Common misconceptions and mistakes
- •
Overresuscitating patients with septic shock
- •
Underresuscitating patients with hemorrhagic shock
- •
Underresuscitating severe pancreatitis
- •
Attempting to initially differentiate isolated right-ventricular (RV) cardiogenic shock from left-ventricular (LV) cardiogenic shock by echocardiogram rather than by chest x-ray (looking for pulmonary edema/pleural effusion)
- •
Missing dependent edema (eg, sacral) during the physical examination
- •
Failing to consider hemorrhage in inpatients (not admitted for bleeding) who develop shock, instead presuming sepsis
Shock
- •
Pathologically low blood pressure (BP) resulting in end organ hypoperfusion
- •
Occurs when the normal homeostatic mechanisms protecting organ perfusion (ie, increased sympathetic activity aimed at increasing cardiac output [CO] and systemic vascular resistance [SVR]) fail, leading to systemic tissue hypoxia and organ injury/dysfunction (specifically):
- •
Acute kidney injury (often acute tubular necrosis with oliguria)
- •
Shock liver (asymptomatic transaminitis or increased international normalized ratio [INR])
- •
Decreased mental status (lethargy to obtundation)
- •
Lactic acidosis from underperfused skeletal muscle and intestine
- •
- •
If not reversed, shock will cause death by pulseless electrical activity (PEA) arrest secondary to overwhelming lactic acidosis
- •
Shock is diagnosed when end organ hypoperfusion is proven in the setting of low BP
- •
Hypoperfusion is evidenced by organ failure and the presence of an elevated serum lactate
- •
- •
Tachycardia is anticipated in all causes of shock not directly related to bradycardia and/or heart block
- •
Individuals with baseline conduction system disease may not mount an appropriate tachycardia
- •
Shock with “relative bradycardia” may require inotropic/chronotropic support
- •
- •
- •
There are four distinct pathophysiologic types of shock, with six cardiogenic subtypes ( Table 18.1 ):
- •
Hypovolemic shock
- •
Hypovolemic shock is caused by one of the following:
- •
Acute blood loss (hemorrhage)
- •
Volume depletion, as seen with gastrointestinal (GI) and renal NaCl loss
- •
Third-spacing physiology, as seen in severe pancreatitis or after a large intraabdominal surgery
- •
- •
Leads to a decreased central venous pressure (CVP), right ventricular end-diastolic pressure (RVEDP), and left ventricular end-diastolic pressure (LVEDP), reducing stroke volume and thus CO
- •
Decreased CO triggers an increase in sympathetic activity, leading to tachycardia and a maximally increased SVR (renin–angiotensin system activation)
- •
- •
Distributive shock
- •
Distributive shock is caused by one of the following:
- •
Sepsis (cytokine mediated)
- •
Anaphylaxis, as seen in allergic-mediated diffuse mast cell degranulation and histamine release
- •
Adrenal crisis, as seen in adrenal insufficiency with provocative stress (eg, bleeding)
- •
Severe pancreatitis (cytokine mediated)
- •
Neurogenic Shock (central nervous system [CNS] mediated, as in spinal cord injury)
- •
- •
Leads to inappropriate arteriolar vasodilation and increased capillary permeability (capillary leak), which decreases SVR and effective circulating volume, causing hypotension
- •
Hypotension triggers an increase in sympathetic activity, leading to tachycardia and an increased CO
- •
Importantly, distributive shock from sepsis often causes concomitant myocardial depression, decreasing CO
- •
- •
- •
LV cardiogenic shock (HFpEF, HFrEF, and mechanical failure)
- •
From LV failure, as seen in acute systolic dysfunction from ischemia, acute diastolic dysfunction from arrhythmia or hypoxemia, or mechanical failure (ie, papillary muscle rupture)
- •
Leads to a decreased CO and an increase in LVEDP, mean pulmonary arterial pressure (mPAP), RVEDP, and CVP
- •
Decreased CO triggers an increase in sympathetic activity, leading to tachycardia and a maximally increased SVR
