the cardiovascular system
TRANSCRIPT
Hypotension & Shock In Critical Care
Tutorials in Intensive Care Medicine Series v4.5,04.01 by Patrick Neligan There are three key problems in intensive care which require immediate attention: hypoxemia, as detected by pulse-oximetery, oliguria, as detected by measurement of urinary output and hypotension, detected by direct and indirect measurement of blood pressure. If ignored, the pathologies behind these symptoms will lead to irreversible organ failure and death. Even as a novice in intensive care, you must be able to deal with these three problems.
Introduction and Overview. Hypotension is a sign of cardiovascular insufficiency. The cardiovascular system is made up of three key elements (figure 1): a pump, tubing and a fluid. The pump propels the fluid, the tubing distributes and collects it. If a patient becomes hypotensive, either the pump is not working properly, there is not enough fluid in the system, or the distribution network is malfunctioning. Under normal conditions, the various components of the cardiovascular system are interdependent, and if one element malfunctions, the others compensate to return the blood pressure to normal. An example of this is when a patient bleeds: the volume of fluid falls, and in response, the blood vessels tighten up (vasoconstrict), and the heart rate rises.
1. Pump
3.1 DistributionSystem
3.2 Exchange System
3.3 CollectionSystem
The Cardiovascular System
2. Fluid
3. Tubing
Figure 1
When there is evidence of end organ insufficiency (confusion, oliguria or lactic academia), then hypotension has caused “shock.” In shock – definitive evidence of hypotension (inadequate blood pressure to maintain tissue perfusion) – at least one element of the cardiovascular system has malfunctioned, and the others have failed to adequately compensate. The simplest way to
describe shock is 1) Pump failure – “cardiogenic” shock, 2) Tubing malfunction- “distributive” shock, & 3) Fluid loss – “hypovolemic shock”. The treatment of shock depends on the cause. The commonest type – hypovolemic – is treated by replacing the fluid that is lost, blood or plasma. Cardiogenic shock is managed by using therapies that improve overall cardiac function. Distributive shock is treated by either loosening up constricted blood vessels or tightening up dilated vessels. It is important to remember that shock is failure of circulation and failure of compensation, and two separate types overlap: e.g. in anaphylaxis, there is distributive shock due to mast cell degranulation and vasodilatation. In this situation the failure is the vasodilatation, but there is failure of compensation as the volume of blood in the vasculature is inadequate to maintain pressure, and the patient becomes “relatively hypovolemic”. The treatment therefore is fluid loading and vasoconstrictors. Learning Objectives
1. To understand the physiological basis of cardiovascular function and why compensation fails in shock.
2. To use deductive reasoning to evaluate the hypotensive patient. 3. To develop a method for resuscitating and monitoring the shocked patient.
What is: Blood Pressure, Hypotension, Shock? • Blood Pressure is Cardiac Output multiplied by Peripheral Resistance
Cardiac Output is Heart Rate times Stroke Volume Hypotension is caused by either Inadequate Cardiac Output or Inadequate Peripheral
Resistance What is Blood Pressure? The cardiovascular system consists of five components: a pump – the heart, a carrier fluid – blood, a distribution system – the arteries, an exchange system – the capillary network, and a collecting system – the venous system. Blood pressure is the driving force that propels blood along the distribution network. Blood pressure is conventionally measured at the level of the aortic arch, where it is greatest. As the arterial tree branches out, the velocity of blood slows, until it moves extremely slowly through the capillary network. The main thrust of blood pressure comes from the contraction of the heart, around the fluid that collects in the left and right ventricles, when the pressure in the ventricles exceeds that in the aorta and pulmonary arteries, blood is projected forward. The amount of blood expelled per cycle is the stroke volume. The stroke volume is determined by the amount of blood in the heart before it starts to contract – the “preload” or end diastolic volume, the force required to overcome resistance to ejection – the “afterload”, and the ability of the heart muscle to deal with the volume “loaded” onto it – the heart muscle “contractility”. The cardiac output is the amount of blood ejected from the heart per minute, the heart rate times the stroke volume. Pressure is calculated simply as force per unit area [P=f/a]. The force in this case is the forward motion of blood, the cardiac output. The area into which the blood is being propelled is the arterial network, principally the arterioles, subdivisions of arteries that act as resistance vessels. Conventionally we call this area “the total peripheral resistance”, as the arterial network exists in a state of tonic vasoconstriction, a function of the sympathetic nervous system. The circulating volume is controlled by a number of reflex systems, extrinsic and intrinsic to the kidney. These effectively assimilate information about perfusion pressure (essentially from baroreceptors in the carotid body and aortic arch), serum osmolality (in the mid brain) and urinary sodium content (in the distal tubule of the nephron).
• Heart Rate, Stroke Volume and Total Peripheral Resistance exist in dynamic equilibrium: these interactions maintain blood pressure. If one of the three
becomes abnormal, the other two compensate. This represents the cardiovascular physiologic reserve.
Blood pressure is maintained by a series of interactive autonomic and humoral reflexes that continually equate heart rate, stroke volume, total peripheral resistance and circulating volume. If there is a malfunction within this system, the other components’ function alters to compensate (after all without an adequate blood pressure vital organs will not perfuse). If a patient becomes hypotensive, compensation has failed, and external intervention is required to correct the problem.
What are these compensatory mechanisms? The heart is responsive to the amount of fluid present in the ventricles at the end of a diastolic filling period. The heart muscles are stretched by the distending fluid, and the degree of stretch is directly related to the stroke volume, this is known as Starling’s Law (figure 2). If the heart rate slows down, then filling time increases, as does filling volume. The stroke volume increases. If the filling volume is reduced due to excessively fast heart rate, stroke volume falls. If the patient has a low preload, due for example to bleeding, the heart rate increases in order to compensate for the lower stroke volume. The objective of all interventions relating to the heart is to optimize stroke volume while minimizing the risk of rate or work related ischemia. The majority of patients who are hypotensive in ICU are so because of overall hypovolemia, the treatment is volume loading in order to place the patient on the most efficient part of the pressure-volume curve.
