Solution: pain on effort/stress? → stable;

Extra Information / Pictures:

Solution: left shoulder, arms, abdomen, neck

Extra Information / Pictures:

Solution: 1. Pericardial pathology 2. Aorta dissection 3. Pulmonary embolism 4. pneumonia, pleuritis 5. MI 6. Gastric, pancreatic, cholecystic, esophageal origin 7. Rheumatic pain (elderly)

Extra Information / Pictures:

⇒ PATHOLOGIES OF FOLLOWING ORIGIN:

cardiac, pulmo + upper gastro

Solution: sharp pain, superficial, ↑with motion/breathing, friction rub

Solution: uninfluenced by position, breathing, medication

Solution: usually ↓ pain more dominated by dyspnea + hypotension

Solution: - Lab - EKG rest - Stress EKG - Holter EKG - in really unsure cases: angiography or angioCT - Echography

DDx ⇒ Pericarditis, pulmonary embolism, aorta dissection

Solution: 1. Heart failure 2. Respiratory origin 3. Effort dyspnea (anemia/fat)

Solution: edema + hypotension

Solution: 1. Echo → systolic + diastolic performance & structural disorders(valve, pericardial, congential, dilation, dyskinesia) 2. EKG 3. Chest Xray → cardiomegaly 4. Stress testing → NYHA classification for effort dyspnea 5. Lab → BNP

Solution: false, there are a lot of other reasons

Extra Information / Pictures:

“Palpitations are differently perceived by patients, they being able to describe rapid heartbeats or heart rhythm irregularities. Irregularities are perceived like sudden pauses in cardiac activity, eventually followed by a strong precordial beat or at the level of throat vessels, usually due to increased preload and contractility following atrial or ventricular extrasystole with increased systolic output. Palpitations may appear without rhythm disorders, within the above mentioned hyperkinetic syndromes but also in case of precordial muscular fasciculation that may result in palpitations (especially in patients with necrosis or hypocalcemia) so suggestive for rhythm disorders. Of course, pulse palpation or auscultation quickly make diagnosis.”

Solution: 1. Lab 2. EKG (rest) + Holter EKG 3. Echo → Underlying cardiac disease for arrhythmias

Extra Information / Pictures:

Certain circumstances → endocavity electromstimulation may trigger arrhythmias

1. Edema
2. Skin color (cyanosis?)
3. Veins (jugular, collaterals, varicosis)
4. Pulse palpation (heart rhythm, irregular/high/low...)

check cardiac impuse → in hemodynamic overload + HF it is displaced

2,5-5h/week moderate exercise OR 30-60min most days

Check out risk factors, PH + FH of CV diseases

• Family history (gene mutations) + PH
• Hypertension + CV diseases
• Dylipidemia
• DM
• Lifestyle
• smoking
• diet
• obesity
• sleep apnea

1. 🧠brain → headache, blurred vision, TIA, motor/sensory defects
2. ❤️heart → palpitation, angina, dyspnea, ankle edema
3. 🥐kidney → thirst, polyuria, nocturia, hematuria
4. 🔴 arteries → cold extr., intermittent claudication

1. Brain → murmurs carotid, motor+sensory defect
2. Retina → fundoscopy abnormalities
3. Heart → apical impulse, arrhythmia, ventricular gallop, crackles (rales) , periph. edema
4. Periph. arteries → ↓pulses, cold extremities, ischmemic skin lesion
5. obesity

→ identify RF, exclude secondary HT + identify end-organ damage

Routine

• Gluc (RF)
• Lipid profile (RF)
• crea + GFR (renal functin
• Uric acid (renal function)
• K+ (renal function)
• Urinanalysis (renal function)
• Hb + Hct (bleeding)

• signs of LVH 📷 + LAD 📷
• might also show signs of ischemia + arrhythmias

• Echocardiogram 📷
• Carotid ultrasound
• Quantitative proteinuria (if dipstick test is positive)
• Ankle-brachial blood pressure index
• Fundoscopy
• Glucose tolerance test (if fasting plasma glucose > 5.6 mmol/L (100 mg/dL))
• Home and 24h ambulatory blood pressure measuring (Fig.3)
• Pulse wave velocity measurement (if available)

