Bifascicular Block:

1. Left anterior fascicular block (LAFB) or left posterior fascicular block (LPFB)

AND

2. Right bundle branch block (RBBB)

 

Trifascicular Block (impending):

1. Left anterior fascicular block (LAFB) or left posterior fascicular block (LPFB)

2. Right bundle branch block (RBBB)

AND

3. First degree AV Block (Delayed conduction through the remaining fascicle)

NOTE: If complete blockage, third degree heart block will occur!

REFERENCES

  1. Life in the Fast Lane
  2. Healio.com

A heart “murmur” is the sound of blood flowing (i.e through a valve).

RIGHT SIDED MURMURS (i.e Tricuspid regurgitation or Pulmonary stenosis) will INCREASE WITH INspiration.

WHY? When inhaling, a more negative intra-thoracic pressure is created. This increases venous return to the right ventricle. More venous return means more blood flow over the valve and an increase in the intensity of the right sided murmur.

Likewise during EXpiration, LEFT SIDED MURMURS (i.e mitral regurgitation) INCREASE. This is due to the expanded lung parenchyma collapsing and the pooled volume of blood in it being squeezed into the left side of the heart.

Exception : MVP and HOCM murmurs DO NOT increase on expiration.

REFERENCES

  1. Chapter 267: Physical Examination of the Cardiovascular System. Patrick T. O’Gara; Joseph Loscalzo. Harrison’s Principles of Internal Medicine, 19e
  2. Chapter 14. The History, Physical Examination, and Cardiac Auscultation. Richard A. Walsh; Robert A. O’Rourke; James A. Shaver. Hurst’s The Heart, 13e

Hypothyroidism has been recognized as a cause of secondary hypertension.

Img Cred: http://circ.ahajournals.org/
Img Cred: http://circ.ahajournals.org/

Previous studies on the prevalence of hypertension in subjects with hypothyroidism have demonstrated elevated diastolic blood pressure values. (hypertension in ~30% of patients)

WHY???

In hypothyroidism, there is endothelial dysfunction and arterial smooth muscle compliance is reduced => leads to increased Systemic Vascular Resistance (SVR).

This appears to be a multi-factorial mechanism (increased adrenergic activity and reduction in endothelial-derived relaxation factor (EDRF) availability). 

REFERENCES

  1. Klein, I and Danzi, S. Thyroid Disease and the Heart. Circulation. 2007;116:1725-1735.
  2. Klein I, Ojamaa K. Thyroid hormone and the cardiovascular system. N Engl J Med. 2001;344(7):501.
  3. Taddei S, Caraccio N, Virdis A, Dardano A, Versari D, Chiadoni L, Salvetti A, Ferrannini E, Monzani F. Impaired endothelium-dependent vasodilatation in subclinical hypothyroidism: beneficial effect of levothyroxine therapy. J Clin Endocrinol Metab. 2003; 88: 3731–3737.

Pleural effusions in patients with congestive heart failure are typically bilateral. However, a unilateral pleural effusion is more commonly seen on the right side.

WHY??? Although multiple theories attempt to explain the right-sided preponderance of pleural effusions, to date, no mechanism has been universally accepted or experimentally proven.

REFERENCES

  1. Woodring JH. Distribution of pleural effusion in congestive heart failure: what is atypical? South Med J. 2005 May;98(5):518-23.
  2. Natanzon A, Kronzon I. Pericardial and pleural effusions in congestive heart failure-anatomical, pathophysiologic, and clinical considerations. Am J Med Sci. 2009 Sep;338(3):211-6. doi: 10.1097/MAJ.0b013e3181a3936f.
  3. Porcel JM. Pleural effusions from congestive heart failure. Semin Respir Crit Care Med. 2010 Dec;31(6):689-97. doi: 10.1055/s-0030-1269828. Epub 2011 Jan 6.

Aortic stenosis (AS) is classically a mid-systolic crescendo-decrescendo murmur that radiates to the carotid.

Features that INCREASE likelihood [1]:

    • Pulsus tardus (late) et parvus (weak) [slow rate of increase of the carotid pulse]
    • Peak murmur intensity is late in systole
    • Diminished S2 intensity or absence of S2
    • Apical-carotid delay or Brachio-radial delay
    • Maximal murmur sound at second right intercostal space

Features that DECREASE likelihood:

  • Absence of a murmur radiating to the right clavicle (likelihood ratio [LR] 0.10; 95% confidence interval [CI] 0.01, 0.44) [2]

REFERENCES

  1. Etchells E, Bell C, Robb K. Does this patient have an abnormal systolic murmur? JAMA. 1997 Feb 19;277(7):564-71.
  2. Etchells E, Glenns V, Shadowitz S, Bell C, Siu S. A Bedside Clinical Prediction Rule for Detecting Moderate or Severe Aortic Stenosis. Journal of General Internal Medicine. 1998;13(10):699-704. doi:10.1046/j.1525-1497.1998.00207.

