Two systematic reviews have assessed the diagnostic accuracy of elements of the medical history, physical examination, or readily available tests in diagnosing HF in adults with undifferentiated dyspnea: 
____________________________________________________________________________
Many features increased the probability of heart failure, with the best feature for each category being the presence of:
(1) the chest radiograph showing pulmonary venous congestion (positive LR = 12.0; 95% CI, 6.8-21.0); 
(2) the sign of the third heart sound (S3) gallop (positive LR = 11; 95% CI, 4.9-25.0); 
(3) past history of heart failure (positive LR = 5.8; 95% confidence interval [CI], 4.1-8.0); 
(4) electrocardiogram showing atrial fibrillation (positive LR = 3.8; 95% CI, 1.7-8.8).
(5) the symptom of paroxysmal nocturnal dyspnea (positive LR = 2.6; 95% CI, 1.5-4.5); 
____________________________________________________________________________
Conversely, findings useful in excluding HF include, in decreasing order: 
  1. A low serum BNP proved to be the most useful test (serum B-type natriuretic peptide <100 pg/mL; negative LR = 0.11; 95% CI, 0.07-0.16).
  2. The chest radiograph not showing cardiomegaly (negative LR = 0.33; 95% CI, 0.23-0.48);
  3. The absence of a past history of heart failure (negative LR = 0.45; 95% CI, 0.38-0.53);
  4. The absence of symptom of dyspnea on exertion (negative LR = 0.48; 95% CI, 0.35-0.67);
  5. No Rales (negative LR = 0.51; 95% CI, 0.37-0.70)
  6. Lack of Any electrocardiogram abnormality (negative LR = 0.64; 95% CI, 0.47-0.88). 

REFERENCES:

  1. Wang CS, FitzGerald JM, Schulzer M, Mak E, Ayas NT. Does This Dyspneic Patient in the Emergency Department Have Congestive Heart Failure? JAMA. 2005;294(15):1944–1956.

SYMPTOMS THAT RULE OUT  (Lowest -LR): 

The absence of pain of sudden onset substantively decreases the probability of dissection (negative LR, 0.3;95% CI, 0.2-0.5).

SYMPTOMS THAT RULE IN (Highest +LR): 

The presence of tearing or ripping pain (positive LR, 1.2-10.8) or pain that migrates (positive LR, 1.1-7.6) may prove useful.

 

FINDINGS THAT RULE IN (Highest +LR): 

Pulse deficits (positive LR, 5.7; 95% CI, 1.4-23.0) or focal neurological deficits (positive LR, 6.6-33.0)

FINDINGS THAT RULE OUT (Lowest -LR): 

A normal aorta and mediastinum on chest radiograph helps exclude the diagnosis (negative LR, 0.3; 95% CI,0.2-0.4) 

 

KEY POINT: No single test definitely rules in or out Aortic Dissection, so diagnostic imaging (CTA) will be necessary!

The presence or absence of a diastolic murmur is not useful (positive LR, 1.4; negative LR, 0.9)

 

REFERENCES

Klompas M. Does This Patient Have an Acute Thoracic Aortic Dissection? JAMA. 2002;287(17):2262–2272. doi:https://doi.org/10.1001/jama.287.17.2262

Functions on the premise of mismatch in coronary perfusion after a vasodilator (e.g dipyridamole) is administered. 

HOW? The coronary vessels with disease burden are already maximally dilated, hence after the addition of the vasodilator, perfusion mismatch occurs as the healthier vessels dilate further.

False NEGATIVES:

  • Caffeine or theophylline can interact with dipyridamole.
  • Severe flow limiting triple vessel disease or LEFT main diseae (may both cause a balanced defect). 

CONTRAINDICATIONS:

  • Severe airway disease (COPD or Asthma)

BONUS: reversal agent to dipyridamole is amiophylline.

REFERENCES

  1. Driessen, Roel S et al. “Myocardial perfusion imaging with PET.” The international journal of cardiovascular imaging vol. 33,7 (2017): 1021-1031. doi:10.1007/s10554-017-1084-4
  2. Burrell S, MacDonald A. Artifacts and pitfalls in myocardial perfusion imaging. J Nucl Med Technol. 2006 Dec;34(4):193-211; quiz 212-4.

 

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.