- •
- •
RV cardiogenic shock (with PH, without PH, and mechanical failure)
- •
From isolated RV failure (systolic dysfunction), occurring with pulmonary hypertension (eg, pulmonary embolism), without pulmonary hypertension (eg, RV infarct), or with mechanical failure as in pericardial effusion with tamponade
- •
Decreased RV stroke volume causes a decrease in RV CO, which leaves the left ventricle underfilled leading to an increased RVEDP and CVP and a decreased LVEDP, LV stroke volume, and LV CO
- •
The decreased CO triggers an increase in sympathetic activity, leading to tachycardia (unless the conduction system is injured as in inferior wall myocardial infarction with RV infarct) and a maximally increased SVR
- •
Table 18.1
Pathophysiologic Types of Shock
Type of Shock and Common Causes
Anticipated Hemodynamics
Red = primary insult
Black = direct consequence
Blue = compensatory neurohormonal response
Anticipated Edema
Anticipated
Echocardiographic Finding
Hypovolemic
- •
Blood loss (GI, spontaneous, postprocedure)
- •
Fluid loss (GI/renal)
- •
Third spacing
- •
Severe pancreatitis
- •
Postoperative abdominal surgery
↓CVP, ↓RVEDP, ↓PAP, ↓ LVEDP, ↓ CO, ↑SVR
No edema
↑RV EF, no PH, nl LA, ↑LV EF
Distributive:
- •
Sepsis without myocardial depression
↓CVP, ↓ RVEDP, ↓ PAP, ↓ LVEDP, ↑CO, ↓SVR
No edema
↑RV EF, No PH, nl LA, ↑LV EF
- •
Sepsis with myocardial depression
↑CVP, ↑ RVEDP, ↑ PAP, ↑ LVEDP, ↓CO, ↓SVR
Pulmonary edema
Peripheral edema
↓RV EF, ↑PAS, ↑ LA, ↓LV EF
- •
Severe pancreatitis with necrosis
- •
Anaphylaxis
- •
Adrenal insufficiency
- •
Severe acidosis pH < 7.2
↓CVP, ↓ RVEDP, ↓ PAP, ↓ LVEDP, ↑ CO, ↓SVR
No edema
↑RV EF, No PH, nl LA, ↑LV EF
LV cardiogenic (systolic dysfunction):
- •
Ischemia, EtOH, viral, tachyarrhythmia (subacute), Takotsubo, idiopathic
- •
Long standing:
- •
Aortic or mitral regurgitation, aortic stenosis, HTN
↑CVP, ↑RVEDP, ↑PAP, ↑ LVEDP, ↓ CO, ↑SVR
Pulmonary edema
Peripheral edema *
↓RV EF, ↑PAS, ↑ LA, ↓LV EF
LV cardiogenic (diastolic dysfunction):
- •
Tachyarrhythmia (acute)
- •
Hypoxemia (PaO 2 < 60 mm Hg)
- •
Volume overload
↑CVP, ↑RVEDP, ↑PAP, ↑ LVEDP, ↓ CO, ↑SVR
Pulmonary edema
Peripheral edema *
↓RV EF, ↑PAS, ↑ LA, ↑LV EF
LV cardiogenic mechanical failure:
- •
Mitral regurgitation (acute)
- •
Aortic regurgitation (acute)
- •
Outflow tract obstruction
- •
Aortic stenosis
- •
HOCM
↑CVP, ↑RVEDP, ↑PAP, ↑ LVEDP, ↓ CO, ↑SVR
Pulmonary edema
Peripheral edema *
Mitral regurgitation
Aortic regurgitation
Aortic stenosis
HOCM
RV cardiogenic, with pulmonary HTN:
- •
Acute PE
- •
CTEPH
- •
IPAH
↑CVP, ↑RVEDP, ↑PAP, ↓LVEDP, ↓ CO, ↑SVR
Peripheral edema *
↓RV EF, ↑PAS, nl LA, ↑LV EF
- •
Mitral stenosis
↑CVP, ↑RVEDP, ↑PAP, ↓LVEDP, ↓ CO, ↑SVR
(Note: PCWP elevated despite nl LVEDP because of increased LAP and PVP)
Pulmonary edema
Peripheral edema *
Mitral stenosis
RV cardiogenic, without pulmonary HTN:
- •
RV infarct
↑CVP, ↑RVEDP, ↓ PAP, ↓ LVEDP, ↓ CO, ↑SVR
Peripheral edema *
↓RV EF, no PH, nl LA, ↑LV EF
RV cardiogenic, without pulmonary HTN mechanical failure:
- •
Pericardial effusion with tamponade
- •
Constrictive pericarditis
- •
Restrictive cardiomyopathy
↑CVP, ↑RVEDP, ↓ PAP, ↓ LVEDP, ↓ CO, ↑SVR
Peripheral edema *
Echo signs consistent with:
- •
Tamponade physiology
- •
Constrictive pericarditis
- •
Restrictive cardiomyopathy
CO , Cardiac output; CTEPH , chronic thromboembolis pulmonary hypertension; CVP, central venous pressure; EtOH , ethyl acohol; GI , gastrointestinal; HOCM , hypertrophic obstructive cardiomyopathy; HTN , hypertension; IPAH , idiopathic pulmonary arterial hypertension; LAP, left atrial pressure; LVEDP, left ventricular end diastolic pressure; PAP, pulmonary artery pressure; PAS , pulmonary artery systolic; PCWP , pulmonary capillary wedge pressure; PE , pulmonary embolism; PVP, pulmonary venous pressure; RVEDP, right ventricular end-diastolic pressure; SVR, systemic vascular resistance.