REGULAR

IRREGULAR

·         Sinus tachycardia

·         AVRT

·         AVNRT

·         Atrial flutter (with fixed block)

·         Atrial tachycardia

·         Atrial fibrillation

·         Atrial flutter (with variable block)

·         Multifocal atrial tachycardia

·         Atrial tachycardia (with variable block)

 

REFERENCES

  1. 276: Supraventricular Tachyarrhythmias. Gregory F. Michaud; William G. Stevenson. Harrison’s Principles of Internal Medicine, 19e

Digoxin [Antiarrhythmic (Class III)] competes with Potassium for binding to cellular Na+/K+ ATPase pumps. Hypokalemia predisposes the patient to Digoxin toxicity. Most common arrhythmia associated with Digoxin toxicity is paroxysmal atrial tachycardia with 2:1 block. However, Bradycardia can occur and presence of a bidirectional ventricular tachycardia is practically pathognomonic for Digoxin toxicity!

HOW?? When potassium levels are low, it allows increased Digoxin binding to ATPase pumps to exert its inhibitory effects.

NOTE: Digoxin toxicity can cause Hyperkalemia (Digoxin inhibits Na+/K+ ATPase, so K+ remains in the plasma). In theory, if you give IV Calcium it can cause an influx of Calcium into the cardiac myocytes resulting in a non-contractile state (the so called “Stone Heart“).

REFERENCES

  1. Levine M et al. The Effects of Intravenous Calcium in Patients wit h Digoxin Toxicity. J Emerg Med. 2011;40(1):41–46.
  2. CHAPTER 124: Toxicology in Adults. Patrick McCafferty Lank; Thomas Corbridge; Patrick T. Murray. Principles of Critical Care, 4e
  3. Chapter 95. Adverse Cardiovascular Drug Interactions and Complications. Ileana L. Piña; Gerard Oghlakian. Hurst’s The Heart, 13e

Entresto is made up of two molecules => Valsartan & Scubitril

  • Valsartan is an ARB (Angiotensin receptor blockers) =>  Angiotensin II AT1 receptor blocker
  • Scubitril => Neprilysin inhibitor
Valsartan-sacubitril-Entresto-Mechanism
Img Credit: Vardeny O, Miller R, Solomon SD

REFERENCES

  1. McMurray JJ, Packer M, Desai AS, et al. Angiotensin-neprilysin inhibition versus enalapril in heart failure. N Engl J Med 2014;371:993-1004
  2. Vardeny O, Miller R, Solomon SD. Combined Neprilysin and Renin-Angiotensin System Inhibition for the Treatment of Heart Failure. JCHF. 2014;2(6):663-670. doi:10.1016/j.jchf.2014.09.001

WHAT IS IT? Drop in blood pressure of more than 10 mmHg during inspiration phase.

  • Technically not “paradoxical”. It is merely an exacerbation of normal breathing physiology (small drop in SBP during inspiration)

HOW IS IT DONE? Done via manual blood pressure cuff; inflate above SBP and then deflate slowly (1-2 mmHg per second); the first Korotkoff sound is heard during expiration and then, finally, during both. If the difference between these two pressure readings is the >10 mmHg, it is pulsus paradoxus.

Diff Dx: Used in the evaluation of cardiac tamponade (LR 3.3), pericarditis, COPD, bronchial asthma, restrictive cardiomyopathy, hemorrhagic shock, massive PE, tricuspid stenosis, and mitral stenosis.

Pulsus-Paradoxus

REFERENCES

  1. Pulsus paradoxus. Olfa Hamzaoui, Xavier Monnet, Jean-Louis Teboul. European Respiratory Journal Dec 2013, 42 (6) 1696-1705; DOI: 10.1183/09031936.00138912
  2. Chapter 8: The Chest: Chest Wall, Pulmonary, and Cardiovascular Systems; The Breasts. DeGowin’s Diagnostic Examination, 10e
  3. Chapter 6: Pulsus Paradoxus. Teaching Rounds: A Visual Aid to Teaching Internal Medicine Pearls on the Wards

Wolff Parkinson White Syndrome (WPW) is a pre-excitation tachyarrhythmia (SVT or Afib) characterized by a shortened PR interval along with a delta wave (a delay in initial deflection of the QRS complex) on the ECG. It occurs due to conduction from the SA node to the ventricle through an accessory pathway that bypasses Wolff-Parkinson-White-Syndrome-WPWthe AV node (aka the bundle of Kent).

Agents such as: β-blockers, adenosine, amiodarone, and calcium channel blockers should be avoided. They act as AV nodal blockers; blocking the heart’s normal electrical pathway. Therefore favoring a 1:1 atrial to ventricle conduction ratio, through the accessory pathway. This has the potential to generate unstable ventricular arrhythmias.

REFERENCES

  1. Chapter 18: Cardiac Rhythm Disturbances. William J. Brady; Thomas S. Laughrey; Chris A. Ghaemmaghami. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 8e