• Hypotension is an indication of 1) An abnormality of Heart Rate, Stroke Volume or Peripheral Resistance, & 2) Failure of the others to compensate.
Figure 2. Starling’s Law
Stro
ke V
olum
e
Left Ventricular End Diastolic Volume
X
Increasing the filling volume of the ventricle leads to a progressive increase in stroke volume, until a point is reached (X), where overstretching of muscle occurs and stroke volume falls. The arrow in the diaphragm indicates what happens with cardiac failure (downwards to the right) – the muscle is less effective, and with inotropes (upwards to the left) – muscle contractility is improved. This diagram is the basis of much of cardiac therapeutics.
In a similar manner, if a patient becomes vasodilated for any reason (anaphylaxis, sepsis etc), then peripheral resistance falls, and heart rate and stroke volume must increase in order to maintain blood pressure. This is sometimes called “high output” cardiac failure, a somewhat incorrect term. In patients with severe sepsis, the cardiac output may increase to 10 –12 litres per minute, in order to maintain blood pressure. If, under these circumstances, the patient remains hypotensive, then either the vasodilatation is excessive, or the heart itself is not able to mount an adequate compensatory response. The interactions of the heart and peripheral vasculature are represented in figure 3.
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TskAi
Figure 3: Cardiovascular Reflexes
Circulating volume falls (due to bleeding)
Stroke Volume falls
Baroreceptors in Aortic Arch and Carotid Sinus sense this.
Impulses sent to along the IX and X nerves are reduced.
The Cardioinhibitory center is inhibited The Cardiostimulatory center is activated
The result is an increase in Sympathetic Output and a reduction in Parsympathetic Output
Increased Heart Rate - Increased Cadiac Contractility Venoconstriction - Vasoconstriction
Activation of the Renal Volume Defense System
Angiotensin, Vasopressin, Aldosterone
What is Shock, and what causes it? • Shock is acute circulatory failure leading to inadequate tissue perfusion and
end organ injury Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion esulting in generalized cellular hypoxia." hock is caused by a disruption to the cardiovascular system, and inadequate compensation to aintain tissue perfusion.
Do you have a method of classifying shock? • Shock is hypotension with end organ injury: it classified as being due to malfunction
of 1) the Pump (cardiogenic), 2 ) the Tubing (distributive), or 3) the Fluid (hypovolemic). • Hypotension and Shock are caused by a problem with Heart Rate, Stroke Volume or
Peripheral Resistance. here are only three types of shock, problems with the heart, sometimes called cardiogenic hock, problems vascular system, known as distributive shock, and loss of circulating volume, nown as hypovolemic shock. lthough textbooks and examiners often emphasize the classification of shock, in the real world,
t is often more effective to use the physiologic approach to shock: • Shock is due to inadequate blood pressure. • Low blood pressure is due to inadequate cardiac output or low peripheral resistance. • Low cardiac output is caused by a problem with heart rate or stroke volume. • Heart rate abnormalities: too fast (tachycardia), too slow (bradycardia).
• Stroke Volume abnormalities: failure to receive, failure to eject. • Low peripheral vascular resistance is due to inappropriate vasodilatation.
What is the significance of Heart Rate?
• The heart rate is a fundamental element of hypotension both in terms of cause (tachyarrhythmias / bradyarrhythmias) and compensation – hypotension should be
accompanied by a tachycardia. The amount of blood pumped from the heart per minute is the cardiac output. It is determined by the volume pumped in each cycle, the stroke volume (end diatolic volume minus the end systolic volume) and the frequency of the cycles, the heart rate. The ability of the heart to both receive and eject blood is a fundamental function of heart rate. Firstly if the rate is excessive, then the heart is unable to either fill or eject efficiently. If, for any reason the stroke volume falls, the heart is able to compensate by increasing the heart rate. The filling of the left ventricle is not just determined by the venous return, 30% of filling is derived from the “atrial kick”, which is lost in atrial fibrillation. In some circumstances, the stroke volume is fixed, such as in mitral and aortic stenosis and in infancy, the cardiac output is rate dependent. If baby’s, who normally have a fast heart rate, become bradycardic, then their cardiac output (and thus their blood pressure) falls. Patients who have permanent pacemakers behave in an opposite manner: if their stroke volume falls, they are unable to increase their heart rate to compensate. Hypotension and bradycardia is a characteristic of excessive vagal activity. Cholinergic agents (particularly anticholinesterases such as neostigmine) will mimic vagotonicity. Other drugs may excessively slow nodal conduction - beta blockers, calcium channel blockers, digoxin etc. Hypotension may be the “egg, not the chicken” - it follow an excessively slow or fast heart rate. Complete heart block may cause hypotension, particularly in the non compliant left ventricle. Tachyarrhythmias will reduce filling time and curtail stroke volume
What is the significance of Stroke Volume? • Low Stroke volume is caused by a problem with reception or a problem with ejection
Problems with reception are: inadequate venous return or cardiac inflow obstruction The heart’s normal tasks are to receive and eject blood. The stroke volume is the amount of blood ejected per cycle. If there is a problem with the stroke volume, it must involve either reception or ejection.
Problems with reception (filling): Inadequate venous return diastolic dysfunction & cardiac inflow obstruction
• Fluid loss is caused by either absolute hypovolemia (e.g.blood loss) or relative hypovolemia (“third spacing”).
