Internal cardio topics Flashcards
(285 cards)
1
Q
what is S3
A
Rapid ventricular filling due to overload
2
Q
Physiological S3
A
Pregnancy
Young children
Athletes
3
Q
S4 heart sound
A
Atrial contrasction in ventricular hyperthrophy
4
Q
what is heart murmurs
A
sound prduced by turbulent bloodflow
5
Q
classificatrion of murmurs
A
Functional: infants, children, pregnancy
Pathological: structural defect
6
Q
Diastolic murmurs
A
Mitral stenosis
Tricuspid stenosis
Aortic regurgitation
Pulmonary regurgitation
7
Q
Aortic regurgitation type of murmur
A
High pitched - Blowing - Early diastyolic - Decresendo murmur
8
Q
Etiology of aortic regurgitation
A
BEAR
Bicuspiod aortic vavle
Endocarditis
Aortic root dilation
Rheumatic fever
9
Q
Pulmonary regurgitation
A
Rar - Early diastolic - Decresendo
10
Q
Pulmonary regurgitation etiology
A
Pulmonary HTN
Dilated cardiomyopathy
11
Q
Mitral stenosis
A
Location: Best heard at the apex.
Characteristics: Low-pitched, rumbling diastolic murmur.
Opening snap, loud S1
Mitral face (flushed cheeks, exertional dyspnea).
Causes: Rheumatic heart disease, mitral annular calcification.
12
Q
Systolig murmurs
A
Aortic stenosis
Pulmonary stenosis
Mitral regurgitation
Mitral valve prolaps
HOCM murmurs
13
Q
Aortic stenosis
A
Description: Harsh, crescendo-decrescendo systolic murmur.
Location: Best heard at the right upper sternal border.
Radiation: May radiate to the carotids.
Causes: Calcific aortic valve, bicuspid aortic valve.
14
Q
Mitral regurgitation
A
Description: Holosystolic murmur.
Location: Best heard at the apex, radiating to the axilla.
Associated findings: S3 gallop
Causes: Mitral valve prolapse, rheumatic heart disease.
15
Q
Pulmonary stenosis
A
Description: Harsh, crescendo-decrescendo systolic murmur.
Location: Best heard at the left upper sternal border.
Associated findings: Pulmonary ejection click.
Causes: Congenital pulmonary valve abnormalities, rheumatic heart disease..
16
Q
Mitral proiolaps
A
Late systolic crescendo murmur with midsystolic click (MC) due to sudden tensing of chordae tendineae as mitral leaflets prolapse into the LA.
Causes: Idiopathic, connective tissue disorders
17
Q
HOCM murmur
A
Crescendo-decrescendo systolic ejection murmur
18
Q
Primary riskfactorsk for CVD divided into?
A
Major non modefiable
Modefiable
19
Q
What are the primary risk factorsk for CVD
A
Major non-modifiable: (AGG)
o Age (old)
o Gender (males)
o Genetics
Major modifiable:
o Smoking
o HTN
o Hyper/dyslipidemia
o DM
o Obesity (abdominal)
Additional risk factors:
o Alcohol consumption
o Exercise, diet
o Uric acid
o Metabolic syndrome
20
Q
Primary prevention of CVD
A
Main tools: lifestyle changes, CV risk factor profile modification.
Development of CHD: preclinical phase lasts for years if properly modefied
21
Q
Secondary prevention in CVD
A
Focuses on slowing the progression of established disease.
Tools: Lifestyle changes, CV risk factor profile modifications, drugs (statins, antiplatelet drugs, ACE-inhibitors, ARB, BB)
22
Q
CVS effects in DM
A
Altered response to arterial injury
Diminished fibrinolysis
Platelet hypercoagulability
Goal: HbAi1c less than 7%.
23
Q
CVS effects in smoking
A
Increased HR and BP
Platelet activation: thromboembolism
Vascular plaques
Increased LDL, + Decreased HDL
Goal: complete cessation
24
Q
Lipid managment in CVD
A
Primary goal: LDL < 1.8 mmol/L
Treatment: Statins
25
BP control goal in CVD
Less than 140/90 mmHg
Less than 130/80 mmHg in DM and CKD
26
Define ischemic heart disease
Plaque building up in coronary arteries.
Ischemia of the heart muscle is usually due to CAD
27
Define CAD
Ischemic heart disease due to narrowing of CA, most commonly due to atherosclerosis, resulting in a mismatch between myocardial oxygen supply and demand
28
What is Angina
chest pain caused by myocardial ischemia due to narrowing of coronary arteries. (necrosis of myocytes has not yet occurred)
29
What is stable angina
occurs upon exertion, mental stress, and/or exposure to cold and usually subsides within 20 minutes of rest or after administration of nitroglycerin
30
Define significantg stenosis of CA
> 50% in the left main and > 70% in other coronaries
31
Clinical features of ischemic heart disease
Asymptomatic/silent MI (in DM)
Angina
Dyspnea
Anxiety
Response to sublingual nitrates (complete, partial, not)
Ischemic ECG changes (in rest)or on a stress ECG
Arrhythmia
Sudden Cardiac Death
32
Dx of ischemic heart disease
Family history, medical history, physical examination
Risk factor evaluation
ECG: ST-depression, Flat/inverse T
Exercise ECG (stress)
CXR
MRI/CT
33
Define stable CAD
Patients are either asymptomatic
Have stable angina
Patients having had a MI but symptomes are under control
34
Factors reducing oxygen supply to heart muscle
Coronary atherosclerosis
Vasospasms
Increased heart rate
Anemia
35
Factors increasing oxygen demand to heart muscle
Increassed Heart rate
Increased Afterload
36
what is the cardinal symptom of CAD
Angina
37
when does CAD become symptomatic
Stenosis > 70%
38
Pain in angina
Typically retrosternal chest pain or pressure that radiates to the left arm, neck, jaw, epigastric region or back
39
treatment of stable CAD (ABCDE)
Aspirin (Clopidogrel if Cl)
Anti-angina treatment (Nit) up to every 30 min or as prophylaxis)
Beta-blockers (or ACEi in proven CVD, or CCB if BB is Cl)
BP control
Cigarette cessation
Cholesterol lowering drugs
Diet
DM control
Education
Exercise
40
when do you do PCI or CABG in CAD
Severe symptoms
Acute change in symptom severity
Failed medical therapy
Worsening left ventricular (LV) dysfunction
41
what drug to avoid in vasospasm angina
Dont give Beta Blockers
42
What composes ACD
Unstable angina, NSTEMI, and STEMI
43
what happens in the heart in unstable angina
Acute myocardial ischemia due to partial occlution of Coronary
No elevation in cardiac markers
Normal ECG
44
what happens in the heart during NSTEMI and what is seen on ECG
Acute myocardial ischemia causing subendocardial infarction
Cardiac markers are seen
ECG: T inversion, ST depression Loss of R
45
causes of ACS
CORONARY ARTERY ATHEROSCLEROSIS
Coronary artery dissection
Coronary artery vasospasm
Coronary artery embolism
Myocarditis
Vasculitis (e.g., polyarteritis nodosa, Kawasaki disease)
Myocardial supply-demand mismatch (e.g, anemia)
46
Clinical triad in right ventricular infarction:
Hypotension, JVD, clear lung fields
47
ECG in ACS NSTEMI
ST depression
Inverted T wave
Loss of R wave
48
Tx of all patients with ACS
Sublingual or IV nitrate (nitroglycerin)
Morphine IV or SC (3-5 mg)
Beta blocker recommended within 24 hours of admission
Early initiation of high statins regardless of baseline chol
Loop diuretic (furosemide) if flash pulmonary edema
Supporitve: IV fluids and oxygen > 90%
49
Treatment of ACS with STEMI
Aspirin (loading dose 300mg)
Clopidogrel or ticagrelor (Loading dose 600mg)
Dual AP therapy should be continued for at least 12 months if PCI with DES was performed
Anticoagulation with heparin or enoxaparin
Continue for the duration of hospitalization or until PCI is performed.
