“All great artists draw from the same resource: the human heart, which tells us that we are all more alike than we are unalike.”- Maya Angelou
4.1 Atherosclerosis
Pathophysiology: It is a slow and progressive pathologic process with buildup of lipid-filled plaques, accompanied with interstitial changes in the walls of medium- and large-sized arteries. This is secondary to years of accumulative arterial wall damage and inflammation.
These plaques can cause chronic narrowing of arteries and limit blood supply, resulting in ischemic complications.
At times the plaques can rupture or ulcerate, leading to acute formation of thrombus which can cause:
Risk factors
Age > 45 years in males and > 55 years in females.
Family hx of symptomatic atherosclerotic disease.
4.1.1 Atherosclerotic Cardiovascular Disease
Background: Atherosclerotic plaques can form virtually anywhere, but usually they form in areas where vascular anatomy predisposes to increased turbulence of blood flow, producing shearing forces that cause continuous microendothelial injury (e.g., in areas of bifurcation of major arteries).
Clinical effects depend on the location of the plaques
4.2 Stable Angina
Pathophysiology: With underlying significant atherosclerotic narrowing of coronary vessel (> 50–70%), cardiac ischemia and chest pain can develop whenever there is increase in oxygen demand. Oxygen demand increases when the heart must work more due to increase in preload, afterload, and/or increase in heart rate.
1 Increase in heart rate not only increases myocardial oxygen demand, but also decreases myocardial blood supply, as heart spends less time in diastole. Note: Most of the myocardial blood supply occurs during diastole.
The following conditions can precipitate chest pain in patients with stable angina by increasing adrenergic activity and cardiac workload:
Cold exposure (epinephrine and norepinephrine are secreted in response to cold to maintain body temperature).
Factors that lower oxygen content in blood may aggravate underlying ischemia, for example, anemia and carbon monoxide poisoning.
Pharmacotherapy of stable angina
Ranolazine: It is indicated only in refractory stable angina (i.e., when symptoms persist despite optimal management). It decreases cardiac oxygen demand by inhibiting Na+ channels and indirectly inhibiting calcium-mediated contraction.
Chest pain
Work-up: Any patient who presents with chest pain needs an electrocardiography (EKG), even if the pain is atypical.
2 Remember you cannot miss a diagnosis like angina or myocardial infarction (MI). It is the leading cause of death in developed countries.
Now, let us say the EKG is normal. When do we investigate further for coronary artery disease (CAD)?
First, we need to answer the following questions:
Typical angina chest pain is crushing, heaving, substernal chest pain, radiating to left arm or jaw, exacerbated by exertion/emotion and relieved by rest. It usually does not have any relation with position or breathing.
Does the patient have any risk factors for atherosclerotic cardiovascular disease (ASCVD)?
See the risk factors listed in the beginning of the chapter.
Let us try some clinical case scenarios:
Silent angina or myocardial infarction (MI): Patients with diabetes (and underlying autonomic neuropathy), postsurgery patients (on analgesia), and elderly patients can have atypical presentation of CAD. They may not present with classical anginal chest pain. These patients can present with the following symptoms:
Sudden onset of shortness of breath.
Profound weakness or diaphoresis.
Jaw pain or left arm pain/heaviness.
This is known as silent angina or MI. Also, these patients are likely to present directly with complications of MI.
Management algorithm of stable angina
Legend: NSIM, next step in management; NSIDx, Next step in diagnosis
aPatients with stable angina typically present after an episode of chest pain, hence baseline EKG can be normal. Also, cardiac enzymes are normal by definition in angina.
bPatients who have high-risk occupations (e.g., pilots, bus drivers, train operators,) and who have presentation suggestive of high probability CAD can proceed directly to coronary catheterization, as missing angina in these cases may be catastrophic. Also, see next section on how to choose the right stress test.
cEarly onset of chest pain or ST wave changes, large areas of ischemia, or hemodynamic instability during stress testing are considered high-risk features.
dIndications for coronary artery bypass grafting (CABG) are:
Left main coronary artery stenosis of > 50%. (As left main artery is considered crucial, the cutoff for significant lesion is lower).