“

Diagnosis of Heart Failure with Reduced Ejection Fraction (HF-REF) requires three conditions to be satisfied:

1. Symptoms typical of heart failure
2. Signs typical of heart failure
3. Reduced left ventricular (LV) ejection fraction

Diagnosis of Heart Failure with Preserved Ejection Fraction (HF-PEF) requires four conditions to be satisfied:

1. Symptoms typical of heart failure
2. Signs typical of heart failure
3. Normal or only mildly reduced LV ejection fraction with LV not dilated
4. Relevant structural heart disease (LV hypertrophy/left atrial enlargement) and/or diastolic dysfunction”

• Øsmoking
• physical activity (20-30min walking 3-5x week; 20min cycling at 70-80% peak HR 5x/week)
• Diet

🥇

1. ACEi/ARB (Ramipril/Valsartan) + ARNI
2. Beta-blockers (Metoprolol, carvedilo, bisoprolol, Nebivolol)
3. Diuretics

🥈

1. Spironolactone

🥉

1. Digoxin
2. Ivabradine (SA node inhibitor)

LVEF <35%→ ICD 📷

‣

💬

LVEF <35% + LBBB (QRS>120ms)→ CRT (aka biventricular pacing) 📷

1. Bridge to transplantation
2. Patient not considered for transplantation (alternative)
‣
Contraindication LVAD?
→ 📷
1. End organ failure (irreversible) → renal+liver
2. mechanical valves
3. severe aortic regurgitation
4. metastasis
5. coagulation + bleeding disorder

• mitral valve repair
• triscupid anuloplasty

• heart transplant → esp. if VO2 is <10ml.kg/min

‣

💬

1. Stage A: High risk + no symptoms:
1. Risk factors
2. Treat hypertension, diabetes, dyslipidemia (pharmacological
2. Stage B: structural heart D + no symptoms:
1. ACEi / ARBs
3. Stage C: structural heart D + previous/current symptoms
1. ACEi/ARB
2. BB
3. Diuretics
4. Spironolactone
5. Ivabradine (↓SA node)
6. Cardiac resynchronization if LBBB
4. Stage D: Refractory symptoms
1. Inotropes (i.e. Digoxin, Dobutamine, Milrinone)
‣
💬

💡
Inotropes = assoc. with ↑ mortality
1. LVAD
2. transplantation

• sympathetic overstimulation
• HF
• endocrine disorder (thyroid)
• resp. failure

• palpitation
• HR > 100

With very fast heart rates the P waves may be hidden in the preceding T wave, producing a 'camel hump' appearance. 📷

• sinus rhythm normal p-wave

Artrial flutter (2:1)

PSVT (no p-waves)

non-sinus stimulus

asymptomatic OR

brief early aprupt heartbeat - pause - followed by a stronger beat

usually no pathological significance (if no afib)

• anxious → BB + sedatives
• >20% extrasystoles on 24h holter → class Ic (Flecainide, Propafenon) or ablation (pulm. veins)

rapid atrial non-sinusoidal acitvation

rate 150-250/min (>150)

Palpitations (suddenly begin + stop and can last sec-hours)

if >200:

chest pain (ischemia due to high demand)

acute HF → syncope (low output syndrome due to ↑HR)

1. Re-entry AV-node: dual slow or fast pathyway (aka AVNRT)

2. accessory pathways (orthodromic vs. antidromic)
3. pathologic foci in the atrium

‣

💬

• No p-waves (overlapped by QRS or T)
• Narrow 150-200/minute QRS tachycardia

→ 📷

preexitation (foci) 📷

but other can be as well → do electrophysiology

some ventricular transmission blocked (usually every second) → atrial tachycardia with block

→ 📷

retrograde p 📷

‣

💬

#1 Vagal + Adenosine

stable → Rate (BB, Verapamil) or Rhythm control (Amiodaron, IC: Propafenone, Flecainide)

unstable → shock

⇒ Ablation for definite prophylaxis

📷

vagal m. = carotid massage, blowing in a syringe in laying position when patient is blowing with high pressure → elevate legs, eye pressure, induce vomiting