50
Scoring system to risk stratify patients with diagnosed ACS
GRACE SCORE
Age, HR, SBP, Creatinine level, CHF
51
Recommended coronary angio in NSTE-ACS:
Depends on severity of the ACS
1. Immidiate - Within 2h
2. Early invasive - within 24h
3. Delayed invasive - within 72h
4. Elective - within 1 week 9
52
STEMI VS NSTEMI
Ischemia is severe enough to cause ST elevations
Transmurtal infarct
ECG: ST elevation, LBBB
Elevated cardiac markers
53
etiology of STEMI
Plaque rupture causing thrombosis leading to complete occlution of coronary artery
54
diagnosis of STEMI
ECG
LABS
TTE
Cardiac CT
55
If ACS symptoms and LBBB on ECG
considered an STEMI because ST elevations cannot be
adequately assessed in the setting of an LBBB.
56
ECG leads corr with infarct location
V1-V2 LAD
V3-V4 Distal LAD
V5-V6 Left cirtcumflex
I, aVL Lateral
II, III, aVF Inferior
57
Important cardiac markers
Serum troponin T:
- most important cardiac-specific marker
- may be measured 3-4 hours after the onset of MI.
CK-MB (creatinin kinase)
- values correlate with the size of the infarct
- reach a maximum after approximately 12-24 hours
- normalize after only 2-3 days, making CK-MB a good marker for evaluating reinfarction.
58
The most commonly occluded coronary arteries
LAD > RCA > LCX.
59
Tx of STEMI interventions
Immediate PCI within < 90 min not more then 120 min
Thrombolytic therapy if PCI > 120 min: Alteplase, Reteplase
CABG if PCI unsuccessful
Aspirin 250mg
Clopidogrel 600mg
Dual AP therapy for 12 months after PCI with DES
60
complications of MI 0-24h
Cardiogenic shock
Sudden cardiac death
Arrhythmias
Acute left HF
61
most likely cause of SCD after MI, can it be prevented?
Fatal ventricular arrhythmia is
Prevention: installation of the ICD device
62
complications of MI 1-3 days
Early infarct-associated pericarditis
63
complications of MI 3-14 days
Papillary muscle rupture
Ventricular septal rupture
Left ventricular free wall rupture
Left ventricular pseudoaneurysm
64
complications of MI weeks to months
1. Atrial and ventricular aneurysms can lead to rupture — cardiac tamponade and mural thrombus formation
2. Dressler syndrom
Pericarditis occurring 2-10 weeks post-MI without an infective cause, but thought to be due to Ab against cardiac muscle
3. Congestive heart failure due to ischemic cardiomyopathy
4. Arrhythmias
65
what is the consequence of papillary muscle rupture 2—7 days after MI
Signs of acute mitral regurgitation: dyspnea, cough, bilateral crackles, hypotension
66
In which MI is ventricular septal defect seen?
Mostly seen 3-5 days after MI in LAD infarct
Acute-onset right HF (jugular venous distention, peripheral edema) due to shunting of blood from L-R
67
pathuphysiology of a left ventricular free wall rupture after MI
Usually occurs 5-14 days after myocardial infarction
Greatest risk during macrophage-mediated removal of necrotic tissue
68
Cardiac cycle cardiac phases and duration?
Systole (0.27s)
Diastole (0.53s)
69
Cardiac cycle phases
Systole
lsovolumetric contraction
Rapid ejection
Reduced ejection
Diastole
Isovolumetric relaxation
Rapid ventricular filling
Reduced ventricular filling (diastasis)
70
What happens in isovolumetric contraction?
Occurs in early systole, directly after the AV valves close and before the semilunar valves open
Ventricle contracts (i.e., pressure increases) with no volume change
LV volume 120ml
LV P: 8-80 mmHg
RV volume 120ml
RV P: 5-25 mmHg
71
What happens in systolic ejection
From ventricle to aorta and pulm artery
Pressure in RV foes from 80-120 mmHg
Volume: ejection of 70 mL SV (50 mL ESV)
72
what happens in Isovolumetric relaxation
Occurs between aortic valve closing and mitral valve opening, no corresponding ventricular volume change until ventricular pressure is lower than atrial pressure and AV valves open
73
what is the Dicrotic notch?
slight increase of aortic pressure in the early diastole that
corresponds to closure of the aortic valve
74
what happens during ventricular filling
Rapid filling (passive filling of 80%)
Reduced filling (atrial systole of 20%)
LVand RV volume: ventricles fill with ~ 70 mL (50 mL — 120 mL)
75
Cardiac catheterization
Dx and Tx of CVS conditions.