1) Inadequate venous return: due to hypovolemia. Inadequate preload or filling pressure occurs as a result of intravascular fluid depletion, which may be due to volume loss, such as bleeding or dehydration, or fluid redistribution – third space losses, such as occurs in bowel obstruction or capillary leak syndrome. Often severe fluid depletion exists before patients become hypotensive, due to the potency of the compensatory mechanism. In this state patients are vulnerable to interventions which may unmask fluid depletion, such as the administration of vasodilators, including anesthetic agents, and aggressive manual ventilation. Patients admitted to intensive care in compensated shock may become severely hypotensive following the administration of even very small doses of propofol or thiopental. There are many warning signs
of under-resuscitation: a lingering tachycardia, cold peripheries or a pulse oximeter that is not reading, oliguria, low CVP, a large base excess on blood gas analysis, a lactic acidosis.
• Cardiac inflow obstruction is caused by a pericardial (tamponade) or intrathoracic process (PEEP), or a lesion within the heart itself (mitral stenosis).
2) Diastolic Dysfunction: loss of left ventricular compliance impairs it’s ability to receive blood. This disorder most commonly results from systolic dysfunction, and as a consequence of myocardial fibrosis – for example due to ischemia or hypertension. Diastolic dysfunction is characterized by the requirement of higher filling pressures to achieve normal filling volumes, while the heart is less compliant and receptive to blood. Aggressive volume loading of patients with diastolic dysfunction frequently results in backward heart failure, causing acute pulmonary edema. 3) Cardiac inflow obstruction: occurs either due to a constriction around the heart, a pericardial or intrathoracic process, or a lesion within the heart itself. Pericardial injuries include pericardial effusion or hematoma constrictive pericarditis – an acute crisis associated with a pericardial injury is called tamponade. Tamponade is diagnosed as a tetrad of shock, clear lung fields, inaudible or muffled heart sounds, and an increase in the jugular venous pulse wavefrom on inspiration. An often forgotten, but extremely common cause of hypotension, is excessive intrathoracic pressure. This can be transmitted from within the alveolar space – as with positive end expiratory pressure (PEEP) and gas trapping in airway obstruction (auto-PEEP), or within the pleural space – Pneumothorax, hemothorax or, if the patient is in extremis, tension Pneumothorax. Intracardiac lesions may also cause inflow obstruction, these include mitral and tricuspid stenosis or thrombosis, and atrial myxoma. Problems with ejection (systolic dysfunction) include pump failure and outflow obstruction
• Pump failure is caused by ischemia, overload, contusion, inflammation 1. Problems with the pump itself: the heart is a muscle, and if there is damage to the muscle it will not pump effectively. This may be due to inadequate functioning muscle mass, as occurs with ischemia, contusion (bruising in trauma), inflammation (myocarditis) and fibrosis, or to excessive stretch, with excessive fluid administration or valvular incompetence (e.g. aortic regurgitation). With each of these, confirmatory evidence may be available, electro-cardiographic or echocardiographic evidence of acute ischemia. The patient may give a good history of chest pain or trauma, cardiac enzymes may be positive, and murmurs may be audible. Do not forget the right ventricle: right ventricular contusion or infarction may be much more difficult to diagnose and the treatment is almost the polar opposite of that of left ventricular failure. The pump may be overwhelmed by excessive volume administration, or valvular (aortic or pulmonary) regurgitation.
• Cardiac outflow obstruction is caused by pulmonary embolism, aortic stenosis, aortic crossclamps
2. Outflow obstruction: there are two major sites that cardiac outflow may be blocked: at the level of the aortic valve (aortic stenosis) or within the low pressure (at thus easily occluded) pulmonary circulation – pulmonary embolism. The former can be diagnosed on the basis of history, ECG and classic murmur. The latter may be more difficult to diagnose. Useful information includes risk (cancer, immobility, deep venous thrombosis, lack of prophylaxis,
pelvic and hip surgery), ECG changes (right sided – RVH, sinus tachycardia, atrial fibrillation, right bundle branch block), occasional chest x-ray findings, and definitive diagnosis on ventilation-perfusion scanning, spiral CT or pulmonary angiography.
Problems with peripheral resistance (distributive shock)
• Shock caused by low peripheral vascular resistance is caused by loss of tonic vasoconstriction (vasoplegia), due to sympathectomy, anaphylaxis or sepsis, leading to
relative hypovolemia. Distributive shock is a problem with the peripheral vascular resistance. Blood vessels are normally kept in a state of tonic vasoconstriction, maintained by the interaction between the baroreceptors and sympathetic nervous system. Under certain circumstances, injuries may reverse this process, blood vessels dilate, and the patient becomes hypotensive. An example of this situation occurs with spinal shock, due to high transection of the spinal cord, or spinal anesthesia, which causes a sympathetic blockade. The patient develops a “relative hypovolemia” – the amount of fluid is the same, but the tubing is bigger. A similar picture occurs in anaphylactic shock: there is extensive mast cell degranulation in response to an allergen, and the histamine release causes vasodilatation. In sepsis the culprit is nitric oxide, excessively produced by inducible nitric oxide synthetase. The vasodilatation is sepsis is accompanied by widespread injury to the microcirculation.
Evaluating and Treating the Hypotensive Patient • Use your knowledge of physiology to find the cause: hypotension is due to a problem of
Heart Rate, Stroke Volume or Peripheral Resistance. The patient is hypotensive, where do I start? We know that if a patient is hypotensive, then there is a problem with heart rate, stroke volume or peripheral resistance. Heart rate may be fast or slow. Stroke volume may be abnormal due to a problem with preload (too little or too much), afterload (too little or too much) or contractility. Peripheral resistance may be too low, or, occasionally, too high.
The Questions to ask: Is this genuine hypotension?
Is the heart rate appropriate for the blood pressure? What is the patient’s volume status (cardiac filling)?
Does the heart contract normally? Is the patient abnormally vasodilated?
