CCU

𝙄𝙤𝙧𝙣 𝘿𝙚𝙛𝙞𝙘𝙞𝙩 𝙞𝙣 𝙃𝙚𝙖𝙧𝙩 𝙁𝙖𝙞𝙡𝙪𝙧𝙚
©️Hᴇᴀʀᴛ Fᴀɪʟᴜʀᴇ Cʜᴀʟʟᴇɴɢᴇ

🟩 𝙞.𝙫. 𝙞𝙧𝙤𝙣 supplementation is now recommended
in HFrEF or HFmrEF, and iron deficiency,
👉to Improve Symptoms and Quality of Life🚴‍♀️

🟨 𝙞.𝙫. 𝙞𝙧𝙤𝙣 supplementation should be considered
in HFrEF or HFmrEF, and iron deficiency,
👉to Reduce the risk of HF Hospitalization🏥
——————————————————————————
Intravenous iron supplementation with
𝙛𝙚𝙧𝙧𝙞𝙘 𝙘𝙖𝙧𝙗𝙤𝙭𝙮𝙢𝙖𝙡𝙩𝙤𝙨𝙚 𝙤𝙧 𝙛𝙚𝙧𝙧𝙞𝙘 𝙙𝙚𝙧𝙞𝙨𝙤𝙢𝙖𝙡𝙩𝙤𝙨𝙚

𝙄𝙧𝙤𝙣 𝙙𝙚𝙛𝙞𝙘𝙞𝙚𝙣𝙘𝙮 𝙬𝙖𝙨 𝙙𝙞𝙖𝙜𝙣𝙤𝙨𝙚𝙙 𝙗𝙮 :-
🔻𝙇𝙤𝙬 𝙩𝙧𝙖𝙣𝙨𝙛𝙚𝙧𝙧𝙞𝙣 𝙨𝙖𝙩𝙪𝙧𝙖𝙩𝙞𝙤𝙣 (

𝐌𝐜𝐂𝐨𝐧𝐧𝐞𝐥𝐥'𝐬 𝐒𝐢𝐠𝐧


𝐌ᴄ𝐂ᴏɴɴᴇʟʟ 𝐬ɪɢɴ thought is often used to tell
if a patient with 𝘼𝙘𝙪𝙩𝙚 𝙋𝙀 𝙝𝙖𝙨 𝙍𝙞𝙜𝙝𝙩 𝙃𝙚𝙖𝙧𝙩 𝙎𝙩𝙧𝙖𝙞𝙣
𝙙𝙪𝙚 𝙩𝙤 𝙢𝙖𝙨𝙨𝙞𝙫𝙚 𝙤𝙧 𝙨𝙪𝙗𝙢𝙖𝙨𝙨𝙞𝙫𝙚 𝙋𝙀.

𝐌ᴄ𝐂ᴏɴɴᴇʟʟ 𝐬ɪɢɴ was first mentioned in 𝟏𝟗𝟗𝟔
the sign had 𝟗𝟒% 𝙨𝙥𝙚𝙘𝙞𝙛𝙞𝙘𝙞𝙩𝙮 for Acute PE

𝐌ᴄ𝐂ᴏɴɴᴇʟʟ 𝐬ɪɢɴ defined as :-
One of the most distinct echo findings in patients with acute pulmonary embolism:
• Distinct regional RV dysfunction
• Mid RV free wall - akinetic, bulging
• Normal RV apex - tethered to LV
• LV apex - hyperkinetic
in the setting of RV strain. (aka enlargement).

See this movie 👇
https://coreultrasound.com/5ms-blog-mcconnells-sign/

S𝐮𝐫­𝐠𝐢­𝐜𝐚𝐥 T𝐢𝐦­𝐢𝐧𝐠 F𝐨𝐫 I𝐧­𝐟𝐞𝐜­𝐭𝐢𝐯𝐞 E𝐧­𝐝𝐨­𝐜𝐚𝐫𝐝𝐢­𝐭𝐢𝐬
🌀 2023 ESC GUIDELINE =================================