Involves the insertion of a catheter into a cardiac vessel or chamber by way of a suitable vascular access.
Once in position, a cardiac catheter can help evaluate:
The blood supply to the cardiac musculature
Open up narrowed or blocked segments by means of a coronary angioplasty with stenting.
76
Cardiac catheterization: the process
Inserted through the Femoral, Radial artery or Brachial artery.
A contrast dye is injected via the catheter, and is visualized with serial x-ray imaging.
77
when do we do a coronary angio?
1. Coronary artery disease
2. Valvular or myocardial diseases with symptoms
3. Recurring chest pain of unidentified cause
4. Preoperative evaluation prior to noncardiac and planned cardiac surgery (CABG).
78
what is right heart catheterization
The passing of a balloon-tipped, multi-lumen catheter (Swan-Ganz catheter) into the right side of the heart and the pulmonary artery to monitor pressure within the heart (intracardiac pressure) and pulmonary arterial pressure(PCWP)
79
indications of a right heart catheterization
1. For patients with heart failure, cardiomyopathy
2. Pulmonary capillary wedge pressure (PCWP) in LVF and mitral stenosis.
3. In suspected pulmonary hypertension to measure mPAP
80
Definitions in cardiology
SV
EF
CO
MAP
SV = EDV - ESV
EF = SV / EDV (50-70%)
CO =HRx SV
MAP: MAP = CO x TPR (normal 90-100 mmHg)
81
heart chamber pressures
RA: <5mmHg
LA (PCWP): <12 mmHg
RV (pulmonary a pressure): 25/5 mm Hg
LV: 8-130 mm Hg
82
what is PCI
cardiac catheterization in which a blocked coronary vessel is opened and appropriate blood flow is restored. A balloon catheter is used to dilate the narrowed section, with/without the placement of a stent to keep it patent.
83
PCI technique
Seldinger technique
1. Percutaneous puncture (radial, femoral, brachial artery)
2. Guide wire insertion
3. Sheath introducer
4. Removal of guide wire
5. Guiding catheter - Angioplasty/Balloon catheter
6. Inflation of balloon with or wothout a stent on the outside of it
84
Indications for CABG
1. High-grade left main coronary artery stenosis
2. Significant stenosis (> 70%) of the proximal LAD artery, with 2-vessel or 3-vessel disease
3. Symptomatic 2-vessel or 3-vessel disease
4. Disabling angina despite maximal medical therapy
5. Poor left ventricular function with myocardium that can
return to function on revascularization
85
Indications for emergency CABAG
1. NSTEMI + ongoing ischemia unresponsive to medical therapy/PC|
2. STEMI with inadequate response to all nonsurgical therapy
3. Significant ongoing ischemia after a failed PCI or previous CABG
86
CI for CABG
There are no absolute contraindications for CABG, dont do it if its not needed.
87
process of CABG
Thoracotomy via a midline sternotomy — cardiopulmonary bypass (heart-lung machine) > cardioplegic arrest of the heart anastomosis of the bypass vessels distal to the coronary artery stenosis using autologous vessels
88
Grafts in CABG
Internal thoracic artery (internal mammary artery)
Internal thoracic artery (internal mammary artery)
Radial artery
89
types of CABG
Traditional CABG (on pump)
Off-pump coronary artery bypass (OPCAB) surgery
Minimally invasive direct, or totally endoscopic CABG
90
result of CABG
Successful grafts typically last 8-15 years and provide an improved chance of survival (decreased 5-year mortality, especially in patients with triple vessel disease)
91
define congestive heart failure
A clinical syndrome in which the heart is unable to pump
enough blood to meet the metabolic needs of the body, characterized by ventricular dysfunction that results in low CO.
92
Types of congestive heart failure
Systolic dysfunction
Diastolic dysfunction
Right heart failure (RHF)
Left heart failure (LHF)
Biventricular (global) HF
Chronic compensated CHF
Acute decompensated CHF
93
Define Systolic dysfunction CHF
Reduced SV, reduced EF, increased EDV
94
Define Diastolic dysfunction CHF
Reduced SV, preserved EF, normal/reduced EDV
Characterized by low myocardial compliance (due to compensatory hypertrophy)
95
Define Right heart failure (RHF)
due to right ventricular dysfunction.
96
Define Left heart failure (LHF)
due to left ventricular dysfunction.
Long-standing LHF is the most common cause of RHF.
97
Define Biventricular (global) CHF
both the left and right ventricle are affected.
