been lowered to 40-50%, owing to the widespread availability of primary PCI. Regarding PCI, it has been demonstrated recently that a "culprit-lesion only strategy" should be followed in the setting of CS. Other important causes of CS to take into account are mechanical complications of myocardial infarction (papillary and ventricular septal rupture as well as rupture of the myocardial free wall leading to tamponade), valvular heart disease (mostly decompensated aortic stenosis) as well as myocarditis and end stage cardiomyopathy.The diagnosis of CS is made by patient history, physical examination, ECG, echocardiography and coronary angiography. Echocardiography should always be performed before coronary angiography because, in the case of mechanical complications, it significantly alters the management of the patients. Patients with clinical signs of CS but paradoxically preserved ejection fraction must be thoroughly evaluated for the presence of a papillary muscle rupture, particularly in the setting of a lateral wall infarction.Noradrenaline and dobutamine are the first-line agents for medical stabilization. When such conventional measures fail, extracorporeal support devices such as ECMO or Impella© may be used. Currently, trials are underway to assess wheter these devices confer a survival benefit in this high-risk population.

[Hemodynamic effects of oral captopril in patients with critical aortic stenosis].

To analyse the hemodynamic and ventricular function effects of oral captopril in severe aortic stenosis. inclusion criteria: patients older than 18 years with critical aortic stenosis. angiotensin-converting enzyme inhibitor used previously contraindication to right catheterisation aortic insufficiency, valvular prosthesis in aortic position, or other valvulopathy. As well as the need for immediate valvular aortic replacement arrhythmia, A-V conduction alterations, or ventilatory support. prospective, no randomized. Swan-Ganz catheter was used. Basal hemodynamic measurements were made on 1, 2, 4, 6 and 8 hours during 48 hours. Captopril was administered 12.5 mg first and then 8 mg tid (6 doses). Neuman-Keuls test was used for multivariate comparisons. Statistical significance was determined with P < 0.05. 22 patients were analyzed. Systemic vascular resistance fell from 1750 Dyn/seg/cm-5 to 1200 (P-0.001), cardiac output increased from 4.1l/min to 5.8 (P-0.001), cardiac index increased from 2.4 l/min/m2 to 2.9 (P-0.009), stroke volume from 47 ml to 64 (P-0.04) and stroke volume index from 27 ml/m2 to 36 (P-0.002). In patients with heart failure (n = 7) the systemic vascular resistance fell from 2050 Dyn/seg/cm-5 to 1463 (P-0.04), cardiac output increased from 2.8l/min to 4.1 (P-0.04), cardiac index from 2.07 l/min/m2 to 2.75 (P-0.04), stroke volume from 46 ml to 64 (P-0.03), pulmonary capillary wedge pressure fell from 19 mmHg to 16 (0.04) and the systolic pulmonary arterial pressure fell from 63 mmHg to 42 (P-0.009). captopril improves the hemodynamic parameters in patients with critical aortic stenosis, principally in those with heart failure.

[Clinical picture of acute pulmonary embolism. Relations to the degree of vascular obstruction].

In 132 consecutive patients treated for pulmonary embolism, duration of symptoms, number of embolic episodes before the diagnosis, circulatory affection (stable circulation (n = 61), reversible shock (n = 60), circulatory collapse (n = 11), electrocardiographic findings and systolic pulmonary pressure (n = 60) were analysed in relation to 1) underlying diseases (orthopedic surgical patients (n = 43), gynecological-abdominal surgical patients (n = 22), preembolic healthy patients (n = 42), miscellaneous medical patients (n = 25)), and 2) the obstruction of the pulmonary vascular bed quantified by a scintigraphic or angiographic score. While embolic score did not differ between the groups of underlying diseases, preembolic healthy patients with deep vein trombosis (n = 30) had longer mean duration of symptoms (14 days), more embolic episodes, (1.7 episode) and higher pulmonary pressure (72 mmHg) than the material on an average with values of 7 days, 0.9 episodes and 57 mmHg, respectively (p less than 0.001). Among patients with reversible shock or circulatory collapse, half had at least one previous embolic episode, one fifth from two to four. Embolic score correlated well with the circulatory affection (p less than 0.001). A high pulmonary pressure correlated with long duration of symptoms and a high number of embolic episodes (p less than 0.002). Sinus tachycardia and electrocardiographic signs of acute right ventricular strain (complete and incomplete right bundle branch block, SIQIIITIII-pattern and inverted T-waves in V2-4) correlated positively to the circulatory affection and inversely to duration of symptoms and number of embolic episodes (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Valve replacement for aortic stenosis with severe congestive heart failure and pulmonary hypertension.

Significant pulmonary hypertension in aortic stenosis is evidence of severe dysfunction of the left ventricle. It is also a predictor of a bad prognosis in the natural course of the disease. This study was performed to evaluate the changes in the hemodynamic parameters of pulmonary circulation at rest and effort in patients who had significant pulmonary hypertension preoperatively and underwent valve replacement. The study consists of 11 male patients with aortic stenosis with an average peak transvalvular gradient of 68 mmHg and impaired left ventricular function (mean ejection fraction 38%). Six patients were in NYHA functional class III, and five were in class IV. The patients underwent Swan-Ganz catheterization before urgent valve replacement. Significant pulmonary hypertension was found in all subjects, and a below normal cardiac index in eight. Urgent valve replacement was performed in all patients: two of them were operated on during pulmonary edema and cardiogenic shock which developed soon after diagnosis-one of them died. Patients were followed up six months after surgery, and all of them showed major clinical improvement (six in NYHA class I, four in class II). Mean pulmonary artery systolic pressure dropped from 77 mmHg preoperatively to 32 mmHg, and the pulmonary artery mean pressure from 47 mmHg to 17 mmHg, pulmonary wedge pressure from 32 mmHg to 9 mmHg, and pulmonary vascular resistance from 4.74 to 1.8 Wood units. The cardiac index came back to normal in all patients (2.18 vs. 3.0 l/min/m2). Swan-Ganz catheterization was also performed during exercise (work load; 50 Watts in three patients, 100 Watts in six patients). The reaction of the hemodynamic parameters on exercise in most patients was almost normal. Our data indicate that in aortic stenosis, even with severe left heart failure, pulmonary hypertension can be fully reversible and a significant improvement in both rest and effort hemodynamic parameters can be expected.

[Physiopathology of anaphylactic and anaphylactoid shock. A cooperative retrospective study].