Do that when PSVT is frequent → within less than 3 month

Step 1: AV node blockers (BB or non-dihydropyridines CCB (Verapamil, Diltiazem)

Step 2: Class IC (Propafenone, Flecainide) or Class III (Sotalol)

Step 3: Amiodaron

Step 4: Ablation

rapid non-sinus activation 200-350 BPM

due to macro-reentry betw. tricuspid + vena cava (classic: counterclockwise; can also be clockwise)

due to ↑intra-atrial pressure, ischemia or inflammation

• right heart damage
• HF + ↑BP
• pulmonary diseases
• heart surgery (scars circuit not normal curcuit)
• sick sinus syndrom (tachy-brady)
• thyrotox
• etc.

• rapid rate palpitation
• refractory to valsalva (+ adenosin )
• symptoms depending on underlying heart diseases (i.e. HF, thromboemolic)

• 2:1 (or 3:1, 4:1) transmission of p-waves
• if 1:1 transmission → Vfib → sudden cardiac death
• F-waves 250-300/min + high amplitude + wide base
• negative in inferior leads + pos. in V1 in counterclockwise
• reverse in clockwise
• if counterclockwise: saw-tooth
• QRS narrow regular (or irregular); rate = 100-150

Treatment: Acute:

• For unstable patients with hypotension, congestive heart failure, or angina, electrical cardioversion is recommended.
• For stable patients, chemical cardioversion (e.g., amiodarone) should be considered along with rate control (e.g., beta-blockers).
• In both cases, anticoagulation is necessary, similar to atrial fibrillation.

Long-term:

• Antiarrhythmic medications are commonly used.
• Radiofrequency ablation via catheter, especially targeting the cavotricuspid isthmus, may be performed. 📷

• RATE CONTROL = BB, NDHP-CCB, Digoxin
• RHYTHM CONTROL

= Amiodarone, Class Ic, Ibu+dofetilide OR

electrical cardioversion (if unstable) OR

Long term = ablation

• Anticoagulation (if >48h after onset, BEFORE cardioversion) → for 3 weeks
• TEE (Transesophageal Echocardiography)

⇒ same as afib

directly ablation

non-sinus rapid chaotic activation of atria

BPM 350-600

ATRIAL FIBROSIS due to

• ↑intra-atrial p
• inflammation
• ischemia
• valvular diseas, congenital diseases, aterial hypertension, cardiomyopathies, congestive heart failure , after heart surgery

paroxysmal not longer than 7 days

persistent in first 3-12 month

permanent >12 month

microcircuit around pulmonary vein

→ no proper atrial contraction due to too rapid stimulation → ↓output by 25-30%

High heart rate 120-180 BPM

→ most of f-waves are blocked by Av-node

thromboembolic

• paroxysmal → sudden palpitations onset with variable duration
• persistent + permanent → reduced palpitation but increase with effort
• fatigue + ↓effort capacity , dizziness
• dyspnea
• LVF + acute pulmonary edema
• decompensation of pre-existing HF

• F-waves >350-600/min (esp in D2+V1)
• QRS narrow + freq: 120-180 BPM
• if >200 → pre-excitation is cause for afib (aka accessory pathyway)

💡

<120 = flutter ; >150 AVNRT or fib; >180 AVNRT; >200 preexcitation

‣

💬

Echo or TEE → thromboembolic risk

1. Unstable → Shock
2. Stable
1. Rate control (AV blocking agents=BB, CCB, Digoxin) or Amiodarone

↓(if conversion to sinus)

2. Rhythm control (Class I, III or electrical shock (to overdrive stimulation))
‣
💬

3. ablation

STEP 1: RATE CONTROL (BB, CCB, Digox)

STEP 2: Ablation (compare: can be #1 for aflutter)

+ anticoagulation

Aflutter prevention → rhythm control (Class IC or III) or directly ablation +- BB +- Anticoagulant

choice depends on STRUCTURAL heart disease:

if no structural ⇒ Class IC preferred

if structural → Class III

Alternative for both: Ablation

• TEE (for direct cardiversion)
• If >48h → oral anticoagulants for 3-4 weeks then conversion

aka ventricles cant handle without atrial contraction

⇒ AV-node ablation + PACE MAKER

regular 200-250 BPM

→ quickly evolves towards Vfib!!!