Left main equivalent (≥ 70% stenosis of proximal left anterior descending coronary artery [LAD] and proximal left circumflex).
More than 70% proximal LAD stenosis + either EF < 50% or demonstrable ischemia on noninvasive testing.
eIn stable angina, percutaneous transluminal coronary angioplasty (PTCA) has been shown to improve symptoms, but not mortality.
fTarget resting HR should be around 55–60 beats per minute. Use beta blocker (preferable) and/or cardioselective calcium channel blocker (e.g. verapamil, diltiazem). If angina is still not controlled, use long-acting nitrates, followed by ranolazine on a step-by-step basis.
For coronary artery bypass grafting (CABG) purpose, internal mammary artery graft is preferred over vein graft as the arterial graft lasts longer.
Patient presents with problematic stable angina symptoms. He is on maximal dose of a beta blocker, full-dose aspirin, sublingual nitroglycerin as needed, and high-intensity statin therapy (BANS therapy). His resting heart rate is 90 beats per minute. What is the NSIM?
Above patient comes back to the office and reports that he continues to have problematic stable angina symptoms. His resting heart rate is 60 beats per minute. What is the NSIM?
In a patient with angina not controlled with optimal medical management, coronary angiography shows 65% proximal left main coronary artery stenosis. What is the NSIM?
How to choose the right stress test?
aWhenever possible, do exercise testing. It allows assessment of functional capacity of the patient. Some patients cannot exercise due to orthopedic or pulmonary issues.
bConditions mentioned below typically have baseline EKG abnormalities (e.g., ST-T wave depression ≥ 1 mm) where EKG cannot be interpreted
3 If patients with these conditions and significantly abnormal baseline EKG, present with symptoms of ongoing ischemia, EKG changes can be obscured. Consider bedside echocardiography to look for hypokinesia or akinesia of the ventricular walls.
• Left bundle branch block (LBBB).
• Certain cardiac drugs, such as digitalis, procainamide, can cause ST-T wave depression.
• Left ventricular hypertrophy with significant ST-T wave abnormalities.
• Wolff–Parkinson–White syndrome.
cExercise Treadmill Test (ETT) is always preferred over other modalities, as it is low cost, easy to do, and does not involve radiation. But this can only be done in patients who can exercise and who have no significant baseline EKG abnormalities.
4 Stress tests in order of preference are ETT > echocardiographic studies > nuclear imaging Nuclear stress imaging involves radiation exposure that is approximately 15-20 times more than an average CT scan of head.
dV-pacing and LBBB can produce false positive results on exercise echocardiogram. In patients with atrial fibrillation, dobutamine can worsen the arrhythmia.
eThe following conditions can present with chest pain. They also predispose to sudden onset of ventricular fibrillation and have higher risk of sudden death on exertion or stress. Dobutamine or exercise stress test are contraindicated in these cases:
fAfter exercise, ischemic areas become hypokinetic which is detected by echocardiography. Note: if patient is known to have has extensive baseline wall motion abnormalities at rest, then echo imaging is not really helpful. In this case nuclear imaging is done. gNuclear stress test includes the use of:
Radionuclide contrast (thallium or technetium-99m) that helps in directly visualizing coronary blood flow; hence it is aka radionuclide myocardial perfusion imaging (rMPI)
Vasodilator (adenosine or dypiridamole
6 Contraindications for adenosine or dipyridamole:
• Active bronchospastic airway disease.
• Sick sinus syndrome and high degree AV block (no pacemaker yet).
Theophylline should be held for 48 hours and no caffeinated drinks for 12 hours before the procedure.
