CARDIAC
In this section, you will learn about the following topics:
Shock
Heart Failure
Acute MI Management
Cardiac Arrest
Hypertension Urgency/Emergency
Pericardial Effusion
SVT, Atrial Fibrillation
Shock
Shock is a life-threatening condition that occurs when there is an inadequate supply of oxygen and nutrients to the body's tissues and organs. It is a medical emergency that requires immediate attention and treatment. There are several types of shock, each with its own unique characteristics and underlying causes. Understanding the different types of shock is crucial for effective management and treatment.
Prior to the 1930s, the main type of shock that was recognized was hypovolemic shock although they did not directly recognize it at the time. They noticed that in trauma patients, if they did not bleed to death, they would often have post-traumatic shock that was called "wound shock". The belief was that the wound would release toxins that resulted in neurogenic vasodilation and blood pooling. Later, more groups came out with the idea that it wasn't necessarily from toxins, but from loss of fluids in general.
In 1934, Dr. Blalock first defined the types of shock:
Hematologic/oligemic
Cardiogenic
Neurogenic
Vasogenic
And later in 1967 Shubin and Weil proposed more types of shock. These were added to those listed above:
Hypersensitivity
Bacteremic
Obstructive
Endocrinologic
Early Developments Of Septic Shock
Dr. Swan and Dr. Ganzs noticed that there were two types of bacteremic shock - "warm shock" which was associated with high cardiac output state and "cold shock" which was associated with a low cardiac output state. They noticed that there was a period of hyperdynamic heart function which was the "warm shock"; if their disease progressed past this it would develop into "cold shock". Even more importantly they noticed that the development of cold shock was associated with death, and therefore death by septic shock was subsequently from a low cardiac output state. At the time, studies they did on animals supported this.
As we know today, septic shock is a high cardiac output state, so why did they believe this?
There was no way to measure CO at bedside
CVP was used as a surrogate for LVEDV (heart function), which we now know is inaccurate and inappropriate
Dr. Wilson first came up with the idea that septic shock was a high CO, low SVR state, but nobody believed him because he didn't have the evidence to back it up.
The Invention Of The SGC
Dr. Forssman was a resident physician who was training cardiologist in 1929. While undergoing training, he became curious - can we see the inside of the heart? Out of his curiosity came the first central venous catheter. Unfortunately he could not find a volunteer, so he decided to do it on himself. He went to the OR; inserted a catheter into his ventricle and climbed up the stairwell to radiology in order to confirm its placement. He was subsequently fired by his group and decided to take up a new gig in urology.
After that time, advancements were made; the first heart cath was done and they began to put catheters into the heart regularly. In 1970 Dr. Swan and Dr. Gans then had the idea to push a pulmonary artery catheter into a dogs heart in order to assess it's cardiac output. It worked! They decided to immediately do it to a patient with MI afterward and they were able to successfully measure heart function. With the invention of the Swan Ganz catheter, we were finally able to get cardiac output.
This is when Dr. Wilson's description of shock as a high cardiac output, low SVR state became more widely accepted. Even later it was shown by Dr. Clavin through portable radionucleide cineangiography that septic shock caused reversible myocardial dysfunction that last for 7-10 days; that CO was indeed high.
New Types Of Shock Emerge
In 1972, Hinshaw and Cox proposed a classification of shock based on hemodynamics. This was primarily due to the invention of the SGC. The previous types of shock were scrapped, and the following were proposed: hypovolemic, cardiogenic, distributive and obstructive. These are the types of shock that we seek to understand in our practice today.
Hypovolemic Shock: Hypovolemic shock is the most common type of shock and occurs when there is a significant loss of blood or fluid volume in the body. This can be caused by severe bleeding, dehydration, or fluid loss from burns or excessive sweating. The reduced blood volume leads to a decrease in oxygen delivery to the tissues, resulting in organ dysfunction. Symptoms of hypovolemic shock include rapid heart rate, low blood pressure, cool and clammy skin, and decreased urine output.
