HF & AHT Flashcards
(28 cards)
Define HF
Clinical syndrome develops when the heart cannot maintain adequate output to meet demand
of the body.
Explain the pathogenesis of HF
Cardiac
output depends on preload and afterload and myocardial contractility
Hypertrophy with dilatation it’s a compensatory mechanism, so it’s called compensated HF,
but in presence of risk factors lead to decompensation with ventricular dysfunction which
lead to activation of sympathetic system and Renin angiotensin system so increase after and
preload by
increase Na and water retention and prolonged sympathetic activation cause
vasoconstriction, cardiac myocyte apoptosis, focal myocardial necrosis and predispose
arrhythmias.
Explain :
Starlings law
Marrys low
Bainbridge low
Starling : CO is affected by preload ,afterload & contractility
-Marry’s low: HR is inversely proportionate to blood pressure.
-Bainbridge reflex: Increased RA pressure causes increased HR.
What are the causes of Na & water retention in HF ?
-Aldosterone.
-Endothelin 1.
-Vasopressin
-Natriuretic peptides
Mention the causes of HF .
1) Reduced in ventricular contractility:
-Segmental dysfunction (myocardial infraction)
-Global dysfunction (Myocarditis, Cardiomyopathy)
2) Ventricular inflow obstruction:
-Mitral and Tricuspid stenosis
3)Ventricular outflow obstruction:
-Left heart failure due to aortic or AHT
-Right heart failure due to Pulmonary stenosis or Pulmonary HTN.
4)Ventricular volume overload:
-Left heart failure due to aortic or mitral regurgitation.
VSD.
-Right heart failure due to Tricuspid regurgitation, ASD.
increase metabolic demand.
5) Arrhythmia:
-Atrial fibrillation. -Tachycardia. -Complete heart block
6) Diastolic dysfunction:(contract and difficult to relax)
-Constructive pericarditis. -Restrictive cardiomyopathy.
-Left ventricular hypertrophy and fibrosis. -cardiac tamponade
Mention the causes of high output HF
Pregnancy
Anemia
Beri beri
Thyrotoxocosia
AV shunt
Pagets disease
Mention the causes of dilated cardiomyopathy .
What is the most common one ?
Idiopathic(most common), Myocarditis, peripartum
cardiomyopathy, DM, Hemochromatosis, Sarcoidosis, scleroderma, Alcohol.
Mention the factors precipitating or aggregating HF in pre excisting heart ds .
- Myocardial ischemia or infarction
- Intercurrent illness
- Arrhythmia
- Inappropriate reduction of therapy
- Administration of a drug with negative inotropic (β-blocker) or fluid-retaining properties (e.g., non-steroidal anti-inflammatory drugs, glucocorticoids)
- Pulmonary embolism
- Conditions associated with increased metabolic demand (e.g., pregnancy, thyrotoxicosis, anemia)
- Intravenous fluid overload
Describe NYHA classification of HF .
Class: I
- Limitation: None
- Clinical Assessment: Ordinary physical activity does not cause undue fatigue, dyspnea, palpitations, or angina.
Class: II
- Limitation: Slight limitation
- Clinical Assessment: Comfortable at rest. Ordinary physical activity (e.g., carrying heavy packages) may result in fatigue, dyspnea, palpitations, or angina.
Class: III
- Limitation: Marked limitation
- Clinical Assessment: Comfortable at rest. Less than ordinary physical activity (e.g., getting dressed) leads to symptoms.
Class: IV
- Limitation: Severe limitation
- Clinical Assessment: Symptoms of heart failure or angina are present at rest and worsened with any activity.
Describe the stages of HF progression according to ACCF ,AHA .
Stage: A
- Description: At risk for heart failure but without structural heart disease or symptoms of heart failure.
Stage: B
- Description: Structural heart disease but without signs or symptoms of heart failure.
Stage: C
- Description: Structural heart disease with prior or current symptoms of heart failure.
Stage: D
- Description: Refractory heart failure requiring specialized intervention (e.g., mechanical circulatory assist devices, intravenous inotropes, or vasodilators).
How to diagnose HF clinically?
Clinically : History ,CP ,exam.
LHF :
_acute : -Pulmonary edema: severe persistent breathlessness, profuse sweating, cyanosis, cold
extremities, poor effort tolerance, expectations of watery frothy blood stained sputum.
_chronic :skeletal muscle atrophy, fatigue, weakness also cardiac cachexia ,nocturia ,chronic cough
On exam : ▪︎Generally: pale, cold, cyanotic extremities, cardiac cachexia, tachycardia/brady, increase diastolic blood pressure or hypotension in cardiogenic shock.
▪︎Locally:
-Inspection:
bulging of pericardium if there is cardiomegaly.