Nuclear vasodilator test is based on this phenomenon. Stenosed coronary arteries, affected by atherosclerosis, are maximally dilated to compensate for decreased blood supply. Administration of a coronary vasodilator causes dilation of normal vessels and redirection of flow, “stealing” blood away from ischemic regions of the heart, resulting in decreased perfusion to these areas.
7 Unlike adenosine or dypiridamole, nitrates cause vasodilation primarily in large epicardial vessels, thus there is less likelihood of coronary steal phenomenon.
Uniform distribution of radioactive thallium at rest but decreased radioactivity in certain areas after dipyridamole or adenosine injection is diagnostic of CAD.
Exercise treadmill test
Preparing for test: Medications that decrease heart rate (e.g., β-blockers, calcium channel blockers) should be withheld 48 hours prior to scheduled exercise treadmill test (ETT), as this might produce false negative result.
Test description: While patient is running on a treadmill or pedaling a bicycle, we monitor patient’s vital signs (e.g., blood pressure, heart rate), and do a realtime EKG to look for signs of ischemia.
Remember these signs of ischemia:
Altered mental status (e.g., confusion), or dizziness.
Shortness of breath (SOB) or chest pain with ST-T wave depression ≥ 1 mm.
• ST-T wave elevation in non-Q wave lead.
Other high-risk features include development of high-grade atrioventricular (AV) block, ven-tricular arrhythmia, and/or left bundle branch block (LBBB).
If any of the above features develop, NSIM is to stop the test. Dx of stable angina is made.
ETT is considered adequate if patient’s heart rate reaches at least 85% of maximal heart rate.
8 The maximal heart rate = 220 – patient’s age. 85% of maximal heart rate = target heart rate for ETT.
If no signs of ischemia develop with target heart rate, then the dx of CAD is unlikely.
If test fails to achieve at least 85% of the maximal heart rate, the test is considered to be in-adequate to rule out CAD.
4.3 Acute Coronary Syndrome
aMorphine is given to alleviate chest pain. Alleviating pain decreases accompanying sympathetic activity, which decreases cardiac myocardial oxygen demand. Morphine also acts as a direct venodilator, reducing the preload. If chest pain persists despite morphine and sublingual nitroglycerin, NSIM is intravenous nitroglycerin.
bIf patient develops chest pain in the setting of acute massive gastrointestinal (GI) bleeding, NSIM is blood transfusion. Do not give aspirin in this setting.
• If patient develops chest pain in the setting of tachyarrhythmia, then controlling heart rate should be the primary goal.
c Aspirin confers the highest mortality benefit. It should be given in all chest pain patients as soon as possible, after excluding active bleeding, even before any diagnostic work-up. The first aspirin tablet should be chewed.
dIf EKG can’t be interpreted due to some preexisting condition (see optimal cardiac stress test chapter), NSIDx is bedside echocardiogram.
9 Note that LBBB (new or old) is not considered a ST-elevation myocardial infarction (STEMI) equivalent anymore, as new studies suggest that only a small number of patients with new LBBB are ultimately diagnosed with acute MI.
eCardiac enzymes are creatine kinase-muscle/brain (CK-MB) and cardiac troponins T or I. They can be normal in early MI, as it can take up to 4 to 12 hours after the MI event for the levels to be abnormal. Hence, normal cardiac enzyme levels cannot exclude MI in the first few hours after MI.
fIn patients who are going for coronary catheterization, anticoagulation with unfractionated heparin or bivalirudin is preferred over low-molecular weight heparin (LMWH) due to easy reversibility and shorter duration of action. In low-risk patients for which conservative strategy is planned LMWH is preferred.
gPlatelet receptor blockers,9 statins, β-blockers,
10 Platelet receptor (adenosine diphosphate receptor) blockers are ticagrelor, clopidogrel, and prasugrel.
11 β-lockers are contraindicated in patients who present with acute congestive heart failure (particularly when patient is β-blocker naïve), hypotension, severe bradycardia, and heart block (other than first degree).
hTwo treatment modalities have been shown to increase survival in STEMI:
Percutaneous transluminal coronary angioplasty (PTCA) with stent placement (aka percutaneous coronary intervention [PCI]).