The pathophysiology of anaphylactic and anaphylactoid shock states suggests that the rapidly initiated, intensive therapeutic measures to be taken must involve: breathing (ventilation) of (with) 100% oxygen, continuous or semi-continuous sympathicomimetic therapy (epinephrine, isoprenalin, orciprenalin) avoiding excessive single doses, rapid intensive volume substitution, control of metabolic acidosis, bronchospasmolytic therapy, in case of laryngospasm intubation, if not possible coniotomy or transtracheal punction. In case of circulatory arrest possibly also cardiac massage, defibrillation, lidocain, cardioversion. In a retrospective study 91 cases of anaphylactic and anaphylactoid shock were analyzed. Cutaneous vascular changes. Vasodilation was reported in 30 cases, vasoconstriction in 15 cases. Hypovolemia. CVP as measured in 23 cases was less than or equal to 2 cmH2O in 12 cases; in 4 of these cases the early finding and in 2 a rather low hematocrit are in favour of venous blood sequestration. In 2 cases the increase of the hematocrit suggests an extravasation of as much as 1,2 and 1,81 of plasma, respectively. Increase of pulmonary arterial pressure. CVP increased in 2 out of 9 cases suggesting a high pulmonary arterial pressure. Decreased cardiac output (CO). In 3 cases CO as determined in a late shock phase diminished by 37--55%. Blood gas changes. PaO2 was as low as 47--61 mmHg in 4 out of 8 cases, PaCO2 being 29--34 mmHg in 2 of them. It suggests an insufficient oxygen transport. Myocardial involvement. Arrhythmias (non sinus-) were found in 38 cases, of which 14 ventricular arrhythmia and 13 asystole. Serious wave deformation concerned QRS (3), AV-block (2), intraventricular blocks (4). 5 times the reaction resulted in myocardial infarction. A localized coronary spasm in anayphylactic shock was observed during a coronary angiography. Respiratory impairment. Severe respiratory impairment was associated with anaphylactic and anaphylactoid shock in 31 cases (26 bronchospasm, 4 apnea, 1 laryngospasm).

[Clinical and hemodynamic efficacy of enalapril in severe congestive heart failure].

Evaluate the clinical and hemodynamic efficacy of enalapril in the treatment of severe congestive heart failure, refractory to the classic therapeutics with diuretics and digitalis. Hospitalized patients (pts) of a cardiac department. 10 pts with a mean age of 57.8 years in whom a Swan-Ganz catheter was placed for 72 hours to monitor the right pressures and cardiac output, with regular control of arterial blood pressure and cardiac frequency. Low doses of enalapril (2.5 mg) were utilized at the start of the treatment and this dose was readjusted depending on the clinic and hemodynamic parameters. the 10 pts had the following characteristics: Basal-mean pulmonary arterial pressure (PAP) 34.1 mmHg, Pulmonary wedge pressure (PWP) 21.1 mmHg, cardiac output (CO) 4.8 l/min, cardiac index (CI) 2.8 l/min/m2. After 72 hours with enalapril treatment, these measurements were: PAP-23.8 mmHg, PWP-12.6 mmHg, CO-5.2 l/min and Cl-3.0 ll/min/m2. These differences were statistically significant. With a follow-up of 18.4 months, there was also a clinical improvement; of the 4 pts in class III, 2 moved to class II and 2 to class I; the 4 pts in class IV 4 moved to class II; two pts had died. In severe heart failure, the addition of enalapril to the classic therapy has allowed the immediate improvement of the clinical and hemodynamic indexes and this improvement was maintained in the follow-up period.

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Abbreviations: (A − a) DO2, alveolar-arterial oxygen difference; FIO2, fraction of inspired oxygen; PaO2, partial pressure of oxygen; WBC, white blood cell count. Mortality rate, % FIGURE 321-1 APACHE II survival curve. Blue, nonoperative; green, (See also Chap. 323) During the initial resuscitation of patients in postoperative. shock, principles of advanced cardiac life support should be followed. most common cause of high-cardiac-output hypotension is sepsis (Chap. 325). Other causes include liver failure, severe pancreatitis, burns and other trauma that elicit the systemic inflammatory response syndrome (SIRS), anaphylaxis, thyrotoxicosis, and peripheral arteriovenous shunts. In summary, the most common categories of shock are hypovolemic, cardiogenic, and high-cardiac-output with decreased SVR (highoutput hypotension). Certainly more than one category can occur simultaneously (e.g., hypovolemic and septic shock).

Invasive hemodynamic monitoring in the postoperative period of cardiac surgery.

To assess the hemodynamic profile of cardiac surgery patients with circulatory instability in the early postoperative period (POP). Over a two-year period, 306 patients underwent cardiac surgery. Thirty had hemodynamic instability in the early POP and were monitored with the Swan-Ganz catheter. The following parameters were evaluated: cardiac index (CI), systemic and pulmonary vascular resistance, pulmonary shunt, central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), oxygen delivery and consumption, use of vaso-active drugs and of circulatory support. Twenty patients had low cardiac index (CI), and, 10 had normal or high CI. Systemic vascular resistance was decreased in 11 patients. There was no correlation between oxygen delivery (DO2) and consumption (VO2), p = 0.42, and no correlation between CVP and PCWP, p = 0.065. Pulmonary vascular resistance was decreased in 15 patients and the pulmonary shunt was increased in 19. Two patients with CI < 2 L/min/m2 received circulatory support. Patients in the POP of cardiac surgery frequently have a mixed shock due to the systemic inflammatory response syndrome (SIRS). Therefore, invasive hemodynamic monitoring is useful in handling blood volume, choice of vasoactive drugs, and indication for circulatory support.

Septic lung and shock lung in man.

Two series of patients were studied by serial measurements of blood gas exchange and pulmonarmonary dysfunction and to evaluate the dangers of respiratory failure in post traumatic patients. There were 27 patients who had sustained profound hemorrhagic shock and massive blood replacement averaging 9.7 liters and 38 patients who suffered general peritonitis or other forms of fulminating nonthoracic sepsis. All were supported by endotrachael intubation and volume controlled ventilators. The overall mortality for the post shock patients without sepsis was 12% while in the septic patients it was 35%. The maximal pulmonary arteriovenous shunt encountered in the post hemorrhagic shock patients at 36 hours averaged 20 plus or minus 8% and was accompanied by high cardiac indices (average 5.1 plus or minus 1.3 L/M-2/min) but no significant rise of pulmonary arterial pressure or peak inspiratory pressure (PIP). Severe pulmonary dysfunction subsequently occurred only in those patients who later became septic. The studies on the septic patients were divided according to the magnitude of the cardiac indices (the high indices averaged 4.8 plus or minus 1.6L/M-2/min) and thelow indices averaged 1.9 plus or minus 1.0 L/M-2/min. In the former, the average maximal shunt of 30 plus or minus 6% was sustained for 4 or more days, accompanied by an elevation of PIP to 36 plus or minus 6 cm H2O and by Pa pressure of 28 plus or minus 5 mm Hg. The patients in low output septic shock usually had an associated bronchopneumonia and had an average venous admixture of 34 plus or minus 8% and PIP values of 41 plus or minus 8 cm H2O. The mean Pa pressure in this group was 29 plus or minus 6 mm Hg.

Cardiac index

Cardiac index (CI) is a haemodynamic parameter that relates the cardiac output (CO) from left ventricle in one minute to body surface area (BSA), thus relating heart performance to the size of the individual. The unit of measurement is litres per minute per square metre (L/min/m2). Calculation The index is usually calculated using the following formula: where CI Cardiac index BSA Body surface area SV Stroke volume HR Heart rate CO Cardiac output Clinical significance The normal range of cardiac index at rest is 2.6–4.2 L/min/m2. The cardiac index is frequently measured and used in both intensive care medicine and cardiac intensive care. The CI is a useful marker of how well the heart is functioning as a pump by directly correlating the volume of blood pumped by the heart with an individual's body surface area. If the CI falls acutely below 2.2 L/min/m2, the patient may be in cardiogenic shock. References Cardiovascular physiology Diagnostic intensive care medicine

[Cardiogenic shock in acute myocardial infarct patients].