1) Is this genuine hypotension? The first thing to ask is: is this genuine hypotension? By this I mean – what is this patient’s normal blood pressure. Remember that the principle objective of targeted therapy is to return the patient to the physiological range: the patient’s vital organs are used to a certain perfusion pressure, below which ischemia may result. Step 1: if the patient is awake, communicating and urinating, then he is probably not hypotensive. In intensive care, patients are often sedated and cannot interact with you, and the urinary output may be the only clinical sign of tissue perfusion. If the patient is being treated with diuretics, then this is lost. The other blunt measure of end organ perfusion is acid base
balance: look at the base excess (is it negative and by how much?); does the patient have a lactic acidosis? Step 2: is this measurement error? When addressing the information on arterial lines and non- invasive cuffs, it is the mean pressure that is likely to be accurate. The systolic pressure may over-read with a tight cuff, or under-read with a damped arterial line trace. Often there is a considerable difference between what is being read by the arterial line and the cuff. Care givers tend to believe the measurement that is closest to the physiological range. This is illogical. If the patient’s arterial line is reading low, and there is no objective evidence of good end-organ perfusion (mentation, urine output), then the patient is hypotensive until otherwise proven. Step 3: go to the notes / obtain a history. You need to establish the patient’s baseline blood pressure. Look for a measurement made at an outpatient appointment or on admssion. Is the patient on antihypertensive medications? If so – has his pressure been controlled: is there evidence of end organ damage – left ventricular hypertrophy with strain on the ECG? If you do not know what the patient’s baseline blood pressure is, then assume a mean arterial pressure of 80mmHg. If you know that the patient has a history of hypertension, then it is wise to aim higher, 90mmHg at least. Regardless of the predetermined target, you must have an endpoint: i.e. drive the blood pressure upwards until the patient starts urinating. If you have confirmed that the patient is indeed hypotensive then: Step 4: look for an iatrogenic cause. If the patient is being treated with agents that lower the blood pressure – propofol, midazolam, morphine, nitroprusside etc, then stop these drugs, and, if necessary, reverse their effects with phenylephrine (a specific vasoconstrictor). Step 5: Use your knowledge of physiology and your skills of deductive reasoning to determine the cause 2) Is the heart rate appropriate?
An 84 year old female is admitted with an episode of loss of consciousness. Her blood premeasurement. Her heart rate is 40. No collateral history is available. How would you evaluate this patient? What investigations would you order and how would you manage this patient?
Primary pathological processes of the heart can cause brady- or tachyhypotension as a secondary process. Hypotension is failure of compensyndrome or complete heart block (for example following an inferior wall mymay cause a bradycardia. If the patient is hypotensive he should have a tachycardia. A slow or normpresence of hypotension is a pathology in it’s own right. You need to determof this relative bradycardia is (often inappropriate beta blockade). Look for p(absence suggests atrial fibrillation or an escape rhythm). Excesssively slowaccelerated using isoproteranol, epinephrine or dobutamine. The patient maypacemaker adjustment.
Clinical Scenario 1.
ssure is 76/44 on cuff
- arrhythmias and sation. Sick sinus ocardial infarction)
al heart rate in the ine what the cause wave on the ECG heart rate may be require pacing, or
Tachycardias causing hypotension must be slowed. If the arrhythmia is acute, then cardioversion is the gold standard. If you are unsure of the origin, correction of magnesium and potassium deficits are indicated, followed by amiodarone intravenously. Alternatives for supraventricular arrhythmias are calcium channel blockers (verapamil and diltiazem) and beta-blockers.
A 74 year old female was admitted to intensive care on Friday evening, following a laobstruction. There was a small amount of fecal soiling intra operatively, but the patient stable. The patient has a 40 pack year history of smoking, type II diabetes, two previous ma permanent pacemaker, and had a right carotid endarterectomy four years ago. During thoperation, she became hypotensive, blood pressure 80/56, heart rate 70. The resident treatment with dobutamine, titrated against blood pressure response to a mean arteWhen you come into work on Monday morning, the patient is still in the intensive care, ewell, and still on dobutamine at 5 mic/kg/min, blood pressure 110/70, heart rate 70. Youday’s admissions, but the patient cannot go out to the floor on inotropes, which the weekendwean. What do you think the pathological process is and how would you manage this patient?
3) What is the patient’s volume status? Unless you suspect an ischemic myocardial event, assume hypovolemia anthere is not an early improvement in blood pressure and urinary output, inserta target CVP (a high one such as 14 or 16mmHg in a ventilated patient), and load. Replace blood loss with blood, and use isotonic fluids (normal salincolloid). If you reach the target without an adequate improvement in blood poutput, start a catecholamine – dopamine, epinephrine or norepinephrine.
How do I use CPick the number based on the best information available (e.g. inmeasurements). Volume load and continue to do so. Three things may happeCVP – keep filling! 2. CVP goes up to target and drops down again – keep fito target and stays there – stop filling, the “tank is full”!
A 79 year old female presents with central abdominal pain radiating through to the back. Bhypertension, treated with nifedipne 20 mg bid and enalapril 10 mg daily. She is cold and cPulse 100. Blood Pressure 100/60. Femoral pulses impalpable. Catheterized: only 10 ml ofHemoglobin 6.0. How would you classify this patients hemodynamic status? How would you manage this patient? The same patient undergoes surgery. On day 3 you are called to review her in the ICU. Hbeen less than 30 ml/hr for the last 6 hours. Her creatinine today is 2.7 (yesterday it was day it was 0.8). Her blood pressure is 90/40. You prescribe 500 ml of hydroxyethyl starch.are called because this has had no response. The nurse suggests renal dose dopamine. How would you manage this patient?