-Palpation:
Apex beat is either displaced in chronic or non displaced in acute HF with heave (LVH).
-Auscultation:
Gallop rhythm tachycardia with 3rd or 4th heart sound.
Crepitation ,Systolic murmur.
Rhonchi in case of bronchospasm.
Cardiac wheeze
▪︎Right heart failure:
Symptoms:
-Cerebral congestion: headache, insomnia, Restlessness.
-Pulmonary congestion: cough, dyspnea.
-Portal congestion: Anorexia, nausea, vomiting.
-hepatic congestion: Pain in Right hypochondrium .
-Renal congestion: oliguria, Nocturia
-Peripheral edema: feet, sacral , ascites.
On examination:
-Raised JVP with positive hepatojugular reflex
-Tender hepatomegaly due to congestion (smooth)
-Dependent pitting edema in ankle, sacrum, ascites, pleural effusion
-Evidence of heart disease: P2 is present in Pulmonary hypertension, functional Tricuspid regurgitation .
How to diagnose HF paraclinically ?
Chest X ray:
-Prominent upper lobe pulmonary vessels.
-Enlargement hilar vessels.
-Enlarged cardiac shadow.
- kerley B lines in costophrenic angle .
-Pleural effusion
-Bat’s wing appearance .
2) Echo:
▪︎Systolic or diastolic impairment, right and left ventricles.
▪︎Ejection fraction.
▪︎Valvular diseases.
▪︎Cardiomyopathy.
▪︎Regional wall motion abnormalities.
▪︎Intracardiac thrombus.
3)ECG:
▪︎Right or left ventricular hypertrophy
▪︎Myocardial ischemia or infraction
▪︎Arrhythmia.
4)CBC : Anemia.
5)LFTs: liver congestion.
6)Urea and creatinine: decrease renal perfusion.
7)Serum electrolytes:
Hypokalemia due to Diuretics.
Hyponatremia indicates poor prognosis.
8)Thyroid function test.
9)Cardiac enzymes: to detect MI if present.
10) B-natriuretic peptide: prognostic marker, used to differentiate cardiac or respiratory cause of dyspnea.
11)Endothelin 1: increase in HF, but NOT a marker for prognosis.
12)cardiac catheterization: to exclude Valvular diseases or to determine presence and extent of coronary artery disease.
- in P.E : ABG : Raise paco2 and decrease pao2
Elevated pulmonary capillary wedge pressure > 20 mmhg
Describe the Mx of P.E
keep pt in rest by Sit him up.
▪︎Continuous monitoring cardiac rhythm, BP, and pulse oximetry.
▪︎Give high flow oxygen
▪︎Ensure continuous positive airway pressure (CPAP) of 5-10mmHg by tight fitting mask.
▪︎Administer nitrates:
IV Glyceryl trinitrate 10-200 microgram /min
Buccal Glyceryl trinitrate 2-5mg
▪︎Administer a loop diuretic:
Furosemide (50-100 mg IV)
▪︎Intravenous opiate: used in distressed patient sparingly.
▪︎Inotropic agent(dubtamine 2.5-10 micrograms/min) in Hypotensive patient.
▪︎Intra aortic Balloon pump : beneficial in patient with cardiogenic pulmonary edema and shock .
Describe modified Framingham criteria in the diagnosis of HF
Major Criteria:
-Paroxysmal nocturnal dyspnea
- Orthopnea
- Elevated jugular venous pressure
- Pulmonary rales
- Third heart sound (S3 gallop)
- Cardiomegaly on chest radiography
- Pulmonary edema on chest radiography
- Weight loss >4.5 kg in 5 days in response to diuretic therapy for presumed heart failure
Minor Criteria:
- Dyspnea on exertion
- Bilateral leg edema
- Nocturnal cough
- Pleural effusion
- Tachycardia (>120 beats per minute)
- Weight loss >4.5 kg in 5 days
Note:
Diagnosis requires 2 major or 1 major and 2 minor criteria to be present and not attributed to another condition.
How to manage chronic HF ?
●General measures:(non drug treatment)
-Education about Good general nutrition with weight reduction, avoidance of high salt foods and added salt ,cessation of alcohol (alcohol induced
cardiomyopathy) and smoking regular exercise within limit of symptoms,
-vaccination(influenza and pneumococcal).
-Screen and treat comorbidities such as hypertension, CAD, DM, sleep disorder breathing.
-Certain drugs are known to make HF worse, should be avoided:
Calcium antagonists, Beta Blocker, NSAIDS, antiarrhythmic agents (all class I agents,
sotalol “class III”) ,Anti-TNF Antibodies.
●Drug treatment :
1)Diuretics:
Increase Na and water excretion, so decrease preload .
increase cardiac efficiency.