Results in the development of both RHF and LHF symptoms
98
Define Chronic compensated CHF
patient has signs
of CHF onechocardiography but is asymptomatic
99
Define Acute decompensated CHF
Sudden deterioration of CHF or new onset of severe CHF due to an acute cardiac condition like MI
100
what type of HF dopes the cardiomyopathies form
DCM - Systolic dysfunction
RCM - Diastolic dysfunction
HCM - Diastolic dysfunction
101
markers in congestive heart failure
BNP > 400
NT-pro BNP > 450
102
gold standard diagnosis of CHF
TTE which check
- Atrial and ventricular size
- IV septal size ( > 11mm indicates hyperthrophy)
- Systolic function (EF)
- Diastolic fuinction ( Diastollc filling)
- Investigating etiologies
103
Define dilated cardiomyopathy L
Left or biventricular dilation with strucxtural and functional systolic dysfunction in the ansence of CAD, valvular hearty disease or congenital heart disease
104
Etiology of DCM
Idiopathic (~ 50%)
Genetic predisposition
Coronary heart disease
Arterial hypertension
Coxsackie B virus myocarditis, SLE
ALcohol, cocain
Radiation
105
Genes in DCM
Mutations of TTN gene, encoding for the intrasarcomeric protein titin (connectin)
Mutations of MYH7 gene, encoding for the B-myosin heavy chain
106
pathophysiology o DCM
1. Causative factors decrease the contractility of myocardium
2. Compensatory mechanisms (Frank-Starling law) are activated to maintain CO - increased EDV (preload) - myocardial remodeling — eccentric hypertrophy
3. Sarcomeres added in series and dilation of the ventricle — reduced myocardial contractilitym ans systolic dysfunction
4. Decreased EF leading to heart failure
107
General symptoms: gradual development of CHF symptoms
Exertional dyspnea
Ankle edema, ascites
Angina pectoris
108
Mitral valve regurgitation or tricuspid valve regurgitation
S3 gallop
Left ventricular impulse displacement
Jugular venous distention
Rales over both lung fields
Palpitations
Diffuse abdominal and peripheral edema
109
x-ray in DCM
Cardiomegaly: left-sided hypertrophy with a balloon appearance
Pulmonary edema: sign of LHF decompensation
110
Define HCM
HCM: without obstruction of the LVOT 30%
HOCM: with LVOT obstruction that is dynamic 70%
111
HCM etiology
Most common hereditary heart disease
AD inheritance with varying penetrance
Most commonly by mutations of the sarcomeric protein genes
Also due to
Chronic hypertension (most common cause of LVH)
Aortic stenosis
Friedreich ataxia, Fabry disease, Noonan syndrome
Amyloidosis
112
Pathophysiology of HCM and HOCM
Hypertrophy of the LV ; most commonly occurs with asymmetrical septal involvement, which leads to diastolic dysfunction (impaired left ventricular relaxation and filling) > reduced SVm > reduced peripheral and myocardial perfusion > cardiac arrhythmia and/or heart failure and increased risk of SCD
113
what happend in the myocardium in both HCM and HOCM
- Increased LV wall thickness with septal predominance, no dilation of left ventricle
- Myofibrillar disarray, interstitial fibrosis, and myocyte hypertrophy
- Concentric hypertrophy: a form of cardiac remodeling characterized by parallel duplication of sarcomeres that leads to thickening of the ventricular wall
114
what can mimick HCM with consentric HT
Hypertension and aortic valve stenosis (due to chronic pressure and volume overload): Chronic hypertension > increased afterload + increased myocardial wall tension > changes in myocardial gene expression > sarcomeres laid down in parallel > increased LV
thickness
115
HOCM Pathomechanism:
LVOT obstruction > increased LV systolic pressure > prolongation of ventricular relaxation > increased LV diastolic pressure exacerbation of HCM with further reduction of CO.
116
cause of murmur in HOCM
Venturi effect: accelerated blood flow through ventricular outflow tract creates negative pressure that pulls the mitral valve towards the septum > increeased outflow tract obstruction.
117
symptomes of HCM
Frequently asymptomatic (especially the nonobstructive type)
Exertional dyspnea
Angina pectoris
Dizziness, lightheadedness, syncope
Palpitations, cardiac arrhythmias
SCD (particularly during or after intense physical activity)
118
Ecco findings in HCM
2. Asymmetrically thickened left ventricular wall (> 15 mm)
3. Typically involving the septum
4. If LV wall thickness > 30 mm high risk of sudden death.
5. Left atrial enlargement with mitral regurgitation
119
pharma in HCM
First-line: Beta blockers
Second-line: Nondihydropyridine CCB - Verapamil
120
when not to give CCB in HCM
should be avoided if there is hypotension or dyspnea at rest
121
Pharmacotherapy to avoid in HCM
High-dose diuretics
Digoxin
Spironolactone
122
General therapy in HCM
Lifestyle modifications
Automated implantable cardioverter defibrillator (AICD)
BB anmd CCB
Surgical septal myectomy if LVOT gradient = 50 mm Hg
Heart transplant: If end-stage non-obstructive HCM + LVEF < 50%.
123
Types of Heart failure
Acute heart failure: rapid onset of new or worsening signs
Acute decompensated heart failure: due to decompensation of preexisting disease (most common)
De novo heart failure: acute heart failure occurring for the first time
124
Etiology of De novo heart failure
Cardiac ischemia from ACS
Myocarditis
Drug-induced cardiomyopathy
Peripartum cardiomyopathy
Thyroid storm
Tachycardia-induced cardiomyopathy
Acute mitral regurgitation after ACS
Bacterial endocarditis
Pulmonary embolism
Pericardial effusion causing tamponade
Aortic dissection
125
Etiology of ADHF
In 40-50% of cases, no trigger is found
Uncontrolled and/or refractory hypertension
New/worsening cardiac ischemia
Arrhythmias (e.g., A.fib with RVR, complete heart block)
Serious infection/sepsis (e.g., pneumoni)
Anemia
Renal failure
Volume overload
Drugs with negative inotropic properties (nondihydropyridine CCBs)
126
Clinical features of acute heart failure are commonly classified as?
According to perfusion and the presence of congestion at rest
Warm dry
Warm cold
Cold dry
Cold wet
127
Clinical symptomes of left sided congestive heart failure
Acute dyspnea
Flash pulmonary edema: rapid, life-threatening accumulation
Signs of increased WOB
Cough (occasionally with frothy, blood-tinged sputum)
Coarse crackles or wheezing on auscultation
Severe cases: central cyanosis
128
Clinical symptomes of right sided congestive heart failure
Peripheral pitting edema
Hepatic venous congestion symptoms: abdominal pain + jaundice
Other symptoms of organ congestion (nausea, loss of appetite)
JVD
Kussmaul sign
129
Non spesific ECG findings in heartfailrue
Acute ischemic changes due to ACS
Atrial fibrillation
Left ventricular hypertrophy
Bundle branch block
Non-specific ST-segment changes
Low voltage QRS
ECG findings may be normal.
130
X-ray findings in pulmonary congestion
Cardiomegaly
Septal lines/Kerley B lines: visible horizontal interlobular septa
Basilar interstitial edema
Dilated pulmonary vessles
Pulmonary effusion
131
How to decide managment of accute hearty failre?
Find out whith type first, and if the patient is hemodydamically stable
Warm dry
Warm cold
Cold dry
Cold wet
132
Cardiogenic shock treatment
DRY+COLD
1. Consider small fluid bolus (250-500 mL) if DRY+COLD
(in WET+COLD)go traight to inotropic agents)
2. Assess fluid respons; consider additional bolus if responsive.
3. If shock persists, start a vasopressor, ideally, norepinephrine.
4. Administer inotropic if hypoperfusion persists despite fluids and vasopressors: DOBUTAMIN
133
Tx of DRY-WARM AHF
Optimize oral therapy.
134
Tx of WET+WARM AHF
Start diuretics
Consider a vasodilator
135
Respiratory support in acute heart failure
Positioning: Ensure the patient is sitting upright.