Flutter → wide + high amplitude, regular 200-250BPM 📷

Fib → irregular chaotic osscillation 250-300 BPM 📷

CPR

T

1. idiopathic fibrosis of conduction system
2. IHD

within AV (and above His) → suprahisian/intranodal

within His (and below AV) → infranodal

intranodal

I° → all p transmitted, PR>200ms (22 in eledery)

II°

• intermittently ommited
• Mobitz I → PR intervals get progressively longer → suddenly one p wave not followed by QRS
• Mobitz II → PR-waves stays the same suddenly no QRS after one p
• 2:1 → only every second p followed by QRS
• advanced → ≥2 p-waves are not transmitted

III° → complete dissociation (R-R distance + P-P distance is REGULAR)

• I + IInd degree with intermittently blocked → asymptomatic
• II° 2:1, advanced II° + III° → regular/irregular rhythm (palpitation)
• Auscultation → ↓HR <40-50
• Systolic BP ↑ (compensatory vasoconstriction)
• LVF
• ↓Output: ↓effort capacity + effort syncope
• Congestion: worsening of underlying heart failure

Mobitz 1 → intranodal

Mobitz 2→ infranodal

2:1 → intranodal (QRS narrow); infranodal (QRS wide)

→ low junctional rhythm(from AV node 40/min) or ventricular escape rhythm (below AV node 10-30/min)

• I° + II° Mobitz I → no therapy
• II° Mobitz II risk for complete heart block → temporary or permanent pacing
• II° 2:1 → temporary or permanent pacing / atropine if intranodal (narrow QRS)
• III° → permanent pacing (except congenital heart block→adapted)

⇒ or drugs if you cant do pacing or for bridging (Adrenaline, Noradrenaline, Dopamine; atropin when intranodal)

single or dual

single → RV or RA

dual → RV + RA

depression/absensce of pulse formation from sinus sode

→ might also exist with AV-block (bi-nodal)

→ sometimes cause SVT

→ See av block

#1 idiopathic degeneration or ischemic heart diseases

#other (inflamm, drugs, cardiomyopathy)

sinus node dysfunction = excessive vagal tonus

1. ↓effort capacity + effort syncope
2. → might lead to asystole + sudden death
3. → bradycardia-tachycardia syndrome → SVT alternating with bradycardia → cardiac + periph ischemia + acute heart failure
4. Pulse <40-50 irregular or regular
5. ↑Systolic BP (compensatory)

1. Sinus bradycardia: 📷
1. <50 BPM; <40 = suggestive for SSS
2. Sinus Pauses. 📷
3. Atrial fib + low ventricular rate (in case of simultaneous AV node imparment - binodal impairment) 📷

4. Permanent sinus arrest - junctional/ventricular escape rhythm 📷

‣

💬

5. Bradycardia-tachycardia syndrome 📷→ alternating bradycardia with episodes of atrial tachycardia/SVT → Permanent cardiac pacing necessary

stress or atropine test → DDx SSS vs node dysfunction due to ↑vagus tone

→ if SSS HR will not exceed 90 BPM under stress + atropine

• HR >40 + asymptomatic → follow up
• If pauses >3s + symptomatic bradycardia/syncope → permanent pacemaking
• symptomatic → emergency drugs / pacemaking
• Drugs or shock for tachycardic episodes
• or ablation/electrophysiology
• drugs: Atropine, Adrenaline, Noradrenaline, Dopamine

sick sinus

AV block

1. Cardiovascular diseases: myocardial infarction, acute myocarditis, constrictive pericarditis, valvulopathies.
2. Endocrine diseases: thyroid insufficiency, suprarenal insufficiency.
3. Neurological disorders.
4. Infections.
5. Toxic agents.

Coronary ischemia causes abnormalities in electrical activity (electrocardiographic ischemic abnormalities; rhythm disorders), heart function (systolic or diastolic dysfunction), and chest pain. These manifestations are associated with coronary artery disease and have clinical implications.