PTCA has been shown to have better outcome than thrombolytics, so whenever available, PTCA is the treatment of choice.
iAbsolute contraindications for thrombolytics are:
Relative contraindications are:
Current use of anticoagulants—the higher the international normalized ratio (INR), the higher the risk of bleeding.
For streptokinase: prior exposure (more than five days previously) or prior allergic reaction to these agents.
jStudies have shown better outcomes in patients transferred to PCI facility immediately after thrombolysis, as rescue PCI may be needed if thrombolysis is not successful. The indicators of successful reperfusion therapy are resolution of chest pain, normalization of ST-segment, and development of transient benign accelerated idioventricular rhythm (reperfusion arrhythmia).
kDifference between unstable angina and non-STEMI is that in unstable angina, cardiac enzymes are not significantly elevated.
lonsider preangiography glycoprotein IIb/IIIa inhibitor (eptifibatide or tirofiban) if patient has persistent chest pain and/or persistent EKG changes despite optimal medical treatment.
mIn selected unstable angina patients, who have no further episodes of chest pain and no troponin elevation, risk stratification with stress test can be done. If stress testing shows high-risk findings or EF of < 40%, coronary angiography is recommended.
4.3.1 Additional Notes on ACS Management
What are the treatment modalities that decrease mortality and increase survival in acute coronary syndrome (ACS) patients?
| |
Have been shown to improve mortality only in patients with EF of ≤ 40% (systolic dysfunction). They reduce ventricular remodeling | |
aPlatelet receptor blockers are ticagrelor, clopidogrel, and prasugrel. Recent recommendations prefer ticagrelor over clopidogrel in most of the clinical situations (except when thrombolytics are given, where clopidogrel is preferred). | |
Patients with CAD may have concomitant vascular impotence (same risk factors) and might be using phosphodiesterase inhibitors, such as sildenafil. Nitrates should not be given within 24 hours of sildenafil use, as it can lead to dangerous hypotension, which can worsen myocardial infarction (MI).
Postinfarct or post-revascularization chest pain is always considered unstable angina and treated as such. Measuring CK-MB level is very helpful for diagnosing reinfarction because it has short half-life and levels return to normal within 3 days.
Complications of coronary angiography or peripheral arterial catheterization
4.3.2 Myocardial Infarction, Arterial Territories, and Complications
Mechanical complications of MI were commonly seen prior to the era of interventional cardiology, but fortunately, they are not that common anymore.
II, III, AVF = inferior wall involvement V1 and V2 = RV involvementa | Complete heart block and p asystole due to AV node infarction | ||||
Hypotension, tachycardia, and JVD with Kussmaul signb | |||||
Within few days/week after acute MI, patient develops acute heart failure and/or cardiogenic shock. This can be due to following factors → | Rupture/dysfunction of posterior papillary muscle of mitral valve with development of acute mitral regurgitation | Pansystolic murmur heart best at mitral area radiating to axilla | |||
Pansystolic murmur heard best at left sternal border with palpable systolic thrill | |||||
The anterior wall constitutes the major contractile portion of left ventricle; hence infarction may lead to following → | Acute heart failure and/ or cardiogenic shock presenting on the first day of MI | Presents with acute pulmonary edema or hypotension (cardiogenic shock), without any characteristic murmur | |||
Low ejection fraction that leads to increased stasis and increased risk of intracardiac thrombus formationc | Development of acute stroke, intestinal ischemia, or acute leg pain in a patient with recent hx of anterior wall MI. (This is a late complication) | ||||
Within few days to 2 weeks after acute MI, patient develops acute heart failure and/or cardiogenic shock → | Free wall rupture resulting in hemopericardium and cardiac tamponade | Hypotension, JVD, pulsus paradoxus,d muffled heart sounds | |||