Oxygen: indicated if SpO2 < 90% or PaO2 < 60 mm Hg
NIPPV: for patients with respiratory distress despite oxygen
136
Indications of invasive mechanical ventilation in HF patients
Hypoxemic respiratory failure unresponsive to NIPPV
Refractory hypoxemia (PaQO2 < 60 mm Hg)
Hypercapnia (PaCO2 > 50 mm Hg)
Acidosis (pH < 7.35)
137
Diuretic treatment in HF patients
Diuretic-naive patients: IV furosemide or bumetanide
Patients already taking diuretics: 1-2 times the patient's usual dose
138
Countinued assesment of diuretic treatment in HF patients
If urinary output is < 100 mL/hour : Consider doubling the dose.
If urinary output is > 100-150 mL/hour
- If congestion then continue dose
- If no congestion then lower dose
139
Options for refractory congestion despite high doses loop diuretics:
Combination therapy with a thiazide diuretic
Addition of a vasodilator
Low-dose dopamine infusion
140
Indication of vasodilator therapy in acute heart failure
Acute heart failure caused by hypertensive emergency
Flash pulmonary edema
Adjuvant to diuretics for symptomatic relief of dyspnea
141
Vasodilator therapy in acute heart failure
IV nitroglycerin
e Sodium nitroprusside
142
when not to give vasodiulators in acute HF
Avoid the use of vasodilators in patients with acute heart failure and hypotension.
143
Mechanical circulatory support indicated in reversible refractory acute heart failure?
ECMO is the most widely used form of mechanical support in AHF
Intra-aortic balloon pump and left ventricular assist device may be useful in certain etiologies like mitral regurgitation.
144
Chronic compensated CHF definition
a clinically compensated type of CHF in which the patient has signs of CHF on echocardiography but is asymptomatic or symptomatic and stable.
145
what is the pathyphysiology of compensated chronic heart failure
1. Increased adrenergic activity : increase HR, BP, and contractility
2. Increase of RAAS: activated following decrease in renal perfusion secondary to reduction of and CO
3. Secretion of BNP
146
mechanismo of aldosteron
Aldosterone secretion incrtease renal Na and H2O resorption > increased preload
147
Mechanism of BNP secretion in HF
ventricular myocyte hormone released in response to increased ventricular filling and stretching casuing increased intracellular smooth muscle cGMP —> vasodilation, hypotension and decreased PCWP
148
General features of Chronic herart failure
Nocturia
Fatigue
Tachycardia, various arrhythmias
S3/S4 gallop on auscultation
Pulsus alternans
Cachexia
149
Kussmaul sign
increased JVP on inspiration and failure of decreased JVP on expiration seen in Right sidedn HF
150
Classification of heart failure
NYHA
Class 1: Nosymptoms of CHF
Class 2: Slight limitations of moderate or prolonged physical activity
Class 3: Marked limitations of physical activity
Class 4: Symptoms at rest
151
Medical treatment in chronic heart failure
Based on the stage of HF +
Diuretics - in volume overload
ACEI - to reduce preload, afterload and improve CO
BB - added once stable on ACEI, good in HT
Aldosteron antagonists - in EF < 35%
Ivabnradin - decrease HR, if no responce to BB, EF < 35%
Hydralazine - if EF < 40%
Digoxin - in HFrEF and symptomes despite BB, ACEI, diuretic and MRA
ARB - persistans symptomes despite first lione drugs
Nesiritide (BNP derivative) - in Acute decompensated HF
152
Drugs improving prognosis of HF
BB, ACEi, and MRA
153
Drugs that improve symptoms of HF
Diuretics and digoxin
(significantly reduce the number of hospitalizations)
154
Contraindicated drugs in HF
NSAIDs: Worsen renal perfusion, Reduce the effect of diuretics, May trigger acute cardiacb decompensation
CCB (verapamil and diltiazem): Negative inotropic effect, Worsen symptoms and prognosis
Antidepressants (citalopram): causes a dose-dependent QT prolongation
155
Non pharma treatment of HF
- Salt restriction (< 3 g/day) in symptomatic patients
- Fluid restriction in patients with edema and/or hyponatremia
- Weight loss and exercise
- Cessation of smoking and alcohol consumption
- Immunization: pneumococcal an influenza vaccine
- Patient education in self-monitoring and symptom recognition
- Daily weight: gain > 2 kg within 3 days requires consultation
156
invasive treatment of HF
Implantable cardiac defibrillator (ICD)
Cardiac resynchronization therapy
Coronary revascularization
Valvular surgery
ECMO
Cardiac transplantation
157
Indication of pacemaker in chronic heart failure
Heart failure 'NYHA class II-IV with EF < 35%
Dilated cardiomyopathy
LBBB with QRS > 150 ms
Can be combined with an ICD
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Types of bradychardia
Respiratory sinus arrhythmia
Sinus bradycardia
Sinus pause or arrest
Tachycardia-bradycardia syndrome
AV blocks
159
Define sinus bradychardia
Physiological (athletes)
Sinus node dysfunction (e.g, sick sinus
syndrome}, hypothyroidism,
hypothermia,
Drugs: BB, CCB
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Define Sinus pause or arrest
May occur in healthy individuals
Underlying cardiovascular disease (e.g,
sick sinus syndrome}
161
Define achycardia-bradycardia syndrome
Abnormal supraventricular impulse
generation and conduction like in sick sinus syndrome
162
Sick sinus syndrom
Degeneration and fibrosis of the SA node and surrounding myocardium (most common cause)
Medication (BB, digoxin, non-dihydropyridine CCB such as verapamil)
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Symptomes of bradychardia
Dizziness, Syncope
Lack of increasing heart rate during physical activity
Adams-Stokes attacks (A sudden loss of consciousness)
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ECG of SSS
Non-respiratory sinus arrhythmia
Bradycardia
Sinus arrest
Sinoatrial pauses
SA block
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Treatment of SSS
Initial therapy for hemodynamically unstable patients
1. First-line: atropine
2. Temporary cardiac pacing
Long-term therapy: lsolated symptoms of bradycardia: pacemaker
166
What is Vagal tone
Associated slowing of heart rate and decreased atrioventricular node electrical conduction.