𝐈𝐧𝐝𝐢𝐜𝐚𝐭𝐢𝐨𝐧𝐬 𝐟𝐨𝐫 𝐒𝐮𝐫𝐠𝐞𝐫𝐲 𝐢𝐧 𝐈𝐧𝐟𝐞𝐜𝐭𝐢𝐯𝐞 𝐄𝐧𝐝𝐨𝐜𝐚𝐫𝐝𝐢𝐭𝐢𝐬
𝐓𝐡𝐞𝐫𝐞 𝐚𝐫𝐞 𝐅𝐨𝐮𝐫 𝐦𝐚𝐢𝐧 𝐫𝐞𝐚­𝐬𝐨𝐧𝐬 𝐭𝐨 𝐮𝐧­𝐝𝐞𝐫­𝐠𝐨 𝐬𝐮𝐫𝐠𝐞𝐫𝐲
𝐢𝐧 𝐭𝐡𝐞 𝐬𝐞𝐭­𝐭𝐢𝐧𝐠 𝐨𝐟 𝐀𝐜𝐮𝐭𝐞 𝐈𝐧𝐟𝐞𝐜𝐭𝐢𝐯𝐞 𝐄𝐧𝐝𝐨𝐜𝐚𝐫𝐝𝐢𝐭𝐢𝐬 𝐈𝐄:

𝐄𝐧𝐮𝐦𝐞𝐫𝐚𝐭𝐞𝐝 𝐢𝐧 𝟒 𝐀𝐥𝐠𝐨𝐫𝐢𝐭𝐡𝐦𝐬 ••••

𝟏️⃣ 𝐇𝐞𝐚𝐫𝐭 𝐅𝐚𝐢𝐥𝐮𝐫𝐞

𝟐️⃣ 𝐏𝐫𝐞­𝐯𝐞𝐧­𝐭𝐢𝐨𝐧 𝐨𝐟 𝐒𝐞𝐩­𝐭𝐢𝐜 𝐄𝐦­𝐛𝐨𝐥𝐢𝐳𝐚­𝐭𝐢𝐨𝐧
(𝐢𝐧 𝐩𝐚𝐫­𝐭𝐢𝐜­𝐮­𝐥𝐚𝐫, 𝐜𝐞𝐫𝐞­𝐛𝐫𝐚𝐥 𝐞𝐦­𝐛𝐨𝐥𝐢)

𝟑️⃣ 𝐔𝐧­𝐜𝐨𝐧­𝐭𝐫𝐨𝐥𝐥𝐞𝐝 𝐈𝐧­𝐟𝐞𝐜­𝐭𝐢𝐨𝐧

𝟒️⃣ 𝐑𝐞𝐬𝐢𝐬𝐭𝐚𝐧𝐭 𝐁𝐚𝐜𝐭𝐞𝐫𝐢𝐚 𝐨𝐫 𝐅𝐮𝐧𝐠𝐢

𝐓𝐢𝐦­𝐢𝐧𝐠 𝐨𝐟 𝐬𝐮𝐫𝐠𝐞𝐫𝐲 𝐜𝐚𝐧 𝐛𝐞
===================
• 𝐄𝐦𝐞𝐫­𝐠𝐞𝐧­𝐜𝐲 (𝐰𝐢𝐭𝐡­𝐢𝐧 𝟐𝟒 𝐡),
• 𝐔𝐫­𝐠𝐞𝐧𝐭 (𝐰𝐢𝐭𝐡­𝐢𝐧 𝟑–𝟓 𝐝𝐚𝐲𝐬) 𝐨𝐫
• 𝐍𝐨𝐧-​𝐮𝐫­𝐠𝐞𝐧𝐭 (𝐰𝐢𝐭𝐡­𝐢𝐧 𝐭𝐡𝐞 𝐬𝐚𝐦𝐞 𝐡𝐨𝐬­𝐩𝐢­𝐭𝐚𝐥­𝐢𝐳𝐚­𝐭𝐢𝐨𝐧).

𝐏𝐫𝐨­𝐩𝐨𝐬𝐞𝐝 S𝐮𝐫­𝐠𝐢­𝐜𝐚𝐥 T𝐢𝐦­𝐢𝐧𝐠
F𝐨𝐫 I𝐧­𝐟𝐞𝐜­𝐭𝐢𝐯𝐞 E𝐧­𝐝𝐨­𝐜𝐚𝐫𝐝𝐢­𝐭𝐢𝐬. 👇
💚class I 💛class IIa. 🧡class IIb

𝐍𝐞𝐮𝐫𝐨𝐥𝐨𝐠𝐢𝐜 𝐂𝐨𝐦𝐩𝐥𝐢𝐜𝐚𝐭𝐢𝐨𝐧𝐬 𝐨𝐟 𝐈𝐧𝐟𝐞𝐜𝐭𝐢𝐯𝐞 𝐄𝐧𝐝𝐨𝐜𝐚𝐫𝐝𝐢𝐭𝐢𝐬.