Acute VSD due to rupture of interventricular septume | Pansystolic murmur heard best at left sternal border with palpable systolic thrill | ||||
Left ventricular aneurysm | Can present with progressive heart failure, systemic cardiac embolism, and/or sustained ventricular tachycardia Look for double apical impulse in physical exam and sustained ST-wave elevation in EKGf | ||||
Horizontal ST-wave depression in V1-V3 might suggest posterior wall STEMI | Nonspecific It is usually associated with complications related to either RCA or left circumflex territory as posterior descending artery can be a branch of either one of these arteries | ||||
aIf ST-T wave elevation in V1 taller than V2, suspect right ventricular infarction. NSIDx is to place EKG leads in right side of the chest. Most specific finding for RV infarction is ST-T wave elevation in right-sided leads. | |||||
bKussmaul sign = paradoxical increase in jugular venous pressure (JVP) on inspiration. | |||||
cWarfarin or newer generation anticoagulants is recommended in patients with EF of < 30% and severe anteroapical wall motion abnormality (high risk of thrombus formation). Anticoagulation is also reasonable in patients with EF of ≤ 40% and severe wall motion abnormalities, particularly if patient has low risk for bleeding. | |||||
dPulsus paradoxus= more than expected fall in systolic blood pressure (≥10 mm Hg) during inspiration. | |||||
eMost specific diagnostic finding for VSD is the presence of left-to-right shunt on right heart catheterization. | |||||
f This aneurysm may enlarge and mature over time; a mature true left ventricular aneurysm rarely ruptures because of the dense fibrosis in its wall. | |||||
Management: Medical treatment with afterload reduction for small- to moderate-sized aneurysm. Consider aneurysmectomy + coronary artery bypass grafting (CABG) for patients with persistent heart failure or intractable ventricular arrhythmias, who failed medical management or percutaneous interventions. In patients with severe left ventricular (LV) dysfunction or presence of a clot, anticoagulation is recommended. | |||||
Abbreviations: AVF, augmented Vector Foot; CXR, chest X-ray; EKG, electrocardiogram; JVD, jugular venous distension; MI, myocardial infarction; VSD, ventricular septal defect. | |||||
Differentiating different causes of acute heart failure and/or cardiogenic shock in acute MI
Free ventricular wall rupture → hemopericardium → cardiac tamponade | ||||||
|---|---|---|---|---|---|---|
RCA (or LADa) | ||||||
Biventricular failure occurs; hence lungs might be clear. They mostly present with hypotension (cardiogenic shock) | ||||||
Might have functional murmur of TR due to tricuspid annular dilatation | Loud holosystolic/ pansystolic murmur heart best at left sternal border. (Sometimes it is best heard at mitral area and can be hard to differentiate from MR) | Loud holosystolic/ pansystolic murmur heart best at mitral area, radiating to axilla | Might have functional murmur of MR due to annular dilatation | |||
Rapid bedside TTE and pericardiocentesis. If pericardiocentesis is bloody, immediate surgery is indicated | NSIDx: emergent TTE. | |||||
aComplete heart block can also occur in extensive anterior wall MI, which has a poorer prognosis. | ||||||
bIn acute pericardial tamponade due to myocardial rupture, the classic sign of big globular heart in CXR might not be evident, as adequate time hasn’t passed by for pericardial stretching to occur. | ||||||
cPulsus paradoxus and Kussmaul sign have very similar causes (e.g. constrictive pericarditis, restrictive cardiomyopathy, pericardial tamponade) | ||||||
Abbreviations: CXR, chest X-ray; IABP, intra-aortic balloon pump; JVD, jugular venous distension; LAD, left anterior descending artery; MI, myocardial infarction; MR, mitral regurgitation; RCA, right coronary artery; TR, tricuspid regurgitation, TTE, transthoracic echocardiography; VSD, ventricular septal defect. | ||||||
4.3.3 Other Complications of Acute Coronary Syndrome Ventricular Fibrillation (VF)
It is the most common cause (MCC) of death in CAD and MI is VF. Arrhythmias usually occur within first 24 hours of MI. Mechanism of arrhythmia is reentrant circuit formation (ischemic/infarct area have different conduction properties than viable/normal myocardium).