Coronary ischemia can result in various electrocardiographic changes indicating myocardial ischemia. These changes may include ST-segment depression or elevation, T-wave inversion, or pathological Q waves. These findings help diagnose myocardial infarction and guide management.

Systolic or diastolic dysfunction can occur due to coronary ischemia. Systolic dysfunction impairs heart muscle contraction, reducing stroke volume and cardiac output. Diastolic dysfunction involves impaired ventricular relaxation or increased stiffness, affecting filling and ventricular compliance.

Chest pain, known as angina, is a common symptom of coronary ischemia. It is described as a pressure-like or squeezing sensation in the chest that may radiate to the left shoulder, arms, abdomen, or neck. Prompt recognition and management of chest pain are crucial for preventing complications and ensuring optimal outcomes.

70%

at what point angina occurs during stress test

• only during exercise or emotional stress
• Ø during rest
• 1-10min (depending on when exercise stopped) → alleviated at rest
• alleviated by sublingual Nitroglycerin
• radiation (neck)
• Levine sign 📷

sinus tachycardia

T → except. sinus tachycardia

• Class 1: ordinary physical activity → angina during exertion (strenuous, sudden or prolonged)
• Class 2: slight limitation ordinary activity. Angina during fast walking or climbing stairs. After large meals, cold, emotional stress
• Class 3: marked limitation. angina walking a normal pace
• Class 4: Invalidating angina, unable to perform any activity without discomfort. Angina may be at rest → transition to unstable angina

inverted t-wave

but 50% → normal ekg

ST-depression 📷→ for pos. dg: ≥1mm

+/- Inverted T-waves

1. Coronary Angiography:
• exclude → CT coronary angiography (in atypical symptoms + low probability)
• coronary angiograph → diagnostic + severity assessment
2. echo → contractility abnormalities during ischemic periods
3. prove → scintigraphy (myocardial)

STEMI → overlapping trombus on unstable plaque → occlusion → myocardial necrosis

NSTEMI → overlapping trombus on unstable plaque → Ø complete occlusion → Ønecrosis or minor subendocardial necrosis

T

• Thrombus
‣

💬

Intraluminal thrombus is formed on the atheroscleroto plaque wich can be ruptured cracked eroder or discecred

• O2 demand/supply mismatch
‣

💬

Embolism or coronary spasm, potension, arrhythmias with haemodynaric instability, severe anemia

• MI death W/o Necrosis enzymes
‣

💬

Death occurred before necrosis enzymes were reacted or dosed, but there were signs.

• Iatrogenic MI
‣

💬

Type 4a: Myocardial infarction caused by percutaneous coronary intervention (PCI) Significant increase in necrosis enzymes is 3-20 times if already elevated, accompanied by symptoms of ischemia, additional ECG alterations, new imaging of myocardial kinetics disorders, or angiographic detection of a complication related to PCI.

Type 4b: Myocardial infarction caused by stent thrombosis.

Type 5: Myocardial infarction caused by coronary artery bypass graft (CABG) surgery. Significant increase in necrosis enzymes 10 times, accompanied by additional ECG alterations.

1. severe angina
1. at rest
2. >1h
3. Ø influenced by nitro
4. radiation
5. painless is diabetic elderly
2. diastolic + systolic HF
1. might be asymptomatic
2. dyspnea
3. pulmonary edema
4. cardiogenic shock
3. palpitation → sinus tachycardia, premature beats, SVT
4. Autonomic symptoms: Sweating, agitation, palor, cold

I → Absence: ØCrackles ØS3

II → Mild: Crackles lower half only, S3

III → Moderate (pulmonary edema): Crackles upper chest

IV → Severe: Cardiogenic shock

• Reperfusion therapy → 🥇PCI or fibrinolysis(when PCI Ø available <2h)
‣
💬

• Drugs ⇒ MONAAS BH

• General measures: Nitrates, analgesics, O2, morphine

→ RV-infarction → fluid + Ønitro
‣
💬

1. Dual platelet: Ass + Tica
2. Heparin/Enoxaparin
3. Adjuvant:
• Statins,
• BB (if ØHF),
• ACEi

⇒ 📷

<40%

venodilation → ↓preload → ↓O2 demand

1. Arrhythmias:
‣

what types of arrhythmia might occur?