To differentiate between various forms of cardiogenic shock (CS) and to elaborate the criteria of its prognosis, the authors examined 284 patients with acute myocardial infarction (MI) and 30 patients of the control group for the peculiarities of the clinical course of the disease in relation to changes in the hemodynamic parameters and oxygen supply to the tissues. CS was shown to develop more frequently in patients over 64 years of age, with a history of MI and with signs of chronic circulation insufficiency of IIA stage. Late CS more commonly took the true form and was associated with a MI relapse. Reflex CS was characterized by the hyperkinetic variant of the hemodynamics while an arrhythmic one by the congestive variant. Patients with the authentic form of CS were divided into 3 subgroups with different hemodynamic reactions to sympathomimetic amines. In the first day of the disease the coefficient of the tissue extraction of oxygen serves as a significant prognostic criterion which should be determined along with the dynamic measurement of the pump and contractile functions of the heart.

Hemodynamic effects of monomeric nonionic contrast media in pulmonary angiography in chronic thromboembolic pulmonary hypertension.

The purpose of this study was to investigate the hemodynamic safety of the monomeric nonionic contrast agent iomeprol for selective pulmonary angiography in chronic thromboembolic pulmonary hypertension (CTPH), and to investigate the effect of periinterventional oxygen administration. Selective pulmonary digital subtraction angiography was performed in 94 patients with CTPH using six bolus injections of iomeprol (posteroanterior, oblique, and lateral projections; both pulmonary arteries; iomeprol, 25 mL at 13 mL/s). Hemodynamics were obtained with Swan-Ganz catheters, and systolic pulmonary artery pressure (PAsyst) was classified into one of three groups: 30 mm Hg or less (control group), greater than 30 but less than or equal to 60 mm Hg (group 1, moderate pulmonary hypertension), and greater than 60 mm Hg (group 2, severe pulmonary hypertension). At baseline, values for PAsyst were 21.4 +/- 2.3 (control group, n = 8), 49.8+/- 8.5 (group 1, n = 18), and 86.5 +/- 18.9 (group 2, n = 68) mm Hg (p < 0.001). Pulmonary vascular resistance indexes (PVRI) were 222 +/- 105 (control), 703 +/- 364 (group 1), and 1,582 +/- 562 (group 2) dyne x s x cm(-5) x m2 (p < 0.001). The mean cardiac indexes were 3.1 (control), 2.8 (group 1), and 2.3 (group 2) L/min/m2 (p < 0.05). Pulmonary capillary wedge pressure (PCw) indicated healthy left heart function. Periinterventional oxygen inhalation improved oxygen saturation in all groups and slightly reduced pulmonary artery pressure and heart rate. Online measurement of pulmonary artery pressure during contrast bolus injection for angiography showed only a minor increase, predominantly in severe pulmonary hypertension (triangle up [difference] PAsyst: 1.3 +/- 1.9 [control], 2.9 +/- 3.4 [group 1], and 3.8 +/- 4.5 [group 2] mm Hg [p < 0.001]). After completion of angiography, right atrial pressure (RAP) and PAsyst were moderately increased: triangle up RAP: 1.4 (control), 2.6 (group 1, p < 0.001), and 3.0 (group 2, p < 0.001) mm Hg; triangle up PAsyst: 3.2 (control), 7.7 (group 1, p < 0.01), and 8.5 (group 2) mm Hg (p < 0.001). PVRI was significantly higher in group 2 (triangle up PVRI: 188 dyne x s x cm(-5) x m2, p < 0.001). Selective pulmonary angiography using iomeprol is safe without critical pressure peaks during selective contrast bolus injection or significant hemodynamic derangement in severe CTPH. Periinterventional oxygen inhalation improved pulmonary circulation.

Hemodynamic determinants of mortality in human septic shock.

To assess the relative importance of cardiac versus peripheral vascular failure in patients dying of septic shock, a series of 42 patients with documented septic shock was retrospectively evaluated. Patients were included in the study if serial hemodynamic and metabolic studies had been performed: the first one within 12 hours after onset of septic shock and the last one within 12 hours (median 2 hours; range 0.1 to 12 hours) before death in nonsurvivors. Nonsurvivors were included only if they died in shock. From the patient records the first, highest, and last measured cardiac indexes (CI) (t = 1, t = 2, and t = 3) with concomitant hemodynamic and metabolic variables were obtained. Group I (n = 21) consisted of survivors and group II (n = 21) of nonsurvivors. Group II was divided into three subgroups: group IIa (n = 4) consisted of nonsurvivors with liver cirrhosis, group IIb (n = 9) patients with final CI less than 4 1 X min-1 X m-2, and group IIc (n = 8) patients with final CI greater than 4 1 X min-1 X m-2. At t = 1 no significant differences in hemodynamic variables were found between groups I and II, and all patients, whether surviving or not, were able to increase CI to similar levels. At t = 3 group II showed a marked decrease in mean arterial pressure and systemic vascular resistance index compared with group I (p less than 0.001), whereas CI did not differ significantly. The nonsurvivors showed progressive lactic acidemia. Even group IIb patients showed persistent vasodilation despite a decrease in CI. Our data suggest that many patients in septic shock die as a result of peripheral vascular rather than cardiac failure, since persistent vasodilation, irrespective of CI, was a major hemodynamic determinant in nonsurvivors, of whom 57% maintained a high CI until shortly before death.

Effects of propranolol on the cardiovascular and renin-angiotensin systems during hypotension produced by sodium nitroprusside in humans.

The authors examined the effects of controlled hypotension induced with sodium nitroprusside (SNP) with and without propranolol on the cardiovascular, pulmonary, and renin-angiotensin systems in 10 consecutive anesthetized patients with kyphoscoliosis undergoing posterior spinal fusion. SNP infusion (4.1 microgram . kg-1 . min-1) alone decreased mean systemic arterial pressure (SAP) by 25 torr +/- 3 SE (P less than 0.001), systemic vascular resistance index (SVRI) by 1113 dyne . sec. cm-5 . m2 +/- 125 SE (P less than 0.001), mean pulmonary artery pressure (PAP) by 6 torr +/- 2 SE (P less than 0.02), pulmonary capillary wedge pressure (PCWP) by 4 torr +/- 1 SE (P less than 0.01), pulmonary vascular resistance (PVR) by 50 dyne . sec . cm-5 +/- 18 (P less than 0.05), and PaO2 by 16 torr +/- 7 SE (P less than 0.05), whereas cardiac index increased by 1.08 l . min-1 . m2 +/- 0.24 SE (P less than 0.01) and heart rate increased 16 beats/min +/- 5 SE (P less than 0.02). After 40 min of hypotension, 0.03 mg/kg propranolol was injected intravenously while the SNP infusion rate was held constant. Ten min later there was a significant decrease in the heart rate (10 beats/min +/- 4 SE, P less than 0.02) and cardiac index (0.65 l . min-1 . m-2 +/- 0.21, P less than 0.02). Plasma renin activity (PRA) increased from 2.37 ng . ml-1 . h-1 +/- 0.7 SE before anesthesia to 6.50 ng . ml-1 . h-1 +/- 1.45 SE (P less than 0.05) after 40 min of nitroprusside infusion. Forty min after propranolol there was a significant reduction in PRA to 4.07 ng . ml-1 . h-1 +/- 0.73 SE (P less than 0.05). Thus propranolol, when given during SNP hypotension, exhibits an early cardiovascular response manifested as a decrease in cardiac output and heart rate and a delayed action of the kidney resulting in an inhibition of renin release.