↑LV EF = Normal or high LV ejection fraction
↓LV EF = Systolic dysfunction
↑RV EF = Normal or hyperdynamic RV function
↓RV EF = Decreased or hypodynamic RV function and/or RV or RA dilation
¥ Pulmonary edema = Interstitial edema, alveolar edema, or pleural effusion
* In cases of acute LV and RV cardiogenic shock, peripheral edema takes hours to become appreciable even though right-sided pressures increase instantly.
- •
Initial Evaluation
- •
History should focus on screening for symptoms of:
- •
Infection (eg, fever, chills, cough, dysuria, abdominal or extremity pain)
- •
Bleeding (eg, hematemesis/coffee-ground emesis, bright-red blood per rectum, melena)
- •
Left-sided heart failure (eg, paroxysmal nocturnal dyspnea, orthopnea, increased edema, weight gain)
- •
Exertional syncope, which is seen in both:
- •
Isolated right-sided heart failure (eg, pulmonary arterial hypertension [PAH])
- •
Left-sided heart failure from outflow tract obstruction (ie, hypertrophic obstructive cardiomyopathy [HOCM])
- •
- •
- •
Physical examination should focus on:
- •
Temperature
- •
Fever and hypotension equal sepsis until proven otherwise
- •
- •
Heart rate
- •
Anticipate sinus tachycardia (relative bradycardia implies conduction system disease or atrioventricular [AV] nodal blockade)
- •
- •
Blood pressure (BP)
- •
Interpret relative to baseline BP:
- •
Patients with long-standing, poorly controlled hypertension may experience end organ hypoperfusion despite an mean arterial pressure (MAP) ≥ 60 mm Hg and/or an systolic blood pressure (SBP) ≥ 90 mm Hg
- •
- •
- •
Mental status
- •
Anticipate delirium and/or globally decreased sensorium with septic shock secondary to poor cerebral perfusion and cytokines
- •
Anticipate globally decreased sensorium in cardiogenic shock secondary to poor cerebral perfusion from decreased cardiac output
- •
Individuals with hemorrhagic shock tend to have a normal mental status despite significant hypotension because cerebral perfusion is maintained by cerebral autoregulation
- •
- •
Ability to lie flat comfortably (unusual in LV mediated cardiogenic shock)
- •
Presence or absence of:
- •
Oxygen requirement (suggesting LHF, pneumonia, or acute respiratory distress syndrom [ARDS])
- •
Heart murmur suggesting valve failure, or a prominent S2 suggesting (pulmonary hypertension [PH]) and/or an S3 suggesting (left-ventricular [LV] dysfunction)
- •
Thoracic edema (ie, crackles, decreased breath sounds with dullness) suggesting LHF
- •
Peripheral edema suggesting HF
- •
- •
Markers of cutaneous perfusion may reflect the underlying systemic vascular resistance (ie, poor perfusion implies a high SVR shock state and good perfusion implies a distributive shock state)
- •
Skin color (hyperemic or pale)
- •
Skin temperature (warm or cool)
- •
- •
- •
Initial diagnostic labs and imaging include:
- •
Complete blood count (CBC) looking for anemia and/or leukocytosis
- •
Coagulation studies looking for coagulopathy
- •
Chemistries with renal and liver indices and an anion gap calculation
- •
Lactate
- •
Arterial blood gas (ABG) to check the pH, screen for respiratory failure, and assess gas exchange
- •
A pH < 7.25 (but typically < 7.20) may cause a low SVR state, in and of itself, as intrinsic (and extrinsic) pressors fail in the acidotic milieu
- •
Shunt physiology (ie, PaO 2 < 200 mm Hg on 100%) is worrisome for either cardiogenic or noncardiogenic pulmonary edema
- •
- •
Troponin test looking for evidence of LV or RV ischemia
- •
ECG looking for ischemia and/or right heart strain (ie, S I, Q III, flipped T in III)
- •
Chest x-ray looking for thoracic fluid and/or pneumonia
- •
Urinalysis looking for infection and/or casts consistent with acute tubular necrosis (ATN)
- •
Bedside echocardiogram looking at global RV and LV size and function, and screening for a pericardial effusion
- •
Differentiating the Types of Shock ( Fig. 18.1 )
- •
First differentiate cardiogenic from noncardiogenic etiologies by looking for the presence or absence of any peripheral and/or thoracic edema (ie, alveolar edema, pulmonary interstitial edema, or pleural effusion)
- •