1. Ventricular arrhythmias
1. Premature ventricular beats
2. Ventricular tachycardia
3. Ventricular fibrillation
‣

How do you treat premature ventricular beats usually? Exceptions?

no treatment mandatory → just monitor

→ except: R-on-T phenomenon or non-sustained VT → lidocaine/amiodarone

‣

How do you treat a unstable patient with ventricular tachycardia?how to you continue when sinus rhythm is restored?

electrical cardioversion

(if cannot be applied or bridging: lidocaine/amiodarone)

→ after sinus rhythm restored → continue with BB+amiodarone

‣

How do you treat Vfib?

defibrillation

2. SVT
‣

When do you need to treat?

if HR > 100BPM

‣

How do you treat?

BB

‣

How do you treat hemodynamically instable PSVT?

if hemodynamically instable →electrical cardioversion

‣

Afib + Aflutter treatment?

BB (+/- amiodaron) if stable

unstable → shock

3. Brady arrhthymias (Sinus bradycardia + AV-block)
‣

How do you treat SSS?

atropin + tempary pacing

‣

How do you treat AV block?

suprahisian → Atropin

infrahisian → pacing

4. LBBB
‣

T/F LBBB often mask ECG aspect of myocardial necrosis

T

→ new onset LBB + chest pain = considered STEMI

2. LVF + pulmonary edema
‣
Treatment of pulm. edema + LVF?
1. Revascularization
2. furosemide
3. Nitrates
4. standard measures → oxygen, morphine, mechanical ventilation
5. ↓ afterload (or ↑afterload if Cardiogenic shock (Killip IV))
1. ACEi
2. NE or dobutamin if BP<90
‣

Cardiogenic shock occurs when more the ...% of LV mass is affected

30%

‣
Treatment cardiogenic shock?
1. (Revascularization)
2. NE, dobutamin, dopamin
3. Volemic support
4. Intra aortic balloon pump
5. ECMO (extracorporal membrane oxygenation)
6. (LVAD)
3. Free wall rupture
‣

Might lead to what complication?

hemopericardium + percardial tamponade

4. Mitral regurgitation (papillary muscle rupture)
5. Interventricular septum perforation
‣

Treatment ISP?

▶️

🥇 ↓ preload + inotropes or 🥈 surgery

1. Morphine + mechanical suppoirt
2. diuretics
3. Nitro
4. inotropic durgs

→ emergency surgery if hemodynamic stabilization is not obtained with drugs!

6. Pericarditis
‣
How do detect pericarditis?
• relapsing chest pain (mimic re-infarct)
• friction rub
• echocardiography
‣

Treatment?

only analgesics + anti-inflammatory drug when pain severe

7. LV true aneurysm
‣

Usually located at ...

the apex

‣

Consequence on LV?

intraventricular "regurgitation" → ↓output → LVF

→ might also lead to Vtach + Vfib

‣
Treatment?
The 4 A’s
‣
💬

• ACEi
• anticoagulation
• aneurysmectomy (in selected cases)
8. LV thrombosis*
‣

Treatment?

oral anticoagulation 2-3month

9. LV pseudoaneurysm
‣

How do you dg?

Echo → communication aneurysm + pericardium

(pseudoaneurysm = left ventricular free wall ruptured contained by adjacent pericardium)

10. Extension of ac. MI*
‣

How do you dg + treat

ECG + enzymes (Esp. CK-MB)→ identical treatment to first time

11. Post-infarction angina*

• lifestyle (classic like angina)
• physical rehabilitation (↑exercise capacity)
• drugs
• Dual antiplatelet (at least 1y)
• “adjuvants of acute MI “
• High dose statins
• ACEi
• BB

unstable angina

non-Q MI

unstable angina → pain at rest but Ø↑enzymes (=Ø necrosis)

NSTEMI → ↑enzymes

T

→ NSTEMI with necrosis

→ unstable w/o necrosis

1. Unstable angina out of progressively worsening stable angina (longer duration)
2. de-novo angina out within first month of stable angina (1month exercitional angina) → ↑↑risk for MI
3. Secondary rest angina = stable plaque + ↑Oxygen demand (↑HR, acute. HF) → precipitate rest angina

