Up to 40% of inferior wall Myocardial infarctions have associated right ventricular involvement. Venodilation and medications that decrease RV filling (i.e nitrates, diuretics) should be avoided.

WHY?

The right ventricle contains less myocardial tissue compared to the left ventricle. It is more dependent on adequate preload (Frank-Starling curve) to assure adequate cardiac function (CO). If there is damage to the right ventricle, preload reduction from nitrates/ diuresis could result in significant hypotension.

REFERENCES

  1. Albulushi A., et al. Acute right ventricular myocardial infarction. Expert Rev Cardiovasc Ther. 2018 Jul;16(7):455-464.
  2. Bouhuijzen LJ, Stoel MG. Inferior acute myocardial infarction with anterior ST-segment elevations. Neth Heart J. 2018 Oct;26(10):515-516.
Ventricular interdependence occurs when there is discordance. This results from the heart ventricles filling out of phase with one another. It is an important physiological manifestation of cardiac tamponade and constrictive pericarditis.

The ventricles experience impaired diastolic relaxation secondary the constrictive pericardium and are unable to fully expand. During inspiration, the right ventricle will fill and shift the interventricular septum to the left reducing its filling capacity. During expiration, the opposite will occur with the interventricular septum moving to the right.
REFERENCES
  1. Santamore WP, Dell’Italia LJ. Ventricular interdependence: significant left ventricular contributions to right ventricular systolic function. Prog Cardiovasc Dis. 1998 Jan-Feb;40(4):289-308.

The Frank-Starling mechanism is a relationship characterizing stroke volume with pre-load. Stroke volume is dependent on the following:

  • Pre-load: changes in pre-load affect the end-diastolic volume/pressure which in turn alter stroke volume
  • Contractility: can be influenced by sympathetic/parasympathetic nervous system changes and electrolytes. Increases in contractility cause decreases in end-systolic volume while decreases in contractility result in increased end-systolic volumes.
  • Afterload: can be altered by changes in vascular resistance or damage to semi-lunar valves of the heart

In a normal heart, increasing pre-load or venous return will result in increased contractility leading to increased stroke volume and ultimately leading to increased cardiac output (CO= Heart Rate x Stroke Volume).

When heart failure occurs, increases in pre-load do not result in a stroke volume sufficient to meet the demands of the body’s peripheral tissues. As a result of the decreasing effective circulating volume of blood, the body responds with multiple ways in an effort to increase tissue perfusion. These include:

  • Activation of renin-angiotensin-aldosterone system
  • Activation of sympathetic nervous system

The systemic vasoconstriction that results from the above mentioned mechanisms can sustain cardiac output in a heart failure patient for a limited time. As the disease progresses, the cardiac output does not increase appropriately despite increased pre-load. Eventually, the increased in left ventricle end diastolic volume/pressure transmits pressure back to the pulmonary veins leading to the symptoms of pulmonary congestion (dyspnea, orthopnea, PND, etc).

REFERENCES:

  1. http://www.cvphysiology.com/Cardiac%20Function/CF003
  2. https://www.healio.com/cardiology/learn-the-heart/cardiology-review/topic-reviews/frank-starling-law

The ST segment on an ECG represents the interval between ventricular depolarization and ventricular repolarization.

Image taken from Wikipedia

When ST elevation is present, it is most important to rule out cardiac ischemia or a myocardial infarction. Other causes of ST elevation include:

  • Coronary Vasospasm (Prinzmetal’s Angina)
  • Acute Pericarditis: typically causes diffuse ST elevation associated with PR depression (reciprocal ST depression and PR elevation seen in leads aVR and V1)
    • Benign Early Repolarization: mild ST elevations with tall T waves, mainly in the precordial leads
  • Left Bundle Branch Block
  • Left Ventricular Hypertrophy (LVH): usually causes ST elevation in leads with deep S waves (V1-V3)
  • Ventricular Aneurysm
  • Brugada Syndrome: ST elevations and Right Bundle Branch Block in V1-V2
  • Raised Intracranial Pressure (ICP): can cause ST elevation or depression

For ECGs showing the conditions above, visit the link in the references.

REFERENCES

  1. https://lifeinthefastlane.com/ecg-library/st-segment/

QT interval is the length between the beginning of the QRS complex (ventricular depolarization) and end of the T wave (ventricular re-polarization).

  • QTc is prolonged if > 440ms in men or > 460ms in women
  • QTc >500ms is associated with increased risk of torsades de pointes
  • QTc is abnormally short if < 350ms
  • A useful rule of thumb is that a normal QT is less than half the preceding RR interval

QTc prolongation can be caused by the following:

REFERENCES

  1. Goldstein, J. N., Dudzinski, D. M., Erickson, T. B., & Linder, G. (2018). Case 12-2018: A 30-Year-Old Woman with Cardiac Arrest. New England Journal of Medicine, 378(16), 1538-1549. doi:10.1056/nejmcpc1800322
  2. QT Interval. Edward Burns, Last updated November 21, 2017.https://lifeinthefastlane.com/ecg-library/basics/qt_interval/
  3. http://www.rxfiles.ca/rxfiles/uploads/documents/qa%20torsadesdepoint.pdf

 

It is quite common to see accompanying acute kidney injury during a congestive heart failure exacerbation. 

WHY?

  1. Renal hypo-perfusion secondary to poor cardiac output.
  2. Renal venous congestion. Increased central venous pressure (CVP) is transmitted into the efferent arteriole, reducing the pressure gradient and subsequently the GFR.  
  3. Neurohumoral mechanisms (i.e RAAS, ADH) which help acutely but are maladaptive in the long term on the kidneys’ GFR.
Pathophysiological mechanisms of worsening renal function in acute heart failure. Img Cred KCJ.

REFERENCES

  1.  Marlies Ostermann, Heleen M. Oudemans-van Straaten and Lui G. Forni. Fluid overload and acute kidney injury: cause or consequence?. Critical Care 201519:443https://doi.org/10.1186/s13054-015-1163-7 
  2. Han SW, Ryu KH. Renal Dysfunction in Acute Heart Failure. Korean Circulation Journal. 2011;41(10):565-574. doi:10.4070/kcj.2011.41.10.565.

Sodium bicarbonate has become the mainstay treatment for arrhythmias caused by TCA toxicity.

The cardiotoxic effects of TCA work via blockade of the rapid sodium channels (see below- stage 0).

There will be a characteristic prolongation of the QRS. Potentiating hemodynamic instability.

HOW DOES BICARBONATE HELP?

The benefit of sodium bicarbonate (NaHCO3) is primarily related the sodium component. Increasing the extracellular sodium concentration results in an increase of the electrochemical gradient across cardiac cell membranes. This in effect works to attenuate the TCA-induced blockade of rapid sodium channels.

Also the alkalization of the blood from bicarbonate shifts TCA towards its non-ionized form, reducing its ability to bind sodium channels.

REFERENCES

  1. Sasyniuk BI, Jhamandas V. Mechanism of reversal of toxic effects of amitriptyline on cardiac Purkinje fibers by sodium bicarbonate. J Pharmacol Exp Ther. 1984;231(2):387.
  2. Bruccoleri RE, Burns MM. A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening. J Med Toxicol. 2016 Mar;12(1):121-9.

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.