[Importance of oximetry parameters in the detection of hypoxia in the early phase of septic shock].

The routinely monitored variables in shock stages include: arterial pressure, heart rate, central venous pressure, pulmonary artery wedge pressure and cardiac index. With vigorous therapy it is possible to bring these values back into the normal range in both survivors and nonsurvivors. The therapeutic goal in septic shock stages is to maximize the values of cardiac index, O2 delivery (DO2) and O2 consumption (CO2). The aim of this study is to determine the relationship between O2 delivery and O2 consumption as an early sign of hypoxia. Fifteen patients with septic shock were treated in order to maximize the value of CI, DO2 and VO2. We compared the levels of these parameters between the survivors and nonsurvivors and found no significant differences after 24 hours. High levels of DO2 and VO2 do not exclude tissue hypoxia in the early stage of septic shock.

Myocardial depression characterizes the fatal course of septic shock.

The relationship between cardiac and vascular abnormalities was studied in 68 patients with established septic shock. At time of hemodynamic evaluation, after initial resuscitation, there was no significant difference in arterial pressure, pulmonary artery pressure, cardiac filling pressures, and cardiac index between the 38 survivors of shock and the 30 patients who died of shock, but the left ventricular stroke work index and the right ventricular (RV) stroke work index were higher in survivors than in those who died (mean +/- SD: 25.0 +/- 9.1 vs 20.1 +/- 9.4 gm/m2 [p less than 0.05] and 6.6 +/- 3.6 vs 4.8 +/- 2.8 gm/m2 [p less than 0.05], respectively). Survivors had also higher thermodilution RV ejection fraction and lower RV end-diastolic volumes than had those who died (43.9% +/- 16.3% vs 31.1% +/- 13.7% [p less than 0.01] and 82 +/- 30 vs 99 +/- 31 ml/m2 [p less than 0.05], respectively). Calculated systemic vascular resistance was similar in the two groups, but vasopressors had been required in 22 (58%) of 38 survivors and 25 (83%) of 30 patients who died (p less than 0.01). Moreover, when the patients were separated into two groups according to their cardiac output, higher or lower than 3 L/min/m2, in both subgroups patients who died had lower blood pressure than had survivors. Blood lactate levels were significantly lower in survivors than in nonsurvivors (5.1 +/- 2.1 vs 8.1 +/- 4.7 mEq/L, p less than 0.01). Final data obtained before recovery of shock or death indicated that the survivors had higher arterial pressure, lower pulmonary artery pressure and right atrial pressure, higher stroke volume, and higher RV ejection fraction than had the patients who died. No survivors but all patients who died had been treated with vasopressors. These data therefore indicate that death as a result of septic shock is characterized by both myocardial depression and altered vascular tone and both are probably interrelated.


The data provided on the characteristics of the murmur (it DECREASES with Valsalva) and the data on left ventricular hypertrophy, lead us to the diagnosis of severe aortic stenosis.

A 58-year-old hypertensive man comes to the emergency department for a 30-second syncope while jogging, with spontaneous recovery and no sequelae. Blood pressure is 135/65 mmHg. Cardiac auscultation shows a loud, intense systolic murmur, which is reduced with Valsalva maneuvers and an attenuated second tone. The ECG shows sinus rhythm at 72 bpm, with criteria of left ventricular hypertrophy and inverted T waves in anterior face. Point out the correct statement:

The clinical picture suggests pulmonary thromboembolism.

The data provided indicate hypertrophic cardiomyopathy with severe obstruction of the left ventricular outflow tract.

These data correspond to severe aortic stenosis.

Aortic dissection should be excluded by contrast-enhanced computed tomography.

[Differential diagnosis of obstructions to left ventricular outflow (author's transl)].

A total of 127 patients with different forms of obstruction to left ventricular outflow are studied. There were eight cases with supravalvular aortic stenosis, 79 with valvular aortic stenosis, 25 with hypertrophic subaortic stenosis, and 15 with subvalvular aortic stenosis. Clinical findings and electrocardiographic, radiographic, and angiohemodynamic data corresponding to these groups are reported, as well as the differential characteristics for each category from a clinical, electrocardiographic and radiographic point of view. The presence of a typical face, asymmetrical carotid and brachial pulses, absence of aortic ejection click and little or no aortic button on the chest roentgenogram reveals a supravalvular aortic stenosis. Valvular aortic stenosis shows aortic ejection click, poststenotic dilation of the ascending aorta, electrocardiographic signs of left ventricular hypertrophy and associated aortic regurgitation. Hypertrophic subaortic stenosis is characterized by a typical arterial pulse, marked "a" wave in the jugular venous pulse, double apical impulse on palpation and appearance or modification of the systolic ejection sound with Valsalva's maneuver.

[Advanced sequelae of apical hypertrophic cardiomyopathy: report of two cases with wall motion abnormalities].

In view of the paucity of reports describing symptoms of increased degree, and deterioration of left ventricular systolic function in patients with apical hypertrophic cardiomyopathy (apical HCM), two cases with congestive heart failure and progressive thinning of previously hypertrophied apical portions of the left ventricle are reported. These were among 13 patients observed from eight to 10 years. Case 1: A 56-year-old man was diagnosed as having apical HCM at the age of 49 years. Severe left ventricular hypertrophy and prominent ST-T changes were observed on ECG during his first admission. His left ventricular end-diastolic pressure (LVEDP) was 24 mmHg and a left ventriculo-gram revealed a decrease in the left ventricular cavity in the apex and marked hypertrophy of the apical wall. Moderate interstitial fibrosis without hypertrophy or disarray of myocytes was observed in a left ventricular endomyocardial biopsy specimen. In two episodes of cardiac arrest he was successfully resuscitated at the age of 50 years. At the age of 55 years, two-dimensional echocardiography revealed thinning and abnormal motion in the apical wall, and a defect in 201T1 accumulation was observed in the same region by perfusion scintigraphy. This patient was readmitted with a diagnosis of cerebral embolism at the age of 56 years. Cardiac catheterization revealed normal LVEDP (8 mmHg), and a left ventriculogram revealed an aneurysm in the left ventricular apex with normal major epicardial coronary arteries. He has been under treatment with antiarrhythmic medications, calcium antagonists and anticoagulants, and has become relatively asymptomatic. Case 2: A 69-year-old-man was diagnosed as having apical HCM after a complete evaluation, including cardiac catheterization, at the age of 59 years. His LVEDP was elevated (17 mmHg), and a left ventricular angiogram revealed marked hypertrophy localized to the apex. Ejection fraction was 64%. A left ventricular endomyocardial biopsy revealed interstitial fibrosis without hypertrophy of myocytes. Thereafter, he has been followed as a New York Heart Association functional class III to IV with occasional elevation of cardiac enzymes but without chest pain or acute changes in his ECGs. However, atrial fibrillation with complete right bundle branch block developed at the age of 60 years. Apical wall thinning and dyskinesis were diagnosed by 2D echocardiography and a defect in the 201T1 accumulation was observed at about 65 years of age. He was readmitted in severe cardiac failure at the age of 69 years, and he was diagnosed as having cardiac asthma with pulmonary capillary wedge pressure of 35 mmHg.(ABSTRACT TRUNCATED AT 400 WORDS)

[Hypertrophic cardiomyopathy manifesting different modes of illness: report of three cases].