Clinical Scenario 2
porotomy for bowel remained reasonably yocardial infarctions, e night following the on call commenced
rial pressure of 70. xtubated, apparently
need the bed for the staff were unable to
d volume load. If a central line, pick continue to volume e, lactated ringers, ressure and urinary
VP as a target? traoperative CVP n. 1. no change in
lling! 3. CVP rises
Clinical Scenario 3
ackground history of lammy. ECG normal. urine in the bladder.
er urinary output has 1.9, and the previous Two hours later you
Which “pressor do I choose”?
If you are sure that this is septic shock - use norepinephrine. If this is anesthesia related or spinal shock (and the patient does not have a bradycardia)– use phenylephrine.
• If this is cardiogenic shock – use dobutamine norepinephrine or an intra-aortic balloon pump.
• If this is anaphylactic shock – use epinephrine. • If the patient is bradycardic and hypotensive – use epinephrine. • If you don’t know what is causing the shock – use epinephrine or dopamine. • If the patient has a history of ischemic heart disease, left ventricular hypertrophy, or a
myocardial ischemic event, the CVP may not be a reliable indicator of left sided pressures, and a pulmonary artery catheter (PAC) is indicated.
What do I look for on the PAC?
You will need to look at the pulmonary capillary wedge pressure (PCWP), which is the left sided equivalent of the CVP, the cardiac index and the strike volume. You need to pick targets for the three of these and adjust the fluids and drugs appropriately. For example: if the cardiac index (CI), stroke volume (SV) and PCWP are low, then the patient needs volume. If the CI and SV are low and the PCWP is high, then the patient needs an inodilator, such as dobutamine. If the CI is low, and the SV and PCWP are high, then the patient needs preload reduction (e.g. nitrates), plus or minus an inotrope. If the CI, SV and PCWP are all high, then the patient may require a vasoconstrictor, such as norepinephrine.
4) Does the heart contract normally (is this pump failure)? There are innumerable causes of cardiogenic shock, as outlined above. You must think about inflow obstruction (cardiac tamponade – jugular veins distend on inspiration and heart sounds cannot be heard), outflow obstruction (pulmonary embolism) and pump failure (acute ischemia or volume overload). There are a medley of clinical signs to fit each diagnosis (e.g. pulmonary embolism – tachycardia, right ventricular strain, hypoxemia and hypocarbia, deep venous thrombosis). It may be necessary to construct, mentally, cardiac pressure volume curves, to optimize cardiac filling (see diagram above), and avoid excessive stretch of myofibrils.
Clinical Scenario 4
A 56 year old male presents to ER. He is cold, clammy, dysphoric and complaining of central chest pain. His pulse is 130, blood pressure is 84/50, lung fields: bilateral crackles, a third heart sound is audible. ECG reveals ST segment elevation leads V2 to V4. What is the diagnosis? How would you classify this patients hemodynamic status? How would you manage this patient? What if the same patient had been admitted with the same symptoms and ST segment elevation in leads II, III and aVf, blood pressure 84/50, heart rate 40?
Clinical Scenario 5 A 63 year old male is admitted to the coronary care unit for thrombolysis following an anterior wall myocardial infarction. Eight hours after admission, and apparent resolution of ischemia, his blood pressure falls precipitously, his pulse rises to 140, his pulse oximeter registers an SpO2 of 88%. On examination, his lung fields are clear, his heart sounds are inaudible and his jugular veins are distended and a pulsation can not be identified. What is your differential diagnosis, and how would you manage this patient?
Clinical Scenario 6 A 43 year old female is admitted to ICU with acute pancreatitis. She develops acute respiratory distress syndrome and is managed with difficulty with high oxygen requirements, prone positioning, high levels of PEEP and vasopressor. On day 29 following admission, the patient, who had been hemodynamically stable, without support, on minimal ventilation settings, acutely deteriorates. Her blood pressure falls to 60/40. SpO2 is 80%, heart sounds are inaudible, heart rate is 45, jugular veins are distended. What is your differential diagnosis and how would you manage this patient?
Clinical Scenario 7 A 42 year old female is transferred from another hospital for chemotherapy. Two days prior to transfer the patient had undergone a laporotomy for a hysterectomy. The procedure was abandoned when the surgeon realized that there was an inoperable tumor present in the pelvis, and there was a considerable amount of blood loss, which continued into the post-operative period. Hours after transfer the patient becomes initially hypoxemic and subsequently hypotensive. Her heart rate is 140, blood pressure is 80/36, ECG shows a sinus tachycardia, SpO2 is 79%. What is your differential diagnosis, and how would you manage this patient?
A 63 year old male is admitted through the ER. He presented with acute shortness of breaBP was 90/50, heart rate 110, PaO2 80 on 100% oxygen. His ECG shows left ventriculawave across his antero-lateral leads. His chest x-ray shows cardiac hypertrophy with bihas a history of hypertension, treated with lisinopril, and has a 40 pack-year history of smWhat is your diagnosis and how would you manage this patient?
A 22 year old male motorcyclist is involved in a accident. He arrives in the ER intubatedblood pressure is 82/40, minimal urinary output, heart rate 130, fractured left acetabulumflail chest on the right, normal cardiac silhouette, grade 2 liver laceration. His hemoglobin1.6, and creatine kinase 1084, MB 15%. ECG: ST segment elevation along anterior leads.What is the diagnosis, and how would you manage this patient?
5) Is the patient abnormally vasodilated? The first thing I do when asked to review a hypotensive patient, is runpatient’s skin peripherally: if they are freezing cold (“shut down”), the chanappropriate compensation to hypovolemia or cardiac insufficiency. If the pacould fry an egg on their skin”), then there is probably abnormal vasoessentially two different possibilities: anaphylaxis to a drug, and sepsis.