β-blockers decrease risk of ventricular arrhythmias.
Lidocaine should NOT be given prophylactically as it can increase risk for asystole.
Automated implantable cardioverter-defibrillator (AICD) placement is indicated in VF and sus-tained ventricular tachycardia (VT) that occur after 48 hours of index-MI.
Know how to differentiate them. Think about the ones that cause pulmonary edema (crackles in exam and CXR with bilateral infiltrates) versus the ones that do not.
Cardioembolic phenomenon
With loss of major contractile portion of the heart that occurs particularly in anterior wall MI, re-sultant stasis increases risk of thrombus formation in the left ventricle.
12 By similar mechanism, intracardiac thrombus can form in:
• Atrial fibrillation (stasis of blood in the left atrium).
• Dilated cardiomyopathy (all of the heart chambers are dilated and hypokinetic).
Post-MI pericarditis: Section 4.6.5, Pericarditis
Patient had an anterior wall MI 3 weeks ago. She now presents with sudden onset left-sided weakness and aphasia. EKG reveals sustained ST-wave elevation.
5. What is the NSIDx to look for the underlying cause?
Other causes of chest pain
4.4 Heart Failure
Definition: Primary life-sustaining work of our heart is to receive blood (diastole) and then to pump it (systole). Heart failure can occur when heart fails to relax adequately to receive enough blood (diastolic failure/dysfunction) or to pump enough blood (systolic heart failure/dysfunction). It might also fail to do both.
Clinical pathophysiology
Increase in backward pressure from left heart failure: Increased pressure in pulmonary vascular system results in fluid leakage into the alveoli, causing gas exchange problem and SOB (shortness of breath).
Depending upon severity of heart failure, SOB can initially be present only on exertion, later progress to paroxysmal nocturnal dyspnea (SOB 1-2 hours after lying down) → orthopnea (SOB immediately after lying flat)
→ SOB at rest.
14 Lying flat increases venous return, thereby increasing preload pressure and putting strain on a weak heart.
Severe left heart failure can cause acute respiratory failure and acute pulmonary edema. Exam may reveal bibasilar crackles and S3. (S3 is one of the most specific finding in heart failure.)
Increase in backward pressure from right heart failure: This results in increased pressure in the systemic veins and presents with jugular venous distension, hepatomegaly, ascites, and bilateral pitting edema.
Decrease in forward cardiac output: All patients with heart failure have symptoms related to decrease in cardiac output. This presents with SOB and limitation of physical activity.
New York Heart Association functional classification of heart failure
MCC of right heart failure is left heart failure, as left heart pathology is more common. Increased left-sided pressure due to left heart failure eventually increases right-sided heart pressure.
Work-up: For any patient who presents with abovementioned clinical features, the NSIDx is transthoracic echocardiography (TTE).