Patients in hypovolemic or distributive shock will not have any edema at presentation (unless they had preexisting heart failure and volume overload)
- •
Patients with LV -mediated cardiogenic shock will have pulmonary edema and peripheral edema
- •
Shock from acute LV failure leads to “flash pulmonary edema,” a sudden rise in LVEDP, causing dyspnea and gas exchange abnormalities (ie, hypoxemia) with radiographic evidence of pulmonary edema, often without obvious peripheral edema at presentation
- •
Peripheral edema and pleural effusion may take hours to become appreciable (despite an immediate elevation in pulmonary artery pressure [PAP], RVEDP, RA and CVP)
- •
- •
Patients with RV -mediated cardiogenic shock (isolated right heart failure) will have peripheral edema only (no pulmonary edema)
- •
Shock from acute RV failure may present without obvious peripheral edema which may take hours to become appreciable (despite an immediate elevation in RVEDP and CVP)
- •
- •
- •
Next asses cutaneous perfusion (ie, warm vs cool extremities)
- •
Distributive shock (a low SVR state) produces warm , cutaneously well-perfused extremities
- •
Both hypovolemic and cardiogenic shock (high SVR states) produce cool, cutaneously poorly perfused extremities
- •
- •
Then obtain a cardiac echocardiogram aimed at globally assessing RV and LV function and right- and left-sided pressures (eg, atrial chamber size and estimated pulmonary artery systolic [PAS] pressure) while ruling out tamponade and acute valve failure:
- •
The echocardiogram is key in differentiating cardiogenic shock from hypovolemic or distributive shock
- •
Distributive and hypovolemic shock states cause the right and left ventricles to be underfilled, appearing on an echocardiogram as hyperdynamic (ie, with an increased ejection fraction)
- •
LV-mediated cardiogenic shock has two possible echocardiographic findings:
- •
Decreased systolic function, a.k.a. HFrEF
- •
Preserved systolic function, a.k.a. HFpEF
- •
Both HFpEF and HFrEF will cause an increase in LA pressure and mPAP
- •
However, echocardiographic evidence of LA enlargement and/or mPAP elevation are not guaranteed
- •
The left atrium may not always enlarge under pressure, and echocardiography may underestimate (or miss) pulmonary hypertension
- •
- •
- •
- •
- •
RV-mediated cardiogenic shock from mechanical failure as a result of pericardial effusion with tamponade physiology or LV-mediated cardiogenic shock as a result of aortic or mitral valve failure, can also be readily identified by echocardiogram
- •
RV-mediated cardiogenic shock (isolated right heart failure) shares the same core echocardiographic findings as LV-mediated cardiogenic shock caused by HFpEF—namely RV dysfunction with preserved LV function
- •
Therefore isolated RV-mediated cardiogenic shock is differentiated from LV-mediated cardiogenic shock due to HFpEF by the presence or absence of pulmonary edema ( not echocardiographic findings)
- •
That said, left atrial enlargement (without mitral valve disease) strongly supports a HFpEF etiology
- •
- •
- •
- •
Mixed physiology shock
- •
Distributive shock with concomitant heart failure occurs relatively commonly, as infection and sepsis can decompensate preexisting heart failure in addition to causing myocardial depression directly (cytokine mediated)
- •
Patients will have warm edematous extremities and varying degrees of pulmonary edema
- •
- •
Hypovolemic shock with preexisting heart failure occurs most commonly when an individual with chronic decompensated heart failure develops hemorrhagic shock or (less commonly) third-spacing physiology
- •
Hypovolemic shock causes low CVP, RVEDP, and LVEDP physiology such that:
- •
Individuals with preexisting volume overload will have mobilized (resolved) all of their pulmonary edema by the time their hypovolemic disease process (eg, GI bleeding) causes shock
- •
Long-standing lower extremity edema, however, may persist and be present at presentation in these individuals because this fluid may be slower to mobilize
- •
- •
Volume depletion and heart failure cannot coexist
- •
Volume depletion is a low total-body sodium content state
- •
Heart failure is a volume-overloaded, high total body sodium content state
- •
- •
- •