====================================
Symptomatic neurologic complications of IE are frequent, and asymptomatic cerebral embolism diagnosed by magnetic resonance imaging (MRI) occurs in many more patients.

Neurologic complications increase mortality
and complicate surgical decision-making.

The most common neurologic complication is Stroke due to septic embolism.

Other Complications include :-
~~~~~~~~~~~~~~~~~~~~~
• Micro- and macro-abscesses,
• lnfectious aneurysms, and
• More general toxic-metabolic encephalopathies,
• Cerebrospinal fluid (CSF) pleocytosis, and
• Seizures.

Neurologic complications influence diagnosis, management, and prognosis. MRI should be obtained in all patients with suspected IE and may identify cerebral abnormalities in many IE patients who do not have neurologic symptoms.

MRI sequences should include diffusion weighted imaging (DWI) and gradient echo (GRE) to detect ischemic and hemorrhagic infarction.

The detection of clinically silent ischemic or hemorrhagic brain lesions may affect
performance or timing of surgery,
choice of valve prosthesis, and
antimicrobial or anticoagulant therapeutic planning.

Neurologists should recommend urgent cerebral angiography in the setting of intracranial hemorrhage so that endovascular treatment of mycotic (infectious) aneurysms can be planned.

Patients with large vegetations by echocardiography should be considered for surgery before embolism occurs.

They should be referred to centers with extensive surgical experience in debridement of infected tissue and infectious disease expertise in antibiotic choice.

Additional indications for surgery
To replace the affected valve include :-
~~~~~~~~~~~~~~~~~~~~~~~~~~~
• Heart failure,
• Difficult-to-treat pathogens (such as fungi),
• Elevated LV or atrial pressure due to valvular regurgitation, and
• Perivalvular abscess.

Patients with cerebral embolism due to IE
Should not be Anticoagulated.

Anticoagulation should be stopped
as soon as a diagnosis of IE is suspected,
particularly if S. aureus infection is likely.

Early surgery is recommended for those with transient ischemic attacks and small infarctions. Neurologists can assist the surgical team by providing neurological preoperative clearance for surgical intervention.

Contraindications to early valve replacement include coma, large cerebral infarctions and intracranial hemorrhage.
——————————————
ESC Recommendations for indications and timing
of cardiac surgery after neurological complications
in active infective endocarditis

▪️After a transient ischaemic attack,
cardiac surgery, if indicated,
is recommended without delay.

▪️After a stroke, surgery is recommended
without any delay in the presence of HF ,
uncontrolled infection, abscess, or persistent
high embolic risk, as long as coma is absent
and the presence of cerebral haemorrhage
has been excluded by cranial CT or MRI.

▪️Following intracranial haemorrhage,
delaying cardiac surgery >1 month, if possible,
with frequent reassessment of the patient's
clinical condition and imaging should considered.

▪️In patients with intracranial haemorrhage and
unstable clinical status due to HF uncontrolled
infection or persistent high embolic risk,
urgent or emergency surgery should considered
weighing likelihood of meaningful neurological outcome.
——————————
CT, computed tomography; HF resonance imaging.

Acute Conditions and AF


Lᴀɴᴅɪᴏʟᴏʟ ɪs ᴀɴ ᴜʟᴛʀᴀ⁻sʜᴏʀᴛ⁻ᴀᴄᴛɪɴɢ,
ʜɪɢʜʟʏ \⁽\ʙᴇᴛᴀ ⁻{1}\⁾⁻sᴇʟᴇᴄᴛɪᴠᴇ ɪɴᴛʀᴀᴠᴇɴᴏᴜs
ʙᴇᴛᴀ⁻ʙʟᴏᴄᴋᴇʀ ᴘʀɪᴍᴀʀɪʟʏ ᴜsᴇᴅ ɪɴ
ᴄʀɪᴛɪᴄᴀʟ ᴄᴀʀᴇ ᴀɴᴅ ᴇᴍᴇʀɢᴇɴᴄʏ sᴇᴛᴛɪɴɢs