167
two classifications of Atrioventricular block (Heart block)
Physiological: when decreased vagal tone
Pathologial
168
Pathophysiology of AV block
Idiopathic fibrosis of the conduction system
Ischemic heart disease
Cardiomyopathy (e.g., due to amyloidosis or sarcoidosis)
Infections
Hyperkalemia (> 6.3 mEq/L)
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Drugs causing AV block
BB, CCB, digitalis
170
First-degree AV block
PR interval > 200 ms
No interruption in atrial to ventricular conduction
Rate of SA node = heart rate
171
1st degree AV block treatment
No treatment, but pacemaker if QRS is wide, if conduction time
from the bundle of His to the ventricles is > 100 ms.
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2nd degree AV block types of
Mobitz I
Mobitz II
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Mobitz type I/Wenckebach
Progressive lengthening of the PR interval until a beat is dropped; regular atrial impulse does not reach the ventricles (a normal P wave is not followed by a QRS-complex)
174
2nd degree AV blocks treatment
Monitoring with transcutaneous pacing pads
If asymptomatic, find underlying cause
If symptoms not reversible ~ permanent pacemaker
Hemodynamically unstable give atropine
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Mobitz type II
Single non-conducted P waves without QRS complexes
The PR interval remains constant.
RR interval = x2
Follows regular patterns: 2:1 3:1 3:2 block
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symptoms of AV blocks
Bradycardia > decreased cardiac output
o Fatigue
o Dyspnea
o Chest pain
© Dizziness, syncope
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Third-degree AV block (complete heart block)
Third-degree AV block is a complete block with no conduction between the atria and ventricles.
AV dissociation: on ECG, P waves and QRS complexes have their own regular rhythm but bear no relationship
Aventricular escape mechanism is generated by sites that are usually located near the AV node or near the bundle of His.
178
what happens when theres is a sudden onset of 3rd AV Block
Sudden onset of a third-degree AV block results in asystole, which lasts until the ventricular escape mechanism takes over. This asystole may lead to Stokes-Adams attacks.
179
symptoms of 3rd degree AV block
Depends on Rate of ventricular escape mechanism and Length of asystole
180
Supraventricular tachycardias
Atrial Fibrillation (AF)
Atrial Flutter
Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
Atrioventricular Reentrant Tachycardia (AVRT)
Wolff-Parkinson-White Syndrome (WPW)
Atrial Tachycardia (focal or multifocal)
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Atrial flutter
Regular rhythm
Rate: atrial 250-350: ventricular < 200
P waves: Occur before every QRS complex,
Sawtooth appearance of regular P waves
Narrow QRS complex
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Atrial fibrillation
Rhythm: irregularly irregular
Rate: Atrial: 350-450 bpm: ventricular < 200
No P-waves
Narrow QRS complex
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Focal atrial tachycardia
Very abrupt onset, Regular rhythm
Rate: 150-250
P wave: morphology depends on the site of
the ectopic focus (same morphology)
Occurs before the QRS complex
Narrow QRS complex
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Multifocal atrial tachycardia (MAT)
Very abrupt onset with rate variation
Rhythm: irregularly irregular
Rate: 150-250
P waves with different morphologies; no single morphology
Narrow QRS complex
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Atrioventricular reentry tachycardia (AVRT)
Very abrupt onset, Regular rhythm
Rate: 150-250
P wave
- Inverted (downgoing in II, Ill and aVF and/or upright in aVR)
- Occur after the QRS complex
- RP interval is shorter than PR interval
ORS complex:
- Orthodromic AVRT: narrow QRS complex
- Antidromic AVRT: wide QRS complex with delta waves
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AV nodal reentry tachycardia
Regular rhythm
Rate: 150-250
P waves occur during (are not visible) or after the QRS complex
RP interval is shorter than PR interval
Narrow QRS complex
187
AVNRT etiology
AVNRT: tachycardia caused by a dysfunctional AV node that contains two electrical pathways
188
AVRT etiology
AVRT: tachycardia caused by an accessory pathway between the atria and ventricles
189
Atrioventricular tachycardia (AVT)
Atrial tachycardia (AT): The atria respond to impulses from an atrial pacemaker outside of the SA node.
A common cause of AT includes digoxin poisoning which typically presents with concomitant AV block.
190
WPW in AVRT
Wolff-Parkinson-White syndrome (WPW): A congenital condition characterized by intermittent tachycardias and signs of ventricular pre-excitation on ECG, which both arise from an accessory pathway known as the “Bundle of Kent”
The bundle of Kent connects the atria and ventricles, bypassing the AV node and leading to a pre-excitation of the ventricles.
191
acute treatment if PSVT
1. Cardioversion: fastest and most effective treatment
2. Carotid sinus massage and valsava maneuver
3. Medical therapy IV adenosine: briefly blocks the AV node
192
Long term treatment if PSVT
Catheter radiofrequency ablation
Medical therapy as second line
193
The general principles of treating atrial fibrillation include:
1. Correcting reversible causes and/or treatable conditions
2. Controlling heart rate and/or rhythm
3. Providing anticoagulation
194
treatment of unstable afib
emergent electrical cardioversion
195
Rate control in afib
1st line: BB: metoprolol, propranolol esmolol
2nd line: digoxin
3rd: Amiodorane
196
rythm control in afib
1st choice: elective electrical cardioversion
2nd choice: pharmacologic cardioversion with
antiarrhythmic drugs such as propafenone
197
risk assessment in afib
CHA2DS2-VASc score
198
anticoagulation in afib when
High thromboembolic risk: start anticoagulation immediately before or after cardioversion
Low thromboembolic risk: consider anticoagulation directly before or after cardioversion
IV heparin or LMWH immediately before cardioversion
followed by warfarin for up to 4 weeks after
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Cardioversion define
The restoration of normal heart rhythm in patients with tachycardia or arrhythmia using electric current
(electric cardioversion) or drugs (chemical cardioversion).
200
types of cardioversion
Synchronized
Pharmacological
201
Define synchronized cardioversion
Synchronized electrical cardioversion is the process by which an abnormally fast heart rate or cardiac
arrhythmia is terminated by the delivery of a therapeutic dose of electrical current to the heart at a specific
moment in the cardiac cycle.
202
Define pharmacological cardioversion
Pharmacologic cardioversion uses medication instead of an electrical shock to convert the cardiac
arrhythmia.