A 72 year old female is admitted complaining of weakness, sweating and dysuria. Her tem130, BP 76/44, warm peripherally, lung fields: reduced air entry bilaterally, oliguria, Hb 18.2, MSU gram -ve bacilli, >105 organisms. What is your diagnosis? How would you classify this patients hemodynamic status? How would you manage this patient?
Clinical Scenario 8
th. On admission his r hypertrophy with T lateral infiltrates. He oking.
Clinical Scenario 9
and hypotensive. His , fractured left femur, is 9.2g/L, creatinine
my hand along the ces are that this is an tient is red hot (“you dilatation. There are
Clinical Scenario 10.
perature is 390C, pulse 6 g/dl, WCC 27, PO2
Clinical Scenario 11
A 27 year old male is involved in an motor vehicle accident. He sustains a burst fracture of T2 with complete neurological deficit below this level. Fours hours following admission his SpO2 is 85%, his blood pressure is 80/40 and his heart rate is 45. How would you classify this patients' hemodynamic status? How would you manage this patient?
It is usually not difficult to separate the two. In anaphylaxis there is often an antecedent history of drug administration, angio-edema, wheezing and a rash (all histamine related). In sepsis the meditor is inducible nitric oxide, the patient may well have a thermoregulatory abnormality, a leucocytosis (or leucopenia), and a source. Treatment is both cases is aggressive volume loading. The single biggest worry in anaphylaxis is loss of airway (bronchospasm and laryngeal edema): the treatment is epinephrine, 100µg doses repeatedly given intravenously, or 1mg given subcutaneously. In sepsis the treatment is fluids, fluids and more fluids, using the strategy described above. If vasopressor are required, then norepinephrine with or without dobutamine is indicated to optimize gut perfusion and myocardial function. Again, if in doubt, use what “God gave you” – epinephrine.
Clinical Scenario 12 A 74 year old man is admitted with hypotension. On admission his ECG demonstrated inverted T waves across his anterior leads, with positive cardiac enzymes. He is admitted to coronary care. He remains hypotensive. A nurse notices a black patch on his right buttock, and calls the intern. Unsure as to the diagnosis, the intern correctly consults the surgeons on call, who make a diagnosis of necrotizing fasciitis and rush the patient to the operating room, where a large debridement takes place. He is returned to you in the surgical intensive care. On admssion, he is ventilated, blood pressure is 90/50, heart rate 120, CVP 12, minimal urinary output, on dopamine 3 mic/kg/minute. How would you evaluate this patient and how would you treat him? Following initial resuscitation: Two hours later, he is still oliguric, blood pressure is 88/50, CVP is 18, heart rate is 140, and he is on dopamine at 15 mic/kg/minute. What will you do now? You insert a PAC which yields a cardiac output of 2.2 liters, stroke volume of 35ml a pulmonary capillary wedge pressure of 18, and a mixed venous oxygen saturation of 56%. What do you think?
Key Points
1. Blood Pressure is Cardiac Output multiplied by Peripheral Resistance. 2. Cardiac Output is Heart Rate times Stroke Volume. 3. Hypotension is caused by either inadequate Cardiac Output or inadequate Peripheral
Resistance 4. Heart Rate, Stroke Volume and Total Peripheral Resistance exist in dynamic equilibrium:
these interactions maintain blood pressure. If one of the three becomes abnormal, the other two compensate. This represents the cardiovascular physiologic reserve.
5. Hypotension is an indication of 1) an abnormality of Heart Rate, Stroke Volume or Peripheral Resistance, & 2) failure of the others to compensate.
6. Shock is acute circulatory failure leading to inadequate tissue perfusion and end organ injury: it classified as being due to malfunction of 1) the Pump (cardiogenic), 2 ) the Tubing (distributive), or 3) the Fluid (hypovolemic).
7. The heart rate is a fundamental element of hypotension both in terms of cause (tachyarrhythmias / bradyarrhythmias) and compensation – hypotension should be accompanied by a tachycardia.
8. Low Stroke volume is caused by a problem with reception or a problem with ejection. 9. Problems with reception are: inadequate venous return or cardiac inflow obstruction. 10. Fluid loss is caused by either absolute hypovolemia (e.g. blood loss) or relative
hypovolemia (“third spacing”). 11. Cardiac inflow obstruction is caused by a pericardial (tamponade) or intrathoracic
process (PEEP), or a lesion within the heart itself (mitral stenosis). 12. Problems with ejection include pump failure (ischemia, overload, contusion,
inflammation) and outflow obstruction (embolism, aortic stenosis, aortic crossclamps). 13. Shock caused by low peripheral vascular resistance is caused by loss of tonic
vasoconstriction (vasoplegia), due to sympathectomy, anaphylaxis or sepsis, leading to relative hypovolemia.
14. Use your knowledge of physiology to find the cause: hypotension is due to a problem of Heart Rate, Stroke Volume or Peripheral Resistance.
15. The Questions to ask: Is this genuine hypotension? Is the heart rate appropriate for the blood pressure? What is the patient’s volume status (cardiac filling)? Does the heart contract normally? Is the patient abnormally vasodilated?