Three cases of hypertrophic cardiomyopathy (HCM) which presented with different modes of appearance of left ventricular hypertrophy are reported. Case 1: A 24-year-old man had three relatives with HCM. At 13 years of age, he showed no electrocardiographic or echocardiographic abnormalities characteristic of HCM. During the ensuing 11 years, he developed asymmetric septal hypertrophy (ASH) and systolic anterior motion of the mitral valve (SAM), with right bundle branch block and T-wave inversion. Cardiac catheterization confirmed the diagnosis of hypertrophic obstructive cardiomyopathy by demonstrating an intraventricular pressure gradient of 25 mmHg. These observations indicate that this case developed abnormal hypertrophy during adolescence on the basis of genetic predisposition of an autosomal dominant trait. Case 2: A 51-year-old woman had three proven and three possibly affected relatives. At 35 years of age, she had a normal electrocardiogram, although the echocardiogram was not available. Now, 16 years later, she had developed ASH with abnormal Q-waves and was diagnosed as having non-obstructive HCM. These suggest that ASH can be manifested as late as during middle-age, even in those with genetic predisposition. Case 3: A 47-year-old woman was diagnosed as having hypertension and her blood pressure was 190/100 mmHg at 40 years of age, though she had no abnormal electrocardiographic findings and heart murmurs. Now, at 47 years of age, she had developed T-wave inversion, ASH, SAM, and an intraventricular pressure gradient of 50 mmHg. Thus, her ASH appeared during middle-age, and was probably provoked by hypertension, though a complete family survey could not be conducted. These three patients' findings indicate that there may be various modes of appearance of left ventricular hypertrophy in HCM. In the majority of patients with genetic predisposition, abnormal hypertrophy may develop during adolescence as in Case 1. In others, it may develop in middle-age, as it did in Case 2. The disease spectrum of HCM may additionally include those who develop abnormal hypertrophy during middle-age, following provocation by hypertension, as in Case 3.

[Functional maneuvers for the diagnosis of hypertrophic cardiomyopathies with and without left ventricular outflow obstruction].

to assess the diagnostic value of the commonly adopted haemodynamic criteria for the diagnosis of obstructive and non-obstructive hypertrophic cardiomyopathy. 16 cases of hypertrophic cardiomyopathy, 7 cases of the non-obstructive form, 16 fixed subaortic stenosis, 8 valvular aortic stenosis, and 7 cases of hypertensive heart disease. left and right heart catheterisation, with particular attention to the pressure gradient and to the aortic pulse pressure by means of simultaneous pressure recording from the left ventricle and aorta under basal conditions, after a ventricular premature beat, during the Valsalva manoeuvre, during amyl nitrite inhalation, and isoproterenol administration. the Valsalva manoeuvre increases significantly (p < 0.001) the pressure gradient, and the aortic pulse pressure in the post-extrasystolic beat decreases significantly (p < 0.001) in patients with hypertrophic obstructive cardiomyopathy. This response is significantly different from that of the other 3 disease groups. If the non-obstructive form is defined by strict criteria (i.e. no gradient above 30 mmHg even after provocative manoeuvres), then it cannot be separated from other forms of secondary left ventricular hypertrophy.

Aortic regurgitation

If there is increased stroke volume of the left ventricle due to volume overload, an ejection systolic 'flow' murmur may also be present when auscultating the same aortic area. Unless there is concomitant aortic valve stenosis, the murmur should not start with an ejection click. There may also be an Austin Flint murmur, a soft mid-diastolic rumble heard at the apical area; it appears when a regurgitant jet of blood from severe aortic regurgitation partially closes the anterior mitral leaflet. Peripheral physical signs of aortic regurgitation are related to the high pulse pressure and the rapid decrease in blood pressure during diastole due to blood returning to the heart from the aorta through the incompetent aortic valve, although the usefulness of some of the eponymous signs has been questioned: Phonocardiograms detect AI by having electric voltage mimic the sounds the heart makes. Characteristics- indicative of aortic regurgitation are as follow:

Pressure overload

Signs and symptoms A forceful apex beat indicates left ventricular pressure overload, while a right ventricular heave suggests right ventricular pressure overload. Other signs provide evidence for specific causes of pressure overload. Hypertension is diagnosed by sphygmomanometry. A narrow pulse pressure is a sign of aortic stenosis. The chest x-ray may show pulmonary hyperaemia in the case of pulmonary hypertension, and pulmonary oligemia in pulmonary stenosis. Pulmonary hypertension is also associated with chronic lung disease. Coarctation of the aorta presents with a significant difference in blood pressure between the upper and lower limbs, a systolic murmur or radiofemoral delay. Causes Any obstruction to the outflow of one of the chambers of the heart can lead to pressure overload. Left ventricular pressure overload Aortic stenosis Hypertension Coarctation of the aorta Right ventricular pressure overload Pulmonary stenosis Pulmonary hypertension Treatment

Heart murmur

Tricuspid valve regurgitation presents as a holosystolic (pansystolic) murmur at the left lower sternal border with radiation to the left upper sternal border. Prominent v and c waves may be seen in the JVP (jugular venous pressure). The murmur will increase with inspiration. Hypertrophic obstructive cardiomyopathy (or hypertrophic subaortic stenosis) will be a systolic crescendo-decrescendo murmur best heard at the left lower sternal border. Valsalva maneuver will increase the intensity of the murmur, as will changing positions from squatting to standing. Atrial septal defect will present with a systolic crescendo-decrescendo murmur best heard at the left upper sternal border due to increased volume going through the pulmonary valve, and is associated with a fixed, split S2 and a right ventricular heave.

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and left ventricles with inspiration (right ventricular systolic pressure increases while left ventricular systolic pressure decreases) are observed. The latter hemodynamic phenomenon is the most specific for constriction. Restrictive cardiomyopathy may be distinguished from constrictive pericarditis by a marked increase in right ventricular and pulmonary artery systolic pressures (usually >60 mmHg), a separation of the left and right ventricular diastolic pressures by and magnitude of the pressure waveforms provide important diag->5 mmHg (at baseline or with acute volume loading), and concordant nostic information; an example of normal pressure tracings is shown changes in left and right ventricular diastolic filling pressures with in Fig. 272-1. In the absence of valvular heart disease, the atria and inspiration (both increase). ventricles are “one chamber” during diastole when the tricuspid and mitral valves are open while in systole, when the pulmonary and aortic Cardiac Output

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CHAPTER 51e Approach to the Patient with a Heart Murmur PART 2 Cardinal Manifestations and Presentation of Diseases FIguRe 51e-2 Maximal intensity and radiation of six isolated systolic murmurs. HOCM, hypertrophic obstructive cardiomyopathy; MR, mitral regurgitation; Pulm, pulmonary stenosis; Aortic, aortic stenosis; VSD, ventricular septal defect. (From JB Barlow: Perspectives on the Mitral Valve. Philadelphia, FA Davis, 1987, p 140.) during the respiratory cycle and the performance of simple bedside maneuvers complete the auscultatory examination. These features, along with recommendations for further testing, are discussed below in the context of specific systolic, diastolic, and continuous heart murmurs (Table 51e-1).