203
placement of pads in synchronized cardioversion
Place one anteriorly just left to the sternum and one posteriorly
to the left of midline.
204
optimal moment in the cardiac cycle for synchronized cardioversion
the R wave of the QRS complex on the ECG.
205
why is it important to time a synchronized cardioversion
Timing the shock to the R wave prevents the delivery of the shock during the vulnerable period
(or relative refractory period) of the cardiac cycle, which could induce ventricular fibrillation.
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when to use synchronized cardioversion
SVT, including atrial fibrillation and atrial flutter. It is also used in the emergent treatment of wide complex tachycardias, including ventricular tachycardia, when a pulse is present.
207
when do you use unsynchronized cardioversion
Pulseless ventricular tachycardia and ventricular fibrillation are treated with unsynchronized shocks referred to as defibrillation.
208
when not to give electrical shock
Electrical therapy is inappropriate for sinus tachycardia, which
should always be a part of the differential diagnosis.
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before a cardioversion
Nothing by mouth: for at least 6 hours
Thyroid function: treat thyrotoxicosis or myxedema first, if the patient is stable.
IV access
Sedation: short general anesthesia (propofol)
Cardioversion: check that no one is in contact with the patient
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cardioversion in intracardiac devices
Pacemakers/AICDs: Position the paddles away from the generator and not in the same
vector as the device.
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complications of cardioversion
Asystole/bradycardia
Ventricular fibrillation
Thromboembolism
Transient hypotension
Skin burns
Aspiration pneumonitis
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Pharmacologic cardioversion
If the patient is stable, Adenosine may be administered first, as the medicine performs a sort of "chemical cardioversion" and may stabilize the heart and let it resume normal function on its own without using electricity.
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classification of antiarrhythmic drugs
Class | - Na-channel blockers — Quinidine, lidocaine
Class Il - BBs
Class Ill - Block outward K-channels — Amiodarone, sotalol
Class IV - CCBs which inhibit AP in AV and SA node
214
Catheter ablation
Ablation is the removal of tissue.
Destruction of small areas of cardiac tissue by means of electrical energy delivered through an intracardiac catheter.
215
how is catheter ablation done
Cells are destroyed by heating > 50 degrees C.
The radiofrequency (RF) generator delivers an alternating current of 500-750 KHz
216
heating in catheter ablation
<50 degrees = transient loss of function
>50 degrees = permanent damage
> 80 degrees = coagulation (thromboembolism!)
217
types of catheter ablation
Radiofrequency (RF) energy:
Cryoablation
218
Cryo-catheter ablation
Liquid nitrous oxide is released into the tip and removes heat
Tissue temperature falls to -30 degrees C, at which stage there is reversible loss of cell function.
The tissue can be further cooled to -60 degrees for 4 minutes to cause permanent destruction.
219
CRT - Cardiac resynchronization therapy
CRT devices pace both the left and right ventricles simultaneously to resynchronize the muscle contraction and improve the efficiency (restore EF) of the weakened heart. Can restore function in e.g. dilative cardiomyopathy. Improves cardiac output and symptoms
220
pacemaker letters
First letter is pacing location
Second letter is sensing location
Third letter is respons (inhibit, trigger, both)
Fourth letter is added features
221
implantation of pacemaker
Most are implanted transvenously using cephalic or subclavian
The ventricular lead is most commonly placed in the RV apex, RV outflow tract or on the septum.
The atrial lead is placed in the right atrial appendage ideally, but anywhere is acceptable.
Pulse generator is placed subcutaneous
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Definit indications for pacemaker
1. Symptomatic 3rd degree heart block
2. Symptomatic advanced 2nd degree heart block
3. BBB.
4. After STEMI in the presence of high degree AV block
5. Symptomatic sinus node dysfunction
6. Symptomatic chronotropic incompetence.
7. Conditions requiring drugs that result in symptomatic bradycardia.
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which type of pacemaker should be used
Afib: VVI(R)
224
Define supraventricular tachycardias
Supraventricular tachycardias (SVTs) are a group of tachyarrhythmias arising from abnormalities in pacemaker activity and/or conduction involving myocytes of the atria and/or AV node.
A tachycardia originating in the following:
Sinus node
AV node
Atrial myocardium
Bundle of His above the bifurcation
225
AVRT reentry tachycardia typed and their bundle
WPW: Kent bundle
LGL: James bundle
226
medical therapy in AVRT
Amiodarone
227
medical therapy AVNRT
Verapamil, BB
228
Respiratory sinus bradycardia
bradycardia on expiration, it is physiological
229
Tachycardia-bradycardia syndrome presents with additional symptoms:
Palpitations
Dyspnea
Angina pectoris
230
what are temporary cardiac pacing
Involves electrical cardiac stimulation to treat a bradyarrhythmia or tachyarrhythmia until it resolves or until long-term therapy can be initiated.
Patients with temporary pacemakers are hospitalized and continuously monitored.
231
which infection can give a AV block
Lyme disease
232
how to treat a hemodynamic stable AV block patient?
monitor transcutaneous pacing pads, or pacemaker
233
Hemodynamically unstable
Atropine
Temporary cardiac pacing (if not responsive to atropine)
234
When does the patient need a heart transplant
Patients with end-stage CHF (NYHA class IV), EF < 20%, and no other viable treatment options
235
when is a ICD used as prophylaxis?
Patients with ischemic heart disease and EF < 30%
Heart failure NYHA class IIEIV with EF < 35%
236
Secondary prophylaxis indications for an ICD device
History of sudden cardiac arrest
Ventricular flutter or ventricular fibrillation
237
Cardiotoxic drugs
Anthracylines:
Doxorucibin
Traztuzumab
238
First line drugs used in heart failure
BB
Diuretics
ACEI
(aldosteron inhibitor)
239
pathophys of afib
Volume overload, hemodynamic stress > atrial hypertrophy and dilatation
Atrial ischemia
Inflammation of the atrial myocardium atal wyocovay
Altered ion conduction by the atrial myocardium
240
what happens in the heart during afib
The atria contract rapidly but ineffectively and in an uncoordinated fashion — stasis of
blood within the atria > risk of thromboembolism and stroke
Irregular activation of the ventricles by conduction through the AV node — tachycardia
241
ECG afib
Irregularly irregular RR intervals
No P-waves
Tachycardia
‘Narrow QRS complex (< 0.12 seconds)
242
treatment of unstable afib
emergent electrical cardioversion
243
afib cardioversion type?