𝐀𝐜𝐮𝐭𝐞 𝐀𝐭𝐡𝐞𝐫𝐨𝐭𝐡𝐫𝐨𝐦𝐛𝐨𝐭𝐢𝐜 𝐌𝐲𝐨𝐜𝐚𝐫𝐝𝐢𝐚𝐥 𝐈𝐧𝐟𝐚𝐫𝐜𝐭𝐢𝐨𝐧 𝐂𝐚𝐧𝐚𝐝𝐢𝐚𝐧 𝐂𝐚𝐫𝐝𝐢𝐨𝐯𝐚𝐬𝐜𝐮𝐥𝐚𝐫 𝐒𝐨𝐜𝐢𝐞𝐭𝐲; 𝐜𝐥𝐚𝐬𝐬𝐢𝐟𝐢𝐜𝐚𝐭𝐢𝐨𝐧


Clinical application
—————————-
CCS stage 1

Aborted MI: ≥ 50% ST-segment resolution of the initial ST-segment elevation on the presenting ECG at either 90 minutes post fibrinolysis or 30 minutes post PCI in pharmacoinvasive and primary PCI patients, respectively.

In addition, a lack of enzyme biomarker increase of cardiac troponin I/T levels ≤ 5 times the upper limit of normal on at least 2 measurements within 24 hours of reperfusion.

Reperfusion ECGs should show no evidence of significant new Q-wave development. Normal reperfusion flow on angiogram.

No microvascular obstruction on contrast perfusion echocardiogram and CMR

———————————————————————-
CCS stage 1(+)
Apparent aborted MI according to all clinically available diagnostic tests, but complete assessment with all diagnostic methods not performed, therefore worse stage cannot be excluded

———————————————————————-
CCS stage 2
"Classic" MI. Infarction progressed with significant cardiomyocyte necrosis, exceeding criteria for aborted MI. No evidence for no-reflow on angiogram, no microvascular obstruction on contrast echocardiography or CMR

———————————————————————-
CCS stage 2(+)
Apparent stage 2 MI according to all clinically available diagnostic tests, but complete assessment for reperfusion injury was not performed and thus injury more severe than stage 2 cannot be excluded

———————————————————————-
CCS stage 3
MI with microvascular obstruction ascertained according to no-reflow on angiogram or perfusion deficit on contrast perfusion echocardiogram or microvascular obstruction on CMR. No hemorrhage detected on CMR

———————————————————————-
CCS stage 3(+)
Apparent stage 3 MI according to all clinically available diagnostic tests, but hemorrhagic infarction cannot be excluded (CMR assessment for hemorrhage nondiagnostic or not performed)

———————————————————————-
CCS stage 4
Hemorrhagic MI, ascertained according to CMR (presently there are no other diagnostic tests for hemorrhagic MI
———————————————————————-
"MC"to be added for presence of mechanical complication (ventricular septal defect, free wall rupture, papillary muscle rupture)

𝙍𝙚𝙥𝙚𝙧𝙛𝙪𝙨𝙚𝙙 𝙈𝙮𝙤𝙘𝙖𝙧𝙙𝙞𝙖𝙡 𝙄𝙣𝙛𝙖𝙧𝙘𝙩𝙞𝙤𝙣 𝙎𝙩𝙖𝙜𝙞𝙣𝙜

Each stage is characterized by a specific type
of tissue injury that defines the stage;
with each progressive stage, a new characteristic,
stage-defining injury is added. The 4 stages are:

Sᴛᴀɢᴇ 1﹕ Aʙᴏʀᴛᴇᴅ MI, ᴄʜᴀʀᴀᴄᴛᴇʀɪᴢᴇᴅ ʙʏ ᴍʏᴏᴄᴀʀᴅɪᴀʟ ᴇᴅᴇᴍᴀ.

Sᴛᴀɢᴇ 2﹕ Cᴀʀᴅɪᴏᴍʏᴏᴄʏᴛᴇ ɴᴇᴄʀᴏsɪs, ᴀʙsᴇɴᴄᴇ ᴏꜰ ᴍɪᴄʀᴏᴠᴀsᴄᴜʟᴀʀ ɪɴᴊᴜʀʏ.