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The mid-systolic, crescendo-decrescendo murmur of congenital pulmonic stenosis (PS, Chap. 282) is best appreciated in the second and third left intercostal spaces (pulmonic area) (Figs. 51e-2 and 51e-4). The duration of the murmur lengthens and the intensity of P2 diminishes with increasing degrees of valvular stenosis (Fig. 51e1D). An early ejection sound, the intensity of which decreases with inspiration, is heard in younger patients. A parasternal lift and ECG evidence of right ventricular hypertrophy indicate severe pressure overload. If obtained, the chest x-ray may show poststenotic dilation of the main pulmonary artery. TTE is recommended for complete characterization. Significant left-to-right intracardiac shunting due to an ASD (Chap. 282) leads to an increase in pulmonary blood flow and a grade 2–3 mid-systolic murmur at the middle to upper left sternal border CHAPTER 51e Approach to the Patient with a Heart Murmur

A catheter-induced syncopal attack in a case of hypertrophic obstructive cardiomyopathy.

A 48-year-old man with hypertrophic obstructive cardiomyopathy (HOCM) was studied by serial cardiac catheterization during incidentally induced syncope. His hospital admission was for repeated syncopal attacks and chest pain. His electrocardiogram showed giant negative T waves (greater than 10 mm) in V3, V4 and V5 leads, and his M-mode echocardiogram disclosed typical asymmetric septal hypertrophy, systolic anterior movement of the mitral valve, and a midsystolic semiclosure of the aortic valve. During cardiac catheterization, we incidentally induced syncope and recorded the serial pressure changes. During syncope, systemic blood pressure dropped without appreciable changes in pulmonary arterial and right ventricular pressures. Although blood pressure was maintained by administering etilefrine and hydrocortisone, syncope persisted. After administration of propranolol, he recovered from syncope. He was on sinus rhythm throughout the examinations. The ejection time (ET) obtained from the aortic pressure curve was extremely short (160 msec) during syncope and prolonged (300 msec) after recovery without significant change in the heart rate. We believe that the prompt intravenous administration of propranolol was very effective in relieving myocardial spasm as a possible cause of syncope.

Handgrip maneuver

Murmurs that are due to forward flowing of blood such as aortic stenosis, and hypertrophic cardiomyopathy decrease in intensity. The effect of reducing the intensity in forward flowing murmurs is much more evident in aortic stenosis rather than mitral stenosis. The reason for this is that there is a larger pressure gradient across the aortic valve. A complementary maneuver for differentiating disorders is the Valsalva maneuver, which decreases preload. See also Valsalva maneuver Preload Afterload References Cardiac procedures

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Systolic murmurs can be early, mid, late, or holosystolic in timing (Fig. 267-5). Acute severe MR results in a decrescendo early systolic murmur, the characteristics of which are related to the progressive attenuation of the left ventricular to left atrial pressure gradient during systole because of the steep and rapid rise in left atrial pressure in this context. Severe MR associated with posterior leaflet prolapse or flail radiates anteriorly and to the base, where it can be confused with the murmur of AS. MR that is due to anterior leaflet involvement radiates posteriorly and to the axilla. With acute TR in patients with normal pulmonary artery pressures, an early systolic murmur that may increase in intensity with inspiration may be heard at the left lower sternal border, with regurgitant cv waves visible in the jugular venous pulse.

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FIGURE 267-5 A. Top. Graphic representation of the systolic pressure difference (green shaded area) between left ventricle and left atrium with phonocardiographic recording of a holosystolic murmur (HSM) indicative of mitral regurgitation. ECG, electrocardiogram; LAP, left atrial pressure; LVP, left ventricular pressure; S1, first heart sound; S2 second heart sound. Bottom. Graphic representation of the systolic pressure gradient (green shaded area) between left ventricle and aorta in patient with aortic stenosis. A midsystolic murmur (MSM) with a crescendo-decrescendo configuration is recorded. AOP, aortic pressure. B. Top. Graphic representation of the diastolic pressure difference between the aorta and left ventricle (blue shaded area) in a patient with aortic regurgitation, resulting in a decrescendo, early diastolic murmur (EDM) beginning with A2. Bottom. Graphic representation of the diastolic left atrial–left ventricular gradient (blue areas) in a patient with mitral stenosis

Main systolic blood flow patterns in the left and right ventricular outflow tracts determined by Doppler echocardiography.

The main blood flow velocity patterns in the LVOT and RVOT were recorded by pulsed Doppler echocardiography in 28 normal healthy cases, in two athletes, and in 85 patients with atrial septal defects, pulmonary regurgitation, tetralogy of Fallot, aortic regurgitation, mitral stenosis, aortic stenosis, mitral regurgitation, hypertrophic cardiomyopathy, ischemic heart disease, and pulmonary hypertension. Blood flow velocities were displayed using a graphic system to form a real time sonogram, using Fast Fourier Transformation. In the normal group, the blood flow velocity was 1.69 KHz in LVOT, and 1.71 KHz in RVOT. In AR and T/F but not MS, there was high blood flow velocity in the LVOT, and the peak of blood flow velocity was shifted to mid-to late systole. In ASD and VSD with a L-R shunt, high blood flow velocity occurred in the RVOT, and the peak velocity shifted to early systole. Pulmonary hypertension occasionally produced a W- or V-shaped curve. In normal subjects, a small "a" wave could be detected in the LVOT recording. The "a" wave began at point B on the AML tracer of the M-mode echocardiography, reached maximum velocity at point C, and returned to zero (baseline) at point C'. The "a" wave was coincident with the R wave of the ECG, and with the Ia of the phonocardiogram (PCG). The normal velocity of the "a" wave was 602 Hz, and the a/H ratio was 0.36. In cases of HCM and IHD, the "a" wave velocity and the a/H ratio correlated with the end diastolic pressure and the peak dP/dT. These data suggest that the Doppler blood flow patterns in the LVOT and RVOT can indicate volume overload in the right and left ventricles, and that the "a" wave velocity and a/H ratio can provide new information concerning cardiac performance.

Valsalva maneuver

Medical diagnostics Cardiology The maneuver can sometimes be used to diagnose heart abnormalities, especially when used in conjunction with an echocardiogram. For example, the Valsalva maneuver (phase II) increases the intensity of hypertrophic cardiomyopathy murmurs, namely those of dynamic subvalvular left ventricular outflow obstruction. At the same time, the Valsalva maneuver (phase II) decreases the intensity of most other murmurs, including aortic stenosis and atrial septal defect. During the first few seconds of the Valsalva maneuver (phase I) the opposite findings will be the case.