▪︎Loop diuretic (Furosemide 5-10mg/hr or 20-40mg BD) : thick ascending loop of Henle “ SE:hypokalemia “
▪︎Thiazides diuretics :early distal tubule. “cause hypokalemia.”.
▪︎Potassium sparing diuretics : late distal tubule and collecting duct
Don’t lead to Hypokalemia.
2)ACE inhibitors:s decrease Na and water retention with decrease systemic vasoconstriction.
Adverse effect: hypotension, renal impairment in bilateral stenosis, hyperkaliemia ,cough
Enalapril 10mg BD(starting dose 2.5mg BD).
Lisinopril 20mg OD(starting dose 2.5mg OD),
Ramipril 10mg OD(starting dose 1.25mg)
You should start by “starting dose” .
3)ARBs:
Adverse effect: Renal dysfunction and hyperkaliemia
Losartan 100mg OD (starting dose 25mg OD).
Candesartan 32mg OD (starting dose 4 mg
OD) .
Valsartan 160mg OD (starting dose 40mg OD).
4) Neprilysin inhibitor +ARB:
used for resistance heart failure
▪︎Sacubitril -Valsartan 97/103mg BD (starting dose 24/26 mg BD) .
5) Vasodilators:
Nitrate reduce preload (Isosorbide dinitrat 20-80mg TDS).
Arterial dilators such as Hydralazine (150-300mg OD) reduce afterload.
Adverse effect: hypotension and pharmacological tolerance ,SL .
6) Beta blockers:
reduces the risk of arrhythmias , sudden death, increase ejection fraction, improve symptoms, decrease hospitalization and mortality “ more effective than ACEI” .
-Bisoprolol 1.25mg OD.
Metoprolol 25mg BD.
Carvedilol 3.25mg BD.
Then, gradually increase for duration 12 weeks to the target dose:
-Bisoprolol 10mg OD, Metoprolol 100mg BD, Carvedilol 25mg BD.
7) Ivabradine(2.5mg-5mg BD):
used for patient with relative high HR >77/min.
NOT effective in patients with atrial fibrillation.
8) Digoxin: heart rate control in patient with severe heart failure (NYHA class III or IV) and atrial fibrillation.
has no effect on long-term survival.
9) Amiodarone: only for symptomatic arrhythmia .
●Non pharmacological treatment:
-Implantable cardiac defibrillators.
-Cardiac resynchronization therapy devices.
-Coronary revascularization.
-Cardiac transplantation
Mention the complications of HF .
1)Renal failure: caused by decrease perfusion ,diuretics.
2)Hypokalemia: caused by Potassium losing diuretic ,Hyperaldosteronism
3) hyperaldosteronism.
4)Hyponatremia: caused by diuretic therapy or improper H2O retention and it’s poor prognostic sign.
5)Impaired liver function: caused by hepatic congestion may lead to jaundice or increase liver enzymes with decrease synthesis of coagulation factors.
6)Thromboembolism: DVT with PE caused by decrease cardiac output with decrease
mobility, systemic embolic caused by arrhythmias, or Intracardiac thrombus.
7)Arrhythmias caused by electrolytes imbalance, underlying cardiac disease with effect of sympathetic activation.
8)Sudden death due to VF.
Regarding cor pulmonale ,explain the followings :
Definition
Types
S&S
O/E
Invest.
Tx
Dilatation and hypertrophy of right ventricle resulting from structural or functional lung
disease.
Types (acute, chronic, hypoxic (COPD), obliterated (Thromboembolic).
○Symptoms:
Fatigue, dyspnea on exertion, syncope, chest pain, palpitation.
abdominal distension .
lower limb edema.
○Signs:
1) Dependent peripheral edema with tender hepatomegaly.
2) Accentuated A wave with prominent V wave of JVP.
3) palpable left parasternal lift (heave).
4) Right sided 4th sound and Accentuated pulmonary component of 2nd heart sound.
5) Murmur of Tricuspid regurgitation.
○Investigations:
☆ECG:
1)Right axis deviation.
2) P-prominent.
3) Right bundle branch block.
4) Right pericardial T wave inversion.
☆Chest X ray:
1) Enlarged pulmonary artery and Right ventricle.
2) Westermark sign(oliguria of lung).
3)Hyperlucency and flat diaphragm.
☆CT scan:
-Main Pulmonary artery diameter >29mm.
☆Doppler echo:
1) measure pulmonary artery pressure
2) measure flow of regurgitate blood through tricuspid valve.
3) measure right ventricle ejection flow.
☆Right heart catheterization:
-Used to diagnosis pulmonary hypertension.
○Treatment:
1) O2 therapy.
2) Phlebotomy for patient and polycythemia HTC>60%.
3) Noninvasive positive pressure ventilation.