Heart failure (HF) classification by ejection fraction
EF ≤ 40% = systolic heart failure (aka heart failure with reduced EF) | EF > 40 %= diastolic heart failure (aka heart failure with preserved EF) | |
|---|---|---|
Note: Almost all causes of diastolic HF, if untreated can lead to systolic HF | Hypertension, valvular heart disease, hypertrophic obstructive cardiomyopathy, restrictive cardiomyopathy, right ventricular infarctiona | |
Extra heart sound heardb | ||
Impaired relaxation of cardiac wall with thickened myocardium | ||
aIn right ventricular (RV) infarction, the primary pathologic mechanism is the failure of the right heart to relax. The systolic function of RV is not that important, as RV is not required to generate a lot of force to pump blood through low-pressure pulmonary system. | ||
b Practice listening to the S3/S4 heart sounds as it is high yield. They are available in Google videos/ YouTube. | ||
Abbreviations: ACE, angiotensin-converting enzyme; ARB, angiotensin receptor blocker; EF, ejection fraction; HTN, hypertension. | ||
4.4.1 Systolic Heart Failure Management
Legend: NSIM, next step in management: ACE-I, angiotensin-converting enzyme inhibitor: ARB, angiotensin receptor blocker
aCardiac resynchronization therapy (CRT): Strongest consideration is given for patients with LBBB morphology and QRS duration of ≥ 150 milliseconds.
How does CRT work? Prolonged QRS interval on EKG signals that left and right ventricles are not working in synchrony. CRT (biventricular pacing) consists of placing pacer leads in both ventricles in order to make them contract simultaneously. Synchronous contractions are more effective, resulting in increased cardiac output.
Automated implantable cardioverter-defibrillator (AICD)
Failing heart is prone to life-threatening ventricular arrhythmias, and AICDs improve survival by cardioverting life-threatening ventricular arrhythmias.
| |
| |
aIn patients with NYHA class IV heart failure and no indication for CRT, AICD alone is not recommended due to poor prognosis. | |
Abbreviations: CRT, cardiac resynchronization therapy; EF, ejection fraction; MI, myocardial infarction; NYHA, New York Heart Association; VT/VF, ventricular tachycardia/ventricular fibrillation. | |
Medications that have been shown to decrease mortality in patients with systolic heart failure
Diuretics and digoxin provide symptomatic benefit and reduce hospitalization rates; however, these medications have not been shown to improve survival.
A 65-year-old male black patient has chronic systolic heart failure with NYHA class II functional status. He was started on an angiotensin-converting enzyme (ACE) inhibitor. In 8 weeks, his creatinine has increased by more than 30% above baseline.
7. What is the NSIM regarding ACE-i?
8. What should be started next?
A 65-year-old male with hx of systolic heart failure, on lisinopril for the last few months, comes in to the clinic with lip swelling for 1 day.
9. What is the likely diagnosis?
4.4.2 Acute Decompensated Heart Failure
Presentation: Hallmark of presentation is worsening SOB (more than baseline). When severe, it can progress to pulmonary edema and acute respiratory failure.
16 CCS: 75-year-old male presents with acute respiratory failure requiring 4 L of oxygen via nasal cannula. Physical exam reveals elevated jugular venous pressure, S3 heart sound and extensive crackles are heard throughout lung. Patient is also bringing up pink frothy sputum at bedside.
Causes of acute decompensation of heart failure
Inadequate diuretic dosage or noncompliance.
Excessive dietary salt intake: The first SIM of heart failure patient is to decrease salt intake.
Myocardial ischemia or infarction.
Thyrotoxicosis (check thyroid-stimulating hormone [TSH] when suspected).
Medications such as nonsteroidal anti-inflammatory drugs (NSAIDs), thiazolidinediones, etc.
Management
For acute presentation with significant worsening of symptoms, NSIDx is EKG, chest X-ray (CXR), and serum brain natriuretic peptide (BNP).
17 Brain natriuretic peptide (BNP) is secreted by the ventricles in response to volume overload and stretching of the cardiomyocytes.
• BNP level of <100 often excludes decompensated heart failure as the etiology for SOB.
• BNP of >400 has high positive predictive value for heart failure as the etiology of SOB.
Note: BNP cannot be used to differentiate in between systolic and diastolic heart failure. Also in morbidly obese patients BNP might be falsely low.
Address underlying factor (e.g., correction of atrial fibrillation with rapid ventricular rate).
For severe cases follow the following management plan:
Loop diuretics (intravenous): Lasix (furosemide), bumetanide, etc. (Furosemide is not only a loop diuretic, but also causes venodilation, thereby decreasing preload, even before the onset of its diuretic action.)
