Korotkoff sounds:

When the cuff pressure is great enough to close the artery during part of the arterial pressure cycle, a sound then is heard with each pulsation. These sounds are called Korotkoff sounds believed to be caused mainly by blood jetting through the partly occluded vessel. The jet causes turbulence in the vessel beyond the cuff, and this sets up the vibrations heard through the stethoscope.

As long as the pressure in the cuff is higher than the systolic blood pressure of the patient, blood doesn’t jet through the completely occluded artery, hence no sound is heard. If the pressure is dropped to a level equal to that of the patient’s systolic blood pressure, the first Korotkoff sound will be heard. As the pressure is further gradually lowered down, following korotkoff sounds are heard:

Phase 1 (K1): Clear tapping sounds representing systolic pressure
Phase 2 (K2): Softer tones
Phase 3 (K3): Louder once again
Phase 4 (K4): Muffled Tones sounds representing diastolic pressure
Phase 5 (K5): Tones cease

Auscultatory Gap:

An auscultatory gap also called as silent gap is the interval of pressure where korotkoff sounds indicating true systolic pressure fade away and reappear at a lower pressure point during the manual measurement of blood pressure by auscultatory method. The auscultory gap happens when the first Korotkoff sound fades out for about 20-50 mmHg only to return. It can result in following erroneous blood pressure reading:

1. Underestimation of systolic blood pressure
2. Overestimation of diastolic blood pressure

Example:

The patient’s actual systolic pressure is 200 with a gap from 170 to 140 and a diastolic of 110. You inflate the cuff to 170 and hear nothing until the manometer reaches 140, which you presume is the systolic pressure. Also if you, inflate the cuff to 200, you may read 170 as the diastolic pressure which is the beginning of auscultatory gap.

When recording a blood pressure with an auscultatory gap, always list your complete findings. eg. BP 200/110 with the auscultatory gap from 170 to 140.

Auscultatory gap has been found to occur due to venous pooling of blood. The auscultatory gap is most likely to appear in the obese arm, especially if the physician pumps up the cuff slowly and traps a great deal of blood in the arm’s venous compartment. Another way to trap blood is to pump the cuff 2nd time immediately after 1st determination, without allowing 1-2 minutes for the trapped blood to escape.

Auscultatory gap in Hypertension

An auscultatory gap is common in elderly hypertensive patients. It occurs in some hypertensive patients only. Auscultatory gaps are related to carotid atherosclerosis and to increased arterial stiffness in hypertensive patients, independent of age.

Types:

3 types of auscultatory gaps, have been identified by using wideband external pulse recording.

1. G1: occurs with cuff pressure just below systolic and is characterized by the presence of K1 and K2 with intermittent disappearance of K2. G1 gaps are related to a phasic decrease of arterial (systolic) pressure.
2. G2: are related to a phasic increase of arterial (diastolic) pressure, occur when cuff pressure is just above diastolic, and are characterized by the presence of K1, K2, and K3 with intermittent disappearance of K2.
3. G3: occurs with cuff pressure between systolic and diastolic and are characterized by an underdeveloped or blunted K2 signal.

Mechanism:

• The mechanism of origin of auscultatory gap has not been understood clearly.
• Cavallani recently showed that the early loss of audible sound during cuff deflation is associated with blunted high frequency K2 signals associated with korotkoff sound (detected by wideband external pulse recording) likely related to the altered physical properties of a stiffer arterial wall.

Precautions:

1. Determining systolic blood pressure by palpatory method before recording the blood pressure with auscultatory method.
2. Inflating the blood pressure cuff to 20-40 mmHg higher than the pressure required to occlude the brachial pulse.

Unfractioned Heparin- is derived from  porcine intestinal mucosa or bovine lung tissue. UFH catalyzises that inactivation of thrombin and factor Xa by inhibiting Anti-thrombin III.  At usual dose it prolongs TT and aPTT and has a minimal effect on PT/INR.

Benefits of UFH-

1. 1. The effect of UFH normalizes within hours of discontinuation
2. 2. It is reversible with Protamine Sulphate.
3. 3. Can be titrated according to aPTT.
4. 4. Dosing is not typically affected by Renal function.

Dosage-

1. DVT prophylaxis- 5000 U SC  Q8-Q12hrly ( aPTT monitoring not necessary)

2. Therapeutic anticoagulation

a. Weight based Heparin dosing-

Bolus- 80 U/kg

Infusion- 18U/kg/hr.

ADJUSTMENTS

aPTT target level may vary depending upon the Hospital standards.

aPTT to be sent 6 hrly after any bolus or dose change.

b. For Acute STEMI patients-

60U/kg bolus ( usually 5000U bolus) followed by 12U/kg/hr(  usu. 1000U/kg/hr)

Dose-adjusted UFH may be administered SC q8hrly ( 12000U UFH) or Q12hr ( 16000U UFH) à  aPTT after 6 hrs.

2. Low-Molecular Heparin-

Produced by chemical and enzymatic cleavage of UFH.  LMW inactivates factor Xa to greater extent. It minimally prolongs aPTT.