4) Pharmacological therapy:
▪︎Diuretics.
▪︎Vasodilators.
▪︎Anticoagulant.
Mention the DDX of peripheral edema
-
Cardiac Failure:
- Pericardial constriction
- Cardiomyopathy
-
Chronic Venous Insufficiency:
- Varicose veins
-
Hypoalbuminaemia:
- Nephrotic syndrome
- Liver disease
- Protein-losing enteropathy .
-
Drugs:
- Sodium retention: fludrocortisone , NSAIDs.
- Increasing capillary permeability: nifedipine, amlodipine.
-
Idiopathic:
- More common in women than men
- Chronic Lymphatic Obstruction
Define hypertension according to Sys & Diastolic BP
Optimal : < 120……. < 80
Normal :< 130…….< 85
High normal :130–139….85–89*
Hypertension :
Grade 1: (mild)140–159…..90–99
Grade 2 :(moderate)160–179…100–109
Grade 3 :(severe)≥ 180≥ …110*
Isolated systolic hypertension
Grade 1 :140–159…..< 90
Grade 2 : ≥ 160……….< 90
Explain the pathogenesis of AHT in large and small artries .
▪︎In large arteries: 《>1mm》:
-The Internal elastic lamina is Thickened
-Smooth muscles is hypertrophied
-Fibrous tissue deposit
lead to dilatation & less complaint wall .
▪︎In small arteries 《<1mm》:
-Hyaline arteriosclerosis occur in wall.
-Lumen become Narrow.
-Aneurysm may develop
Mention the causes of AHT
Primary idiopathic .
Secondary Hypertension :
- Alcohol
- Obesity
- Pregnancy
- Renal disease:
- Parenchymal renal disease, particularly glomerulonephritis
- Renal vascular disease
- Polycystic kidney disease
- Endocrine disease:
- Phaeochromocytoma
- Cushing’s syndrome
- Primary hyperaldosteronism (Conn syndrome)
- Glucocorticoid-suppressible hyperaldosteronism
- Hyperparathyroidism
- Acromegaly
- Primary hypothyroidism
- Thyrotoxicosis
- Congenital adrenal hyperplasia due to 11β-hydroxylase or 17α-hydroxylase deficiency
- Liddle syndrome
- 11β-hydroxysteroid dehydrogenase deficiency
- Drugs : -Oral contraception. -Corticosteroids. -NSAIDS.
-Sympathomimetic agents. -Amphetamines, Cocaine.
-Antidepressants. -Erthropiotien
- Coarctation of the aorta
- Neurological ds : raised ICP ,GBS ,Dysautonomia.
Mention the causes of isolated Systolic hypertension.
Aging
Anemia
AV shunt
Thyrotoxicosis
Aortic regargetation
How to diagnose AHT clinically ?
A-history : age ,Dm ,family H ,alcohol ,drug history …
B- Symptoms :
1- asymptomatic
2–symptoms related to increase blood pressure:
Headache [ suboccipital ,pulsating ,in early morning, subside during day ].
, Dizziness, vertigo, tinnitus, syncope, chronic fatigue, epistaxis.
3-Symptoms of secondary cause: Cushing, acromegaly….
4-Symptoms of complication:
1) CNS: Cerebral infraction, lacunar infraction, TIA, Cerebral hemorrhage, SAH.
2)Eyes: Hypertensive retinopathy
3) vascular: due to dilitation :
aortic aneurysm, aortic dissection ,AR
Due to atherosclerosis :
-Coronary arteries: IHD
-Carotid: stroke
-Renal artery: stenosis
-Lower limb: ischemia.
Or due to rupture small arterioles: Hematuria, epistaxis.
4) Cardiac:
Diastolic/ systolic HF, ischemia , arrhythmia(AF).
5) Renal:
▪︎Renal artery stenosis
▪︎Hematuria
▪︎Glomerulonephritis
▪︎Renal failure
6) Malignant and accelerated hypertension
C-Examination :
1) increased blood pressure may be the only sign .
2) finding of secondary cause:
-Coarctation of aorta»_space; Radio femoral delay
-Polycystic kidney»_space; palpable enlarged kidney .
-Renal artery stenosis»_space;abdominal bruit
-Cushing syndrome»_space;facial characteristics
3) Finding of risk factor:
Central obesity
Hyperlipidemia (xanthelasma)
4) Finding of complication:
- Retinopathy
5) Nonspecific finding:
▪︎Left ventricular heave
▪︎Left ventricular thrust
S3 ,S4 …..
Mention the investigations required in all pt with AHT .
-Urine analysis for RBCs, protein, glucose…
- Kidney function test, electrolytes (hypokalemia alkalosis)
-Blood glucose
-Lipid profile
-Thyroid function test
-ECG