1. intense + prolonged pain (strong nerve-ending stimulation
2. ↓syst+diastol. performance (in the ischemic area)
1. ↓contractability
2. ↓EF+Output
3. rhythm disorder + cardiac arrest

• angina at rest (+during minimal physical exertion)
• broader irradiation of pain than stable angina
• >10-15min
‣

Difference of angina pain: stable, unstable/NSTEMI, STEMI

stable 1-10min

unstable/NSTEMI >10-15min

STEMI >60min

• ↑HR (mild) during minimal exercision+emotional stress
• signs of LV failure
• dyspnea + orthpnea
• vegetative symptoms (palor, sweating)
• SINUS arrhythmia → palpitation
• most cases also: prematue VB, Vtach, Vfib
‣

T/F sinus arrhythmia is always present in NSTEMI/unstable angina

T

• ↑BP (anxiety + pain)

inverted T +/- ST-depression 📷 📷⇒ Øpathological Q

+/- rhythm disorders

TROPONIN

↑ → NSTEMI confirmed

normal → unstable angina

1. Echo → LV performance, contractability (global +segmental), diastolic function ⇒ all affected by signif. ischemia
2. Coronary angiography
1. first day for high risk
2. next few days for medium risk
3. in low risk: stabilization → exercise stress test → if positive with high-risk criteria → coro

NAAS BH

1. Dual anticoagulation (Ass + Tica)
2. i.v. unfract. Heparin or Enoxaparine or Fondaparinux
3. Nitates (sublingual, LAN, Nitro patches, iv. nitro) → pain control, if not enough add other analgesic i.e.opioids
4. BB → max. tolerated dose (200mg metoprolol)
1. if contraindicated → NDHP-CCB instead
2. or add DHP-CCB if BB+LAN not enough
5. ACEi
6. Statins (Atorvastatin 80mg)

• in NSTEMI
• in medium + high-risk unstable angina
• in low-risk + positive stress test (with high-risk criteria)

1. 12month dual platelet
1. NOAKs if dilated LV, afib or ↑risk for ACS
2. BB
3. ACEi
4. Statins
5. Nitrates if still angina

prinzmetal = spontanous + promt resolution of ST elevation after pain relief (usually <15min)

ST depression → RESOLVE during pain → appear again after pain relief

Hypertrophy → diastolic dysfunction +/- ventricle outflow obstruction

→ ischemia

‣

💬

Mainly idiopathic

1/3 familiar

T

1. non-obstructive (non-septal)→ eqally distributed hypertrophy (like in HT). 📷
2. obstructive → assymetrical hypertrophy of interventricular septum 📷 → subvalvular aortic stenosis (septum bulges into aortic outflow tract) → drag effect aspiration of mitral valve → ant. mitral valve in systole (SAM) 📷→ more stenosis

severity of asymmetric hypertrophy

abnormal relaxation

during exercise

(sinus tachycardia → ↓diastolic pressure → more obstruction of the outflow)

↑in LV diastolic pressure + LVH + Myocardial ischemia

obstructive hypertrophic (but the other one as well to lesser degree)

• ↑HR → ↑interventricular septum contractility → ↑obstruction
• ↓LV volume → more obstruction

Low output during exercise + congestion + arrhythmias

‣

💬

• exercise syncope
• exercise cerebral ischemia
• exercise angina pectoris
• acute LVF → ac. pulmonary edema
• Rhythm disorders
‣

Which rhythm disorder?

• PB
• non-sustained tachycardia → vfib → sudden cardiac death
• afib

‣

T/F afib is highly symptomatic in obstructive hypertrophic cardiomyopathy

TTTT!!!

restore sinus rhythm as qucik as possible

• systolic ejection murmor (in obstructive type)
• ↑during exercise (due due ↑HR )
• mitral regurgitation murmur
• S4

↑HR (exercise)

fails to increase

• LVH
• Left atrial hypertrophy (bifid p-wave)
• Afib + ventricular arrhythmias
• sometimes pathologic Q + T-inversion (signs of ischemia)

pulmonary congestion

LVH