Exercise intolerance

Hazards Certain conditions exist where exercise may be contraindicated or should be performed under the direction of an experienced and licensed medical professional acting within his or her scope of practice. These conditions include: Decompensated heart failure Recent myocardial infarction Hypertrophic cardiomyopathy or cardiomyopathy from recent myocarditis Active or suspected myocarditis or pericarditis Low left-ventricular ejection fraction (LVEF) Severe aortic stenosis Unstable ischemia Unstable arrythmia Irregular or resting pulse greater than 100 bpm Resting systolic blood pressure >200 mm Hg or resting diastolic blood pressure >110 mm Hg Severe pulmonary hypertension Chronic fatigue syndrome Suspected or known dissecting aortic aneurysm Recent systemic or pulmonary embolus Pneumothorax and haemoptysis Thrombophlebitis

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Figure 271e-12 A 70-year-old patient with known cardiac murmur and progressive shortness of breath and a recent episode of syncope. Echocardiography shows severe calcific aortic stenosis. A heavily calcified aortic valve (arrow) is shown in the parasternal long-axis views (top panels) and short-axis view (bottom left). Doppler interrogation shows a peak transaortic velocity of 5.2 m/s consistent with a peak instantaneous gradient of 109 mmHg and a mean gradient of 66 mmHg, and a corresponding aortic valve area of <0.6 cm2 (lower right). Ao, aorta; LA, left atrium; LV, left ventricle; RV, right ventricle. (See Videos 271e-8, 271e-9, and 271e-10.)

Increased intensity of the murmur of hypertrophic obstructive cardiomyopathy with carotid sinus pressure.

In a prospective study murmurs increased in intensity with carotid sinus pressure in 18 of 26 patients with hypertrophic obstructive cardiomyopathy (HOCM) (sensitivity, 69.2 percent for the 26 patients, 85.7 percent for the 21 patients in whom heart rate and blood pressure decreased with carotid sinus pressure). On the other hand, the murmur remained constant or decreased in all but one of 104 patients with valvular aortic stenosis, mitral insufficiency, hypertrophic nonobstructive cardiomyopathy, and systolic murmurs of miscellaneous origins (specificity, 99 percent; positive predictive value, 94.7 percent). Catheterization, indirect arterial pressure tracings, and echocardiographic studies indicated that carotid sinus pressure-induced bradycardia was associated with increased left ventricular outflow tract obstruction. The carotid sinus pressure-induced increase in the murmur is probably multifactorial: decreased aortic pressure and impedance; increased contractility immediately on sudden slowing of heart rate; further increase in obstruction as the mitral valve systolic anterior movement is enhanced; and delayed vasodilatation maintaining the obstruction even after return of heart rate to precarotid sinus pressure values. An increase in a systolic murmur with carotid sinus pressure is characteristic of HOCM.

Vital Sign Assessment -- Clinical Significance -- Pulse Rate

Assessing whether the rhythm of the pulse is regular or irregular is essential. The pulse could be regular, irregular, or irregularly irregular. Changes in the rate of the pulse, along with changes in respiration are called sinus arrhythmia. In sinus arrhythmia, the pulse rate becomes faster during inspiration and slows down during expiration. Irregularly irregular pattern is more commonly indicative of processes like atrial flutter or atrial fibrillation. We should also be checking for the radial and the femoral pulse simultaneously. If there is any delay between the pulses, it could indicate conditions like the coarctation of the aorta. Assessing the volume of the pulse is equally essential. A low volume pulse could be indicative of inadequate tissue perfusion; this can be a crucial indicator of indirect prediction of the systolic blood pressure of the patient. If we can palpate the radial pulse, the systolic blood pressure is generally more than 80 mmHg. If we can palpate the femoral pulse, the systolic blood pressure is more than 70 mmHg, and if we can palpate the carotid pulse, the systolic blood pressure is more than 60 mmHg. [10] Checking for symmetry of the pulses is important as asymmetrical pulses could be seen in conditions like aortic dissection, aortic coarctation, Takayasu arteritis, and subclavian steal syndrome. Besides the above-stated parameters, amplitude and rate of increase is also an important consideration. Low amplitude and low rate of increase could be seen in conditions like aortic stenosis, besides weak perfusion states. High amplitude and rapid rise can be indicative of conditions like aortic regurgitation, mitral regurgitation, and hypertrophic cardiomyopathy.

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Diagnosis Due to the unstable condition of these patients, supportive therapy must be initiated simultaneously with diagnostic evaluation (Fig. 326-2). A focused history and physical examination should be performed, blood specimens sent to the laboratory, and an electrocardiogram (ECG) and chest x-ray obtained. Etiologies of Cardiogenic Shock or Pulmonary Edema Acute myocardial infarction/ischemia LV failure Ventricular septal rupture Papillary muscle/chordal rupture–severe MR Ventricular free wall rupture with subacute tamponade Other conditions complicating large MIs Post-cardiac arrest Post-cardiotomy Refractory sustained tachyarrhythmias Acute fulminant myocarditis End-stage cardiomyopathy LV apical ballooning Takotsubo’s cardiomyopathy Hypertrophic cardiomyopathy with severe outflow obstruction Aortic dissection with aortic insufficiency or tamponade Severe valvular heart disease Other Etiologies of Cardiogenic Shockb RV failure due to:

Cardiac examination

Finally the sacrum and ankles are checked for pitting edema which is caused by right ventricular failure in isolation or as part of congestive cardiac failure. Auscultation One should comment on S1 and S2 – if the splitting is abnormal or louder than usual. S3 – the emphasis and timing of the syllables in the word Kentucky is similar to the pattern of sounds in a precordial S3. S4 – the emphasis and timing of the syllables in the word Tennessee is similar to the pattern of sounds in a precordial S4. If S4 S1 S2 S3 Also known as a gallop rhythm. diastolic murmurs (e.g. aortic regurgitation, mitral stenosis) systolic murmurs (e.g. aortic stenosis, mitral regurgitation) pericardial rub (suggestive of pericarditis) The base of the lungs should be auscultated for signs of pulmonary oedema due to a cardiac cause such as bilateral basal crepitations.

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It is usually of grade 1 or 2 intensity but may be absent when the cardiac output is severely reduced despite significant obstruction. The intensity of the murmur increases during maneuvers that increase cardiac output and mitral valve flow, such as exercise. The duration of the murmur reflects the length of time over which left atrial pressure exceeds left ventricular diastolic pressure. An increase in the intensity of the murmur just before S1, a phenomenon known as presystolic accentuation (Figs. 51e-1A and 51e-6), occurs in patients in sinus rhythm and is due to a late increase in transmitral flow with atrial contraction. Presystolic accentuation does not occur in patients with atrial fibrillation.

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Palpation may reveal cardiac enlargement and abnormal contraction of the cardiac impulse (left ventricular dyskinesia). Auscultation can uncover arterial bruits, a third and/or fourth heart sound, and, if acute ischemia or previous infarction has impaired papillary muscle function, an apical systolic murmur due to mitral regurgitation. These auscultatory signs are best appreciated with the patient in the left lateral decubitus position. Aortic stenosis, aortic regurgitation (Chap. 283), pulmonary hypertension (Chap. 304), and hypertrophic cardiomyopathy (Chap. 287) must be excluded, since these disorders may cause angina in the absence of coronary atherosclerosis. Examination during an anginal attack is useful, since ischemia can cause transient left ventricular failure with the appearance of a third 1582 and/or fourth heart sound, a dyskinetic cardiac apex, mitral regurgitation, and even pulmonary edema. Tenderness of the chest wall, localization of the discomfort with a single

Heart murmur

Abrupt standing Squatting, by increasing afterload and increasing preload. Handgrip maneuver, by increasing afterload Valsalva maneuver. One study found the Valsalva maneuver to have a sensitivity of 65%, specificity of 96% in detecting hypertrophic obstructive cardiomyopathy (HOCM). Both standing and Valsalva maneuver will decrease venous return and subsequently decrease left ventricular filling, resulting in an increase in the loudness of the murmur of hypertrophic cardiomyopathy, since outflow obstruction is increased by decreasing preload. Alternatively, squatting increases systemic vascular resistance, increasing afterload and helping to hold the obstruction in a more open configuration, decreasing the murmur. Maximum handgrip exercise also results in a decrease in the loudness of the murmur. Post ectopic potentiation

77-year-old female with syncope.