Cardiogenic Shock: Cardiogenic shock occurs when the heart is unable to pump enough blood to meet the body's demands. This can be caused by a heart attack, severe heart failure, or other conditions that impair the heart's ability to function properly. In cardiogenic shock, the heart's pumping ability is compromised, leading to decreased blood flow to the organs. Symptoms of cardiogenic shock include low blood pressure, rapid and weak pulse, shortness of breath, and fluid retention.
Distributive Shock: Distributive shock is characterized by a widespread dilation of the blood vessels, leading to a decrease in blood pressure and inadequate tissue perfusion. There are several subtypes of distributive shock, including septic shock, anaphylactic shock, and neurogenic shock.
Septic shock occurs as a result of a severe infection, usually caused by bacteria. The infection triggers a systemic inflammatory response, leading to widespread vasodilation and increased permeability of blood vessels. This causes a drop in blood pressure and impaired organ function. Symptoms of septic shock include high fever, rapid breathing, altered mental status, and decreased urine output.
Anaphylactic shock is a severe allergic reaction that can be triggered by certain foods, medications, or insect stings. It causes a release of histamine and other chemicals, leading to widespread vasodilation and increased permeability of blood vessels. This results in a rapid drop in blood pressure and can lead to life-threatening complications if not treated promptly. Symptoms of anaphylactic shock include hives, swelling of the face and throat, difficulty breathing, and a rapid pulse.
Neurogenic shock occurs as a result of damage to the spinal cord or disruption of the autonomic nervous system. This leads to a loss of sympathetic tone, causing widespread vasodilation and a decrease in blood pressure. Symptoms of neurogenic shock include low blood pressure, bradycardia (slow heart rate), and warm and dry skin.
Obstructive Shock: Obstructive shock occurs when there is a physical obstruction that prevents adequate blood flow to the heart or from the heart to the rest of the body. This can be caused by conditions such as pulmonary embolism, cardiac tamponade, or tension pneumothorax.
Pulmonary embolism occurs when a blood clot or other material blocks the blood vessels in the lungs, preventing proper oxygenation of the blood. This leads to increased pressure in the right side of the heart and a decrease in cardiac output.
Cardiac tamponade occurs when fluid accumulates in the pericardial sac, compressing the heart and preventing it from filling properly. This leads to a decrease in cardiac output and inadequate tissue perfusion.
Tension pneumothorax occurs when air accumulates in the pleural space, causing the lung to collapse and putting pressure on the heart and great vessels. This can lead to a decrease in cardiac output and impaired blood flow.
Symptoms of obstructive shock can vary depending on the underlying cause but may include chest pain, shortness of breath, rapid heart rate, and low blood pressure. Treatment varies based on the type of shock.
See our core content (shock) podcast: Pulmcast: Core Content Shock
Resources to complete:
Part 1: The Differentiating Different Types
FCCS Ch. 7
Identification and Treatment of Cardiogenic Shock
Marino 3rd ed: Ch 12-14; 4th ed: Ch 11-12
Pulmcast - Core Content: Shock
Part 2: In-Depth Interpretation And Management
FCCS Ch. 6
Marino 3rd ed: Ch. 9, 10; 4th ed: Ch 7-10
Vasopressors
EmCrit Podcast 138: Vasopressor Basics
AHA 2008: Inotropes and Vasopressors (Drive)
Pulmcast: Peripheral Vasopressor - Are my days of placing central lines over? Not yet?
Heart Failure
Heart failure is a chronic condition that occurs when the heart is unable to pump enough blood to meet the body's needs. It is a serious and progressive condition that affects millions of people worldwide. To understand heart failure, it is important to have a basic understanding of the anatomy and physiology of the heart. The heart is a muscular organ located in the chest, slightly to the left. It consists of four chambers: two atria and two ventricles. The atria receive blood from the body and lungs, while the ventricles pump blood out to the rest of the body.
The heart's pumping action is controlled by electrical signals that regulate the heart rate and rhythm. These signals ensure that the heart contracts and relaxes in a coordinated manner, allowing for efficient blood circulation. Any disruption in this process can lead to heart failure.
