Tuesday, May 25, 2021

Heart Failure(HF)

1. intro

2. pathophysio

3. Signs and Symptoms

4. Classifications: NYHA

5. Investigations

6. Management

HF is a structural or physiological abnormality of the heart resulting in its inability to meet the metabolic demands of the body or its ability to do so only at higher than normal filling pressure

Population:

EF <40% HFrEF

EF>50% HRpEF

EF: 40-50: HFmrEF

Pathophysio

Acute heart failure Signs and Symtoms

4 types of symptoms to show which type of HF belongs to.

warm and wet: adequate perfusion but congested (lungs/peripheral) - volume overload
cold and dry - hypoperfuse, dehydrated - pump failure
cold and wet - hypoperfuse and congested
ward and dry - adequate perfusion and dehydrated - mild HF/ compensated stage of HF

what is reperfusion? The restoration of blood back into tissue

- Elevated jugular venous pressure

is a manifestation of abnormal right heart dynamics, mostly commonly reflecting elevated pulmonary capillary wedge pressure from left heart failure. This usually implies fluid overload, indicating the need for diuresis.

Left and Right sided heart failure differences:

NYHA:

I- no limitation ,

II: slight limitation, comfortable at rest, activity causes fatigue

III: dmarked limitation: less than ordinary activity causes sx

IV: unable to carry out physical activity without discomfort.

Imvestigations (Ix):

- access HR, rhythm,
QRS morphology /durarion/voltage,
evidence of ischemia, LVhypertrophy/ arrthymia

chest radiography:

pulmonary congestion, cardiomegaly , or other lung pathology

Echo

to determine type of HF
- assess LV chamber size, thicknesss
- diastolic fx
myocardial ischemia test: treadmill exercise, stress echocardio,

invasive:

coronary angiography

others: holter, pulmonary function test

Blood Ix:

FBC
RP
LFT
CBS
FLP
HbA1c
Natiuretic Peptides/BNP:

peptide hormones synthesized by the heart, brain and other organs. to reduce arterial pressure by decreasing blood volume and systemic vascular resistance

- the higher the number= heart could not pump the way it should
- release when cardiac myocytes are strained
- useful to rule out acute dypsnea
- NP can increase also when pt have AF/ CRF/ age/ obese/ ARNI
- significant if >400, age >50: >450, age 50-75 :>900, age>75: >1800

inflammation of muscle, indicates level of damage or disease of skeletal muscle

TFT
infective screening
iron study,

- to check Tsat: Fe/TIBC x100, if <20% : inadequate iron supply

urine test: UFEME/ C+S
blood gas:

- hypoxemia: paO2<60
- hypercapnia: PaCO2>50
- Acidosis: pH<7.35

Management(Mx):

Acute HF:

stabilise hemodynamics
maintain o2 and perfusion of organs
relieve symptoms and signs
treat u/l cause or aggravating factors

Treatments:

1. non pharma, pharma

Diuretics
ACEI
ARB
Beta blockers
MRA
Statins

2. Surgery
3. Device therapy
- catheter ablation/pacemaker therapy

Common drugs used:

dopamine: improve renal perfusion and promote diuresis / increase BP
dobutamine: peripheral hypoperfusion n pulmonary congestion
Ivabradine: slows the heart rate to allow more perfusion to the heart
thiazides: hydrochlorothiazides: promote natiuresis and diuresis

ROF : 1-1.5L/day

To watch out for

- worsen symptoms, readmission rate

- increase in cardiovascular event rate

- increase in bleeding risk and stroke rate

- adverse effects due to pharmacotherapy

References:

1. Malaysia CPG for HF

Sunday, May 2, 2021

Pulmonary embolism (PE)

it is not complete but do include key points that we need to know to work in ward.

pathophysio:

it results from DVT - venous thromboembolism
venous stasis, endothelial injury and hypercoagulability.

bridging:

egfr>30: s/c clexane BD
egFR 15-30 - s/c clexane OD
eGFR <15 - IVI heparin (kena monitor coag 6 hourly)

Warfarin affects the APTT & PT value
Clexane - APTT (to help INR reaches the aim faster)

Aim INR 2-3, once INR >2, off clexane, bridging complete

1st to 3rd days for warfarin just trial with dose 5mg/5mg/3mg,

4th day start adjusting dose base on INR

- pharmacist has special counsellor or booklet for the patient to understand the use of warfarin. with constant follow up and also diet suggestions (no green leafy veges)

BOOKLET LINK: for BM, Eng, Chinese

Investigations(Ix):

1. ECG :

look for ST changes S1Q3T3

- deep S wave in lead I, Q wave in lead 3, T inversion in lead 3

- ST depression, RBBB

- P. pulmonale

2. blood Ix: trop t and ck stat

3. basic supportive tx: HFM, transfer to acute bed

request for :

- CXR : hamptoms hump: wedgemark sign, westermark sign: pulmonary oligaemia in the affected segment

- CTPA : thrombi within pulmonary

https://epos.myesr.org/poster/esr/ecr2020/C-04154

- V/Q scan:

for those who have clot in the past, and have a previous episode before, or those who has acute kidney damage/ckd.
clear cxr

- ultrasound for lower limb: to rule out lower limb DVT due to long sitting/surgery...

- start DAPT

4. echo:

- look for RV dilation and hypokinesia. - acute rv failure--> increase afterload, rv cannot unload sufficiently causing rv dilated. impinge on LV cause LV to decrease output and supply to CA
- it increases o2 demand which CA could not meet, results in ischemia and necrosis

MASSIVE PE:

HYPOTENSION BP<50 for at least >15MINUTES, HR <40 - usually with evidence of MI and hyocardial dysfunction

Well's score for PE

low<2, mid 2-6, high >6
1. clinical signs of DVT -3
2. previous surgery / long traveeling>4hrs -1.5
3. previous DVT and PE- 1.5
4. HR>100 - 1.5
5. other diagnosis seem less likely -3
6.hemoptysis -1
7. cancer -1

Management (Mx):

anticoagulant

- without hypotension: LWMH, fonda/ DOACS
- unstable/ bleeding: parental anticoag 5-10d, switch to warfarin overlap 3-7d before discontinue heparin when INR >2 for >2d
- continue anticoag for 3-6months

thrombolytic therapy:

STK 25mu if pt high risk massive PE/ with cardiopulmonary arrest.

other mx:

1. rivaroxaban 15mg BD for 21d then 20mg OD
2. dabigatran (expensive)

Reference:

1. anticoagulant protocol malaysia

Med4yu

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