A 77-year-old female was referred for evaluation of an episode of syncope while eating breakfast. There was no history of fall, syncope, prodrome, dyspnoea, chest discomfort or palpitations. Medical history was notable for hyperlipidaemia and treated hypertension. Blood pressure was 140/90 mm Hg, pulse 85  beats per minute (BPM). No murmurs were present on cardiac examination. ECG revealed normal sinus rhythm with left ventricular (LV) hypertrophy (see online supplementary figure S1). Holter monitor demonstrated rare premature ventricular complexes (<1% of beats), without heart block or ventricular tachycardia. Transthoracic echocardiogram is shown in figure 1. Which of the following is the explanation for the flow indicated by the yellow arrow? Aortic stenosisCoronary artery flow, indicative of coronary fistulaHypertrophic cardiomyopathy with apical pouchHypertensive heart diseaseMitral stenosis.

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Tricuspid regurgitation (TR) with normal pulmonary artery pressures, as may occur with infective endocarditis, may produce an early systolic murmur. The murmur is soft (grade 1 or 2), is best heard at the lower left sternal border, and may increase in intensity with inspiration (Carvallo’s sign). Regurgitant “c-v” waves may be visible in the jugular venous pulse. TR in this setting is not associated with signs of right heart failure. Mid-Systolic Murmurs Mid-systolic murmurs begin at a short interval after , end before S (Fig. 51e-1C), and are usually crescendo-decrescendo in configuration. Aortic stenosis is the most common cause of a mid-systolic murmur in an adult. The murmur of AS is usually loudest to the right of the sternum in the second intercostal space (aortic area, Fig. 51e-2) and radiates into the carotids. Transmission of the mid-systolic murmur to the apex, where it becomes higher-pitched, is common (Gallavardin effect; see above).

[The clinical significance of the audible and mechanographic manifestations of mitral valve prolapse].

Graphic techniques were employed to examine 82 patients with mitral valve prolapse verified on echocardiography. In addition to the known acoustic symptoms, enhancement of tones III, IV and V was identified, especially in transmitral regurgitation, together with inverted alternating of the components of tones I and II. Mitral click (OS) was discovered in one third of the examined. Uninterrupted protodiastolic and presystolic murmurs were found more seldom. They were more well-defined on the phonocardiogram recorded from the esophagus, at the level of the mitral valve. The right and left ventricular apex cardiography made it possible to diagnose hyperdynamia of the left atrium, the shortening of isometric relaxation of the left ventricle on elongation of this phase of the right ventricle. Both the curves had the M-like deformation in the systole. On the apex cardiogram of the left ventricle, the O point was always low, and the OF amplitude (rapid ventricular filling) was increased. During regurgitation, the OF transformed to an anomalous positive wave (a "surge"). Simultaneous alterations in the jugular phlebogram and in both apex cardiograms reflect changes in all four heart chambers. In part of the examined, pulmonary hypertension was established with the aid of indirect techniques. Esophagoatriography turned out diagnostically instrumental, since in some of the patients it enabled identification of systolic expansion of the entire posterior wall of the left atrium (regurgitation).

Cardiac stress test

Absolute contraindications to cardiac stress test include: Acute myocardial infarction within 48 hours Unstable angina not yet stabilized with medical therapy Uncontrolled cardiac arrhythmia, which may have significant hemodynamic responses (e.g. ventricular tachycardia) Severe symptomatic aortic stenosis, aortic dissection, pulmonary embolism, and pericarditis Multivessel coronary artery diseases that have a high risk of producing an acute myocardial infarction Decompensated or inadequately controlled congestive heart failure Uncontrolled hypertension (blood pressure>200/110mm Hg) Severe pulmonary hypertension Acute aortic dissection Acutely ill for any reason Indications for termination: A cardiac stress test should be terminated before completion under the following circumstances:

Pulsus bisferiens

Pulsus bisferiens, also known as biphasic pulse, is an aortic waveform with two peaks per cardiac cycle, a small one followed by a strong and broad one. It is a sign of problems with the aorta, including aortic stenosis and aortic regurgitation, as well as hypertrophic cardiomyopathy causing subaortic stenosis. Pathogenesis In hypertrophic cardiomyopathy, there is narrowing of the left ventricular outflow tract (LVOT) due to hypertrophy of the interventricular septum. During systole, the narrowing of the LVOT creates a more negative pressure due to the Venturi effect and sucks in the anterior mitral valve leaflet. This creates a transient occlusion of the LVOT, causing a midsystolic dip in the aortic waveform. Towards the end of systole, the ventricle is able to overcome the obstruction to cause the second rise in the aortic waveform.

Man in his 50s with chest pain and dyspnoea.

A man in his 50s with sudden-onset chest pain and dyspnoea was transferred to the emergency room. He had a history of aortic valve replacement due to aortic regurgitation with a mechanical valve 6 years previously. Heart rate was 90 bpm, and blood pressure was too low to measure. In the emergency room, he presented with severe dyspnoea and a chest X-ray showed severe lung congestion (figure 1A). ECG showed complete left bundle branch block. His respiratory status rapidly worsened, and he went into cardiopulmonary arrest. After cardiopulmonary resuscitation, transthoracic echocardiography was performed (figure 1B, online supplementary video 1).DC1SP110.1136/heartjnl-2017-312477.supp1Supplementary file 1 heartjnl;104/10/868/F1F1F1Figure 1(A) Chest X-ray. (B) Colour Doppler image from apical five-chamber view. What is the most likely cause of the patient's cardiopulmonary arrest?Myocardial infarction in left main trunkAortic dissectionProsthetic valve thrombosisProsthetic valve embolisationPulmonary embolism.

T wave

Hypertrophic cardiomyopathy is the thickening of the left ventricle, occasionally right ventricle. It may be associated with left ventricular outflow tract obstruction or may not be associated with it in 75% of the cases. ECG would be abnormal in 75 to 95% of the patients. Characteristic ECG changes would be large QRS complex associated with giant T wave inversion in lateral leads I, aVL, V5, and V6, together with ST segment depression in left ventricular thickening. For right ventricular thickening, T waves are inverted from V1 to V3 leads. ST and T waves changes may not be apparent in hypertrophic cardiomyopathy, but if there is presence of ST and T waves changes indicates severe hypertrophy or ventricular systolic dysfunction. According to Sokolow-Lyon criterion, the height of R wave in V5 or V6 + the height of S wave in V1 more than 35 mm would be suggestive of left ventricular hypertrophy.