Clinical Scenarios Clinical Scenario 1. An 84 year old female is admitted with an episode of loss of consciousness. Her blood pressure is 76/44 on cuff measurement. Her heart rate is 40. No collateral history is available. This patient’s heart rate is inappropriately low for the blood pressure. The most likely scenario is that the patient has a bradyarrhythmia, and is unable to mount a stroke volume sufficient to maintain blood pressure. This would occur for example if her myocardium lacked elasticity, such as with myocardial fibrosis, or with outflow obstruction, such as with aortic stenosis or mitral stenosis. A vaso-vagal episode would manifest in the same way. The essential immediate test is an electrocardiograph, which would show complete heart block, with an escape rhythm, or a sinus bradycardia. The treatment is atropine: this reverses vagally mediated bradycardia, and will reassert the blood pressure. If this is not successful, then the use of more potent chronotropes (such as isoproteranol), or external pacing may be necessary. Other things to think about here are: inferior wall myocardial infarction causing complete heart block, hypothyroidism, and overdosing on nodal blocking drugs – beta blockers, calcium channel blockers and digoxin. Clinical Scenario 2. A 74 year old female was admitted to intensive care on Friday evening, following a laporotomy for bowel obstruction. There was a small amount of fecal soiling intra operatively, but the patient remained reasonably stable. The patient has a 40 pack year history of smoking, type II diabetes, two previous myocardial infarctions, a permanent pacemaker, and had a right carotid endarterectomy four years ago. During the night following the operation, she became hypotensive, blood pressure 80/56, heart rate 70. The resident on call commenced treatment with dobutamine, titrated against blood pressure response to a mean arterial pressure of 70. When you come into work on Monday morning, the patient is still in the intensive care, extubated, apparently well, and still on dobutamine at 5 mic/kg/min, blood pressure 110/70, heart rate 70. You need the bed for the day’s admissions, but the patient cannot go out to the floor on inotropes, which the weekend staff were unable to wean. The perioperative process almost certainly stirred up some inflammatory mediators, leading to peripheral vasodilatation. This woman was unable to compensate for reduced peripheral resistance by increasing her cardiac output, because this is essentially fixed – by her pacemaker. The patient’s pacemaker rate was reset at 90 beats/minute, and the patients no longer required dobutamine one hour later. Clinical Scenario 3. A 79 year old female presents with central abdominal pain radiating through to the back. Background history of hypertension, treated with nifedipne 20 mg bid and enalapril 10 mg daily. She is cold and clammy. ECG normal. Pulse 100. Blood Pressure 100/60. Femoral pulses impalpable. Catheterized: only 10 ml of urine in the bladder. Hemoglobin 6.0. This woman is in hypovolemic shock, secondary to hemorrhage, in addition there is relative hypotension (this patient is normally hypertensive). Low cardiac output, high peripheral resistance. Ensure a patent airway and adequate ventilation and administer oxygen. Large bore i.v. access is obtained: this patient requires urgent surgery (leaking abdominal aortic aneurysm). Perioperative management involves aggressive volume loading (preferably after application of an aortic crossclamp). The same patient undergoes surgery. On day 3 you are called to review her in the ICU. Her urinary output has been less than 30 ml/hr for the last 6 hours. Her creatinine today is 2.7 (yesterday it was 1.9, and the previous day it was
0.8). Her blood pressure is 90/40. You prescribe 500 ml of hydroxyethyl starch. Two hours later you are called because this has had no response. The nurse suggests renal dose dopamine. How would you manage the low urinary output following surgery? This patient is hypotensive. I would aim to correct this. I would further volume load this patient to a CVP of 15 -16 cmH2O. If she doesn't increase both her blood pressure and urine output, I would start epinephrine or dopamine to increase MAP to 100 mmHg. There is no indication for dialysis at this time. "Renal dose dopamine" is scientifically unproven, and it would be unwise to force renal perfusion in a hypotensive patient, as this may provoke acute tubular necrosis. This patient requires a physiologic renal perfusion pressure, not a diuretic. Clinical Scenario 4 A 56 year old male presents to ER. He is cold, clammy, dysphoric and complaining of central chest pain. His pulse is 130, blood pressure is 84/50, lung fields: bilateral crackles, a third heart sound is audible. ECG reveals ST segment elevation leads V2 to V4 The diagnosis is cardiogenic shock secondary to acute myocardial infarction. The heart muscle is unable to eject the end diastolic volume, stroke volume falls and the body behaves as if it is reacting to hypovolemia by vasoconstriction and fluid retention. The cardiac output is low, the peripheral resistance is high. The management is: Oxygen therapy, minimal 40%, intavenous morphine and aspirin 325mg to chew. Ideally thrombolysis or percutaneous angioplasty are performed, to reperfuse ischemic myocardium – hopefully re-establishing muscle functionality. If this fails, then intra-aortic balloon counterpulsation or dobutamine may be required. Clinical Scenario 5 A 63 year old male is admitted to the coronary care unit for thrombolysis following an anterior wall myocardial infarction. Eight hours after admission, and apparent resolution of ischemia, his blood pressure falls precipitously, his pulse rises to 140, his pulse oximeter registers an SpO2 of 88%. On examination, his lung fields are clear, his heart sounds are inaudible and his jugular veins are distended and a pulsation can not be identified. The differential diagnosis is left ventricular failure, Pneumothorax, valvular incompetence or cardiac tamponade. The latter is the most likely scenario, presumably as a result of cardiac rupture. Drainage of the pericardium is urgent. Clinical Scenario 6 A 43 year old female is admitted to ICU with acute pancreatitis. She develops acute respiratory distress syndrome and is managed with difficulty with high oxygen requirements, prone positioning, high levels of PEEP and vasopressor. On day 29 following admission, the patient, who had been hemodynamically stable, without support, on minimal ventilation settings, acutely deteriorates. Her blood pressure falls to 60/40. SpO2 is 80%, heart sounds are inaudible, heart rate is 45, jugular veins are distended. This patient has a tension pneumothorax. The differential diagnosis is sepsis and myocardial dysfunction. The acute onset, hemodynamic insufficiency and absence of heart sounds support the diagnosis. The other signs that may be present are absence of breath sounds on one side, and tracheal deviation away from that side. Urgent placement of a chest drain is required. Clinical Scenario 7 A 42 year old female is transferred from another hospital for chemotherapy. Two days prior to transfer the patient had undergone a laporotomy for a hysterectomy. The procedure was abandoned when the surgeon realized that there was an inoperable tumor present in the pelvis, and there was a considerable amount of blood loss, which continued into the post-operative period. Hours after transfer the patient becomes initially hypoxemic and subsequently hypotensive. Her heart rate is 140, blood pressure is 80/36, ECG shows a sinus tachycardia, SpO2 is 79%. What is your differential diagnosis, and how would you manage this patient?