Heart failure can be classified into two main types: systolic heart failure and diastolic heart failure. Systolic heart failure occurs when the heart's ability to contract and pump blood is impaired. Diastolic heart failure, on the other hand, occurs when the heart's ability to relax and fill with blood is compromised.
Echocardiography is a key diagnostic tool for heart failure. It uses ultrasound waves to create detailed images of the heart's structure and function. This non-invasive test provides valuable information about the heart's size, shape, and pumping ability. Echocardiography can assess the ejection fraction, a measure of the heart's pumping efficiency, and identify any structural abnormalities, such as valve dysfunction or ventricular hypertrophy. Measuring cardiac biomarkers, such as troponin and brain natriuretic peptide (BNP), can help differentiate heart failure from other cardiac conditions and assess disease severity.
Signs and symptoms of acute heart failure exacerbations involve shortness of breath, pulmonary edema, leg swelling, fatigue/weakness, persistent cough or wheezing, and reduced appetite.
Medications play a crucial role in the treatment of heart failure. They are used to alleviate symptoms, improve heart function and prevent further damage to the heart. A common slew of medications you’ll see heart failure on is GDMT (guideline directed medical therapy). This is specifically for patients with reduced ejection fraction, and consists of four main drug classes:
ACEI or ARB
Beta Blocker - primarily bisoprolol, carvedilol, or metoprolol (evidence based)
Agents with mortality benefit (MRA) - think Spironolactone
SGLT-2 inhibitor - like Empagliflozin, Dapagliflozin (cannot use in type 1 diabetes)
Can consider adding diuretic dose as needed
In acute heart failure exacerbations, hypoxemia can often develop due to pulmonary edema. Treatment of this involves diuretics and respiratory support (often with the aid of non-invasive ventilation like BiPAP). If acute heart failure progresses, it can result in cardiogenic shock.
Resources to complete:
MedCram: Heart Failure parts 1-3
FOAMCast Episode 7: Heart Failure
EmCrit Podcast Episode 1: SCAPE (Sympathetic Crashing Acute Pulmonary Edema)
Acute MI Management
Acute myocardial infarction (MI), commonly known as a heart attack, is a serious and life-threatening condition that occurs when there is a sudden blockage of blood flow to the heart muscle. This blockage is usually caused by a blood clot that forms in one of the coronary arteries, which supply oxygen-rich blood to the heart.
During an acute MI, the heart muscle is deprived of oxygen and nutrients, leading to damage or death of the affected heart tissue. The severity of the heart attack depends on the location and extent of the blockage, as well as the duration of the blood flow interruption. The most common symptom of an acute MI is chest pain or discomfort, often described as a crushing or squeezing sensation. This pain may radiate to the left arm, jaw, neck, or back. Other symptoms may include shortness of breath, nausea, vomiting, lightheadedness, and cold sweats. However, it is important to note that not all individuals experience the same symptoms, and some may even have atypical or silent heart attacks, especially in older adults or individuals with diabetes.
Diagnosing an acute MI involves a combination of clinical evaluation, medical history, and diagnostic tests. The healthcare provider will assess the patient's symptoms, perform a physical examination, and order tests such as an electrocardiogram (ECG), blood tests to measure cardiac enzymes, and imaging tests such as a coronary angiography or cardiac MRI.
The primary goal of treatment for an acute MI is to restore blood flow to the affected coronary artery as quickly as possible. This is usually achieved through a procedure called percutaneous coronary intervention (PCI), commonly known as angioplasty. During PCI, a catheter with a balloon at its tip is inserted into the blocked artery and inflated to open the artery and restore blood flow. In some cases, a stent may also be placed to keep the artery open. In addition to PCI, medications are also administered to manage the symptoms, stabilize the heart, and prevent further complications. These medications may include aspirin, nitroglycerin, beta-blockers, ACE inhibitors, and antiplatelet drugs such as clopidogrel.