Morphine: Consider this in patients who appear very short of breath (distress) It decreases accompanying sympathetic activity and acts as a direct venodilator.
Nitroglycerin paste, IV nitroglycerin, or nitroprusside drip, can be used to decrease preload, particularly in patients acute severe heart failure and in presence of comorbidities such as severe HTN, acute mitral regurgitation, etc.
Oxygen (high flow) → BIPAP → intubation (depending upon severity).
Position patient to keep the head of bed elevated: A simple technique of increasing the angle of the patient’s bed to > 45 degrees decreases venous return and improves symptom.
Further management
In hospitalized patients with severe acute heart failure who are not responding to aggressive high-dose diuretics, consider hemodialysis with ultrafiltration to remove extra fluid.
The following modalities can be considered in patients with progressive severe heart failure, especially in patients with signs of end-organ dysfunction in the setting of a low cardiac output, as a bridging therapy for heart transplantation:-
Electrolyte abnormalities in patients with heart failure
This is common because of concurrent use of diuretics and associated comorbidities.
Hyperkalemiaa | Can be caused by ACE-i, ARB, and/or potassium-sparing diuretics |
Hypokalemiaa | Can be caused by all diuretics except the potassium sparing ones. |
Neurohormonal activation leads to increase in ADH and renin-aldosterone activity, which results in excess water retention and hyponatremia. It is often associated with severe heart failure and poor prognosis. | |
aAbnormal potassium level can precipitate arrhythmias and worsen heart failure. | |
Abbreviations: ACE-i, angiotensin-converting enzyme inhibitor; ADH, antidiuretic hormone; ARB, angiotensin receptor blocker. | |
4.5 Arrhythmias
Presentation: Depending on the severity of underlying arrhythmia, brady/tachyarrhythmias can present with missed heartbeat, palpitations, chest pain, SOB, exercise intolerance, presyncope (dizziness), and syncope. Very severe arrhythmias can present with sudden onset clinical deterioration and hemodynamic instability.
Work-up: NSIDx for suspected arrhythmia is EKG. If EKG is unremarkable, NSIDx is Holter or event loop monitoring.
4.5.1 Acute Tachyarrhythmias
Difference in electrical conduction can occur between normal and abnormal myocardium (e.g., due to ischemia, fibrosis, accessory pathway). This can, at times, create an electrical positive feedback loop that can cause persistent action potential propagation and development of arrhythmia.
Increased automaticity: This can occur with excessive adrenergic stimulation, muscarinic blockade, etc.
Algorithm: Approach to Management of Acute Tachyarrhythmias
Legend: NSIM, next step in management; DOC, drug of choice
aIn presence of “danger” signs, NSIM is always electrical cardioversion.
bWhen pulse is present, NSIM is to do synchronized cardioversion, which delivers shock during systole. When cardioversion is not properly synchronized to systole, it can trigger dangerous ventricular tachycardia.
cIf pulse is absent, there is nothing to synchronize cardioversion with; hence no need for synchronization.
dWide-complex tachycardia with AV dissociation (atria and ventricles beat independently of each other in their own rhythm and rate) is pathognomonic for ventricular tachycardia. Amiodarone is the drug of choice (DOC). Other choices are lidocaine, procainamide, and sotalol.
eFor narrow complex tachycardia look at the EKG to determine next plan of action:
fIn SA or AV nodal reentrant tachycardia (SANRT or AVNRT), primary micro-reentrant circuit occurs inside the SA node or the AV node. If we block the SA or AV node (even for short period of time), you can terminate the arrhythmia.
20 Sinus tachycardia and SA nodal re-entrant tachycardia may be virtually indistinguishable by looking at EKG; pointers to the latter are abrupt initiation and termination of rhythm and its responsiveness to vagal stimulation or adenosine.
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