1st choice: elective electrical cardioversion
2na choice: pharmacologic cardioversion with
antiarrhythmic drugs such as flecainide, propafenone,
244
drugs used i ryth control of afib
BB
CCB
digoxin
amiodoran
245
pharmacological cardioversion
first give amiodarone to slow down heart ryth
then give adenosin as the cardioversion drug
246
ventricular arrhythmia etiology
Idiopathic
Cardiovascular disease (CAD, myocarditis)
Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia)
Side effect of certain drugs (digoxin, psychiatric medications)
Caffeine, alcohol
247
ventricular arrhythmias
premature ventricular beats
ventricular tachy
torsades de point
Vfib
248
weight of the heart
approx. 300-500 g
249
vertebra behind the heart
T5-T8
250
posteriormorst part of the heart
The left atrium is the posteriormost part of the heart, located directly in front of the esophagus. It can
be visualized using TEE.
251
anterior most part of the heart
The right ventricle is the anteriormost part of the heart and is at greatest risk of injury following chest
trauma.
252
Common site for the development of thrombi in patients with atrial fibrillation
Right auricle
Left auricle (left atrial appendage)
253
what is the cardiac skeleton
e Consists of four fibrous rings (annuli fibrosi cordis) that surround the atrioventricular and arterial
orifices
254
the pappilary muscles
(two in the left ventricle; three in the right ventricle)
Derive from the myocardium
Extend from the ventricular walls and the septum
Contract during systole and thereby tighten the chordae tendineae: prevent prolapse of valve leaflets and regurgitation
255
what are the chorda tendinae
fibrous cords that support the AV valves and connect them to the papillary muscles
256
Subvalvular apparatus
chorda and pappilary muscles
257
does the semilunar valves have subvalvular apparatur?
three crescent-shaped cusps without subvalvular apparatus
258
Coronary arterial dominance
Right-dominant (85% of the pop): PDA supplied by the RCA
Left-dominant (~ 8% of the pop): PDA supplied by the LCX
e Codominant (balanced; ~ 7% of people): PDA supplied by both RCA and LCX
259
what supplies the conduction system of the heart?
The RCA supply the sinus and AV node so that stenosis or
occlusion of this vessel often leads to cardiac arrhythmias!
260
wher does the coronary sinus drain?
Drains into the right atrium between the IVC orifice and the right atrioventricular orifice
261
where is the AV node
in the Koch triangle
262
conduction branches after the bundle of his`
2 Tawara branches
263
Cardiac stress test
Stress is applied to the heart either by physical exercise or with pharmacological agents
264
pharma agents in cardio stess test
Dobutamine, adenosine
Dobutamine is indicated: COPD/asthma, high grade AV block
Adenosine is indicated: unable to exercise, LBBB, and post MI.
265
imaging modalities in cardiac stress test
CG, Echo, and SPECT perfusion imaging.
266
indication of coronary stress test
Diagnosis of CAD
Post MI patients treated with thrombolytics (pre-discharge)
Pre- and post-revascularization
Evaluation of arrhythmias; optimizing pacemaker
Preoperative evaluation of selective patients
Cardiopulmonary stress testing to evaluate CHF for transplant.
Evaluate valvular lesions in asymptomatic patients
267
CI of cardiac stress test
Fever
Pericarditis or myocarditis
Severe aortic stenosis with symptoms
Aortic dissection
Severe uncontrolled HTN
Decompensated HF, unstable angina or acute phase MI
268
what ECG signs do we look for on a cardio stress test?
Max ST increase or decrease
ST-slope
Leads showing ST changes: time of onset, duration of ST deviation into recovery
269
what is a positive cardio stress test
Positive stress test is manifested by 2mm ST depression or a decrease in BP (which normally should go up)
270
timing of echo measurements in cardiac stress test?
What do you mesure?
Incase of exercise: rest + immediately post-stress.
Incase of dobutamine: rest + low-dose + peak-dose + post administration
you look at wall motion and LVEF
Wall motion index above 2 high = risk for further cardiac events.
271
SPECT perfusion imaging stress test
Used to diagnose coronary disease by evaluating perfusion.
Involves administration of radiolabeled perfusion tracers at rest, and during stress.
The radiolabeled perfusion tracer emits gamma photons detected by a gamma camera
Myocardial tracer uptake is proportional to blood flow
Radiolabeled: Thallium — taken up like K* into myocytes.
272
what does Unfractionated
heparin (UFH) do? Antidote
activation of anti-thrombin III - decrease thrombin and factor X
Protamine
273
what does LMWH (Enoxaparin) do?
Antidote?
CI?
Acts on factor Xa predominantly
Protamine sulfate
Cl: renal insufficiency
274
what does fondaparinux do?
Antidote?
Factor X inhibitor
NOT reversible
275
Direct antithrombin inhibitors?
antidote?
Dabgatran
AD: Idarusizumab
276
Direct factor X inhibitors
Antidote:
Apixaban
Rivaroxaban
AD: Andexanet
277
Antiplatelet drugs?
Aspirine
Clopidogrel
Abciximab
278
thrombolytic agents
streptokinase
reteplase
Alteplase
279
PE etiology
Deep vein thrombosis (most common cause)
Fat embolism
Air embolism
Amniotic fluid embolism
Others: bacterial embolism, pulmonary tumor embolism
280
DD i pulmonary embolism
D-dimer levels Normal levels: < 500 ng/mL
If = 500 ng/mL: Further testing is required
If the patient is > 50 years of age, adjust for age: age x 10 ng/mL = cut off value in ng/mL
High sensitivity, Low specificity
281
TX PE
Massive PE: thrombolytic therapy or thrombectomy (last resort)
Submassive and nonmassive PE: anticoagulation or IVC filter
282
Localization of aortic dissection
Ascending aorta: ~ 65% of cases
Descending aorta, distal to the left subclavian artery: 20%
Aortic arch: 10% of cases
Abdominal aorta: 5% of cases
283
An aortic dissection is..
is a tear in the inner layer of the aorta that leads to a progressively growing hematoma in the intima-media space.
284
acquired causes of aortic dissectionn
HTN
Trauma
Vasculitis
Pregnancy
285