Sᴛᴀɢᴇ 3﹕ Cᴀʀᴅɪᴏᴍʏᴏᴄʏᴛᴇ ɴᴇᴄʀᴏsɪs ᴘʟᴜs MVO.Mɪᴄʀᴏ ᴠᴀsᴄᴜʟᴀʀ Oʙsᴛʀᴜᴄᴛɪᴏɴ

Sᴛᴀɢᴇ 4﹕ Cᴀʀᴅɪᴏᴍʏᴏᴄʏᴛᴇ ɴᴇᴄʀᴏsɪs, MVO,
ᴀɴᴅ IMH ⁽"ʜᴇᴍᴏʀʀʜᴀɢɪᴄ MI"⁾

𝙃𝙄𝙂𝙃𝙇𝙄𝙂𝙃𝙏𝙎

▫️Not all reperfused MIs are the same.

▫️Severity of myocardial injury from reperfused
MIs can staged as per recent CCS classification.

▫️Therapies/interventions to overcome post-MI
complications need to address CCS stages
of tissue injury.

▫️With each progressive CCS Stage,
ischemia/reperfusion injury becomes more
severe: there is progressive loss of salvageable
myocardium and IS is larger with each stage.

▫️Hemorrhagic MI leads to infarct expansion
post reperfusion, and adds a new type of injury
induced by reperfusion therapy, leading to
chronic iron-mediated inflammatory

▫️The stages build on each other, reflecting
progression of severity of tissue injury.

▫️Timely reperfusion can halt tissue injury at
an earlier stage and prevent progression to
a more severe stage of injury.

▫️Hemorrhagic infarction is the worst stage and
a cause of infarct expansion and risk factor
for mechanical complications.

▫️Wall motion abnormalities and ECG changes
also depend on size of the affected myocardium.

Adapted from Kumar et al.'

𝐏𝐫𝐞𝐥𝐨𝐚𝐝 vs 𝐀𝐟𝐭𝐞𝐫𝐋𝐨𝐚𝐝
𝐂𝐚𝐫𝐝𝐢𝐚𝐜 𝐏𝐞𝐫𝐟𝐨𝐫𝐦𝐚𝐧𝐜𝐞

𝐄𝐂𝐆 𝐃𝐢𝐥𝐞𝐦𝐦𝐚𝐬

𝐋𝐞𝐟𝐭 𝐌𝐚𝐢𝐧 𝐂𝐨𝐫𝐨𝐧𝐚𝐫𝐲 𝐀𝐫𝐭𝐞𝐫𝐲 𝐎𝐜𝐜𝐥𝐮𝐬𝐢𝐨𝐧


𝙀𝘾𝙂 𝙛𝙚𝙖𝙩𝙪𝙧𝙚𝙨

▫️Widespread horizontal ST depression,
most prominent in leads I, II and V4-6
▫️ST elevation in aVR ≥ 1mm
▫️ST elevation in aVR ≥ V1

𝙎𝙏 𝙚𝙡𝙚𝙫𝙖𝙩𝙞𝙤𝙣 𝙞𝙣 𝙖𝙑𝙍 𝙣𝙤𝙩 𝙨𝙥𝙚𝙘𝙞𝙛𝙞𝙘 𝙛𝙤𝙧 𝙇𝙈𝘾𝘼 𝙤𝙘𝙘𝙡𝙪𝙨𝙞𝙤𝙣
and may indicate other conditions such as:

▫️Proximal left anterior descending occlusion
▫️Severe triple-vessel disease
▫️Diffuse subendocardial ischemia

🌊 𝙈𝙚𝙘𝙝𝙖𝙣𝙞𝙨𝙢 𝙤𝙛 𝙎𝙏 𝙚𝙡𝙚𝙫𝙖𝙩𝙞𝙤𝙣 𝙖𝙑𝙍 𝙞𝙨 𝙢𝙪𝙡𝙩𝙞𝙛𝙖𝙘𝙩𝙤𝙧𝙞𝙖𝙡:

• Reciprocal to ST depression in I,II, aVL and V4-V6

• aVR directly records electrical activity from
the right upper portion of the heart (the right
ventricular outflow tract and the basal portion
of the interventricular septum)

• Diffuse subendocardial ischemia with ST
depression in lateral leads produces reciprocal
change in aVR and infarction of the basal septum

The absence of STE in aVR almost entirely
excludes a significant LMCA lesion.

Sinus tachycardia is an often presentation
of LMCA occlusion, as patients do usually develop cardiogenic shock.