Clinical Scenario 8 A 63 year old male is admitted through the ER. He presented with acute shortness of breath. On admission his BP was 90/50, heart rate 110, PaO2 80 on 100% oxygen. His ECG shows left ventricular hypertrophy with T wave across his antero-lateral leads. His chest x-ray shows cardiac hypertrophy with bilateral infiltrates. He has a history of hypertension, treated with lisinopril, and has a 40 pack-year history of smoking. What is your diagnosis and how would you manage this patient? This patient has acute left ventricular failure with pulmonary edema Clinical Scenario 9 A 22 year old male motorcyclist is involved in a accident. He arrives in the ER intubated and hypotensive. His blood pressure is 82/40, minimal urinary output, heart rate 130, fractured left acetabulum, fractured left femur, flail chest on the right, normal cardiac silhouette, grade 2 liver laceration. His hemoglobin is 9.2g/L, creatinine 1.6, and creatine kinase 1084, MB 15%. ECG: ST segment elevation along anterior leads. What is the diagnosis, and how would you manage this patient? Cardiac Contusion. Systolic dysfunction. Intra-aortic balloon counterpulsation. Clinical Scenario 10 A 72 year old female is admitted complaining of weakness, sweating and dysuria. Her temperature is 390C, pulse 130, BP 76/44, warm peripherally, lung fields: reduced air entry bilaterally, oliguria, Hb 16 g/dl, WCC 27, PO2 8.2, MSU gram -ve bacilli, >105 organisms. This woman has urosepsis, probably with gram negative septicaemia, leading to septic shock. Hers is a problem with peripheral resistance – vasodilatation plus or minus microcirculatory dusfunction, with relative hypovolaemia. When describing the treatment of patients, start with airway and move on to breathing and circulation (ABC). 1. Oxygen therapy / mechanical ventilation if necessary 2. Fluid loading with colloid / crystalloid, to a target: improvement in blood pressure, specified CVP. 3. Norepinephrine infusion, if fluid loading is inadequate. Clinical Scenario 11 A 27 year old male is involved in an motor vehicle accident. He sustains a burst fracture of T2 with complete neurological deficit below this level. Fours hours following admission his SpO2 is 85%, his blood pressure is 80/40 and his heart rate is 45. This unfortunate young man has spinal shock as a result of disruption of both the spinal cord and the sympathetic tract. He is hypotensive due to loss of sympathetic tone to the lower part of his body, and bradycardic, due to loss of his cardioaccelerator nerves. He has relative hypovolemia, and inability to compensate. The treatment, initially is airway protection and volume loading, with blood/colloid, as necessary. If this is insufficient to restore the blood pressure, this patient will require a systemic sympathetic analogue to tighten up his blood vessels and increase his heart rate: the choice is either dopamine or epinephrine. Clinical Scenario 12. A 74 year old man is admitted with hypotension. On admission his ECG demonstrated inverted T waves across his anterior leads, with positive cardiac enzymes. He is admitted to coronary care. He remains hypotensive. A nurse notices a black patch on his right buttock, and calls the intern. Unsure as to the diagnosis, the intern correctly consults the surgeons on call, who make a diagnosis of necrotizing fasciitis and rush the patient to the operating room, where a large debridement takes place. He is returned to you in the surgical intensive care. On admssion, he is ventilated, blood pressure is 90/50, heart rate 120, CVP 12, minimal urinary output, on dopamine 3 mic/kg/minute. This is a very tricky situation – the double whammy shock: cardiogenic and septic. I assume that this patient had a very tight coronary stenosis, and when he developed sepsis, the associated hypotension caused acute myocardial infarction. The use of dopamine as an inotrope is reasonable, although the current dose appears inappropriately low: we don’t know whether the
shock (this is shock as the patient is oliguric) is due to vasodilatation or due to myocardial insufficiency. The initial management is to fluid load him to a targeted CVP, and if this does not successfully increase blood pressure and urinary flow, to increase the dose of inotropes. Two hours later, he is still oliguric, blood pressure is 88/50, CVP is 18, heart rate is 140, and he is on dopamine at 15 mic/kg/minute. What will you do now? The fluid loading appears complete, but the dopamine is having a diasaterous effect: the last thing a patient needs following a myocardial infarction is a tachycardia of 140. I would insert a pulmonary artery catheter (PAC) to find out what this patient’s left sided filling pressures are and what his cardiac output is. You insert a PAC which yields a cardiac output of 2.2 liters, stroke volume of 35ml a pulmonary capillary wedge pressure of 18, and a mixed venous oxygen saturation of 56%. What do you think? The low cardiac ouput is a result of a very low stroke volume, which appears inappropriate in the setting of sepsis (his ejection fraction must be very low indeed): the patient is in cardiogenic shock, with a probable peripheral vasoplegia. He appears fully volume loaded. What we need is an agent that will cause peripheral vasoconstriction – to bring the total peripheral resistance back towards normal, improve cardiac contractility and slow down the heart simultaneously, without increasing myocardial oxygen demand. An intra-aortic balloon pump may be a good idea (there is no access to the femoral areas following surgery). An alternative strategy is to put the patient on a combination of dobutamine and norepinephrine – the former titrated against cardiac output, the latter against blood pressure. Using this strategy on dobutamine 5 mic/kg/min and norepinephrine 2.0 mic/min, the patient’s blood pressure rose to 120/70, cardiac output to 4.5 litres / min, stroke volume of 70ml and starts putting out urine.
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