Caution required in patients with deranged RFT, obesity, pregnancy—facter Xa assay may be needed.

These are only partially reversible with Protamine.

Lepirudin ( Refludan, recombinant hirudin) – direct thrombin inhibitor that is used for treatment of HIT.( Heparin Induced Thrombocytopenia )

By Dr Sujit Shrestha ( Reference – various sources including Washington manual, internet)

Unstable angina

NSTEMI or Acute Non Q web MI

Acute MI

Conventionally ACS refers to UA and NSTEMI

Pathophysiology:

• Plaque rupture → Platelet adhesion to expose collagen in coronary arteries → Activation of platelets → Platelet aggregation → thrombus formation → ACS
• Coronary spasm → Decreased Myocardial circulation → ACS

Stable and Unstable Plaque are the 2 forms of plaque in pathogenesis of ACS.

1. Stable Plaque are more hemodynamically significant and produces reversible MI. It usually manifest as chronic stable angina.
2. Unstable Plaque are hemodynamically insignificant, angiographically unimpressive and prone to rupture causing occlusive thrombus and development of MI.

Most AC event develop upon atheromatous plaque.

UNSTABLE ANGINA:-

• Rest Angina- occurs without any exertion or provocation and genreally lasts for 20 minutes or longer.
• Increasing Angina- means ‘ Distinctly more frequent ,longer duration and /or decreased threshold’ in a patient with previously diagnosed Angina.
• Severity increases by 1 or more CCS class atleast upto CCS class III.

NSTEMI-

• NSTEMI differs from UA in severity and both may be indistinguishable at presentation. Ischemia can be severe enough to damage the myocardium though Cardiac markers may not be raised upto several hours of onset of pain. Only 1/4 of these patients will develop Acute Q wave MI.

Investigations:-

ECG/ EKG – ECG must be done within 10 minutes of arrival in ER of all suspected cases. ECG must be repeated as per required and when pain recurrs. 0.05mV of ST segment change in limb leads and 0.1 mV in other leads are significant. T wave changes may be seen. A normal ECG does not rule out ACS completely.

Cardiac markers-

• CKMB, more specific CKMB1 and 2. CKMB2 : CKMB1 ratio >1.5 or CKMB2 level >1 U/L suggest Myocardial injury. rise within 4 hours after MI, peak at 18-24 hours, and subside over 3-4 days. CKMB levels within  reference range does not exclude myocardial necrosis.
• Troponin I and T are equally sensitive and indicates focal necrosis. No CKMB but raised Trop levels in Angina suggests microinfarctions.
• Myoglobin- negative results are helpful.
• LDH is a late marker.

Other Biochemical Markers- CRP, IL-6,sCD40 ligand, myeloperoxidase, pregnancy-associated plasma protein-A, choline, placental growth factor, cystatin C, fatty acid binding protein etc have been suggested.

Imaging Studies-

• Chest X-Ray- pulmonary edema, aneurysms.
• ECHO- limited value, detects wall motion abnormalities. LVH and Valvular HD may be detected.
• Recent advances include CT coronary angiography and CT coronary artery calcium scoring.
• Technetium-99m (99mTc) tetrofosmin single-photon emission computed tomography (SPECT)

Coronary Angiography Video Animation-

Treatment-

Treatment of ACS with Drug doses.

Normally after 30 minutes to 2 hours of lying in bed for sleep, the patient wakes up with feeling of intense suffocation or chocking sensation. Classically he sits upright gasping in bed with legs hanging by bed or rushes to open the window to get cool air, hoping it will relieve his symptom. Profuse sweating occurs and it may be accompanied by a dry, repetitive cough which is due to ‘ Acute Interstitial edema’.  This may resolve with in 30 minutes  and sometimes may end fatally.

Proposed Mechanisms:-

• There is redistribution of blood volume from the lower extremities and splanchnic beds to the lungs in supine posture. In patients there is a significant reduction in vital capacity and pulmonary compliance with resultant shortness of breath. Additionally, in congestive heart failure the pulmonary circulation may already be overloaded, and there may be reabsorption of edema fluid from previously dependent parts of the body.The failing left ventricle is suddenly unable to match the output of a more normally functioning right ventricle; this results in pulmonary congestion.
• Other theories include decreased responsiveness of the respiratory center in the brain.
• Decreased adrenergic activity in the myocardium during sleep.

Pulmonary congestion decreases when the patient assumes a more erect position, and this is accompanied by an improvement in symptoms.

PND is the earliest symptoms of Acute left heart failure. ‘Cardiac asthma’ is said to be closely related to PND.

Clinical examination at the time of attack of PND:-

a. Severe dyspnea and orthopnea: Tachypnea may be present.

b. Anxious and pale with profuse sweating.

c.Central cyanosis

d. Pulse- tachycardia, feeble

e.Blood pressure may be high.

f. Jugular venous pulse is raised.

g.Heart- S3 gallop rhythm can be heard, signs of underlying heart disease.

h. Lungs- Vesicular breath sound with prolonged expiration, Crepitations – basal , ronchi

References: (Bedside Clinics in Medicine, Ncbi.nlm.nih.gov)

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