Resources to complete:
FCCS Ch. 10
Marino 3rd ed: Ch. 17; 4th ed: Ch 16
Mayo Clinic: ACS part 1 Kumar (Drive)
Mayo Clinic: ACS part 2 Kumar (Drive)
Cardiac Arrest
Cardiac arrest is the loss of heart activity when the heart stops beating suddenly, causing lack of blood flow to the brain and other organs. Naturally, cardiac arrest is often sudden and dramatic. When cardiac arrest occurs, it is essential to initiate cardiopulmonary resuscitation (CPR) and ACLS protocol immediately. Survival rates for cardiac arrest vary depending on several factors, including the promptness of CPR and defibrillation, the underlying cause of the arrest, and the overall health of the individual. Immediate CPR and early defibrillation can significantly improve the chances of survival.
Resources to complete:
FCCS Ch. 3, FCCS Appendix 4
Marino 3rd ed: Ch. 15-16; 4th ed: Ch 17
Running a code
Pulmcast: The Anatomy of a Code
Targeted Temperature Management NEJM article (Drive)
Emcrit Podcast 126: Targeted Temperature Management
Hypertension Urgency/Emergency
Hypertensive urgency refers to a situation where blood pressure levels are severely elevated but do not cause immediate organ damage. In this condition, blood pressure readings are typically above 180/120 mmHg. However, unlike hypertensive emergency, there are no signs of acute end-organ damage. The symptoms of hypertensive urgency may include severe headache, shortness of breath, nosebleeds, and anxiety. It is important to note that these symptoms are not specific to hypertensive urgency and can be present in other conditions as well.
Hypertensive emergency, on the other hand, is a critical condition characterized by severely elevated blood pressure levels that lead to acute end-organ damage. In this situation, blood pressure readings are usually above 180/120 mmHg, and there is evidence of organ dysfunction or damage. The organs most commonly affected by hypertensive emergency include the brain, heart, kidneys, and eyes. Symptoms may vary depending on the affected organ, but common signs include severe headache, chest pain, shortness of breath, confusion, blurred vision, and seizures.
While the immediate goal is to lower blood pressure rapidly, it is important to avoid excessively lowering it, as this can lead to complications such as organ hypoperfusion. Blood pressure is typically reduced by no more than 25% within the first hour and gradually over the next 24 to 48 hours. This is often done with a continuous drip in order to offer better control. In our ICUs we often use Cardene (nicardipene).
Resources to complete:
EmCrit Podcast 190: Emergencies with a side of Hypertension
Pericardial Effusion
Pericardial effusion poses unique challenges in the ICU, often requiring urgent intervention. In this setting, the healthcare team is tasked with assessing the effusion's size and its impact on cardiac function. Depending on the severity and underlying causes, interventions can range from pericardiocentesis, a procedure to drain excess fluid, to surgical approaches like pericardial window creation. The goal is to relieve the pressure on the heart and restore normal cardiac function swiftly. Close collaboration between critical care specialists, cardiologists, and interventional teams is paramount in addressing pericardial effusions effectively in the ICU.
Resources to complete:
SVT, Atrial Fibrillation
The management of supraventricular tachycardia (SVT) is a common challenge. You must swiftly assess and address this rapid heart rhythm in critically ill patients. Treatment may involve vagal maneuvers, administration of medications like adenosine, or synchronized cardioversion to restore a normal heart rate and rhythm.
Managing AFib in this setting involves a comprehensive approach, including identifying and addressing underlying causes, such as electrolyte imbalances or sepsis. You may use rate or rhythm control strategies, administer anticoagulants to reduce the risk of thromboembolic events, and closely monitor hemodynamics. In some cases, electrical cardioversion may be necessary.
Resources to complete:
Marino 3rd ed: Ch. 18; 4th ed: Ch 15
FOAMCast Episode 34: Tachyarrhythmia’s
Pulmcast: The Irregular Irregularities of Atrial Fibrillation
Emcrit Podcast 20: The Crashing Atrial Fibrillation Patient
ACLS:
PulmCrit: Treatment of Hemodynamically Stable New Onset AFib in Critical Illness (Drive)
Electrophysiology: VT Diagnosis Wellens (Drive)